Tag Archives: Diabetes

Is Your Diabetes Curable or Just Treatable?

Can Your Diabetes be Cured or Just Treated?

Diabetes can be the worst scourge to ever hit mankind. It’s complications have magnified in the last 30 years or so and have set more souls up for shortened lives, than any other disorder, as this disorder is the gateway to future drug use and continued treatments, ultimately until death. The death is always premature. The grain industry and the pharmaceutical industry has made certain of this with a passion seldom matched by even our greatest artists, athletes and musicians, they are inflicting their will upon an unsuspecting public.

The desire of these industries to dominate our food supply and our pharmaceutical supply is ginormous. Their motivation has pushed them to force as many farmers as they can to grow their GMO seed, simply to sell more of their Roundup Herbicide. You know how dangerous that is by now. You should know that 1.3 million tons of it has been sprayed on your food or on feed for feed lots that goes directly into your meat. It’s this desire that has made carbs more glycemic today than they’ve ever been in history. This is what’s driving the diabetes pandemic today.              Get the book now!

The whole premise behind these posts is to prove that the only way you can prevent these horrendous diseases, is to stop the glycation that is responsible for them and the only way you can stop the glycation is to stop feeding it. It’s really a simple solution, just not an easy one because of the addiction factor. However, YOU and only YOU have control over this and it all depends on what YOU put in you mouth when you eat.

I’ll admit that that can be hard when you have a whole industry trying to get you to eat more of what it is that glycates. This is because they are connected to another industry that feeds off of the unsuspected that buy into this ruse, all those whom the glycation affects, the public.                                    Get the whole story!

With over 123,250 studies and reports available when I searched for diabetes and carbs on PubMed, it appears that this has been known for some time. There are studies on diabetes and carbohydrates dating from 1946. How could it have taken this long to put these pieces together?

The good news here, is that there is a cure for diabetes. Thank you Dr Davis for pointing it out for us. If you’re tired of treating your diabetes and poking yourself all the time, all one has to do to cure it or avoid it in the first place, is to not eat the food that is responsible for creating it and that is the starchy carbohydrates.

From PMC and PubMed,

Evidence of your carb intake and Diabetes

The only way out of this dilemma is to curb the carb usage completely. The following reports detail how carb ingestion leads directly to type2 diabetes, which ultimately leads to every modern disorder or disease;

The first one I looked at was from 1952; This study was so old, they still called glucose dextrose;

This was a difficult study to read and it only showed 8 diabetic patients. It didn’t mention which type they were either. It basically showed that an increase in carbohydrate consumption led to added glycogen and far stored in the body, clearly showing the link between carbs and fat. This study is older than I. Why have I not heard anything about it? Where were the warnings? Where they too afraid of upsetting an industry, so safeguard the public’s health?

This again is evidence that carbs and diabetes were being researched in 1945, as this report is from May,1945.

This is PubMed’s explanation of carbohydrates and how the glycemic index works. It helps to know how diabetics are thinking and how they need to keep track of the glucose levels in their blood.

  • Issues in Nutrition:Carbohydrates.

Carbohydrates include sugars, starches, and dietary fibers. Resistant starches resemble fiber in their behavior in the intestinal tract, and may have positive effects on blood glucose levels and the gut microbiome. Fibers are classified as soluble and insoluble, but most fiber-containing foods contain a mixture of soluble and insoluble fiber. Soluble fiber has been shown to lower low-density lipoprotein cholesterol levels. Many artificial sweeteners and other sugar substitutes are available. Most natural sources of sweeteners also are energy sources. Many artificial sweeteners contain no kilocalories in the amounts typically used. Sugar alcohols may have a laxative effect when consumed in large amounts. Glycemic index and glycemic load are measurements that help quantify serum glucose response after ingestion of particular foods. These measurements may be affected by the combination of foods consumed in a given meal, and the glycemic index may vary among individuals eating the same meal. Eating foods with a low glycemic index may help prevent development of type 2 diabetes. There is no definitive evidence to recommend low-carbohydrate diets over low-fat diets for long-term weight loss; they are equally effective.

They stop short of say that if you don’t eat carbs you can avoid diabetes, so let me be the first to tell you, you don’t need to eat carbohydrates. Carbs, the way they’re grown today, makes them as dangerous as arsenic.

This article published online on Dec 10, 2016 disputes the importance large amounts of carbohydrates in the diet;

Carbohydrates are essential nutrients that are used as a primary source of energy. Carbohydrate utilization should be properly controlled, as abnormal regulation of carbohydrate metabolism is associated with diseases, such as diabetes, cardiovascular diseases, and stroke. These metabolic syndromes have become a serious problem in developed countries, and there is an increased need for research examining the influence of carbohydrates on animal physiology. Diets enriched in glucose, a major carbohydrate, are also associated with accelerated aging in several model organisms, including yeast and Caenorhabditis elegans (C. elegans). Genetic factors that mediate the effects of high glucose diets on aging have been identified during the last decade, mostly through the use of C. elegans. In this review, we describe studies that determine the effects of carbohydrate-enriched diets on aging by focusing on the mechanisms through which evolutionarily conserved pathways mediate the lifespan-altering effects of glucose in C. elegans. These include the insulin/insulin-like growth factor-1, sterol-regulatory element-binding protein, and AMP-activated protein kinase signaling pathways. We also discuss the effects of various carbohydrates and carbohydrate-derived metabolites on aging in model organisms and cultured mammalian cells. Finally, we discuss how dietary carbohydrates influence health and aging in humans.

Would you consider this evidence that carbs should be, for the most part, limited to small portions…as small as possible.

  • Effect of type and amount of dietary carbohydrate on biomarkers of glucose homeostasis and C reactive protein in overweight or obese adults: results from the OmniCarb trial.

OBJECTIVE:

The glycemic index (GI) of dietary carbohydrate is thought to affect glucose homeostasis. Recently, the Effect of Amount and Type of Dietary Carbohydrates on Risk for Cardiovascular Heart Disease and Diabetes Study (OmniCarb) trial reported that a low-GI diet did not improve insulin sensitivity. We conducted this ancillary study of the OmniCarb trial to determine the effects of GI and carbohydrate content on glucose homeostasis and inflammation.

RESEARCH DESIGN AND METHODS:

OmniCarb was a randomized cross-over feeding study conducted in overweight or obese adults without diabetes (N=163). Participants were fed each of 4 diets for 5 weeks with 2-week washout periods. Weight was held constant. Diets were: high GI (GI≥65) with high carbohydrate (58% kcal), low GI (GI≤45) with low carbohydrate (40% kcal), low GI with high carbohydrate, and high GI with low carbohydrate. We measured glycated albumin (GA), fructosamine, and high sensitivity C reactive protein (CRP) at baseline and following each dietary period. These biomarkers were compared within-person between diets.

RESULTS:

The study population was 52% female and 50% black. Mean age was 53 (SD, 11) years; mean body mass index was 32 (SD 6) kg/m2. Reducing GI had no effect on GA or fructosamine, but increased fasting glucose in the setting of a high-carbohydrate diet (+2.2 mg/dL; p=0.02). Reducing carbohydrate content decreased GA in the setting of a high-GI diet (-0.2%; p=0.03) and decreased fructosamine in the setting of a low-GI diet (-4 µmol/L; p=0.003). Reducing carbohydrate while simultaneously increasing GI significantly reduced both GA (-0.2%; p=0.04) and fructosamine (-4 µmol/L; p=0.009). Neither reducing GI nor amount of carbohydrate affected insulin or CRP.

CONCLUSIONS:

Reducing carbohydrate, regardless of high or low GI, decreased GA and fructosamine. This suggests that reducing carbohydrate content, rather than GI, is a better strategy for lowering glycemia in adults at risk for diabetes.

Would you consider this as evidence that carbs should be, for the most part, limited to small portions…as small as possible. Need I say more?

  • [Composition of macronutrients in the diabetic diet].

The diabetic diet is one of the pillars of diabetes treatment. The rapid development of knowledge relating to the treatment of diabetes also includes diet. The paper focuses on the importance of a diet in the treatment of type 2 diabetes and prevention of atherosclerosis. Its main goal is to assess the impact of a composition of macronutrients on individuals with type 2 diabetes. The paper is divided into several parts, each of which ends with a conclusion. The first part examines weight reduction. The diet aimed at a weight loss is effective, it can effectively prevent diabetes, it leads to improvements in glucose control and reduction of the risk factors for atherosclerosis, however it will not impact on cardiovascular morbidity and mortality until after more than 20 years. The second part deals with “healthy” foods. The studies exploring this area are not convincing. The only really rational component of food in relation to atherosclerosis is dietary fibres. Important is a balanced diet combined with regular physical activities. The third part focuses on the composition of macronutrients. It turns out that, considering a low-calorie diet, the effects of high- and low-carbohydrate diets on people with diabetes are similar with regard to weight loss and lowering of HbA1c, however the low-carbohydrate diet is associated with lower glycemic variability and a reduced need for anti-diabetic drugs. We do not know how the comparison of the two extreme diets would come out regarding individuals with a high energy diet. Currently it is useful to focus on the quality of individual macronutrients. Choose foods containing carbohydrates with a low glycemic index and high fibre foods, prefer fats that contain a low proportion of saturated fatty acids. The fourth part discusses the recent recommendation of the Czech Diabetes Society regarding the composition of macronutrients in the diabetic diet. As compared with the diet proposed earlier, lower intake of fibre-rich carbohydrates and higher intake of proteins and fats with a low content of saturated fatty acids is now recommended. Experts’ recommendations on this subject are included. Key words: atherosclerosis – diabetic diet – HbA1c – macronutrients – low-carbohydrate diet – obesity – dietary fibres – high-carbohydrate diet – health food.

  • Adverse effects on insulin secretion of replacing saturated fat with refined carbohydrate but not with monounsaturated fat: A randomized controlled trial in centrally obese subjects.

BACKGROUND:

Current dietary guidelines recommend the replacement of saturated fatty acids (SAFAs) with carbohydrates or monounsaturated fatty acids (MUFAs) based on evidence on lipid profile alone, the chronic effects of the mentioned replacements on insulin secretion and insulin sensitivity are however unclear.

OBJECTIVE:

To assess the chronic effects of the substitution of refined carbohydrate or MUFA for SAFA on insulin secretion and insulin sensitivity in centrally obese subjects.

METHODS:

Using a crossover design, randomized controlled trial in abdominally overweight men and women, we compared the effects of substitution of 7% energy as carbohydrate or MUFA for SAFA for a period of 6 weeks each. Fasting and postprandial blood samples in response to corresponding SAFA, carbohydrate, or MUFA-enriched meal-challenges were collected after 6 weeks on each diet treatment for the assessment of outcomes.

RESULTS:

As expected, postprandial non-esterified fatty acid suppression and elevation of C-peptide, insulin and glucose secretion were the greatest with high-carbohydrate (CARB) meal. Interestingly, CARB meal attenuated postprandial insulin secretion corrected for glucose response; however, the insulin sensitivity and disposition index were not affected. SAFA and MUFA had similar effects on all markers except for fasting glucose-dependent insulin tropic peptide concentrations, which increased after MUFA but not SAFA when compared with CARB.

CONCLUSION:

In conclusion, a 6-week lower-fat/higher-carbohydrate (increased by 7% refined carbohydrate) diet may have greater adverse effect on insulin secretion corrected for glucose compared with isocaloric higher-fat diets. In contrast, exchanging MUFA for SAFA at 7% energy had no appreciable adverse impact on insulin secretion.

Carboholics and Diabetics; This is your warning to steer clear of carbs, if you want to control your diabetes. There is no literature that can  definitively prove that you must eat carbs to survive.

Are these enough reports to prove how directly influence diabetes? After reading this can you see the logic in controlling your diabetes by controlling your carb intake? Where are the warnings from the FDA and the USDA? Don’t they care about what they’re recommending? Don’t they understand because of their recommendations, they sending millions of Moms and Dads, sisters and brothers, husbands and wives to their slow, expensive, painful deaths?

These are free reports that are available to everyone. All you have to do is search for them at the National Library of Medicine in the National Institute of Health. There are literally 100s of thousands of reports on the effects of glycation that remain hidden in the PubMed and PMC databases except to the few who look through them.  The only ones looking through this database are the drug companies looking for more ways to make money. Nobody is looking to warn anyone of the dangers of this food.

My question is why? The answer I get is, “there’s no money in it”. That’s is why I said in my first book, it would be a shame if profits and money weren’t the primary motivating factors in our society, but they are, and we have to live with it. That’s why I choose not to buy into it. It’s the same choice you have.

Is Your Dementia Curable or Just Treatable?

Can Your Dementia or Alzheimer’s, Osteoarthritis, IBS/ IBD, or Other Disease of Inflammation be Cured or Just Treated?

This poses an interesting question osteoarthritis and dementia have something in common? Yes they do. They are diseases of inflammation and inflammation is caused by glycation. It’s these glycative cytokines and plaques that are responsible for all the damage that is responsible for all diseases of inflammation. They are also related to IBS, IBD, Lupus, Psoriasis, COPD, and every other disease that is influenced by inflammation, which would include most heart diseases and cancer. I posted those entries on different pages because of the extent of each one. That alone tells me to stay clear of anything that creates glycation.

Unfortunately, like arthritis, much of the damage has already been done and can’t be undone.  However you can stop the decline immediately and start some recovery. Just realize that the recovery will take twice as long as it took for you to create this quagmire in the first place. That only means that you must stop the glycation as soon as possible. (I suggest immediately, with a 3 day water only fast.) This will give your body more time to repair the damage.

Since the body needs proteins and cholesterol to operate, and doesn’t need the sugar, that leaves only one type of food to be responsible for glycation, carbs. I’ve learned through my research that the body can create all the glucose it needs with a process called gluconeogenesis. Gluconeogenesis is a process your body goes through whenever is needs glucose and has none readily available.

I produces this glucose with your own glycogen. That’s what your body turns glucose into when you eat it. That is what makes me question our need to eat glucose. If you body can create what it needs, why eat it? You can live perfectly well without it because your body can make it.

Why then, were we fed the line, for 50 years that we had to make grains (the foundation of glucose in the body) the largest part of our diet? Could it be because these studies started about 60 years ago? They intensified 30 years ago when Monsanto took over GD Searle pharmaceuticals. This was also about the time when the whole grain ruse started, convincing the public to consume massive amounts of this carcinogenic, atherosclerotic, inflammatory food. Do you wonder now, why all the disease exists?

When you cure a disease, you have nothing to treat. Where’s the money flow in our medical industry? It flows through the treatment process. Every hospital proves this, every weight loss clinic proves this, every orthopedic clinic proves this. Actually, every clinic proves this. If a cure was found for all modern disease, what would it do to the health and medical industries? Reduce it to treating emergencies only?  In several other posts, I show you how reducing carb consumption will reduce emergencies as well. (That’s where this really gets good.) It has something to do with its effect on your emotions.

Because of the growing list on the Real Poisoning of America – Glycation, it’s become evident that I need to display a different post for the different types of damage that glycation induces. For all forms of dementia, I’ll reserve this notice for that purpose only. All reports Of CVDs and other heart disorders will be located on the Atherosclerosis page.  Cancers will be on a separate post as well with all other diseases and disorders inflammation is responsible for.

The whole premise behind these posts is to prove that the only way you can prevent these horrendous diseases, is to stop the glycation that is responsible for them and the only way you can stop the glycation is to stop feeding it. It’s really a simple solution, just not an easy one because of the addiction factor. However, YOU and only YOU have control over this and it all depends on what YOU put in you mouth when you eat.

I’ll admit that that can be hard when you have a whole industry trying to get you to eat more of what it is that glycates. This is because they are connected to another industry that feeds off of the unsuspected that buy into this ruse, all those whom the glycation affects, the public.

Probably the first condition to hit you will be IBS of IBD, Irritable Bowel Syndrome or Inflammatory Bowel Disease. It was just submitted in this year;

Prevalence and Impact of Inflammatory Bowel Disease-Irritable Bowel Syndrome on Patient-reported Outcomes in CCFA Partners.

Abstract

BACKGROUND:

Inflammatory bowel disease (IBD) patients with persistent symptoms despite no or minimal inflammation are frequently described as having an overlap of IBD and irritable bowel syndrome (IBD-IBS). Limited data are available on how IBS impacts the individual patient with IBD. In this study, we aimed to evaluate the prevalence of IBD-IBS and investigate its impact on patient-reported outcomes.

METHOD:

We performed a cross-sectional analysis within the CCFA Partners Study. Bivariate analyses and logistic regression models were used to investigate associations between IBD-IBS and various demographic, disease factors, and patient-reported outcomes including anxiety, depression, sleep disturbances, pain interference, and social satisfaction.

RESULTS:

Of the 6309 participants included, a total of 1279 (20%) reported a coexisting IBS diagnosis. The prevalence of IBD-IBS in this cohort was similar within disease subtypes. A diagnosis of IBD-IBS was associated with higher narcotic use compared with those with no IBS diagnosis for both Crohn’s disease, 17% versus 11% (P < 0.001) and ulcerative colitis/indeterminate colitis, 9% versus 5% (P < 0.001). Quality of life, as measured by Short Inflammatory Bowel Disease Questionnaire (SIBDQ) was lower in patients with IBD-IBS compared with those without. IBD-IBS diagnosis was associated with anxiety, depression, fatigue, sleep disturbances, pain interference, and decreased social satisfaction.

CONCLUSIONS:

In this sample of patients with IBD, high prevalence of concomitant IBS diagnosis was observed. IBD-IBS diagnosis was associated with increased narcotic use and adverse patient-reported outcome. Appropriate diagnosis, treatment, and counseling may help improve the functional status of IBD-IBS patients and decrease narcotic use.

My appropriate treatment for this disorder isn’t a treatment. Those always lead to more treatments. I propose a cure. All the inflammation involved in these disorders can be controlled by your intake of carbs, meaning, by going keto you can avoid all inflammation. How fat would that go to providing relief?

IBS and IBD aren’t the only inflammatory disorders, there are several others such as Lupus;

BACKGROUND:

Early diagnosis is important for the outcome of lupus nephritis (LN). However, the pathological type of lupus nephritis closely related to the clinical manifestations; therefore, the treatment of lupus nephritis depends on the different pathological types.

OBJECTIVE:

To assess the level of monocyte chemotactic protein (MCP-1), fractalkine (Fkn), and receptor for advanced glycation end product (RAGE) in different pathological types of lupus nephritis and to explore the value of these biomarkers for predicting the prognosis of lupus nephritis.

METHODS:

Patients included in this study were assessed using renal biopsy. Class III and class IV were defined as the proliferative group, class V as non-proliferative group, and class V+III and class V+IV as the mixed group. During the follow-up, 40 of 178 enrolled patients had a poor response to the standard immunosuppressant therapy. The level of markers in the different response groups was tested.

RESULTS:

The levels of urine and serum MCP-1, urine and serum fractalkine, and serum RAGE were higher in the proliferative group, and lower in the non-proliferative group, and this difference was significant. The levels of urine and serum MCP-1 and serum RAGE were lower in the poor response group, and these differences were also significant. The relationship between urine MCP-1 and urine and serum fractalkine with the systemic lupus erythematosus disease activity index was evaluated.

CONCLUSION:

The concentration of cytokines MCP-1, fractalkine, and RAGE may be correlated with different pathology type of lupus nephtitis. Urine and serum MCP-1 and serum RAGE may help in predicting the prognosis prior to standard immunosuppressant therapy.

Do you have Lupus? Were you told not to eat your bagels for breakfast? If you weren’t, then it’s probably because someone needed you back for treatment.

This following report dated

Background/Purpose: HMGB1, which may act as a proinflammatory mediator, has been proposed to contribute to the pathogenesis of multiple chronic inflammatory and autoimmune diseases including systemic lupus erythematosus (SLE); however, the precise mechanism of HMGB1 in the pathogenic process of SLE remains obscure.

Method: The expression of HMGB1 was measured by ELISA and western blot. The ELISA was also applied to detect proinflammatory cytokines levels. Furthermore, nephritic pathology was evaluated by H&E staining of renal tissues. Results: In this study, we found that HMGB1 levels were significantly increased and correlated with SLE disease activity in both clinical patients and murine model. Furthermore, gain- and loss-of-function analysis showed that HMGB1 exacerbated the severity of SLE. Of note, the HMGB1 levels were found to be associated with the levels of proinflammatory cytokines such as TNF-α and IL-6 in SLE patients. Further study demonstrated that increased HMGB1 expression deteriorated the severity of SLE via enhancing macrophage inflammatory response. Moreover, we found that receptor of advanced glycation end products played a critical role in HMGB1-mediated macrophage inflammatory response.

Conclusion: These findings suggested that HMGB1 might be a risk factor for SLE, and manipulation of HMGB1 signaling might provide a therapeutic strategy for SLE.

Listed below from PubMed or PMC or the FDA are reports of studies done on the effects of glycation and its influence in osteoporosis or any disease influenced by inflammation.

Abstract

Only three decades ago adipose tissue was considered inert with little relationship to insulin resistance. Similarly bone has long been thought purely in its structural context. In the last decade, emerging evidence has revealed important endocrine roles for both bone and adipose tissue. The interaction between these two tissues is remarkable. Bone marrow mesenchymal stem cells give rise to both osteoblasts and adipocytes. Leptin and adiponectin, two adipokines secreted by fat tissue, control energy homeostasis, but also have complex actions on the skeleton. In turn, the activities of bone cells are not limited to their bone remodeling activities, but also to modulation of adipose sensitivity and insulin secretion. This review will discuss these new insights linking bone remodeling to the control of fat metabolism and the association between diabetes mellitus and osteoporosis.

Conclusion

Chronic hyperglycemica profoundly affects multiple tissues and directly affects the frequency of complications in diabetes mellitus. Hypoinsulinemia is the primary hormonal disturbance leading to T1DM, whereas insulin resistance causing hyperglycemia is the principal event in T2DM. As discussed, bone mineral density is a relatively poor surrogate for defining bone structure during long standing hyperglycemia. Low bone mass is often detected in T1DM although the pathogenesis is likely to be multifactorial. On the other hand, BMD can be low, normal or increased in T2DM. Yet both forms of diabetes are associated with an increased risk of fracture. In part, higher rates of fracture can be related to neuropathic, nephropathic and retinopathic changes that lead to a greater risk of falling. In addition, low body weight, hypoinsulinemia, low serum levels of IGF-I and altered gonadal steroids favor a catabolic state in the skeleton of Type I diabetics. The presence of obesity and T2DM, although associated with increased cortical bone mass, does not translate to a lower fracture risk, and paradoxically may enhance risk. Hyperglycemia can lead to degenerative changes in bone quality through advanced end product glycation, which particularly affects collagen cross-linking. Not surprisingly, one of the classic late clinical features of diabetes mellitus, i.e. vascular calcification, is associated with lower bone mass and impaired bone strength. Those two processes may be linked to reduced renal function and aberrant deposition of calcium in blood vessels rather than in the appropriate collagen matrix. Notwithstanding the potential numerous insults associated with sustained hyperglycemia, several recent developments suggest there is now a greater awareness of the skeleton as both a target of diabetic complications, and a potential pathogenetic factor in the disease itself.

The following study looked at the brains of Alzheimer’s disease patients. It’s dated Jan 3 2017. Theyu officially label Alzheimer’s disease as type 3 diabetes;

Abstract

The brain of patients with Alzheimer disease (AD) showed the evidence of reduced expression of insulin and neuronal insulin receptors, as compared with those of age-matched controls. This event gradually and certainly leads to a breakdown of the entire insulin-signaling pathway, which manifests insulin resistance. This in turn affects brain metabolism and cognitive functions, which are the best-documented abnormalities in AD. These observations led Dr. de la Monte and her colleagues to suggest that AD is actually a neuroendocrine disorder that resembles type 2 diabetes mellitus. The truth would be more complex with understanding the role of Aβ derived diffusible ligands, advanced glycation end products, and low-density lipoprotein receptor-related protein 1. However, now it’s known as “brain diabetes” and is called type 3 diabetes mellitus (T3DM). This review provides an overview of “brain diabetes” focusing on the reason why the phenomenon is called T3DM.

Evidence of inflammation’s role in myasthenia gravis, dated Jan 3, 2017; I used to have a granddaughter with myasthenia gravis, as I recall at that time, there was no cause. I guess the cause wasn’t known then. It’s a nice thing that it is now, but who suggesting that we remove the instigating factor from this equation, the glucose that is responsible for the glycation? I can’t believe that there are only a few of us;

Abstract

This study describes specific patterns of elevated inflammatory proteins in clinical subtypes of myasthenia gravis (MG) patients. MG is a chronic, autoimmune neuromuscular disease with antibodies most commonly targeting the acetylcholine receptors (AChRab), which causes fluctuating skeletal muscle fatigue. MG pathophysiology includes a strong component of inflammation and a large proportion of patients with early onset MG additionally present thymus hyperplasia. Due to the fluctuating nature and heterogeneity of the disease, there is a great need for objective biomarkers as well as novel potential inflammatory targets. We examined the sera of 45 MG patients (40 AChRab seropositive and 5 AChRab seronegative), investigating 92 proteins associated with inflammation. Eleven of the analysed proteins were significantly elevated compared to healthy controls, out of which the three most significant were: matrix metalloproteinase 10 (MMP-10; p = 0.0004), transforming growth factor alpha (TGF-α; p = 0.0017) and extracellular newly identified receptor for advanced glycation end-products binding protein (EN-RAGE) (also known as protein S100-A12; p = 0.0054). Further, levels of MMP-10, C-X-C motif ligand 1 (CXCL1) and brain derived neurotrophic factor (BDNF) differed between early and late onset MG. These novel targets provide valuable additional insight into the systemic inflammatory response in MG.

The following report was submitted Dec 29 2016 and explains the damage that oxidative stress, apoptosis, autophagy and inflammation play in kidney disease;

Diabetic kidney disease (DKD) can occur in approximately 30-40% of both type 1 and type 2 diabetic patients. The well-established features of DKD include increased serum glucose levels along with chronic low-grade inflammation, OxS, increased advanced glycation end products, sorbitol accumulation, increased hexosamine, and protein kinase C pathway activation. On the other hand, accumulating evidence suggests that novel pathways including apoptosis and autophagy might also play important roles in the pathogenesis and progression of DKD. In this review, the integrated mechanisms of inflammation, oxidative stress, apoptosis, and autophagy are discussed in the pathogenesis as well as progression of DM and DKD.

This following report dated Feb 2017 shows the importance of sRAGE involved in lung infections and other inflammatory precursors to lung cancer;

Abstract

BACKGROUND:

The membrane-bound isoform of the receptor for advanced glycation end products (FL-RAGE) is primarily expressed by alveolar epithelial cells and undergoes shedding by the protease ADAM10, giving rise to soluble cleaved RAGE (cRAGE). RAGE has been associated with the pathogenesis of several acute and chronic lung disorders. Whether the proteolysis of FL-RAGE is altered by a given inflammatory stimulus is unknown. Pseudomonas aeruginosa causes nosocomial infections in hospitalized patients and is the major pathogen associated with chronic lung diseases.

CONCLUSIONS:

These data are the first to suggest that inhibition of FL-RAGE shedding, by affecting the FL-RAGE/cRAGE levels, is a novel mechanism for controlling inflammation to acute P. aeruginosa pneumonia. sRAGE in the alveolar space sustains inflammation in this setting.

Below is evidence that the destruction of glycation starts before you were ever born, thank to your mother’s glucose ingestion. This is where your addiction began. Do you think if she knew how much harm she was inflicting, she would do it again? That would depend on her addiction;

Abstract

Ectopic calcifications in intervertebral discs (IVDs) are known characteristics of IVD degeneration that are not commonly reported but may be implicated in structural failure and dysfunctional IVD cell metabolic responses. This study investigated the novel hypothesis that ectopic calcifications in the IVD are associated with advanced glycation end products (AGEs) via hypertrophy and osteogenic differentiation. Histological analyses of human IVDs from several degeneration stages revealed areas of ectopic calcification within the nucleus pulposus and at the cartilage endplate. These ectopic calcifications were associated with cells positive for the AGE methylglyoxal-hydroimidazolone-1 (MG-H1). MG-H1 was also co-localised with Collagen 10 (COL10) and Osteopontin (OPN) suggesting osteogenic differentiation. Bovine nucleus pulposus and cartilaginous endplate cells in cell culture demonstrated that 200 mg/mL AGEs in low-glucose media increased ectopic calcifications after 4 d in culture and significantly increased COL10 and OPN expression. The receptor for AGE (RAGE) was involved in this differentiation process since its inhibition reduced COL10 and OPN expression. We conclude that AGE accumulation is associated with endochondral ossification in IVDs and likely acts via the AGE/RAGE axis to induce hypertrophy and osteogenic differentiation in IVD cells. We postulate that this ectopic calcification may play an important role in accelerated IVD degeneration including the initiation of structural defects. Since orally administered AGE and RAGE inhibitors are available, future investigations on AGE/RAGE and endochondral ossification may be a promising direction for developing non-invasive treatment against progression of IVD degeneration.

From the study report itself, dated Nov 2016;

Ectopic calcifications were present in human IVDs of various degeneration stages and often co-localised with MG-H1… dochondral ossification. There is a need for non-invasive therapies to prevent or reverse early degenerative IVD changes. Currently there is a phase 3 clinical trial using the orally bioavailable RAGE inhibitor Azeliragon (TTP488; trial for Mild Alzheimer’s disease), suggesting additional anti-AGE drugs are available. A clinical study further reported that restriction of oral AGE intake reduced systemic AGE levels and improved insulin resistance in humans with type 2 diabetes (Uribarri et al., 2011), suggesting that effects of AGEs might be reversible. Importantly, we observed indications for endochondral ossifications in human IVDs already in grade II IVDs, a stage at which preventative treatment could still inhibit further degeneration. In conclusion, accumulation of the AGE MG-H1 was associated with endochondral ossifications, hypertrophy and osteogenic differentiation in human IVDs and mechanistic investigations on IVD cells showed a direct relationship involving RAGE, suggesting that AGE/RAGE could be a potential therapeutic target. Further investigations in animal experiments are warranted to assess whether targeting AGEs via the AGE/RAGE axis can potentially provide a non-invasive treatment option for preventing progression of IDD

This report makes me wonder, how long will it take until the FDA or the USDA to wake up and realize that what they’re recommending everyone eat is actually what’s making everyone sick. Then I think about who controls the FDA and the USDA, it somehow nullifies my curiosity, I know who is responsible. A multinational chemical company intent on bolstering their profits at whatever cost may be brought about their actions.

It’s when those actions bolster the profits of another related industry that I get bothered. When I see people conned into consuming foods that make them sicker every day, I get a little upset. When I see this, I see my mother dying because she bought into this ruse herself. This makes this ruse the most danger con game ever to hit mankind.

The following report submitted Mar 2 2009 details the beginning of glycation from the fundamental elements of glucose, glyoxal and methylglyoxal, and their roles in aging and disease;

  • Protein and nucleotide damage by glyoxal and methylglyoxal in physiological systems – role in ageing and disease

Glyoxal and methylglyoxal are potent glycating agents. Glycation of proteins is a complex series of parallel and sequential reactions collectively called the Maillard reaction. It occurs in all tissues and body fluids. Early stage reactions in glycation of protein by glucose lead to the formation of fructosyl-lysine (FL) and N-terminal amino acid residue-derived fructosamines. Later stage reactions form stable end-stage adducts called advanced glycation endproducts (AGEs). FL degrades slowly to form AGEs – and also glyoxal and methylglyoxal. In contrast, glyoxal and methylglyoxal react with proteins to form AGE residues directly and relatively rapidly. 

Glycation by glyoxal and methylglyoxal, and the related influence of Glo1, are now emerging as playing a critical role in ageing and disease processes – vascular complications associated with diabetes renal failure, Alzheimer’s disease, and tumourigenesis and multidrug resistance in cancer chemotherapy. They may also have roles in pathologic anxiety, autism, obesity and other disorders. 

Again, this is just one of 804 return reports from a search of Lymphoma and glycation. To think that one has nothing to do with the other is what the FDA and the USDA seem to be doing in the continued recommendations to eat the food that does the glycating. If you were to tell me that the influence of Monsanto’s execs in the offices and agencies had nothing to do with these decisions to alert the public about the dangers in what they’re eating, I’d have to tell you that you are completely misinformed. Can I sell you some ocean front property in Kansas?

Does this mean that you’re stupid? Absolutely not. It just means that you’ve been duped like everyone else. It’s really easy to do. All you have to do is taste the food. One taste and you’re hooked. Since it doesn’t kill you immediately, it’s assumed safe. This assumption is what’s killing America and the rest of the world. This is the most deadly assumption to make, bread is safe to eat. Bread nowadays is deadly.

The next report I looked at was from Nov 10, 2016 and it displays the extent this industry will go to, to simply allow this addiction to kill as many people as it possibly can, by it to continue. Its purpose is to show the benefits of Bazedoxifene, a new drug being tested for reducing apoptosis and oxidative stress, when all they have to do is to recommend the cessation of the consumption of grains and sugar that leads to the glycation that is responsible for all these diseases. They’re not interested in arresting it or abating it. Their sole interest is to expand its influence, to addict more and more people. This appears to be done solely to increase the profits of the pharmaceutical industry. It explains the benefits of a new drug that the industry wants to impose upon the people, probably in the guise of helping the people;

  • Bazedoxifene Ameliorates Homocysteine-Induced Apoptosis and Accumulation ofAdvanced Glycation End Products by Reducing Oxidative Stress in MC3T3-E1 Cells.

Abstract

Elevated plasma homocysteine (Hcy) level increases the risk of osteoporotic fracture by deteriorating bone quality. However, little is known about the effects of Hcy on osteoblast and collagen cross-links. This study aimed to investigate whether Hcy induces apoptosis of osteoblastic MC3T3-E1 cells as well as affects enzymatic and nonenzymatic collagen cross-links and to determine the effects of bazedoxifene, a selective estrogen receptor modulator, on the Hcy-induced apoptosis and deterioration of collagen cross-links in the cells. Hcy treatments (300 μM, 3 mM, and 10 mM) increased intracellular reactive oxygen species (ROS) production in a dose-dependent manner. Propidium iodide staining showed that 3 and 10 mM Hcy induced apoptosis of MC3T3-E1 cells. Moreover, the activities of caspases-8, 9, and 3 were increased by 3 mM Hcy. The detrimental effects of 3 mM Hcy on apoptosis and ROS production were partly reversed by bazedoxifene and 17β estradiol. In addition, real-time PCR, immunostaining and Western blot showed that 300 μM Hcy decreased the expression of lysyl oxidase (Lox). Furthermore, 300 μM Hcy increased extracellular accumulation of pentosidine, an advanced glycation end product. Treatment with bazedoxifene ameliorated Hcy-induced suppression of Lox expression and increase in pentosidine accumulation. These findings suggest that high-dose Hcy induces apoptosis of osteoblasts by increasing oxidative stress, and low-dose Hcy decreases enzymatic collagen cross-links and increases pentosidine accumulation, resulting in the deterioration of bone quality. Bazedoxifene treatment effectively prevents the Hcy-induced detrimental reactions of osteoblasts. Thus, bazedoxifene may be a potent therapeutic drug for preventing Hcy-induced bone fragility.

Even though we’ve had an idea of the damage of glycation and what causes it for over 30 years, This industry is still concentrating on making new drugs. Drugs always have side effects that lead to more drugs, yet this is this industry’s modus operandi. They don’t know how to operate otherwise. It’s the ties to the grains industry that I object to and the power we’ve given to these industries, simply to allow the public to continue to feed their addiction. You might as well tell us to stand in front of a racing bus or semi. You’re basically selling us the same thing, future time in the hospital;

Abstract

Elevated plasma homocysteine (Hcy) level increases the risk of osteoporotic fracture by deteriorating bone quality. However, little is known about the effects of Hcy on osteoblast and collagen cross-links. This study aimed to investigate whether Hcy induces apoptosis of osteoblastic MC3T3-E1 cells as well as affects enzymatic and nonenzymatic collagen cross-links and to determine the effects of bazedoxifene, a selective estrogen receptor modulator, on the Hcy-induced apoptosis and deterioration of collagen cross-links in the cells. Hcy treatments (300 μM, 3 mM, and 10 mM) increased intracellular reactive oxygen species (ROS) production in a dose-dependent manner. Propidium iodide staining showed that 3 and 10 mM Hcy induced apoptosis of MC3T3-E1 cells. Moreover, the activities of caspases-8, 9, and 3 were increased by 3 mM Hcy. The detrimental effects of 3 mM Hcy on apoptosis and ROS production were partly reversed by bazedoxifene and 17β estradiol. In addition, real-time PCR, immunostaining and Western blot showed that 300 μM Hcy decreased the expression of lysyl oxidase (Lox). Furthermore, 300 μM Hcy increased extracellular accumulation of pentosidine, an advanced glycation end product. Treatment with bazedoxifene ameliorated Hcy-induced suppression of Lox expression and increase in pentosidine accumulation. These findings suggest that high-dose Hcy induces apoptosis of osteoblasts by increasing oxidative stress, and low-dose Hcy decreases enzymatic collagen cross-links and increases pentosidine accumulation, resulting in the deterioration of bone quality. Bazedoxifene treatment effectively prevents the Hcy-induced detrimental reactions of osteoblasts. Thus, bazedoxifene may be a potent therapeutic drug for preventing Hcy-induced bone fragility.

This displays the true despair of this problem, an industry more intent on driving profits than healing the people they affect. Their only interest is in making more drugs to allow the continuation of an addiction that’s putting more people in the hospital than any other one thing. To me, that is the definition of criminal behavior. This is a clear indication of legal extortion….and we allow it to continue, to feed our addiction.

This next report dated Oct 18, 2016, shows the influence of Metformin on the AGE population in our blood. It turns out to be another way to get you to take more drugs, as this drug encourages increased levels of CML (another AGE).

Abstract

Metabolic syndrome (MetS) is considered one of the most important public health problems. Several and controversial studies showed that the role of advanced glycation end products (AGEs) and their receptor in the development of metabolic syndrome and therapeutic pathways is still unsolved. We have investigated whether plasma pentosidine, carboxymethyl-lysine (CML), and soluble receptor for advanced glycation end products (sRAGE) levels were increased in patients with MetS and the effect of metformin in plasma levels of pentosidine, CML, and sRAGE. 80 control subjects and 86 patients were included in this study. Pentosidine, CML, and sRAGE were measured in plasma by enzyme-linked immunosorbent assay (ELISA). Plasma pentosidine, CML, and sRAGE levels were significantly increased in patients compared to control subjects (P < 0.001, P < 0.001, and P = 0.014, resp.). Plasma levels of pentosidine were significantly decreased in patients who received metformin compared to untreated patients (P = 0.01). However, there was no significant difference between patients treated with metformin and untreated patients in plasma CML levels. Plasma levels of sRAGE were significantly increased in patients who received metformin and ACE inhibitors (P < 0.001 and P = 0.002, resp.). However, in a multiple stepwise regression analysis, pentosidine, sRAGE, and drugs treatments were not independently associated. Patients with metabolic syndrome showed increased levels of AGEs such as pentosidine and CML. Metformin treatment showed a decreased level of pentosidine but not of CML. Therapeutic pathways of AGEs development should be taken into account and further experimental and in vitro studies merit for advanced research.

The purpose of this study was to look at Metformin’s effect on two different AGEs, pentosidine and CML. Again the emphasis is on finding ways to keep the glycating substances in the diet and offering treatment only, not in finding a cure. That would involve removing the glycating substances from the diet and that would hurt the grain industry. Their treatment though, involves the continuation of their prescribed drug regimen. This is why they pay the prettiest reps to sell their drugs to all the doctors who prescribe them.

Dated May 2016 is this report on the role of DAMP in inflammation, cancer and tissue repair;

Abstract

PURPOSE:

This review aimed to take stock of the current status of research on damage-associated molecular pattern (DAMP) protein. We discuss the Janus-faced role of DAMP molecules in inflammation, cancer, and tissue repair. The high-mobility group box (HMGB)-1 and adenosine triphosphate proteins are well-known DAMP molecules and have been primarily associated with inflammation. However, as we shall see, recent data have linked these molecules to tissue repair. HMGB1 is associated with cancer-related inflammation. It activates nuclear factor kB, which is involved in cancer regulation via its receptor for advanced glycation end-products (RAGE), Toll-like receptors 2 and 4. Proinflammatory activity and tissue repair may lead to pharmacologic intervention, by blocking DAMP RAGE and Toll like receptor 2 and 4 role in inflammation and by increasing their concentration in tissue repair, respectively.

METHODS:

We conducted a MEDLINE search for articles pertaining to the various issues related to DAMP, and we discuss the most relevant articles especially (ie, not only those published in journals with a higher impact factor).

FINDINGS:

A cluster of remarkable articles on DAMP have appeared in the literature in recent years. Regarding inflammation, several strategies have been proposed to target HMGB1, from antibodies to recombinant box A, which interacts with RAGE, competing with the full molecule. In tissue repair, it was reported that the overexpression of HMGB1 or the administration of exogenous HMGB1 significantly increased the number of vessels and promoted recovery in skin-wound, ischemic injury.

IMPLICATIONS:

Due to the bivalent nature of DAMP, it is often difficult to explain the relative role of DAMP in inflammation versus its role in tissue repair. However, this point is crucial as DAMP-related treatments move into clinical practice.

Another study proving the role of glycation in the pathogenesis of arthritis proves once again how inflammation is the result of glycation, something you have control over:

  • The potential role of advancedglycation end products (AGEs) and soluble receptors for AGEs (sRAGE) in the pathogenesis of adult-onset still’s disease.

BACKGROUND:

Accumulating evidence has demonstrated a pathogenic role of advanced glycation end products (AGEs) and receptors for AGEs (RAGE) in inflammation. Soluble RAGE (sRAGE), with the same ligands-binding capacity as full-length RAGE, acts as a “decoy” receptor. However, there has been scanty data regarding AGEs and sRAGE in adult-onset Still’s disease (AOSD). This study aimed to investigate AGEs and sRAGE levels in AOSD patients and examine their association with clinical characteristics.

METHODS:

Using ELISA, plasma levels of AGEs and sRAGE were determined in 52 AOSD patients, 36 systemic lupus erythematosus(SLE) patients and 16 healthy controls(HC). Their associations with activity parameters and disease courses were evaluated.

RESULTS:

Significantly higher median levels of AGEs were observed in active AOSD patients (16.75 pg/ml) and active SLE patients (14.80 pg/ml) than those in HC (9.80 pg/ml, both p < 0.001). AGEs levels were positively correlated with activity scores (r = 0.836, p < 0.001), ferritin levels (r = 0.372, p < 0.05) and CRP levels (r = 0.396, p < 0.005) in AOSD patients. Conversely, significantly lower median levels of sRAGE were observed in active AOSD patients (632.2 pg/ml) and active SLE patients (771.6 pg/ml) compared with HC (1051.7 pg/ml, both p < 0.001). Plasma sRAGE levels were negatively correlated with AOSD activity scores (r = -0.320, p < 0.05). In comparison to AOSD patients with monocyclic pattern, significantly higher AGEs levels were observed in those with polycyclic or chronic articular pattern. With treatment, AGEs levels declined while sRAGE levels increased in parallel with the decrease in disease activity.

CONCLUSION:

The elevation of AGEs levels with concomitant decreased sRAGE levels in active AOSD patients, suggests their pathogenic role in AOSD.

Juvenile arthritis is shown in this study to be the product of glycation, again something you have control over by what goes in your body for food. If you or your child suffers from this, your only cure is to stop the glycation. The older you are the less you can reverse. But if you’re young enough, you may be able to reverse a majority of it.

Background

The involvement of high mobility group box-1 (HMGB1) in various inflammatory and autoimmune diseases has been documented but clinical trials on the contribution of this pro-inflammatory alarmin in children with juvenile idiopathic arthritis (JIA) and systemic lupus erythematosus (SLE) are basically absent. To address the presence of HMGB1 and a soluble receptor for advanced glycation end products (sRAGE) in different subtypes of JIA and additionally in children with SLE, we enrolled a consecutive sample of children harvested peripheral blood as well as synovial fluids (SF) at diagnosis and correlated it with ordinary acute-phase reactants and clinical markers.

Methods

Serum and synovial fluids levels of HMGB1 and sRAGE in total of 144 children (97 with JIA, 19 with SLE and 27 healthy controls) were determined by ELISA.

Results

The children with JIA and those with SLE were characterised by significantly higher serum levels of HMGB1 and significantly lower sRAGE levels compared to the healthy controls. A positive correlation between serum HMGB1 and ESR, CRP, α2 globulin was found while serum sRAGE levels were inversely correlated with the same inflammatory markers in children with JIA. Additionally, high level of serum HMGB1 was related to hepatosplenomegaly or serositis in systemic onset JIA.

Conclusion

The inverse relationship of the HMGB1 and its soluble receptor RAGE in the blood and SF indicates that inflammation triggered by alarmins may play a role in pathogenesis of JIA as well as SLE. HMGB1 may serve as an inflammatory marker and a potential target of biological therapy in these patients. Further studies need to show whether the determination of HMGB1 levels in patients with JIA can be a useful guideline for detecting disease activity.

What’s important is that you stop the glycation as soon as possible to arrest to glycation. The secret to this cure is an end to all glycation. The magic of this cure is the end of the hunger cycle.

Are these enough reports to prove how directly influence diabetes? After reading this can you see the logic in controlling your diabetes by controlling your carb intake? Where are the warnings from the FDA and the USDA? Don’t they care about what they’re recommending? Don’t they understand because of their recommendations, they sending millions of Moms and Dads, sisters and brothers, husbands and wives to their slow, expensive, painful deaths?

These are free reports that are available to everyone. All you have to do is search for them at the National Library of Medicine in the National Institute of Health. There are literally 100’s of thousands of reports on the effects of glycation that remain hidden in the PubMed and PMC databases except to the few who look through them.  The only ones looking through this database are the drug companies looking for more ways to make money. Nobody is looking to warn anyone of the dangers of this food.

My question is why? The answer I get is, “there’s no money in it”. That’s is why I said in my first book, it would be a shame if profits and money weren’t the primary motivating factors in our society, but they are, and we have to live with it. That’s why I choose not to buy into it. It’s the same choice you have.

Glycation – The Real Poisoning of America

The Real Poisoning of America – Glycation

Of the causes of death below from Wikipedia, Ischaemic heart disease @ 7.4 million ranks right at the top. This is the result of glycation, 5 of the following 8 are also caused by non-enzymatic glycation. Hence my proposal, control the glycation and you control all modern diseases.

According to Wikipedia;

It is estimated that of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes because they have aged prematurely. Glycation is responsible for aging and the more of that, that you allow to happen in your body, the quicker your age. That is why keeping glycation to a minimum is what’s going to help you live longer and healthier. Even though aging may not be able to be reversed completely, it can be slowed dramatically by eating the right diet.  (Deep down you know that to be true. It’s just so hard to stick to when you have to.)

Leading causes of preventable death worldwide as of the year 2001, according to researchers working with the Disease Control Priorities Network (DCPN) and the World Health Organization (WHO). (The WHO’s 2008 statistics show very similar trends.) Imagine what they are right now, 8 years later and what they will be eight years from now, if nothing is done about it. Think it might be time for a cure?

The top 10 causes of preventable death, ones influenced by glycation are in red. Although it may me difficult to stop all glycation in the body, due to its commonality, you can control a major portion of it. Excessive Carbohydrate Consumption, the primary cause of glycation is controllable. Failure to control your consumption leads directly to any of the following disorders in red ;

  1. Ischaemic heart disease @ 7.4 mil
  2. Stroke@ 6.7 mil
  3. COPD @ 3.1 mil
  4. Lower Respiratory infection @ 3.1mil
  5. Trachea bronchus, lung infection@1.6 mil
  6. HIV/AIDS@1.5 mil
  7. Diarrheal diseases@1.5 mil
  8. Diabetes mellitus@1.5 mil
  9. Road injury@1.3 mil
  10. Hypertension@1.1 mil

40% of these deaths or 16.7 million are directly linked to ECC, Excessive Carbohydrate Consumption, making them the most preventable causes of death. 16.7 million deaths each and every year amounts to over 45,750 people each and every day. That includes approximately 1830 Americans each and every day. We have full control of this. All it would take is to say no to the sugar and grain industries. This one response would allow over 1830 more Americans to stay alive, every day. The cessation of carb consumption could add an additional 10-20 years to their lives, simply by eliminating the primary cause of inflammation, glucose. The continuation of carb consumption will, by contrast, prove the destructive power of sugar, by eventually killing its hosts.

Glycation is a common everyday experience that you accelerate with a carbohydrate diet. The more carbs you eat, the more glycation you’ll get to deal with. Glycation is controllable by controlling what you put in your mouth to eat. Although not totally responsible for some of these cancers, they would not exist if the glycation didn’t exist. This is the basis of my contention that if you eliminate the reason for the glycation, you eliminate the reason for inflammation, which in turn will eliminate the reason for these diseases, thereby eliminating the disease. It’s really not hard to see, once you take a good look at it; carb consumption is responsible for the inflammation that builds in the blood that is responsible for 90% of all modern diseases. Remove the inflammation by removing the sugar, which means removing the carbs. A simpler solution doesn’t exist and this cure can be yours.

These Are the Smoking Gun Articles Of

Evidence That The FDA Are Ignoring.

They’re Putting Your Health and Life at Risk.

48 of the 11667 studies done on glycation are below. These research studies were chosen from 231 studies that I examined for evidence of what glycation does to the body. By going through only 7% of these studies, I was able to find enough damning evidence to condemn this food 31 times over. By this ratio, I’ll end up finding at the least 850 more studies showing damage that glycation does.

I chose to search glycation because I know that it’s at the root of all modern diseases from cancer to CVDs to arthritis to dementia including Alzheimer disease. The following studies are the proof of what glycation does, and with sugar being the primary instigator of glycation, removal of sugar from the diet will eliminate everything it’s responsible for. These AGEs are responsible for all modern diseases and thus, are the reason for this book. When you eat carbs, you need to know what those carbs do to your body.

Foundation of Glycation

The study that piqued my interest initially was the report on RAGEs,

This report can be found on PubMed at Receptor for advanced glycation endproductsmediated inflammation and diabetic vascular complications. It explains how glycation turns your body’s fuel (cholesterol) and proteins (hemoglobin) into AGEs before they can be used for fuel and body repair.

“Exposure of amino residue of proteins to reducing sugars, such as glucose, glucose 6‐phosphate, fructose, ribose and intermediate aldehydes, results in non‐enzymatic glycation, which forms reversible Schiff bases and Amadori compounds. A series of further complex molecular rearrangements then yield irreversible advanced glycation end‐products (AGE). The aldehydes, highly reactive AGE precursors, are produced by both enzymatic and non‐enzymatic pathways. The enzymatic pathways include a route of myeloperoxidase in inflammatory cells, such as activated macrophages, which produces hypochlorite, then reacting with serine to generate glycolaldehyde.” Study Link

I’d be willing to bet that you had no idea that carb consumption is behind Amyotrophic Lateral Sclerosis (ALS). Guess what? it is. Here is your proof that MCT fats are beneficial in combating ALS;

  • Metabolic Therapy with Deanna Protocol Supplementation Delays Disease Progression and Extends Survival in Amyotrophic Lateral Sclerosis (ALS) Mouse Model

also known as Lou Gehrig’s disease, is a neurodegenerative disorder of motor neurons causing progressive muscle weakness, paralysis, and eventual death from respiratory failure. There is currently no cure or effective treatment for ALS. Besides motor neuron degeneration, ALS is associated with impaired energy metabolism, which is pathophysiologically linked to mitochondrial dysfunction and glutamate excitotoxicity. The Deanna Protocol (DP) is a metabolic therapy that has been reported to alleviate symptoms in patients with ALS. In this study we hypothesized that alternative fuels in the form of TCA cycle intermediates, specifically arginine-alpha-ketoglutarate (AAKG), the main ingredient of the DP, and the ketogenic diet (KD), would increase motor function and survival in a mouse model of ALS (SOD1-G93A). ALS mice were fed standard rodent diet (SD), KD, or either diets containing a metabolic therapy of the primary ingredients of the DP consisting of AAKG, gamma-aminobutyric acid, Coenzyme Q10, and medium chain triglyceride high in caprylic triglyceride. Assessment of ALS-like pathology was performed using a pre-defined criteria for neurological score, accelerated rotarod test, paw grip endurance test, and grip strength test. Blood glucose, blood beta-hydroxybutyrate, and body weight were also monitored. SD+DP-fed mice exhibited improved neurological score from age 116 to 136 days compared to control mice. KD-fed mice exhibited better motor performance on all motor function tests at 15 and 16 weeks of age compared to controls. SD+DP and KD+DP therapies significantly extended survival time of SOD1-G93A mice by 7.5% (p = 0.001) and 4.2% (p = 0.006), respectively. Sixty-three percent of mice in the KD+DP and 72.7% of the SD+DP group lived past 125 days, while only 9% of the control animals survived past that point. Targeting energy metabolism with metabolic therapy produces a therapeutic effect in ALS mice which may prolong survival and quality of life in ALS patients.

 What does that say about what the grain industry has told you about milk fat? They’ve condemned milk fats when they’re the healthiest fats you can eat. What the industry doesn’t like is that milk fats keep you from needing drugs, something the industry doesn’t want you to know.
Arthritis is a Result of Glycation From Inflammation

The following report is the evidence of glucose’s involvement in arthritis. By being responsible for glycation, the glucose from broken carbs, again, is directly responsible for arthritis, just like if was in the 4,000 yr old ice mummy recovered from a receding glacier.

 “Glycated, oxidized and nitrated proteins and amino acids were detected in synovial fluid and plasma of arthritic patients with characteristic patterns found in early and advanced OA and RA, and non-RA, with respect to healthy controls. In early-stage disease, two algorithms for consecutive use in diagnosis were developed: (1) disease versus healthy control, and (2) classification as OA, RA and non-RA. “  Study Link

Alzheimer’s and Parkinson’s – a Result of Glycation

The following report shows the effects that AGEs have on the body in the diseases it promotes.

“Vast evidence supports the view that glycation of proteins is one of the main factors contributing to aging and is an important element of etiopathology of age-related diseases, especially type 2 diabetes mellitus, cataract and neurodegenerative diseases. Counteracting glycation  can therefore be a means of increasing both the lifespan and health span. In this review, accumulation of glycation products during aging is presented, pathophysiological effects of glycation are discussed and ways of attenuation of the effects of glycation are described, concentrating on prevention of glycation. The effects of glycation and glycation inhibitors on the course of selected age-related diseases, such as Alzheimer’s disease, Parkinson’s disease and cataract are also reviewed.”   Study Link

This study looks at the damaging effects of glycation along with the protective effects of certain phytochemicals (anti-oxidant producing agents).

“Reducing sugars can react non-enzymatically with amino groups of proteins and lipids to form irreversibly cross-linked macroprotein derivatives called as advanced glycation end products (AGEs). Cross-linking modification of extracellular matrix proteins by AGEs deteriorate their tertiary structural integrity and function, contributing to aging-related organ damage and diabetes-associated complications, such as cardiovascular disease (CVD). Moreover, engagement of receptor for AGEs, RAGE with the ligands evoke oxidative stress generation and inflammatory, thrombotic and fibrotic reactions in various kinds of tissues, further exacerbating the deleterious effects of AGEs on multiple organ systems. So the AGE-RAGE axis is a novel therapeutic target for numerous devastating disorders. Several observational studies have shown the association of dietary consumption of fruits and vegetables with the reduced risk of CVD in a general population. Although beneficial effects of fruits and vegetables against CVD could mainly be ascribed to its anti-oxidative properties, blockade of the AGE-RAGE axis by phytochemicals may also contribute to cardiovascular event protection. Therefore, in this review, we focus on 4 phytochemicals (quercetin, sulforaphane, iridoids, and curcumin) and summarize their effects on AGE formation as well as RAGE-mediated signaling pathway in various cell types and organs, including endothelial cells, vessels, and heart.”

Glycation, Amyloid Plaque and Neurodegenerative Disorders

This report examines the nature of amyloid plaque and glyoxal (Glyoxal is an inflammatory compound formed when cooking oils and fats are heated to high temperatures). It’s also made in your body when you body breaks down glucose.

“Glyoxal, a highly reactive α-oxoaldehyde, increases in diabetic condition and reacts with proteins to form advanced glycation end products (AGEs). In the present study, we have investigated the effect of glyoxal on experimental rat hemoglobin in vivo after external administration of the α-dicarbonyl compound in animals. Gel electrophoretic profile of hemolysate collected from glyoxal-treated rats (32mg/kg body wt. dose) after one week exhibited the presence of some high molecular weight protein bands that were found to be absent for control, untreated rats. Mass spectrometric and absorption studies indicated that the bands represented hemoglobin. Further studies revealed that the fraction exhibited the presence of intermolecular cross β-sheet structure. Thus glyoxal administration induces formation of high molecular weight aggregates of hemoglobin with amyloid characteristics in rats. Aggregated hemoglobin fraction was found to exhibit higher stability compared to glyoxal-untreated hemoglobin. As evident from mass spectrometric studies, glyoxal was found to modify Arg-30β and Arg-31α of rat hemoglobin to hydroimidazolone adducts. The modifications thus appear to induce amyloid-like aggregation of hemoglobin in rats. Considering the increased level of glyoxal in diabetes mellitus as well as its high reactivity, the above findings may be physiologically significant.

In view of its inflammatory function in innate immunity and its ability to detect a class of ligands through a common structural motif, rage is often referred to as a pattern recognition receptor.”     Study link

This report examines the relationship of high mobility group box 1 (HMGB1) and the effects it has on the body. HMGB1 is one of the most prevalent RAGE’s, as near as I can tell. It comes up in more studies…

RAGE and Inflammation
·        HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia.

Infectious and sterile inflammatory diseases are correlated with increased levels of high mobility group box 1 (HMGB1) in tissues and serum. Extracellular HMGB1 is known to activate Toll-like receptors (TLRs) 2 and 4 and RAGE (receptor for advanced glycation end products) in inflammatory conditions. Here, we find that TLR5 is also an HMGB1 receptor that was previously overlooked due to lack of functional expression in the cell lines usually used for studying TLR signaling. HMGB1 binding to TLR5 initiates the activation of NF-κB signaling pathway in a MyD88-dependent manner, resulting in pro-inflammatory cytokine production and pain enhancement in vivo. Biophysical and in vitro results highlight an essential role for the C-terminal tail region of HMGB1 in facilitating interactions with TLR5. These results suggest that HMGB1-modulated TLR5 signaling is responsible for pain hypersensitivity.” Study Link

I see HMGB1 come up in almost all modern diseases. This must be the most popular RAGEs.

COPD, Lung Cancer and RAGE

The proof that carb consumption also contributes to lung cancer is in the following report. The underlying cause is inflammation.

·        The Ser82 RAGE Variant Affects Lung Function and Serum RAGE in Smokers and sRAGE Production In Vitro.”

Abstract

INTRODUCTION:

Genome-Wide Association Studies have identified associations between lung function measures and Chronic Obstructive Pulmonary Disease (COPD) and chromosome region 6p21 containing the gene for the Advanced Glycation End Product Receptor (AGER, encoding RAGE). We aimed to (i) characterize RAGE expression in the lung, (ii) identify AGER transcripts, (iii) ascertain if SNP rs2070600 (Gly82Ser C/T) is associated with lung function and serum sRAGE levels and (iv) identify whether the Gly82Ser variant is functionally important in altering sRAGE levels in an airway epithelial cell model.

METHODS:

Immunohistochemistry was used to identify RAGE protein expression in 26 human tissues and qPCR was used to quantify AGER mRNA in lung cells. Gene expression array data was used to identify AGER expression during lung development in 38 fetal lung samples. RNA-Seq was used to identify AGER transcripts in lung cells. sRAGE levels were assessed in cells and patient serum by ELISA. BEAS2B-R1 cells were transfected to over express RAGE protein with either the Gly82 or Ser82 variant and sRAGE levels identified.

RESULTS:

Immunohistochemical assessment of 6 adult lung samples identified high RAGE expression in the alveoli of healthy adults and individuals with COPD. AGER/RAGE expression increased across developmental stages in human fetal lung at both the mRNA (38 samples) and protein levels (20 samples). Extensive AGER splicing was identified. The rs2070600T (Ser82) allele is associated with higher FEV1, FEV1/FVC and lower serum sRAGE levels in UK smokers. Using an airway epithelium model overexpressing the Gly82 or Ser82 variants we found that HMGB1 activation of the RAGE-Ser82 receptor results in lower sRAGE production.

CONCLUSIONS:

This study provides new information regarding the expression profile and potential role of RAGE in the human lung and shows a functional role of the Gly82Ser variant. These findings advance our understanding of the potential mechanisms underlying COPD particularly for carriers of this AGER polymorphism.  Study Link

I wonder if the ACS, American Cancer Society will take this information and realize what foods are responsible for this report showing how RAGEs have a role in COPD and ultimately lung cancer? Will it provoke a response from the ACS on the consumption of the foods responsible for this RAGE? Will they issue a warning or are they more concerned with an industry that depends on this disorder, the pharmaceutical industry, or maybe an industry that provokes this disorder, the grain industry?

You may ask though, shouldn’t smoking play a larger role in this equation? I submit that if the glycation never existed in the first place, the smoking wouldn’t play as large of a role as it does with the inflammation in the body. It takes the glycation to create the RAGE responsible for lung cancer, yet no one knows of glycation or its effects from the FDA, the USDA or the CDC. Who are they trying to protect? Why isn’t glycation considered a disease?

Skin Cancer and Glycation

In the following study the emergence of the HMGB1 RAGE in head and the skin cancer, neck squamous cell carcinoma;

·        “Clinical Value of High Mobility Group Box 1 and the Receptor for Advanced Glycation End-products in Head and Neck Cancer: A Systematic Review.”

Introduction High mobility group box 1 is a versatile protein involved in gene transcription, extracellular signaling, and response to inflammation. Extracellularly, high mobility group box 1 binds to several receptors, notably the receptor for advanced glycation end-products. Expression of high mobility group box 1 and the receptor for advanced glycation end-products has been described in many cancers. 

Objectives To systematically review the available literature using PubMed and Web of Science to evaluate the clinical value of high mobility group box 1 and the receptor for advanced glycation end-products in head and neck squamous cell carcinomas. 

Data synthesis A total of eleven studies were included in this review. High mobility group box 1 overexpression is associated with poor prognosis and many clinical and pathological characteristics of head and neck squamous cell carcinomas patients. Additionally, the receptor for advanced glycation end-products demonstrates potential value as a clinical indicator of tumor angiogenesis and advanced staging. In diagnosis, high mobility group box 1 demonstrates low sensitivity. 

Conclusion High mobility group box 1 and the receptor for advanced glycation end-products are associated with clinical and pathological characteristics of head and neck squamous cell carcinomas. Further investigation of the prognostic and diagnostic value of these molecules is warranted.” Study Link

Cataracts and Glycation

Although the study above was published in Oct 2016, this kind of evidence has been around for over 20 years. These reports started showing up in 1984;

We have examined the nonenzymatic glycation of human lens crystallin, an extremely long-lived protein, from 16 normal human ocular lenses 0.2-99 yr of age, and from 11 diabetic lenses 52-82-yr-old…the nonenzymatic glycation of nondiabetic lens crystallin may be regarded as a biological clock…The glucitol-lysine (Glc-Lys) content of soluble and insoluble crystallin was determined after reduction with H-borohydride followed by acid hydrolysis, boronic acid affinity chromatography, and high pressure cation exchange chromatography…Over an age range comparable to that of the control samples, the diabetic crystallin samples contained about twice as much Glc-Lys.

Cardiovascular Disease and RAGE

This study shows glycations implication in cardiovascular disease;

·        Therapeutic interventions for Advanced Glycation-End Products and its Receptor-Mediated Cardiovascular Disease.

“Advanced glycation end products (AGEs) are heterogeneous group of molecules formed from non-enzymatic reaction of reducing sugars with amino group of proteins, lipids, and nucleic acid. Interaction of AGEs with its cell-bound receptor (RAGE) results in generation of oxygen radicals, nuclear factor kappa-β, pro-inflammatory cytokines and cell adhesion molecules, and is involved in the pathophysiology of cardiovascular diseases (CVD). Circulating soluble forms of RAGE (sRAGE) and endo-secretory RAGE (esRAGE) compete with RAGE for ligand binding and function as a decoy. This paper describes the endogenous and exogenous (high dietary AGEs, cooking food under high dry heat, elevated pH, and long period) sources of AGEs. AGE-RAGE-mediated CVD includes atherosclerosis, coronary artery disease, carotid artery disease, hypertension, peripheral vascular diseases, heart failure, cardiomyopathy, and microangiopathy. The therapeutic intervention with reduction in AGEs and RAGE, and elevation in sRAGE has been reported for the treatment of AGE-RAGE-mediated CVD. Reduction in levels of AGEs can be achieved by reduction in consumption of food containing or creating low amount of AGEs, cooking food at low temperature, moist heat, and shorter duration. AGE formation can be reduced with drugs, vitamins and stoppage of cigarette smoking. Statins, telmisartan, and curcumin have been used for suppression of RAGE. Statins, ACE-inhibitors, Rosiglitazone and vitamin D have been used to increase levels of sRAGE. Finally exogenous administration of sRAGE can be helpful in amelioration of CVD. In conclusion, AGE-RAGE-mediated CVD could be attenuated with reduction in consumption of AGEs, suppression of RAGE and elevation of sRAGE.”

Dangers of Statins

Statins are the most dangerous in the above equation as they unbalance your cholesterol which puts everything in your body out of balance. It’s your cholesterol that regulates a good portion of your hormones. You should already know how much your hormones affect your emotions, energy, intelligence, aging, and basic proper functioning of your body, right down to digesting carbs (insulin). Granted insulin is made in the pancreas, although other more influential hormones are made in your fat which is what statins reduce. Side effects of statins include; Common statin-related side effects (headaches, stomach upset, abnormal liver function tests and muscle cramps) were similar to other statins. Side effects of statins include muscle pain, increased risk of diabetes mellitus, and abnormalities in liver enzyme tests. Additionally, they have rare but severe adverse effects, particularly muscle damage. As of 2010, a number of statins are on the market: atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin. Several combination preparations of a statin and another agent, such as ezetimibe/simvastatin, are also available. In 2005 sales were estimated at $18.7 billion in the United States.

Side effects ultimately lead to other drugs down the road. It’s inevitable. This is how the pharmaceutical corporations make as much money as they do. And you gladly give it to them, simply to keep up your addiction and later to fight your CVD or cancer. How much sense this make to you?

What concerns me more than anything else is the fact the atorvastatin in the best selling pharmaceutical in history, with sales of $12.4 billion in 2008. With all of the side effects listed above, how many patients taking these drugs will not ever have to use any more pharmaceuticals. This is the way they guarantee a return consumer. I know. (I was one of them. I won’t be any more due to my keto diet.)

The best-selling statin is atorvastatin, which in 2003 became the best-selling pharmaceutical in history. The manufacturer Pfizer reported sales of US$12.4 billion in 2008. Pfizer and Monsanto were under one roof at in 2003. That was the year Pfizer started their divesture of Monsanto. (Maybe it was the lawsuits that were starting to pile up, that they didn’t appreciate.) I wonder how many law suits Pfizer has against itself for its pharmaceutical statins. Below are the contraindications for atorvastatin (Lipitor);

Contraindications

The side effects of Lipitor are even longer and include diarrhea, dyspepsia, myalgia and nausea. Are you on statins? Did you read over your drug disclosure? Were you told that you could cure this without drugs? Were you ever told that this disorder started in your diet of carbs? The earliest report in the PMC I found was dated Jan, 1974 and simply stated that weight reduction was important to controlling hyperlipoproteinemia, a fancy word for high amounts of apolipoproteins in the body which indicate levels of cholesterol.

According to a study completed in 1995;

Population studies linking low cholesterol to noncoronary mortalities do not demonstrate cause-and-effect relations. In fact, based on current studies, the opposite is more likely to be the case. Drug intervention, however, should be used conservatively, particularly in young adults and the elderly. Drugs should be used only after diet and lifestyle interventions have failed. The evidence linking high blood cholesterol to coronary atherosclerosis and cholesterol lowering to its prevention is broad-based and definitive. Concerns about cholesterol lowering and spontaneously low cholesterols should be pursued but should not interfere with the implementation of current public policies to reduce the still heavy burden of atherosclerosis in Western society.

Another study from 1994 showed the rethinking of the low-fat hi-carb diet that has been pushed for over 40 years (probably at the insistence of Monsanto). Since they owned GD Searle at the time it makes me wonder, was their intent to hook us on more drugs? Even as recent Dec 31, 2016 the dept of research at Kaiser Permanente Southern California, Pasadena came to the conclusion; Statin use rather than cholesterol level was associated with lower mortality risk in patients with pancreatic cancer. Statins appear to improve survival through a lipid-independent mechanism. Apparently they’re rethinking their strategies. I have a strategy, don’t eat carbs. I go keto and let the fasting take care of the illnesses. If it can work for me it can work for you.

Our medical industry has had research for over 20 years on the benefits of cholesterol and the dangers of lowering it, yet because of our dependence on grains and sugar and Monsanto’s influence in the FDA and USDA, the recommendations from the USDA’s agency for food labeling to food safety to Myplate, the CCNP and at least 3 other agencies in the USDA alone, the CDC, the ADA, the ACS still recommend that you keep whole grains in your diet, regardless of the studies completed that show their danger. Why? Monsanto is in the crop seed industry owning over 15 crop seed companies, all wanting to sell GMO seed ready to handle Roundup herbicide to farmers contracted by Monsanto waiting to plant their next crop. They’ll spray their crops according to their contract with Monsanto. It then goes on your table.

This article appeared 22 years ago in PubMed in Aug, 1994. Even then low cholesterol was being questioned, yet in some corners, it’s still promoted today;

Although hypercholesterolemia is associated with increased liability to death from heart disease, it is as frequently associated with increased overall life expectancy as with decreased life expectancy. These findings are incompatible with labeling hypercholesterolemia an overall health hazard. Moreover, it is questionable if the cardiovascular liability associated with hypercholesterolemia is either causal or reversible. The complex relationships between diet, serum cholesterol, atherosclerosis and mortality and their interactions with genetic and environmental factors suggest that the effects of simple dietary prescriptions are unlikely to be predictable, let alone beneficial. These cautions are borne out by numerous studies which have shown that multifactorial primary intervention to lower cholesterol levels is as likely to increase death from cardiovascular causes as to decrease it. Importantly, the only significant overall effect of cholesterol-lowering intervention that has ever been shown is increased mortality.

With Monsanto’s influence in the FDA, the USDA, the EPA and who knows what else, who’s to protect our food supply? You have to protect yourself. Monsanto has proven they can’t self regulate their industry and keep us safe. The best way to start being safe is to not eat their food, which happens to include all grains. If you don’t buy them, that may send the message.

Direct Influence of Glycation in Cancer

More evidence of its influence in cancer is when this HMGB1 RAGE rears its ugly head again, influencing cancer;

·        Blockade of High Mobility Group Box 1 (HMGB1) augments anti-tumor T-cell response induced by peptide vaccination as a co-adjuvant.

“High Mobility Group Box 1 (HMGB1) is a member of the damage-associated molecular patterns (DAMPs), which cause inflammation and trigger innate immunity through Toll-like receptors (TLRs) 2/4 and the receptor for advanced glycation end products (RAGE). We examined the effect of glycyrrhizin, a selective inhibitor of HMGB1, on the induction of cytotoxic T-lymphocytes (CTLs) in mice. B6 mice, either OT-1 spleen cell-transferred or untransferred, were immunized with an s.c. injection of OVA257-264 peptide with topical imiquimod, and glycyrrhizin was mixed with the antigen peptide. Proliferation of OT-1 cells after immunization was enhanced by glycyrrhizin. The effect of glycyrrhizin was confirmed in other adjuvant systems, such as CpG oligonucleotide and monophosphoryl lipid A (MPL), but glycyrrhizin was not effective in Freund’s incomplete adjuvant system. The augmenting effects of glycyrrhizin were also observed in other synthetic HMGB1 inhibitors, i.e., gabexate mesilate, nafamostat, and sivelstat. Thus the effects are common to the HMGB1 inhibitors. Induction of CTLs detected by IFN-γ ELISPOT assay was similarly augmented by glycyrrhizin. In a therapeutic vaccine model, glycyrrhizin inhibited the growth of s.c. transplanted EG.7 tumors. Expression of inflammatory cytokines in the skin inoculation site was downregulated by glycyrrhizin. These results suggest that HMGB1 inhibitors might be useful as a co-adjuvant for peptide vaccination with an innate immunity receptor-related adjuvant. This article is protected by copyright. All rights reserved.” Study Link

Were you ever told that this could happen if you continued your diet of bread, corn, soy and other carbs? (Neither was I.)

This is evidence of glycation’s effect on the kidneys:

·        AGEs/sRAGE, a novel risk factor in the pathogenesis of end-stage renal disease.

“Interaction of advanced glycation end products (AGEs) with its cell-bound receptor (RAGE) results in cell dysfunction through activation of nuclear factor kappa-B, increase in expression and release of inflammatory cytokines, and generation of oxygen radicals. Circulating soluble receptors, soluble receptor (sRAGE), endogenous secretory receptor (esRAGE) and cleaved receptor (cRGAE) act as decoy for RAGE ligands and thus have cytoprotective effects. Low levels of sRAGE and esRAGE have been proposed as biomarkers for many diseases. However sRAGE and esRAGE levels are elevated in diabetes and chronic renal diseases and still tissue injury occurs. It is possible that increases in levels of AGEs are greater than increases in the levels of soluble receptors in these two diseases. Some new parameters have to be used which could be an universal biomarkers for cell dysfunction. It is hypothesized that increases in serum levels of AGEs are greater than the increases in the soluble receptors, and that the levels of AGEs is correlated with soluble receptors and that the ratios of AGEs/sRAGE, AGEs/esRAGE and AGEs/cRAGE are elevated in patients with end-stage renal disease (ESRD) and would serve as an universal risk marker for ESRD. The study subject comprised of 88 patients with ESRD and 20 healthy controls. AGEs, sRAGE and esRAGE were measured using commercially available enzyme linked immune assay kits. cRAGE was calculated by subtracting esRAGE from sRAGE. The data show that the serum levels of AGEs, sRAGE, cRAGE are elevated and that the elevation of AGEs was greater than those of soluble receptors. The ratios of AGEs/sRAGE, AGEs/esRAGE and AGEs/cRAGE were elevated and the elevation was similar in AGEs/sRAGE and AGEs/cRAGE but greater than AGEs/esRAGE. The sensitivity, specificity, accuracy, and positive and negative predictive value of AGEs/sRAGE and AGEs/cRAGE were 86.36 and 84.88 %, 86.36 and 80.95 %, 0.98 and 0.905, 96.2 and 94.8 %, and 61.29 and 56.67 % respectively. There was a positive correlation of sRAGE with esRAGE and cRAGE, and AGEs with esRAGE; and negative correlation between sRAGE and AGEs/sRAGE, esRAGE and AGES/esRAGE, and cRAGE and AGES/cRAGE. In conclusion, AGEs/sRAGE, AGEs/cRAGE and AGEs/esRAGE may serve as universal risk biomarkers for ESRD and that AGEs/sRAGE and AGEs/cRAGE are better risk biomarkers than AGEs/esRAGE.” Study Link

Breast Cancer and RAGE

This is the evidence that breast cancer is influenced by glycation;

·        Increased Expression of the Receptor for AdvancedGlycation End-Products (RAGE) Is Associated with Advanced Breast Cancer Stage.

“Abstract

BACKGROUND:

The receptor for advanced glycation end-products (RAGE) is a multiligand transmembrane receptor that is overexpressed in various pathological conditions including cancers. However, the expression pattern of RAGE in breast cancer tumors is still not completely clear.

METHODS:

In this study, we investigated the expression levels of RAGE in 25 fresh-frozen breast cancer samples and corresponding noncancerous tissue samples collected from breast cancer patients, by real-time polymerase chain reaction (PCR). Additionally, we performed immunohistochemistry on breast cancer specimens.

RESULTS:

The results indicate a high expression of the RAGE-encoding gene in the cancerous tissues. RAGE expression at the mRNA and protein levels was statistically significantly up-regulated in advanced-stage and triple-negative breast tumors and node-positive tissues compared with other tissues (p < 0.001). A significant association between RAGE expression and tumor size was observed (p = 0.029).

CONCLUSIONS:

Overexpression of RAGE in advanced-stage tumors may be a useful biomarker for diagnosis and the prediction of breast cancer progression.” Study Link

I’m only sorry that I could include studies and reports for all forms of cancer, but with they’re being so many of them, that’s a virtually impossible task.

Evidence of bone density decline from glycation;

·        AdvancedGlycationEnd Products, Diabetes, and Bone Strength.

“Diabetic patients have a higher fracture risk than expected by their bone mineral density (BMD). Poor bone quality is the most suitable and explainable cause for the elevated fracture risk in this population. Advanced glycation end products (AGEs), which are diverse compounds generated via a non-enzymatic reaction between reducing sugars and amine residues, physically affect the properties of the bone material, one of a component of bone quality, through their accumulation in the bone collagen fibers. On the other hand, these compounds biologically act as agonists for these receptors for AGEs (RAGE) and suppress bone metabolism. The concentrations of AGEs and endogenous secretory RAGE, which acts as a “decoy receptor” that inhibits the AGEs-RAGE signaling axis, are associated with fracture risk in a BMD-independent manner. AGEs are closely associated with the pathogenesis of this unique clinical manifestation through physical and biological mechanisms in patients with diabetes mellitus.” Study link

Evidence of Alzheimer’s disease from glycation;

Genetic association between RAGE polymorphisms and Alzheimer’s disease and Lewy body dementias in a Japanese cohort: a case-control study.

“Abstract

BACKGROUND/AIMS:

Interaction of receptor for advanced glycation end products (RAGE) with amyloid-β increases amplification of oxidative stress and plays pathological roles in Alzheimer’s disease (AD). Oxidative stress leads to α-synuclein aggregation and is also a major contributing factor in the pathogenesis of Lewy body dementias (LBDs). Therefore, we aimed to investigate whether RAGE gene polymorphisms were associated with AD and LBDs.

METHODS:

Four single nucleotide polymorphisms (SNPs)-rs1800624, rs1800625, rs184003, and rs2070600-of the gene were analyzed using a case-control study design comprising 288 AD patients, 76 LBDs patients, and 105 age-matched controls.

RESULTS:

Linkage disequilibrium (LD) examination showed strong LD from rs1800624 to rs2070600 on the gene (1.1 kb) in our cases in Japan. Rs184003 was associated with an increased risk of AD. Although there were no statistical associations for the other three SNPs, haplotypic analyses detected genetic associations between AD and the RAGE gene. Although relatively few cases were studied, results from the SNPs showed that they did not modify the risk of developing LBDs in the Japanese population.

CONCLUSION:

Our findings suggested that polymorphisms in the RAGE gene are involved in genetic susceptibility to AD. Copyright © 2016 John Wiley & Sons, Ltd.”  Study Link

With the above evidence showing its involvement in brain diseases, how does this information get hidden? Doesn’t anyone of authority examine these reports?  More evidence below of cancer causing agents from glycation leaving me to wonder; is anyone looking out for our benefit?

·        M2 macrophages do not fly into a “RAGE”.

“Tumor-associated macrophages (TAMs) are key elements in orchestrating host responses inside tumor stroma. This population may undergo a polarized activation process, thus rendering a heterogeneous spectrum of phenotypes, where the classically activated type 1 macrophages (M1) and the alternative activated type 2 macrophages (M2) represent two extreme phenotypes. In this commentary, based on very recent research findings, we intend to highlight how complex could be the crosstalk among all components of tumor stroma, where the coexistence of non-natural partners may even skew the canonical responses that we can expect.”  Study Link

This is where your addiction starts with this evidence of glycation causing agents in baby food. This is indicative of the glucose in the formula. Ask yourself why this is done, if glucose is capable of doing this much harm;

·        “Protein breakdown and release of β-casomorphins during in vitro gastro-intestinal digestion of sterilized model systems of liquid infant formula.”

“Protein modifications occurring during sterilization of infant formulas can affect protein digestibility and release of bioactive peptides. The effect of glycation and cross-linking on protein breakdown and release of β-casomorphins was evaluated during in vitro gastro-intestinal digestion (GID) of six sterilized model systems of infant formula. Protein degradation during in vitro GID was evaluated by SDS-PAGE and by measuring the nitrogen content of ultrafiltration (3kDa) permeates before and after in vitro GID of model IFs. Glycation strongly hindered protein breakdown, whereas cross-linking resulting from β-elimination reactions had a negligible effect. Only β-casomorphin 7 (β-CM7) was detected (0.187-0.858mgL(-1)) at the end of the intestinal digestion in all untreated IF model systems. The level of β-CM7 in the sterilized model systems prepared without addition of sugars ranged from 0.256 to 0.655mgL(-1). The release of this peptide during GID was hindered by protein glycation.” Study Link

This study explains that it’s the glycative results are what drives inflammation and  in type 1 diabetics, this was just released Oct15, 2016. Watch to see if you’ll hear anything about it. If you don’t, it’s probably because Big Pharma has something to say about it;

·        The Receptor for AdvancedGlycationEndproducts Drives T Cell Survival and Inflammation in Type 1 Diabetes Mellitus.

“The ways in which environmental factors participate in the progression of autoimmune diseases are not known. After initiation, it takes years before hyperglycemia develops in patients at risk for type 1 diabetes (T1D). The receptor for advanced glycation endproducts (RAGE) is a scavenger receptor of the Ig family that binds damage-associated molecular patterns and advanced glycated endproducts and can trigger cell activation. We previously found constitutive intracellular RAGE expression in lymphocytes from patients with T1D. In this article, we show that there is increased RAGE expression in T cells from at-risk euglycemic relatives who progress to T1D compared with healthy control subjects, and in the CD8+ T cells in the at-risk relatives who do versus those who do not progress to T1D. Detectable levels of the RAGE ligand high mobility group box 1 were present in serum from at-risk subjects and patients with T1D. Transcriptome analysis of RAGE+ versus RAGE T cells from patients with T1D showed differences in signaling pathways associated with increased cell activation and survival. Additional markers for effector memory cells and inflammatory function were elevated in the RAGE+ CD8+ cells of T1D patients and at-risk relatives of patients before disease onset. These studies suggest that expression of RAGE in T cells of subjects progressing to disease predates dysglycemia. These findings imply that RAGE expression enhances the inflammatory function of T cells, and its increased levels observed in T1D patients may account for the chronic autoimmune response when damage-associated molecular patterns are released after cell injury and killing.”

Study Link

Evidence of the role of AGEs in the process of neurodegenerative diseases;

·        “Impact of Non-Enzymatic Glycation in Neurodegenerative Diseases: Role of Natural Products in Prevention.”

“Non-enzymatic protein glycosylation is the addition of free carbonyls to the free amino groups of proteins, amino acids, lipoproteins and nucleic acids resulting in the formation of early glycation products. The early glycation products are also known as Maillard reaction which undergoes dehydration, cyclization and rearrangement to form advanced glycation end-products (AGEs). By and large the researchers in the past have also established that glycation and the AGEs are responsible for most type of metabolic disorders, including diabetes mellitus, cancer, neurological disorders and aging. The amassing of AGEs in the tissues of neurodegenerative diseases shows its involvement in diseases. Therefore, it is likely that inhibition of glycation reaction may extend the lifespan of an individual. The hunt for inhibitors of glycation, mainly using in vitro models, has identified natural compounds able to prevent glycation, especially polyphenols and other natural antioxidants. Extrapolation of results of in vitro studies on the in vivo situation is not straightforward due to differences in the conditions and mechanism of glycation, and bioavailability problems. Nevertheless, existing data allow postulating that enrichment of diet in natural anti-glycating agents may attenuate glycation and, in consequence may halt the aging and neurological problems.” Study Link

The following is evidence of glycations role in cardiovascular disease;

·        “Advanced Glycation End-Products Induce Apoptosis of Vascular Smooth Muscle Cells: A Mechanism for Vascular Calcification.”

“Vascular calcification, especially medial artery calcification, is associated with cardiovascular death in patients with diabetes mellitus and chronic kidney disease (CKD). To determine the underlying mechanism of vascular calcification, we have demonstrated in our previous report that advanced glycation end-products (AGEs) stimulated calcium deposition in vascular smooth muscle cells (VSMCs) through excessive oxidative stress and phenotypic transition into osteoblastic cells. Since AGEs can induce apoptosis, in this study we investigated its role on VSMC apoptosis, focusing mainly on the underlying mechanisms. A rat VSMC line (A7r5) was cultured, and treated with glycolaldehyde-derived AGE-bovine serum albumin (AGE3-BSA). Apoptotic cells were identified by Terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) staining. To quantify apoptosis, an enzyme-linked immunosorbent assay (ELISA) for histone-complexed DNA fragments was employed. Real-time PCR was performed to determine the mRNA levels. Treatment of A7r5 cells with AGE3-BSA from 100 µg/mL concentration markedly increased apoptosis, which was suppressed by Nox inhibitors. AGE3-BSA significantly increased the mRNA expression of NAD (P)H oxidase components including Nox4 and p22(phox), and these findings were confirmed by protein levels using immunofluorescence. Dihydroethidisum assay showed that compared with cBSA, AGE3-BSA increased reactive oxygen species level in A7r5 cells. Furthermore, AGE3-induced apoptosis was significantly inhibited by siRNA-mediated knockdown of Nox4 or p22 (phox). Double knockdown of Nox4 and p22 (phox) showed a similar inhibitory effect on apoptosis as single gene silencing. Thus, our results demonstrated that NAD (P)H oxidase-derived oxidative stress are involved in AGEs-induced apoptosis of VSMCs. These findings might be important to understand the pathogenesis of vascular calcification in diabetes and CKD.”

Evidence of glycation in mental disorders like schizophrenia;

·        “The regulation of soluble receptor for AGEs contributes to carbonyl stress in schizophrenia.

“Our previous study showed that enhanced carbonyl stress is closely related to schizophrenia. The endogenous secretory receptor for advanced glycation end-products (esRAGE) is a splice variant of the AGER gene and is one of the soluble forms of RAGE. esRAGE is considered to be a key molecule for alleviating the burden of carbonyl stress by entrapping advanced glycation end-products (AGEs). In the current study, we conducted genetic association analyses focusing on AGER, in which we compared 212 schizophrenic patients to 214 control subjects. We also compared esRAGE levels among a subgroup of 104 patients and 89 controls and further carried out measurements of total circulating soluble RAGE (sRAGE) in 25 patients and 49 healthy subjects. Although the genetic association study yielded inconclusive results, multiple regression analysis indicated that a specific haplotype composed of rs17846798, rs2071288, and a 63 bp deletion, which were in perfect linkage disequilibrium (r2 = 1), and rs2070600 (Gly82Ser) were significantly associated with a marked decrease in serum esRAGE levels. Furthermore, compared to healthy subjects, schizophrenia showed significantly lower esRAGE (p = 0.007) and sRAGE (p = 0.03) levels, respectively. This is the first study to show that serum esRAGE levels are regulated by a newly identified specific haplotype in AGER and that a subpopulation of schizophrenic patients are more vulnerable to carbonyl stress. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.” Study Link

Evidence of glycation in renal disease and kidney cancer;

·        Growth arrest specific 2-like protein 1 expression is upregulated in podocytes through advanced  glycation end-products.

“BACKGROUND:

Growth arrest specific 2-like protein 1 (GAS2L1) protein is a member of the GAS2 family of proteins, known to regulate apoptosis and cellular cytoskeleton reorganization in different cells. Recently we identified that Gas2l1 gene expression in podocytes is influenced by advanced glycation end product-bovine serum albumin(AGE-BSA).

METHODS:

The study was performed employing cultured podocytes and diabetic (db/db) mice, a model of type 2 diabetes. Akbuminuria as well as urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion as measured with specific ELISAs. Gene expression was analyzed via semiquantitative and real-time polymerase chain reaction. The protein levels were determined by western blotting and immunostaining.

RESULTS:

We found that the Gas2l1α isoform is expressed in podocytes. Treatment with AGE-BSA induced Gas2l1α and Gas2 mRNA levels compared with controls incubated with non-glycated control BSA (Co-BSA). Moreover, application of the recombinant soluble receptor of AGEs (sRAGE), a competitor of cellular RAGE, reversed the AGE-BSA effect. Interestingly, AGE-BSA also increased the protein levels of GAS2L1α in a RAGE-dependent manner, but did not affect the GAS2 expression. Periodic acid-Schiff staining and albuminuria as well as urinary NGAL excretion revealed that db/db mice progressively developed diabetic nephropathy with renal accumulation of Nε-carboxy-methyl-lysine (immunohistochemistry, western blots). Analyses of GAS2L1α and GAS2 proteins in diabetic mice revealed that both were significantly elevated relative to their non-diabetic littermates. In addition, GAS2L1α and GAS2 proteins positively correlated with the accumulation of AGEs in the blood plasma of diabetic mice and the administration of sRAGE in diabetic mice reduced the glomerular expression of both proteins.

CONCLUSIONS:

We show for the first time that the protein expression of GAS2L1α in vitro and in vivo is regulated by the AGE-RAGE axis. The suppression of AGE ligation with their RAGE in diabetic mice with progressive nephropathy reversed the GAS2L1α expression, thus suggesting a role of GAS2L1α in the development of diabetic disease, which needs to be further elucidated. © The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA.” Study Link

Methylglyoxal is what makes up pyruvic acid which is a foundation for energy expenditure. It comes from glycogen which comes from glucose and can be made into lipids to be used for cholesterol or glucose to be used by your brain when it the ketones aren’t enough to power all lobes in the brain. This the link from glucose to disease through its conversion to AGEs, advanced glycation endproducts as explained by this study published Sep, 2016;

“Glucose and fructose metabolism originates the highly reactive by product methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE). The MG has been implicated in classical diabetic complications such as retinopathy, nephropathy, and neuropathy, but has also been recently associated with cardiovascular diseases and central nervous system disorders such as cerebrovascular diseases and dementia. Recent studies even suggested its involvement in insulin resistance and beta-cell dysfunction, contributing to the early development of type 2 diabetes and creating a vicious circle between glycation and hyperglycemia. Despite several drugs and natural compounds have been identified in the last years in order to scavenge MG and inhibit AGE formation, we are still far from having an effective strategy to prevent MG-induced mechanisms. This review summarizes the endogenous and exogenous sources of MG, also addressing the current controversy about the importance of exogenous MG sources. The mechanisms by which MG changes cell behavior and its involvement in type 2 diabetes development and complications and the pathophysiological implication are also summarized. Particular emphasis will be given to pathophysiological relevance of studies using higher MG doses, which may have produced biased results. Finally, we also overview the current knowledge about detoxification strategies, including modulation of endogenous enzymatic systems and exogenous compounds able to inhibit MG effects on biological systems.”  Study Link

Evidence of glycations influence in pancreatic cancer;

·        AdvancedGlycationEnd Products Impair Glucose-Stimulated Insulin Secretion of a Pancreatic β-Cell Line INS-1-3 by Disturbance of Microtubule Cytoskeleton via p38/MAPK Activation.

Advanced glycation end products (AGEs) are believed to be involved in diverse complications of diabetes mellitus. Overexposure to AGEs of pancreatic β-cells leads to decreased insulin secretion and cell apoptosis. Here, to understand the cytotoxicity of AGEs to pancreatic β-cells, we used INS-1-3 cells as a β-cell model to address this question, which was a subclone of INS-1 cells and exhibited high level of insulin expression and high sensitivity to glucose stimulation. Exposed to large dose of AGEs, even though more insulin was synthesized, its secretion was significantly reduced from INS-1-3 cells. Further, AGEs treatment led to a time-dependent increase of depolymerized microtubules, which was accompanied by an increase of activated p38/MAPK in INS-1-3 cells. Pharmacological inhibition of p38/MAPK by SB202190 reversed microtubule depolymerization to a stabilized polymerization status but could not rescue the reduction of insulin release caused by AGEs. Taken together, these results suggest a novel role of AGEs-induced impairment of insulin secretion, which is partially due to a disturbance of microtubule dynamics that resulted from an activation of the p38/MAPK pathway.” Study Link

In my estimation this is the worst manifestation of bread in the diet. Amyloid plaque is at the root of most modern diseases, ranging from cancer to heart disease to arthritis to Alzheimer’s disease and Parkinson’s disease;

·        Glycationinduced generation of amyloid fibril structures by glucose metabolites.

“The non-enzymatic reaction (glycation) of reducing sugars with proteins has received increased interest in dietary and therapeutic research lately. In the present work, the impact of glycation on structural alterations of camel serum albumin (CSA) by different glucose metabolites was studied. Glycation of CSA was evaluated by specific fluorescence of advanced glycation end-products (AGEs) and determination of available amino groups. Further, conformational changes in CSA during glycation were also studied using 8-analino 1-nephthlene sulfonic acid (ANS) binding assay, circular dichroism (CD) and thermal analysis. Intrinsic fluorescence measurement of CSA showed a 22 nm red shift after methylglyoxal treatment, suggesting glycation induced denaturation of CSA. Rayleigh scattering analysis showed glycation induced turbidity and aggregation in CSA. Furthermore, ANS binding to native and glycated-CSA reflected perturbation in the environment of hydrophobic residues. However, CD spectra did not reveal any significant modifications in the secondary structure of the glycated-CSA. Thioflavin T (ThT) fluorescence of CSA increased after glycation, illustrated cross β-structure and amyloid formation. Transmission electron microscopy (TEM) analysis further reaffirms the formation of aggregate and amyloid. In summary, glucose metabolites induced conformational changes in CSA and produced aggregate and amyloid structures.”

This is more evidence of glycation’s involvement in Alzheimer’s disease. This report was submitted on Aug 24 2016, have you heard anything about this yet? Who doesn’t want you to know? Who has interests in selling your medication for memory loss? How would you learn this information if you didn’t see it here? Do you know where to look for it? Do you even know to look for it? Am I fishing or can this be a conspiracy?

·        HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers of neuroinflammation and progression to neurodegeneration in Alzheimer’s disease.

“BACKGROUND:

The blood-brain barrier (BBB) dysfunction represents an early feature of Alzheimer’s disease (AD) that precedes the hallmarks of amyloid beta (amyloid β) plaque deposition and neuronal neurofibrillary tangle (NFT) formation. A damaged BBB correlates directly with neuroinflammation involving microglial activation and reactive astrogliosis, which is associated with increased expression and/or release of high-mobility group box protein 1 (HMGB1) and thrombin. However, the link between the presence of these molecules, BBB damage, and progression to neurodegeneration in AD is still elusive. Therefore, we aimed to profile and validate non-invasive clinical biomarkers of BBB dysfunction and neuroinflammation to assess the progression to neurodegeneration in mild cognitive impairment (MCI) and AD patients.

METHODS:

We determined the serum levels of various proinflammatory damage-associated molecules in aged control subjects and patients with MCI or AD using validated ELISA kits. We then assessed the specific and direct effects of such molecules on BBB integrity in vitro using human primary brain microvascular endothelial cells or a cell line.

RESULTS:

We observed a significant increase in serum HMGB1 and soluble receptor for advanced glycation end products (sRAGE) that correlated well with amyloid beta levels in AD patients (vs. control subjects). Interestingly, serum HMGB1 levels were significantly elevated in MCI patients compared to controls or AD patients. In addition, as a marker of BBB damage, soluble thrombomodulin (sTM) antigen, and activity were significantly (and distinctly) increased in MCI and AD patients. Direct in vitro BBB integrity assessment further revealed a significant and concentration-dependent increase in paracellular permeability to dextrans by HMGB1 or α-thrombin, possibly through disruption of zona occludins-1 bands. Pre-treatment with anti-HMGB1 monoclonal antibody blocked HMGB1 effects and leaving BBB integrity intact.

CONCLUSIONS:

Our current studies indicate that thrombin and HMGB1 are causal proximate proinflammatory mediators of BBB dysfunction, while sTM levels may indicate BBB endothelial damage; HMGB1 and sRAGE might serve as clinical biomarkers for progression and/or therapeutic efficacy along the AD spectrum.” Study Link

More evidence of the damaging effects of glycation was submitted July15, 2016. Have you heard anything about this report yet?

“The incidence of food allergy has increased dramatically in the last few decades in westernized developed countries. We propose that the Western lifestyle and diet promote innate danger signals and immune responses through production of “alarmins. Alarmins are endogenous molecules secreted from cells undergoing nonprogrammed cell death that signal tissue and cell damage. High molecular group S (HMGB1) is a major alarmin that binds to the receptor for advanced glycation end-products (RAGE). Advanced glycation end-products (AGEs) are also present in foods. We propose the “false alarm” hypothesis, in which AGEs that are present in or formed from the food in our diet are predisposing to food allergy. The Western diet is high in AGEs, which are derived from cooked meat, oils, and cheese. AGEs are also formed in the presence of a high concentration of sugars. We propose that a diet high in AGEs and AGE-forming sugars results in misinterpretation of a threat from dietary allergens, promoting the development of food allergy. AGEs and other alarmins inadvertently prime innate signaling through multiple mechanisms, resulting in the development of allergic phenotypes. Current hypotheses and models of food allergy do not adequately explain the dramatic increase in food allergy in Western countries. Dietary AGEs and AGE-forming sugars might be the missing link, a hypothesis supported by a number of convincing epidemiologic and experimental observations, as discussed in this article.” Study Link

The author  of this report isn’t fully aware of what causes glycation. He still thinks that protein and fat are important as they are what gets glycated, but they’re not the important factor in this equation. It’s the glucose that’s important, as it’s the glucose that does the glycating. If one were to remove the glucose, they’d remove the glycation.

Again no alert about this evidence of the influence of glycation in dementia submitted in Aug 2016 from the Oxford Journal of Gerontology;

·        Inflammatory Biomarkers Predict Domain-Specific Cognitive Decline in Older Adults.

“BACKGROUND:

Vascular risk factors, including inflammation, may contribute to dementia development. We investigated the associations between peripheral inflammatory biomarkers and cognitive decline in five domains (memory, construction, language, psychomotor speed, and executive function).

METHODS:

Community-dwelling older adults from the Ginkgo Evaluation of Memory Study (n = 1,159, aged 75 or older) free of dementia at baseline were included and followed for up to 7 years. Ten biomarkers were measured at baseline representing different sources of inflammation: vascular inflammation (pentraxin 3 and serum amyloid P), endothelial function (endothelin-1), metabolic function (adiponectin, resistin, and plasminogen activating inhibitor-1), oxidative stress (receptor for advanced glycation end products), and general inflammation (interleukin-6, interleukin-2, and interleukin-10). A combined z-score was created from these biomarkers to represent total inflammation across these sources. We utilized generalized estimating equations that included an interaction term between z-scores and time to assess effect of inflammation on cognitive decline, adjusting for demographics (such as age, race/ethnicity, and sex), cardiovascular risk factors, and apolipoprotein E ε4 carrier status. A Bonferroni-adjusted significance level of .01 was used. We explored associations between individual biomarkers and cognitive decline without adjustment for multiplicity.

RESULTS:

The combined inflammation z-score was significantly associated with memory and psychomotor speed (p < .01). Pentraxin 3, serum amyloid P, endothelin-1, and interleukin-2 were associated with change in at least one cognitive domain (p < .05).

CONCLUSION:

Our results suggest that total inflammation is associated with memory and psychomotor speed. In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals. © The Author 2016. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved.”        Study Link

Are you beginning to wonder why we’ve never been informed of these dangers? Evidence below of glycation in lung cancer was submitted on Aug9, 2016. I’ve not heard anything about this. Doesn’t the ACS care? They’re still recommending carbs in the diet, so they must not;

“Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 μmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4-16 μmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-β1. CML or pentosidine at 2-16 μmol/L up-regulated the protein expression of AGE receptor, p47(phox), intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4-16 μmol/L. These two AGEs at 2-16 μmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4-16 μmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis.” Study Link

This is the evidence of your back problems being caused by glycation. This study shows how the inflammatory responses to glycation causing vertebral disk degeneration;

“Inflammation and cytokines have been recognized to correlate with intervertebral disc (IVD) degeneration (IDD), via mediating the development of clinical signs and symptoms. However, the regulation mechanism remains unclear. We aimed at investigating the regulatory role of interleukin (IL)β and high mobility group box 1 (HMGB1) in the inflammatory response in human IVD cells, and then explored the signaling pathways mediating such regulatory effect. Firstly, the promotion to inflammatory cytokines in IVD cells was examined with ELISA method. And then western blot and real time quantitative PCR were performed to analyze the expression of toll-like receptors (TLRs), receptors for advanced glycation endproducts (RAGE) and NF-κB signaling markers in the IL-1β- or (and) HMGB1-treated IVD cells. Results demonstrated that either IL-1β or HMGB1 promoted the release of the inflammatory cytokines such as prostaglandin E2 (PGE2), TNF-α, IL-6 and IL-8 in human IVD cells. And the expression of matrix metalloproteinases (MMPs) such as MMP-1, -3 and -9 was also additively up-regulated by IL-1β and HMGB1. We also found such additive promotion to the expression of TLR-2, TLR-4 and RAGE, and the NF-κB signaling in intervertebral disc cells. In summary, our study demonstrated that IL-1β and HMGB1 additively promotes the release of inflammatory cytokines and the expression of MMPs in human IVD cells. The TLRs and RAGE and the NF-κB signaling were also additively promoted by IL-1β and HMGB1. Our study implied that the additive promotion by IL-1β and HMGB1 to inflammatory cytokines and MMPs might aggravate the progression of IDD.”  Study Link

Even unborn babies are not immune to the effects if glycation;

·        Accumulation of AdvancedGlycationEnd Products Involved in Inflammation and Contributing to Severe Preeclampsia, in Maternal Blood, Umbilical Blood and Placental Tissues.

 

Ovarian cancer is a consequence of glycation;

S100B is one of the members of the S100 protein family and is involved in the progression of a variety of cancers. Ovarian cancer is driven by cancer stem-like cells (CSLCs) that are involved in tumor genesis, metastasis, chemo-resistance and relapse. We then hypothesized that S100B might exert pro-tumor effects by regulating ovarian CSLCs stemness, a key characteristic of CSLCs. First, we observed the high expression of S100B in ovarian cancer specimens when compared to that in normal ovary. The S100B upregulation associated with more advanced tumor stages, poorer differentiation and poorer survival. In addition, elevated S100B expression correlated with increased expression of stem cell markers including CD133, Nanog and Oct4. Then, we found that S100B was preferentially expressed in CD133+ ovarian CSLCs derived from both ovarian cancer cell lines and primary tumors of patients. More importantly, we revealed that S100B knockdown suppressed the in vitro self-renewal and in vivo tumorigenicity of ovarian CSLCs and decreased their expression of stem cell markers. S100B ectopic expression endowed non-CSLCs with stemness, which has been demonstrated with both in vitro and in vivo experiments. Mechanically, we demonstrated that the underlying mechanism of S100B-mediated effects on CSLCs stemness was not dependent on its binding with a receptor for advanced glycation end products (RAGE), but might be through intracellular regulation, through the inhibition of p53 expression and phosphorylation. In conclusion, our results elucidate the importance of S100B in maintenance of ovarian CSLCs stemness, which might provide a promising therapeutic target for ovarian cancer. Stem Cells 2016.”  Study Link

This study looks at the AGEs responsible for inflammatory bowel disease and Rheumatoid arthritis;

Neutrophils and monocytes belong to the first line of immune defence cells and are recruited to sites of inflammation during infection or sterile injury. Both cells contain huge amounts of the heterodimeric protein S100A8/A9 in their cytoplasm. S100A8/A9 belongs to the Ca2+ binding S100 protein family and has recently gained a lot of interest as a critical alarmin modulating the inflammatory response after its release (extracellular S100A8/A9) from neutrophils and monocytes. Extracellular S100A8/A9 interacts with the pattern recognition receptors Toll-like receptor 4 (TLR4) and Receptor for Advanced Glycation Endproducts (RAGE) promoting cell activation and recruitment. Besides its biological function, S100A8/A9 (also known as myeloid related protein 8/14, MRP8/14) was identified as interesting biomarker to monitor disease activity in chronic inflammatory disorders including inflammatory bowel disease and rheumatoid arthritis. Furthermore, S100A8/A9 has been tested successfully in pre-clinical imaging studies to localize sites of infection or sterile injury. Finally, recent evidence using small molecule inhibitors for S100A8/A9 also suggests that blocking S100A8/A9 activity exerts beneficial effects on disease activity in animal models of autoimmune diseases including multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease. This review will provide a comprehensive and detailed overview into the structure and biological function of S100A8/A9 and also will give an outlook in terms of diagnostic and therapeutic applications targeting S100A8/A9.        Study Link

HMGB1 is a label that’s been assigned to a type of AGE or RAGE. It’s importance lies in its ability to create pain in your body. This is one of over 4976 warnings and notices of what glycation does to the body that available for your perusal on the effects of glycation on PubMed;

Neuropathic pain (NPP) is intolerable, persistent, and specific type of long-term pain. It is considered to be a direct consequence of pathological changes affecting the somatosensory system and can be debilitating for affected patients. Despite recent progress and growing interest in understanding the pathogenesis of the disease, NPP still presents a major diagnostic and therapeutic challenge. High mobility group box 1 (HMGB1) mediates inflammatory and immune reactions in nervous system and emerging evidence reveals that HMGB1 plays an essential role in neuroinflammation through receptors such as Toll-like receptors (TLR), receptor for advanced glycation end products (RAGE), C-X-X motif chemokines receptor 4 (CXCR4), and N-methyl-D-aspartate (NMDA) receptor. In this review, we present evidence from studies that address the role of HMGB1 in NPP. First, we review studies aimed at determining the role of HMGB1 in NPP and discuss the possible mechanisms underlying HMGB1-mediated NPP progression where receptors for HMGB1 are involved. Then we review studies that address HMGB1 as a potential therapeutic target for NPP.             Study Link

The following study was completed in July 2010, explaining the health benefits of calorie restriction. This is what was being researched over 120 years ago, as ketonuria was noticed in the urine of fasting patients, giving them ketonemia. This is a condition that best serves healing in the body for multiple reasons and has been shown to heal many diseases, simply from fasting. Since 500BC fasting has been used to cure many diseases with astonishing success. This is what’s known as ketosis today and is what your body goes through as a healing, fat burning type of metabolism. It uses your own fat to provide everything from hormones to glucose, through gluconeogenesis, the perfect glucose for the body as it made from your fat, making it a clean glucose source;

The societal impact of obesity, diabetes, and other metabolic disorders continues to rise despite increasing evidence of their negative long-term consequences on health span, longevity, and aging. Unfortunately, dietary management and exercise frequently fail as remedies, underscoring the need for the development of alternative interventions to successfully treat metabolic disorders and enhance life span and health span. Using calorie restriction (CR)—which is well known to improve both health and longevity in controlled studies—as their benchmark, gerontologists are coming closer to identifying dietary and pharmacological therapies that may be applicable to aging humans. This review covers some of the more promising interventions targeted to affect pathways implicated in the aging process as well as variations on classical CR that may be better suited to human adaptation.

Another report submitted Nov, 08 to the Official Journal of the International League Against Epilepsy, basically said the same thing while they were looking for the best way to approach putting the body into ketosis;

The ketogenic diet (KD) is a 90% fat diet that is an effective treatment for intractable epilepsy. Rapid initiation of the KD requires hospital admission because of the complexity of the protocol and frequent mild and moderate adverse events. The purpose of the study was to compare the efficacy of a gradual KD initiation with the standard KD initiation preceded by a 24- to 48-h fast.

Perhaps the most damning report against aging was issued in January of 1984, yet nothing was mentioned about this report; it was one of the first indications of what glycation does to the body and with a major cause of glycation being glucose or sugar, I have to wonder why the FDA didn’t say anything about it then. Why weren’t we, at least, informed about this study? Industry concerns?

·       Collagen aging in vitro by nonenzymatic glycosylation and browning.

Aging and diabetes mellitus are associated with cross-linking and nonenzymatic glycosylation of collagen. Incubation of tendon fibers with reducing sugars results in increased breaking time in urea similar to that seen in aging, and in nonenzymatic glycosylation and browning. Effect of a sugar is proportional to the amount of sugar available in the open chain form. The increase in breaking time correlates with the appearance of chromophores characteristic of crosslinked browning products. Collagen altered by nonenzymatic browning may play a role in some age-like major complications of diabetes.   Study Link

This evidence of glycation’s role in atherosclerosis was in this study submitted in May 1988. Was this publicized? Did you hear about this? Did the FDA know?

Adhesion of bovine endothelial cells on fibronectin and collagen before and after nonenzymatic glycation in vitro has been studied. Nonenzymatic glycation of these proteins reduced their ability to bind endothelial cells. Furthermore, nonenzymatically glycated fibronectin failed to bind to normal and nonenzymatically glycated gelatin and to fibrin. So gelatin and fibrin Sepharoses can be used to separate highly glycated fibronectins from fibronectins with a low degree of nonenzymatic glucose substitution. Sodium dodecylsulfate polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidences for the role of nonenzymatic glycation of proteins in the development of vascular complications in long-term diabetes and of atherosclerosis.              Study Link

This shows the damage done by glycation on the blood. I posted this study because I wanted to note what the first sentence states, that this damage, at the time of publication, had been known for 20 years. The date on this study is marked as July 29, 1988. That means that his damage was discovered in 1968, 48 years ago.

The association between elevated levels of glycated haemoglobins and diabetes mellitus has been known for twenty years [92]. Since then the determination of glycated haemoglobins has become a valuable tool for the objective assessment of long-term glycaemia in diabetic patients. The marked clinical interest in reliable measurements of glycated haemoglobins has stimulated the development and perfection of the necessary methodology. Limitations of the techniques have led to investigation of the underlying causes. Some of them led to the recognition of processes that were not known to occur in vivo before, such as glycation at sites other than the amino terminus of the beta-chains, modification of haemoglobin by reactants other than glucose or the existence of labile haemoglobin adducts. With ideal methodology these features would have gone unnoticed. Furthermore, the determination of glycated haemoglobin in large populations of diabetic patients has lead to the discovery of new, clinically silent mutant haemoglobins. Today, the routine determination of glycated haemoglobins in diabetic patients probably represents the broadest screening for mutant haemoglobins. The experience with glycated haemoglobins shows that overcoming difficulties in their determination, and progress in biomedical research, are closely intertwined.

This study shows how proteins exposed to glucose undergoes oxidative stress, the basis of aging;

Studies have shown that glycation in vitro is complicated by the ability of glucose to oxidise, in the presence of trace amounts of transition metal, generating protein-reactive ketoaldehydes, hydrogen peroxide and diverse free radicals. Protein exposed to glucose undergoes fragmentational and conformational alterations, and these, as well as thiol oxidation, appear to be caused by hydroxyl radicals. Glycofluorophore formation is dependent upon ketoaldehyde formation. It is suggested that glucose autoxidation contributes to oxidative stress in pathophysiology associated with diabetes and ageing via this newly described process of “autoxidative glycosylation”.

The following report from Oct 30 1981 shows the effects of glycation on cholesterol, LDL particles particularly and how it leads to atherosclerosis ;

Atherosclerosis occurs at an accelerated rate in patients with diabetes mellitus. Since some proteins undergo nonenzymatic glycosylation in diabetic patients and because certain chemical modifications of low density lipoproteins produced alterations in their interactions with certain cultured cells, a fact that may be relevant to atherogenesis, we investigated the effect of in vitro glycosylation on cell-related properties of low density lipoproteins. Glycosylation was carried out by incubating LDL (1-10 mg LDL-protein/ml) with glucose (0-100 mM) in 0.5 M phosphate buffer, pH 8.0, at 37 degrees C. The amount of glucose incorporated into LDL after 1-2 wk of incubation was estimated to be in the range of 1-10 mol/mol LDL-protein. Amino acid analysis of glycosylated LDL showed that glucose was covalently bound to lysine residues. In studies with cultured human fibroblasts, glycosylated LDL was internalized and degraded significantly less than control LDL, in proportion to the estimated degree of glycosylation (12% of control for the most extensively glycosylated LDL). Glycosylation of LDL also impaired significantly its ability to stimulate cholesteryl ester synthesis by cultured fibroblasts. Glycosylated LDL did not stimulate cholesteryl ester synthesis in rat peritoneal macrophages. If glycosylation of LDL occurs in diabetic patients, some pathophysiologic consequences related to the increased incidence of atherosclerosis in these patients may result.

Study Link

In 1981 this was discovered, yet it’s been 35 years since then and yet few people are aware of this. My question is, why?  Maybe I should ask the sugar industry.

The following study shows the how the adhesive qualities of glucose creates fibrinogen, which becomes a target for glycation;

·        Polymerisation and crosslinking of fibrin monomers in diabetes mellitus

Polymerisation and crosslinking of fibrin monomers was studied in 35 healthy volunteers and in 42 poorly controlled diabetic patients. Polymerisation did not show any difference between control subjects (n = 10) and diabetic patients (n = 11) (p greater than 0.1), although fibrinogen was 35% more glycated in the diabetic patients (p less than 0.001). Alpha chain crosslinking in the diabetic patients, however, was impaired as is shown from an increase in intermediate alpha polymers with a concomitant decrease in alpha monomer disappearance. A significant positive correlation was found between the degree of glycation of fibrinogen and the defective alpha chain polymerisation (r = 0.86, p less than 0.005). These results were consistent with the results of thrombin and reptilase experiments. The reaction rate with reptilase did not show any difference between the two groups (p greater than 0.1), whereas the reaction rate with thrombin was significantly slower in the diabetic group compared to the control subjects (p less than 0.001). Purified fibrin clots obtained from the diabetic patients were more susceptible to plasmin than clots obtained from control subjects. It is concluded that in poorly controlled diabetic patients polymerisation of fibrin monomers is normal, but crosslinking of the alpha chains is impaired, leading to a higher susceptibility of the clots to plasmin degradation.

From Wikipedia on Fibrinogen;

Fibrinogen (factor I) is a glycoprotein in vertebrates that helps in the formation of blood clots. It consists of a linear array of three nodules held together by a very thin thread which is estimated to have a diameter between 8 and 15 Angstrom (Å). The two end nodules are alike but the center one is slightly smaller. Measurements of shadow lengths indicate that nodule diameters are in the range 50 to 70 Å. The length of the dried molecule is 475 ± 25 Å.[2]

·        Effect of  of low-density lipoprotein on the immunological determination glycation of apolipoprotein B.

Non-enzymatic glycation of low-density lipoprotein (LDL) may contribute to the premature atherogenesis of patients with diabetes mellitus. To assess whether  glycation of apolipoprotein B, the predominant protein of LDL, interferes with the ability to immunologically quantify this protein, we prepared and purified glycated LDL by incubating normal plasma samples with high concentrations of glucose. Although both the plasma and the LDL specimens incubated with glucose contained significantly more glycated protein than control specimens, the quantitative interaction of an apolipoprotein B-specific antibody with glycated vs nonglycated LDL was not significantly different. We conclude that apolipoprotein B can be accurately quantified immunologically despite the presence of clinically excessive degrees of LDL glycation.

Study Link

I included the following study from November 1989 because of its explanation of how glycation is responsible for inflammation;

·        Changes in concanavalin A-reactive proteins in inflammatory disorders.

Quantitative changes of concanavalin A (Con A)-reactive proteins in serum samples obtained from rats with induced inflammation and from patients with inflammatory and autoimmune diseases were examined by use of lectin blots. Treatment of rats with a single dose of fermented yeast to induce inflammation caused an extensive increase in Con A-reactivity. These changes were time dependent and were similar in both sexes of the animals. When we examined serum samples obtained from patients with various inflammatory disorders for their Con A-reactive proteins as compared with normal donors, we noted that the Con A-reactivity increased in patients with rheumatoid arthritis and systemic lupus erythematosus. Among all the glycoproteins examined by lectin blots with use of Con A, a set of five proteins was selected for detailed analysis by densitometric scanning. These included alpha 2-macroglobulin, P-150, P-95, P-40, and P-35, of Mr 180,000, 150,000, 95,000, 40,000, and 35,000, respectively, by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions. Densitometric scanning analysis of the lectin blots revealed that the Con A-reactivity of these proteins increased during inflammation. Because alpha 2-macroglobulin is not an acute-phase protein in humans, an increase in Con A staining of this protein suggested that altered glycation is associated with autoimmune diseases. Thus, study of changes in Con A-reactive proteins in human sera may facilitate our understanding of the etiology and pathophysiology of autoimmune diseases.                  Study Link

·        Clinical Value of High Mobility Group Box 1 and the Receptor for Advanced Glycation End-products in Head and Neck Cancer: A Systematic Review.

Abstract Introduction High mobility group box 1 is a versatile protein involved in gene transcription, extracellular signaling, and response to inflammation. Extracellularly, high mobility group box 1 binds to several receptors, notably the receptor for advanced glycation end-products. Expression of high mobility group box 1 and the receptor for advanced glycation end-products has been described in many cancers. Objectives To systematically review the available literature using PubMed and Web of Science to evaluate the clinical value of high mobility group box 1 and the receptor for advanced glycation end-products in head and neck squamous cell carcinomas. Data synthesis A total of eleven studies were included in this review. High mobility group box 1 overexpression is associated with poor prognosis and many clinical and pathological characteristics of head and neck squamous cell carcinomas patients. Additionally, the receptor for advanced glycation end-products demonstrates potential value as a clinical indicator of tumor angiogenesis and advanced staging. In diagnosis, high mobility group box 1 demonstrates low sensitivity. Conclusion High mobility group box 1 and the receptor for advanced glycation end-products are associated with clinical and pathological characteristics of head and neck squamous cell carcinomas. Further investigation of the prognostic and diagnostic value of these molecules is warranted.”

“Diabetes is frequently associated with cardiovascular diseases (coronary heart disease, cerebrovascular disease, peripheral vascular disease), and several risk factors have been proposed. Recent studies have strengthened the importance of chronic hyperglycemia because this modifies a variety of circulating substances including lipoproteins, and the glycosylated ones can be involved in the process of accelerating atherosclerosis. In this review, previous studies indicating the significance of glycosylated lipoproteins in the progression of atherosclerosis were overviewed. We also discussed AGE (advanced glycation end products) which may play an important role of atherogenesis in diabetes.”The most recent study, submitted in October 2016 reveals some of the known damage that glycation is responsible for;

·        Relationship between plasma glycation with membrane modification, oxidative stress and expression of glucose trasporter-1 in type 2 diabetes patients with vascular complications.

BACKGROUND OF STUDY:

Enhanced protein glycation in diabetes causes irreversible cellular damage through membrane modifications. Erythrocytes are persistently exposed to plasma glycated proteins; however, little are known about its consequences on membrane. Aim of this study was to examine the relationship between plasma protein glycation with erythrocyte membrane modifications in type 2 diabetes patients with and without vascular complications.

METHOD:

We recruited 60 healthy controls, 85 type 2 diabetic mellitus (DM) and 75 type 2 diabetic patients with complications (DMC). Levels of plasma glycation adduct with antioxidants (fructosamine, protein carbonyl, β-amyloids, thiol groups, total antioxidant status), erythrocyte membrane modifications (protein carbonyls, β-amyloids, free amino groups, erythrocyte fragility), antioxidant profile (GSH, catalase, lipid peroxidation) and Glut-1 expression were quantified.

RESULT:

Compared with controls, DM and DMC patients had significantly higher level of glycation adducts, erythrocyte fragility, lipid peroxidation and Glut-1 expression whereas declined levels of plasma and cellular antioxidants. Correlation studies revealed positive association of membrane modifications with erythrocyte sedimentation rate, fragility, peroxidation whereas negative association with free amino groups, glutathione and catalase.

CONCLUSION:

Our data suggest that plasma glycation is associated with oxidative stress, Glut-1 expression and erythrocyte fragility in DM patients. This may further contribute to progression of vascular complications.

More evidence of the role glucose plays in brain degradation;

Protein glycation is an age-dependent posttranslational modification associated with several neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases. By modifying amino-groups, glycation  interferes with folding of proteins, increasing their aggregation potential. Here, we studied the effect of pharmacological and genetic manipulation of glycation on huntingtin (HTT), the causative protein in Huntington’s disease (HD). We observed that glycation increased the aggregation of mutant HTT exon 1 fragments associated with HD (HTT72Q and HTT103Q) in yeast and mammalian cell models. We found that glycation impairs HTT clearance thereby promoting its intracellular accumulation and aggregation. Interestingly, under these conditions autophagy increased and the levels of mutant HTT released to the culture medium decreased. Furthermore, increased  glycation enhanced HTT toxicity in human cells and neurodegeneration in fruit flies, impairing eclosion and decreasing life span. Overall, our study provides evidence that glycation modulates HTT exon-1 aggregation and toxicity, and suggests it may constitute a novel target for therapeutic intervention in HD.

Evidence of the glycative effects in Cataracts was know in the fall of 1974, yet nothing was said that I can remember, but then I was just getting out of Jr College then;

J Clin Invest. 1984 Nov;74(5):1742-9.

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

We have examined the nonenzymatic glycation of human lens crystallin, an extremely long-lived protein, from 16 normal human ocular lenses 0.2-99 yr of age, and from 11 diabetic lenses 52-82-yr-old. The glucitol-lysine (Glc-Lys) content of soluble and insoluble crystallin was determined after reduction with H-borohydride followed by acid hydrolysis, boronic acid affinity chromatography, and high pressure cation exchange chromatography. Normal lens crystallin, soluble and insoluble, had 0.028 +/- 0.011 nanomoles Glc-Lys per nanomole crystallin monomer. Soluble and insoluble crystallins had equivalent levels of glycation. The content of Glc-Lys in normal lens crystallin increased with age in a linear fashion. Thus, the nonenzymatic glycation of nondiabetic lens crystallin may be regarded as a biological clock. The diabetic lens crystallin samples (n = 11) had a higher content of Glc-Lys (0.070 +/- 0.034 nmol/nmol monomer). Over an age range comparable to that of the control samples, the diabetic crystallin samples contained about twice as much Glc-Lys. The Glc-Lys content of the diabetic lens crystallin samples did not increase with lens age.

This study look at the effects of glycation on your eyes and the cataracts is responsible for. Yes glycation and a glucose diet will buy you cataracts. My mother had two of them. A good who loved to eat her bread had cataracts in both of her eyes as well. What’s interesting, this person was always complaining of headaches and stomach aches, both manifestations of an ECC diet. Again, here is more evidence of the glycative and addictive effects of a grain diet.

The following report provides evidence of glycation’s role in Leukemia.

Extracellular HMGB1 promotes differentiation of nurse-like cells in chronic lymphocytic leukemia.

“Chronic lymphocytic leukemia (CLL) is a disease of an accumulation of mature B cells that are highly dependent on the microenvironment for maintenance and expansion. However, little is known regarding the mechanisms whereby CLL cells create their favorable microenvironment for survival. High-mobility group protein B-1 (HMGB1) is a highly conserved nuclear protein that can be actively secreted by innate immune cells and passively released by injured or dying cells. We found significantly increased HMGB1 levels in the plasma of CLL patients compared with healthy controls, and HMGB1 concentration is associated with absolute lymphocyte count. We therefore sought to determine potential roles of HMGB1 in modulating the CLL microenvironment. CLL cells passively released HMGB1, and the timing and concentrations of HMGB1 in the medium were associated with differentiation of nurse-like cells (NLCs). Higher CD68 expression in CLL lymph nodes, one of the markers for NLCs, was associated with shorter overall survival of CLL patients. HMGB1-mediated NLC differentiation involved internalization of both receptor for advanced  glycation end products (RAGE) and Toll-like receptor-9 (TLR9). Differentiation of NLCs can be prevented by blocking the HMGB1-RAGE-TLR9 pathway. In conclusion, this study demonstrates for the first time that CLL cells might modulate their microenvironment by releasing HMGB1.”         Free PMC Article

J Clin Invest. 1984 Nov;74(5):1742-9.

After searching these last few disorders I got a yen to search any disorder & glycation, and glycation turned up in everything except halitosis. The following report shows its involvement in stomach ulcers. I originally searched just ulcers and got back 30 studies showing involvement. The first few studies in the list were reports on foot ulcers, so I search stomach ulcers and found 3 studies, the following report was the first;

High-mobility group box 1 (HMGB1) was initially discovered as a nuclear protein that interacts with DNA as a chromatin-associated non-histone protein to stabilize nucleosomes and to regulate the transcription of many genes in the nucleus. Once leaked or actively secreted into the extracellular environment, HMGB1 activates inflammatory pathways by stimulating multiple receptors, including Toll-like receptor (TLR) 2, TLR4, and receptor for advanced glycation end products (RAGE), leading to tissue injury. Although HMGB1’s ability to induce inflammation has been well documented, no studies have examined the role of HMGB1 in wound healing in the gastrointestinal field. The aim of this study was to evaluate the role of HMGB1 and its receptors in the healing of gastric ulcers. We also investigated which receptor among TLR2, TLR4, or RAGE mediates HMGB1’s effects on ulcer healing. Gastric ulcers were induced by serosal application of acetic acid in mice, and gastric tissues were processed for further evaluation. The induction of ulcer increased the immunohistochemical staining of cytoplasmic HMGB1 and elevated serum HMGB1 levels. Ulcer size, myeloperoxidase (MPO) activity, and the expression of tumor necrosis factor α (TNFα) mRNA peaked on day 4. Intraperitoneal administration of HMGB1 delayed ulcer healing and elevated MPO activity and TNFα expression. In contrast, administration of anti-HMGB1 antibody promoted ulcer healing and reduced MPO activity and TNFα expression. TLR4 and RAGE deficiency enhanced ulcer healing and reduced the level of TNFα, whereas ulcer healing in TLR2 knockout (KO) mice was similar to that in wild-type mice. In TLR4 KO and RAGE KO mice, exogenous HMGB1 did not affect ulcer healing and TNFα expression. Thus, we showed that HMGB1 is a complicating factor in the gastric ulcer healing process, which acts through TLR4 and RAGE to induce excessive inflammatory responses.                                  Free PMC Article

 

  • Nonenzymatic glycation of human lens crystallin. Effect of aging and diabetes mellitus.

Garlick RLMazer JSChylack LT JrTung WHBunn HF.

This study looked at the effects of glycation on your eyes and the cataracts it’s responsible for. Yes glycation and a glucose diet will buy you cataracts. My mother had two of them. A good friend who loved to eat her bread had cataracts in both of her eyes as well. What’s interesting, this person was always complaining of headaches and stomach aches. Both of those manifestations are from an ECC diet. Again, here is more evidence of the glycative and addictive effects of a grain diet. In all, there were 3,629 studies on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to March, 1984. Incidentally, that was one month after I was released from the hospital after spending a month in a coma and suffering two strokes while comatose. I could have never come back this far without Dr Perlmutter’s help. Again, I have to thank you, Dr Perlmutter.

I found this study done Sep 5, 2014 on autism and environmental factors. The only factor that mirrored the rise in autism was the use of glyphosate herbicides. Note the similarity.  For me, this is enough to shut down the use of Roundup and all generic versions. Will the USDA recommend this? Knowing who runs the USDA, I seriously doubt it. Although it has little to do with glycation, it expresses the danger of the herbicide that’s used on virtually all grains today.

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Temporal trend in autism compared to temporal trend in U.S. application of glyphosate to genetically-modified corn and soy crops, as estimated from US Department of Agriculture data (see Additional file 1 ).
 The author of this last report tries to dance around the issue of the glyphosate herbicide’s relationship to autism, but the evidence is clear.

They’ve had some of this evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create? It’s those AGEs that are at the root of all modern diseases. If this was uncovered starting 30+ years ago, why have we just found out about it from the bestselling books from two doctors? Is someone trying to hide something? My guess is yes. This is Monsanto’s path to power and freedom. They’ve politically engineered their freedom to wreak whatever havoc they can on your health by masturbating your taste buds with their glucose laden products, to grant them power by buying into their pharmaceutical cycle in the very near future. By near, I mean, it only takes a couple days before you’re indebted. (That means addicted.) If you want true power and freedom, you can have it in two weeks to two months. That’s how long it takes to break the addiction.

Each and every one of these 11,000+ studies have been vetted and examined by the NIH and PubMed for whom I thank.

You have two choices;

  1. Continue to masturbate your taste buds and collect these diseases and disorders in return.
  2. Cut out as much as possible the starchy carbohydrates, (grains) and live free from dependence.

You need to realize that the comfort in comfort food, brings massive discomfort in the future, starting immediately, with a process called glycation. This is the real poisoning of America and we can correct it. It lies within our power, each and every one of us can correct this. I offer a cure, not a therapy or treatment, My cure simply involves removal of all glycating substances from the diet to eliminate this problem of glycation so that it never affects the body The glycating substances = carbs, sugar, glucose, fructose.

The above reports on the effects of glycation appeared in many cases, over 30 years ago in PubMed. I’ve only showed you 47 reports out of 11,750 studies to date detailing the damaging effects of Excessive Carbohydrate Consumption, the primary cause of glycation, why doesn’t the FDA or the USDA say anything about that? The 42nd   study, submitted in November, 1989 shows how it causes inflammation, and with inflammation a factor in so many diseases, it truly is a wonder that the FDA and USDA never even issued anything so simple as a warning. The FDA’s involvement in this issue is mostly explained by their influence from the one industry, where they get most of their execs from, Monsanto.

From every form of cancer to Alzheimer’s disease to heart disease and cardiovascular disease to arthritis to hypertension to high cholesterol these food sources (sugar and grains) are responsible for each and every one of these disorders. These studies are proof of exactly what sugar does to the body. To cure the glycation factor in these diseases, the best way is to eliminate it as much as possible. To do that you must eliminate its source and to eliminate the source, you have to eliminate the grains and sugar. Thank you Dr Davis and Dr Perlmutter for bringing this to my attention.

In all, there were 3,629 studies in the FDA’s database on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to march, 1984. Incidentally, that was one month after i was released from the hospital after spending a month in a coma and suffering two strokes while comatose. I could have never come back this far without Dr Perlmutter’s help. Again, i have to thank you, Dr Perlmutter. The above, reports on the effects of glycation, appeared, in many cases over 30 years ago in PubMed. With 11,667 studies to date detailing the damaging effects of Excessive Carbohydrate Consumption, the primary cause of glycation, why doesn’t the FDA say anything? The last study, submitted in November, 1989 shows how it causes inflammation and with inflammation a factor in so many diseases, it truly is a wonder that the FDA never even issued anything as simple as a warning. The FDA’s involvement in this issue is largely explained by the influence they receive from the one industry where they get a good portion of their execs from, Monsanto.

With having the evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create? It’s those AGEs that are at the root of all modern diseases. If this was uncovered 30+ years ago, why have we just found out about it from the bestselling books from two doctors? They weren’t published in 2010 and 2012 and they had to dig this information our of the archives. Is someone trying to hide something? In who’s best interest would it be to hide this information? The grain industry? My guess is yes.

From every for of cancer (with the possible exception of brain cancer, which I suspect is influenced by glycation simply because of the inflammation factor) to Alzheimer’s disease to heart disease and cardiovascular disease to arthritis to hypertension to high cholesterol these food sources (sugar and grains) are responsible for each and every one of these disorders. These studies are proof of exactly what sugar does to the body. To cure the glycation factor in these diseases, the best way is to eliminate it as much as possible. To do that you must eliminate its source and to eliminate the source, you have to eliminate the grains and sugar. Thank you Dr Davis and Dr Perlmutter for bringing this to my attention. It would have been nice if someone could have done it 20 or 30 years ago. For that, I thank the FDA, the USDA and Monsanto. Don’t allow them to be in your driver’s seat. As long as you remain on your carbohydrate diet, they’re in the driver’s seat for your health. Give up the carbs and put yourself back in the driver’s seat. You are the only one who can change yourself. Enable yourself to do so.

 

 

 

Documentaries worth watching;

  1. Food, Inc
  2. Food Matters
  3. Food Beware (French)
  4. Genetically Modified Foods
  5. David vs Monsanto
  6. Of the Land
  7. Hungry for Change
  8. That Sugar Film
  9. Fathead
  10. Love Paleo
  11. Heal Yourself
  12. Fresh
  13. Who Wants to Live Forever
  14. Overfed and Undernourished
  15. My Big Fat Body
  16. Facing the Fat
  17. Fat
  18. Just Eat It; A Food Waste Story

Our Celebration of Our Addiction to Sugar and the Price We Pay For It.

Our Celebration of Our Addiction to Sugar and the Price We Pay For It.

It’s not hard to see how much you enjoy celebrating your addiction to carbs. It’s displayed in everything that’s said and done, in all aspects of the food industry. It’s boldly advertised everywhere you go. Soon after following this celebration of addiction that you love to express, comes a parade of drugs that you’ll be taking to treat all of the symptoms that come from succumbing to your addiction. This simple equation displays the need that we have to curb the influence of the grain and pharmaceutical industry on our health.

Our Addiction is Displayed Everywhere

Enjoy Coca Cola SignFailure to control this influence will not only lead more disease and illness, but more to greater health costs overall. How Drink Coca Cola Signare we ever going to learn to live healthy and kick this habit, before it destroys our society? How are we ever going to put an end to diabetes? Or an end to Alzheimer’s disease? Or cancer? Or heart disease? Or arthritis? Or hypertension? Hyperlipidemia? High Cholesterol? I would like to show just how our celebration of addiction to sugar is not only destroying our individual lives, it has the possibility of destroying our entire civilization, if we don’t curb is influence.

An Addiction That Leads to More Addictions

bakery-bread-pastry-badges-labels-25965021

I intend to show you how this industry hooks you in the first place, how they keep you hooked so in the future you’re forced to buy into their drug habit. This drug habit involves NSAIDS (aspirin, Motrin, Advil, Aleve), anti-inflammatories, antacids, anti-gas and bloating, (Pepto Bismol, Gaviscon, Alka Seltzer) and we’re just starting with the OCDs. For prescription medicine, we’re looking at all opioids (Oxycontin, Oxycodone, Vicodin, Percocet), which again are addictive.  More prescription NSAIDS like Celebrex, Relafen, Relifex, and Gambaran. We know that by the existing opioid abuse epidemic how dangerous these drugs are. Do you think this happened by chance?

The Worst Consequence of Carbs

Other prescription medicines that you’re doomed to need if you continue your carbohydrate consumption (especially for those who allow ECC to control them), includes but are not limited to statins, vasoactive agents, fibrates, CETP Inhibitors, and niacin, just for starters. Statins are, by far, the far worst of these medications.

After spending 15 years giving care to and for seniors, I have seen the ravages statin drugs have taken on their bodies. They slowly rob their users from their mental faculties, then their muscles, then their lives. What it takes away from its users is in no way replaced by the treatment it offers. They are nothing more than invitations to a need to take more and more drugs. It seems that the drug industry has found ways to make you buy more of their wares.

This industry promotes that high cholesterol has something to do with heart disease, which couldn’t be further from the truth and that high cholesterol is dangerous. This couldn’t be further from the truth. Cholesterol isn’t the problem. Cholesterol is healthy. Your body has to use it to stay alive. Taking cholesterol away from your body only leads to more medication. I can see where this would benefit the drug industry.

Cholesterol, your body’s fuel

High cholesterol isn’t a heart problem. It’s a diet problem. Your diet is responsible for your high cholesterol. Your major food source is your primary source of cholesterol and that is where the problem begins. Your high carbohydrate diet produces cholesterol in your body that is not clean cholesterol, meaning that it is dirty fuel, as cholesterol is your body’s fuel. This is cholesterol you don’t need. You need clean cholesterol that’s been produced by fat. That is what powers our bodies.

Cholesterol is your body’s fuel source. It’s cholesterol that enters the cell to be used for fuel, so what’s important is the kind of cholesterol that your body uses. Is it clean or dirty cholesterol? Cholesterol from carbohydrates is a dirty sticky fuel due to the nature from which this cholesterol comes from. It comes from a sticky, icky, gooey, gluey substance, sugar and its residue after it’s burned is just as sticky. This is what leads to plaque, the basis of most all cancers, heart diseases and all dementias.

I’ve only talked about heart medications so far, I haven’t even touched on cancer medication or cholesterol medication (many of which are related to heart medications like statins), nor have I covered other prescription medication for arthritis, high blood pressure, and memory loss. The list goes on and on. What a quagmire this has turned out to be. But I’m going to try to make some sense out of this quagmire, so that we’re left with just a small puzzle leaving you wondering, like me, why?

I’ve already proven how the discontinuance of these foods leads only to better health and how continued consumption of these foods, only leads to a path of illness and disease. What I don’t know, did this industry know what these foods do from the studies that have come out over the last 70+ years? Or did they remain electively ignorant of the reports? Or did they influence the cover-up of these reports? With as many reports that have come out, I seriously doubt it. There are just so many of them (701) that it’s easy to miss most of them. Later I’ll show you how this industry has had its problems in the courts. Some of it is not pretty.

I’ll list just a few of the studies that have shown this damage going back over 70 years. The earliest study I found in 701 studies done over the years, was completed in 1939. I looked through page after page of studies that started in the 60’s, 70’s & 80’s. They seem to grow in number as time goes on. Studies have exploded since the turn of this century, as more and more people are starting to recognize the true dangers this food imposes on its consumers. Yet the majority of the addicted choose to remain ignorant to it dangers, as they’re impotent in ignoring its lures. They are all controlled by their hormones which are controlling their emotions. This is a common trait of carbolism. The addicted have little to no choice in the matter. The need to feed the addiction is no less than that of any other addiction, which forces the addicted to continue to feed the addiction. It’s the way addiction works, it’s the way carbolism works.

Celebration of sugar addiction

We’re inundated with the commercialism of addiction on a daily basis. You see advertising for these foods and drinks everywhere. How many snack food companies are there? How many cereal companies are there? How many soft drink companies are there? How many beer and spirits companies are there? How many commercials do you see each day from these industries? All of those commercials are luring you into their web of addiction. The grain industry has found ways to infect our society, like cockroaches

We all know who profits from this today, but have you ever connected that with who is going to profit from it 10, 20, 30 years from now, the pharmaceutical industry? It seems that the grain industry’s intent is to do nothing more than to fuel the drug industry. Whether it is their intent, it is and has been the result. How long it continues to be, depends on how long we continue allow our addictions to exist.

Drug companies, right now, are foaming at the mouth for all the business the food industry has sent them. (Pun intended.) Nobody is interested in breaking this addiction. What more could they ask for, a captive audience, all set up to need what they need to feed your addiction at a cost that they set. You get to pay it or deal with your pain. Many times you have to pay it, just to stay alive. Do you wonder why medical costs keep going up or why insurance costs so much? If everyone would stop buying into this ruse, and found their cure, what would happen to the pharmaceutical industry? A huge drop in demand for their drugs would lower the price for the drugs as well as the treatments. It’s not hard to see the benefit that would have.

The underlying cause of sugar addiction

First off, let’s define it. Dictionary.com defines addiction;   Noun, the state of being enslaved to a habit or practice or to something thatis psychologically or physically habit-forming,  as  narcotics,  to  such anextent that its cessation causes severe trauma.-

Wikipedia defines Addiction is a medical condition characterized by compulsive engagement in rewarding stimuli, despite adverse consequences.”

I personally define addiction as a compulsion to consume a substance that the body craves but doesn’t need because it actually harms the body. This definition rings true for heroin and opioids, sugar and alcohol, cigarettes and tobacco, the three most abused substances in the civilized algorithm, although not in that order. The worst of these addictions is that of sugar and alcohol, with sugar being by far, the meanest and vilest scourge ever committed upon the human race.

Baby FormulasIt starts with the placement of sugar and carbs in the baby food that’s sold throughout the industry. It’s obvious to me why they put it in baby food.  That’s because it’s so palatable and goes down so easy making the food more palatable so babies would be less likely to not consume it. What baby doesn’t love the taste of sugar? This taste for sugar soon turns into an addiction requiring it be fed to the body, every other hour or so. Whether or not this was the intended consequences of the marketing of this food, this consequence has become America’s newest death sentence. By showing how this addiction affects the body in Carbs; The Newly Discovered Death Sentencethe evidence proves how dangerous this food is to human physiology. Yet we continue to celebrate our addiction to it simply to enhance profits. Profits for the Grain industry as well as the drug industry are driven by our insatiable appetites for these foods, which is driven by their unending advertising.

The major reason this addiction continues is due to the manner in which it is and has been promoted. The desire to create more and more ways and forms to entice everyone to eat and drink more of this deadly food is nothing short of astounding.  It continues to amaze me how inventive we are at finding ways to kill ourselves with our own taste buds. Studies have been done, books have been written, the public have been warned, but it continues to happen. Every time I turn around I see another new way to kill ourselves in another appealing commercial. All this advertising encouraging us to consume more and more or their blood glucose raising, diabetes causing, HBP causing, dementia causing foods is the driving force of this addiction and consequent expense.

woman-eats-bag-doritosA carbohydrate diet requires that you feed it almost on an hourly basis. A ketogenic diet, on the other hand, allows you to go all day without eating much of anything. Here’s the secret, carboholics don’t like to go hungry. They do almost anything they can to not go hungry. Those on a ketogenic diet, don’t mind going hungry. Actually, to us it’s not going hungry. It’s simply going without eating. The hunger doesn’t exist as much, as the cycle of addiction has been broken. We feel the hunger pangs and many times, welcome them, because we know that is where we build our better health. We do this by building Ghrelin throughout our systems, because we know that Ghrelin works to build our immunity as well as making us a little smarter by increasing our brain power, through the addition of BDNF in our brains. Remember BDNF is that stuff that’s the foundation of new brain cells. Remember the Nrf2, that ramps up the production of your anti-oxidants? Those are both benefits of Ghrelin in your system.

Your celebration of your addiction to this sugar is the industry’s celebration of profits, both in the food they sell us and the drugs we buy to relieve the pain. For them, it’s a win-win situation. For the public who buys into this, it’s a no win situation. This is the prescription for future medications, if you’re in your teen and twenties. In your thirties, you’ll start buying their headache and stomach ache medication. In your forties, it’ll become  insulin or anti-diabetes medication, then in your 50’s and 60’s and beyond, pick your poison, heart disease, cancer, Alzheimer’s disease. Any one or all of these are going to hit you when you least expect it. I know. I’ve experienced it. I pray that you heed my words and don’t experience it yourselves.

Targeted Advertising

coke & Pepsi cansAlmost everything I see advertised on channels marketing to younger viewers is encouraging everyone to buy more soda, energy drinks (most of which are laden with sugar), snack chips and cereals. Then when you’re a few years older the ads are aimed at selling you crackers and pastas. Then  into your 40’s, 50’s and 60’s the ads are all aimed at selling you treatments and drugs for all the diseases and illnesses that your lifetime of consumption has brought you, drugs for diabetes, heart disease, cancer, arthritis, dementia, HBP, high cholesterol, etc, etc, etc. How long do I need to go on? Did I mention headaches or stomach aches?

When I watch programming on TV appealing to older viewers, like news broadcasts, I’m inundated with the commercials they show for drugs to treat heart disease (for there is no cure, only treatment), to treat cancer (again no cure), diabetes, high cholesterol, high blood pressure, arthritis, diabetes and obesity. Drug companies are doing their best to sell their drugs to us to treat (not cure) us, for the illness and pain that they cause. And we buy it. We buy into it big time. We’ve bought into it our entire lives. The biggest problem here is most people are still buying into it. And they’re buying into it in massive quantities, evidenced by to pandemics of obesity, diabetes, Alzheimer’s disease, heart disease, cancer, arthritis, HBP, etc, etc. What’s being spent now, not just on snacks and beverages, but on staples like flour and sugar, pasta and cereal will be tripled, quadrupled, quintupled and even more, in payments to the pharmaceutical companies in the future, after your done paying the price for the damage all your years of consumption will cause.  The only way to getting as close to a cure as you can, is to give them up as completely as possible, otherwise, continuance will only incur the need for drugs.

The drugs they’ll be pushing on you, for heart disease or cancer, or even just for your headaches and stomach aches will be an array of side effect causing chemicals that will ultimately make it necessary for you to purchase more of their drugs to counteract the side effects of the drugs you’ve been taking for your treatment. You see proof of this everywhere. I experienced it myself when I was on 12 different medications just to treat an underlying chronic pain problem. I had to take diuretics for my high blood pressure, anti-depressants because “they worked on the same receptors in the brain that the pain used”, NSAIDS for the headaches I always used to get, opioids for the chronic pain I live with from the car accident. The diuretics were for my high blood pressure caused by my pain, or so I thought. After I quit the bread, the pain subsided. Maybe not completely, but enough to encourage me to quit all grains. When it subsided even more, I decided to quit all carbs. My biggest benefit was the loss of my high blood pressure along with 30 lbs of weight.

When they advertise new drugs, the precautions and side effects of the drugs they want to sell you, take up more of the commercials, they show, than the explanations of their benefits. I have to wonder where the regulation is. Is it for the consumer (which it’s supposed to be) or is this regulation for the benefit of the industry? How can drugs with that many precautions and side effects still be approved for sale? It appears to me that this industry has the FDA under their spell.

Which does it appear to be, to you? This industry is still allowed to market foods of disease and death while marketing treatments for those diseases and illnesses. Who knew that these industries are related? Before I started this, I didn’t. I had to uncover this information, so I’ll show you how all this is connected and it’s connected to take your money. Their manner of taking your money is clearly hazardous to your health. This is something you need to know, because nothing is more important than your health.

The industry that feeds you sugar, prescription-drugs-assortment-bottles-containing-bottle-foreground-open-pills-spilled-out-onto-black-surface-36701776pills-3489144

forces you to buy their sister industry’s drugs.


The food industry which also includes the grain industry, which includes the crop seed industry that provides the farmers with the seed they need to grow the grains that they sell us to put on our tables for us to eat, is related to the pharmaceutical industry that makes all the drugs for all the diseases that these foods create. My question is how could we allow an industry responsible for our food, be also responsible for the diseases their food creates?

What we’ve allowed these related industries to do, in a nutshell, is drain our wallets at the grocery store by influencing us to buy their sodas, fruit drinks, snack foods, pastas, breads, cereals and crackers, while draining our wallets again at the pharmacy to buy their drugs that treat the symptoms of the diseases their food is responsible for.

  1. For the food we’re sold through their marketing….(and their advertising is pure magic to see and it’s so easy to buy into). Their product tastes better than anything in the world. How much more could you can ask for than a worldwide customer base that’s addicted to your wares. Because it’s addictive (like tobacco), you only have to make it more appealing than that of its competitors, of which it has plenty because the addiction is so strong. That makes it more deadly than heroin, simply because it’s as prevalent as water. In some places, more prevalent.
  2. We also get to pay their associates for the drugs we need to combat the diseases that their food has given us. And pay them we do. We’ll pay them anything to get out of the pain that we’ve been inflicted with, from eating the food they so happily sold to us. We just don’t connect that pain we feel with the food we’ve grown up with. But it is connected. It’s connected in a big way. They first connected themselves toward the end of the 20th century with mergers and acquisitions bringing chemical, pharmaceutical and crop seed companies under one roof.

The Perfect Sugar Ruse

This disturbs me and it disturbs me big-time.  The company that produces the crop seed for the food I’m supposedly going to eat is the same pharmaceutical company that makes drugs for the illnesses and diseases this food is responsible for? If it legal? It isn’t illegal. it happens and you buy into it..

This industry is so intent on keeping us addicted that sugar or corn syrup is quite often the #1 or #2 ingredient in baby food, meaning that if you’re not one of the few that are raised on their mother’s milk, and had to grow up on baby food, you’re condemned to an addiction that our grain and pharmaceutical industry has imposed upon you.

It’s not surprising that we’ve ignored this addiction for as long as we’ve had it. We’ve ignored it because we grew up with it. Everyone has it, so as far as everyone is concerned, there is no addiction. After all how can you be addicted to something that you need to survive? How can you live without something that you need to survive? That’s where the question lies, in whether or not, it’s something you need to survive. Do you really need this food or can you live without it. You can live without it and you should live without it. To do this, you make your body not need it. Sounds simple, doesn’t it? It is simple, it just isn’t easy. This is one case where simple is not easy.

We’ve made it so easy for this industry to increase our addiction that we look forward to finding new way to inflict more harm on our bodies. And this industry is more than happy to oblige us with their new creations to further our addiction. It’s a win –win situation for them. They couldn’t ask for anything more. We’re paying one side for what we eat the other side for drugs. Monsanto does the best at this.

Monsanto’s involvement

monsanto-evil-seed-corporate-greed-sign-asheville-north-carolina-usa-may-anti-accusing-being-gmo-protest-41136878According to Wikipedia; “Monsanto scientists were among the first to genetically modify a plant cell, publishing their results in 1983;[3] five years later, the company conducted the first field tests of genetically engineered crops. Increasing involvement in agricultural biotechnology R&D in general dates from the installment of Richard Mahoney as Monsanto’s CEO in 1983.[12] This involvement increased under the leadership of Robert Shapiro, appointed CEO in 1995, leading ultimately to divestment of product lines unrelated to agriculture.[12]” This divestment of product lines is their introduction into pharmaceuticals. Did they know at this time, what their food was doing to their consumers? Had they seen any of the reports that started coming out in 1939 and continued until today? Are they aware of any of them now? It appears not, or they’re choosing to be electively ignorant. I think it’s the latter. Their history tells us it’s the latter.

From Wikipedia; “In 1985, Monsanto acquired G. D. Searle & Company, a life sciences company focusing on pharmaceuticals, agriculture, and animal health. In 1993, Monsanto’s Searle division filed a patent application for Celebrex,[39][40] which in 1998 became the first selectiveCOX‑2 inhibitor to be approved by the U.S. Food and Drug Administration (FDA).[41]Celebrex became a blockbuster drug and was often mentioned as a key reason for Pfizer‘s acquisition of Monsanto’s pharmaceutical business in 2002.[42] Celebrex and arthritis, did they know the connection? What causes arthritis? Was this industry aware of the studies that started coming out in the 50’s and 60’s about the dangers of their product?

“In 1996, Monsanto purchased Agracetus, the biotechnology company that had generated the first transgenic varieties of cotton, soybeans, peanuts, and other crops, and from which Monsanto had already been licensing technology since 1991.[44]Monsanto first entered the maize seed business when it purchased 40% of DEKALB in 1996; it purchased the remainder of the corporation in 1998.[45] In 1998 Monsanto purchased Cargill‘s international seed business, which gave it access to sales and distribution facilities in 51 countries.[45] In 2005, it finalized the purchase of Seminis Inc, a leading global vegetable and fruit seed company, for $1.4 billion.[46] This made it the world’s largest conventional seed company at the time. Again, I have to wonder if they had seen the studies of what their products were doing to their consumers?

“In 2007, Monsanto and BASF announced a long-term agreement to cooperate in the research, development, and marketing of new plant biotechnology products.[47][48]” “Through a series of transactions, the Monsanto that existed from 1901 to 2000 and the current Monsanto are legally two distinct corporations. Although they share the same name and corporate headquarters, many of the same executives and other employees, and responsibility for liabilities arising out of activities in the industrial chemical business, the agricultural chemicals business is the only segment carried forward from the pre-1997 Monsanto Company to the current Monsanto Company. This was accomplished beginning in the 1980s:

  • 1985: Monsanto purchased D. Searle & Company for $2.7 billion in cash.[49][50] In this merger, Searle’s aspartame business became a separate Monsanto subsidiary, the NutraSweet Company. CEO of NutraSweet, Robert B. Shapiro, served as CEO of Monsanto from 1995 to 2001.[51]
  • 1996: Monsanto acquiredAgracetus, a majority interest in Calgene, creators of the Flavr Savr tomato, and 40% of DeKalb Genetics Corporation. It purchased the remainder of DeKalb in 1998.[52][53]
  • 1997: Monsanto spun off its industrial chemical and fiber divisions intoSolutia[12][54]In January, Monsanto announced the purchase of Holden’s Foundations Seeds, a privately held seed business. By acquiring Holden’s, Monsanto became the biggest American producer of foundation corn, the parent seed from which hybrids are made.[55] The combined purchase price was $925 million. Also, in April, Monsanto purchased the remaining shares of Calgene.
  • 1999: Monsanto sold off NutraSweet Co.[12]In December, Monsanto merged with Pharmacia & Upjohn,[12] and the agricultural division became a wholly owned subsidiary of the “new” Pharmacia; the medical research divisions of Monsanto, which included products such as Celebrex, were rolled into Pharmacia.[56]
  • 2000 (October): Pharmacia spun off its Monsanto subsidiary into a new company,[12]the “new Monsanto”.[57]Monsanto agreed to indemnify Pharmacia against any liabilities that might be incurred from judgments against Solutia. As a result, the new Monsanto continues to be a party to numerous lawsuits that relate to operations of the old Monsanto. Pharmacia was bought by Pfizer in a deal announced in 2002 and completed in 2003.[58][59])
  • 2005: Monsanto acquired Emergent Genetics and its Stoneville and NexGen cotton brands. Emergent was the third largest U.S. cotton seed company, with about 12 percent of the U.S. market. Monsanto’s goal was to obtain “a strategic cotton germ plasm and traits platform.”[60]The vegetable seed producer Seminis was purchased for $1.4 billion.[61]
  • 2007: In June, Monsanto purchasedDelta & Pine Land Company, a major cotton seed breeder, for $1.5 billion.[62] As a condition for approval from the Department of Justice, Monsanto was obligated to divest its Stoneville cotton business, which it sold to Bayer, and to divest its NexGen cotton business, which it sold to Americot.[63]Monsanto also exited the pig breeding business by selling Monsanto Choice Genetics to Newsham Genetics LC in November, divesting itself of “any and all swine-related patents, patent applications, and all other intellectual property”.[64]:108
  • 2008: Monsanto purchased the Dutch seed companyDe Ruiter Seeds for €546 million,[65] and sold its POSILAC bovine somatotropin brand and related business to Elanco Animal Health, a division of Eli Lilly in August for $300 million plus “additional contingent consideration”.[66]
  • 2012: Monsanto purchased for $210 million Precision Planting Inc., a company that produced computer hardware and software designed to enable farmers to increase yield and productivity through more accurate planting.[67]
  • 2013: Monsanto purchased San Francisco-basedClimate Corp for $930 million.[68]Climate Corp. makes more accurate local weather forecasts for farmers based on data modelling and historical data; if the forecasts were wrong, the farmer was recompensed.[69]
  • 2015 Monsanto tried to buySyngenta for US$46.5 billion but failed.[70]
  • 2016Bayer offered to buy Monsanto for US$62 billion.[71]

Monsanto’s involvement in the pharmaceutical industry and the agrosciences has grown to a monopolistic proportions.  It not only controls

It’s not just crop seed that they manufacture; they also are responsible for the chemicals sprayed on the crops grown from their seed. Since it’s been genetically modified to withstand the effects of their herbicide, roundup, I’ve always wondered how much of those chemicals get into our food through this process. Roundup is a glyphosate herbicide, meaning that it’s an enzyme inhibitor, that’s not good for human health.  For me, it’s just not healthy enough, especially for the problems I already live with. More chemicals in my body is not what I need to keep it healthy. You may want to chance it, but pesticides and herbicides in our diet have been linked to bladder cancer. Why would I want to chance that, just for the taste of something sweet or salty? You only think you’re craving the salt, when in all actuality, you’re craving the carbs that come with the salt. The salt isn’t addictive, the carbs are. Evidenced below is just a little of Monsanto’s bio-chemical industry.

Because they’re so good at manufacturing the chemicals for the herbicides and pesticides, they can manufacture GMO seed that is resistant to these chemicals. Though the plant may be resistant to the chemicals, does that mean that your body is? I don’t think so.

How glyphosate-based herbicides & GM seed combine to make consumption of grains dangerous.

Again according to Wikipedia; “Monsanto chemist John E. Franz repurposed the chemical glyphosate as a systemic herbicide in 1970.[89] Monsanto’s last commercially relevant United States patent on glyphosate expired in 2000, and since then glyphosate has been marketed in the United States and worldwide by many agrochemical companies, in different solution strengths and with various adjuvants, under dozens of trade names.[90][91][92][93] As of 2009, sales of glyphosate represented about 10% of Monsanto’s revenue due to competition from other producers of other glyphosate-based herbicides;[94] their Roundup products (which include GM seeds) represented about half of Monsanto’s gross margin.[95]

Glyphosate is an enzyme inhibitor, used not only in herbicides, but also in many drugs. They allow the drug to be more specific to the treatment and incur fewer side effects, for the patient. Don’t think that ingestion of Glyphosate now through your grain intake will prevent side effects of medications in the future. I can virtually guarantee that it won’t.

biplane-crop-duster-spraying-farm-field-14911079Wikipedia say about glyphosate; “Glyphosate is absorbed through foliage, and minimally through roots,[6][7][8] and transported to growing points. It inhibits a plant enzyme involved in the synthesis of three aromatic amino acids: tyrosine, tryptophan, and phenylalanine. Therefore, it is effective only on actively growing plants and is not effective as a pre-emergence herbicide. An increasing number of crops have been genetically engineered to be tolerant of glyphosate (e.g. Roundup Ready soybean, the first Roundup Ready crop, also created by Monsanto) which allows farmers to use glyphosate as a postemergence herbicide against weeds. The development of glyphosate resistance in weed species is emerging as a costly problem. While glyphosate and formulations such as Roundup have been approved by regulatory bodies worldwide, concerns about their effects on humans and the environment persist.[5][9]

“Many regulatory and scholarly reviews have evaluated the relative toxicity of glyphosate as an herbicide. The German Federal Institute for Risk Assessment toxicology review in 2013 found that “the available data is contradictory and far from being convincing” with regard to correlations between exposure to glyphosate formulations and risk of various cancers, including non-Hodgkin lymphoma (NHL).[10]

A 2014 review article reported a significant association between B-cell lymphoma and glyphosate occupational exposure.[11] In March 2015 the World Health Organization‘s International Agency for Research on Cancer classified glyphosate as “probably carcinogenic in humans” (category 2A) based on epidemiological studies, animal studies, and in vitro studies.[9][12][13] However in 2016 a joint meeting of the United Nations (FAO) Panel of Experts on Pesticide Residues in Food and the Environment and the World Health Organization (WHO) Core Assessment Group on Pesticide Residues (JMPR) concluded that based on the available evidence “glyphosate is unlikely to pose a carcinogenic risk to humans from exposure through the diet”.[86]

Are you glyphosate resistant? Can your body withstand the changes that glyphosate forces upon your body every time  you have a sandwich? With Glyphosate being coated on the wheat that your bread is made from, how can you guarantee that none of it is in your body? How can you guarantee that it’s not affecting your physiology? Can you guarantee that it’s not affecting the actions of enzymes in your body that regulate your health? What guarantees do you have that this won’t initiate more trips to your doctor?

Acetylcholine is an important chemical in the body that’s important for brain function and muscle function throughout the body as Acetylcholine is a neurotransmitter. For Acetylcholine to act as a neurotransmitter, it needs multiple enzymes that function in the central nervous system and the peripheral nervous system, for Acetylcholine works as a neurotransmitter as well as a neuromodulator.

The body uses the enzyme acetylcholinesterase to help activate muscles by inhibiting the action of  acetylcholine , and if glyphosate herbicides (Roundup weed killer used on more farms than any other weed killer) are enzyme inhibitors, how can the ingestion of grains laden with these herbicides, not effect the function of the enzymes in your body since you consume them every time you eat bread products of any sort?

These Glyphosate herbicides are enzyme inhibitors that have the ability to alter or stop the cell signaling capabilities of enzymes. If they can do this to plants, where is the guarantee that it won’t affect your body? Chances are, they’re going to change how your body operates and in the long run be the precursor to many diseases. It’s crucial for the body’s proper function that the actions of certain enzymes are never altered. Where’s the guarantee that these enzyme inhibiting herbicides that your wheat has been sprayed with, won’t affect your health? There is none.

According to Wikipedia; “Acetylcholine receptor agonists and antagonists can either have an effect directly on the receptors or exert their effects indirectly, e.g., by affecting the enzyme acetylcholinesterase, which degrades the receptor ligand. Agonists increase the level of receptor activation, antagonists reduce it.” I would consider an enzyme inhibitor an antagonist as it inhibits enzyme function.

It’s a little clearer to see now, how the altering of how enzymes work, in our bodies can have an effect on our health. I can see how this could come from a diet high in grains because how of much Roundup is sprayed on grain that’s milled into flour. I can also see how this could present a huge gain for the pharmaceutical industry. Is this really the intent of Monsanto, the maker of Roundup, the widest used herbicide on the planet? Or is it just negligence? I have to wonder because of their previous ties with Pharmacia & Upjohn, makers of Celebrex. These are just a few of thousands of enzymes and cell signaling proteins that are effected by this enzyme inhibitor.

I for one would not like to have this inhibitor flowing through by blood mucking up my system. Who knows what enzymes it’s going to inhibit in your body? Fortunately for me, I don’t have to worry about that, as carbs aren’t in my diet. They don’t get a chance to muck up anything in my body anymore, I’ve gone keto and I’m not going back.

It looks to me like Monsanto is trying to lock up not only our digestive problems but the resolve of those digestive problems. They like to persuade you to buy their food products which you are more than happy to do, then they get your money again when you purchase your Celebrex to ease the pain of the arthritis given you by their grains.

It’s not only Monsanto, Bayer has its own interest in the area of crop science, as explained by Wikipedia, “ in 2002, Bayer AG acquired the Dutch seed company Nunhems, which at the time was one of the world’s top five seed companies.[53][54]:270 In 2006, the U.S. Department of Agriculture announced that Bayer CropScience’s Liberty Link genetically modified rice had contaminated the U.S. rice supply. Shortly after the public learned of the contamination, the E.U. banned imports of U.S. long-grain rice and the futures price plunged. In April 2010, a Lonoke County, Arkansas jury awarded a dozen farmers $48 million. The case is currently on appeal to the Arkansas Supreme Court. On 1 July 2011 Bayer CropScience agreed to a global settlement for up to $750 million.[55] In September 2014, the firm announced plans to invest $1 billion in the United States between 2013 and 2016. A Bayer spokesperson said that the largest investments will be made to expand the production of its herbicide Liberty. Liberty is used to kill weeds which have grown resistant to Monsanto’s product Roundup[56]

Bayer’s involvement

bayer-20901226“Bayer’s four divisions, are related in their concerns to their contribution to our food industry as well as their contribution to the pharmaceutical industry.  Bayer Pharmaceuticals, Bayer crop Science, Bayer Animal Health, and Bayer Consumer Health are all related to our health. They too like to charge us for the food they market to us, then charge us for medication to treat the symptoms of the diseases that their foods are responsible for. Their divested interests are Lanxess (Bayer Chemicals AG) Diagnostics Division, Diabetes Devices Division, Covestro (Bayer Material Science).

Astra Zenica / Syngenta’s involvement

“Zeneca Agrochemicals was part of AstraZeneca, and formerly of Imperial Chemical Industries. ICI was formed in the UK in 1926. Two years later, work began at the Agricultural Research Station at Jealotts Hill near Bracknell.[9]” “In 2004, Syngenta Seeds purchased Garst, the North American corn and soybean business of Advanta, as well as Golden Harvest Seeds.[10][11] On 5 December 2004, the European Union ended a six-year moratorium when it approved imports of two varieties of genetically modified corn sold by Monsanto and its Swiss rival, Syngenta.[12]

AstraZeneca owned by Syngenta, again is evidence of this industrial control over our lives. Syngenta is a Swiss biotechnology company that operates globally. According to Wikipedia; “Syngenta AG is a global Swiss agribusiness that produces agrochemicals and seeds. As a biotechnology company, it conducts genomic research. It was formed in 2000 by the merger of Novartis Agribusiness and Zeneca Agrochemicals. As of 2014 Syngenta was the world’s largest crop chemical producer, strongest in Europe.[2] As of 2009 it ranked third in seeds and biotechnology sales.[3] Sales in 2015 were approximately US$13.4 billion, over half of which were in emerging markets.[1]

The three agrichemical companies above are the largest in the world, controlling a majority of the foods we eat along with the medications we take. I’ve laid out the evidence of what their foods do to the human body, yet they continue to produce the seed for the crops to make the food they want us to put on our table to eat. They also produce the aspirin everybody takes for the headaches they get from eating their bread.

I’ve said before how convenient we’ve made it for this industry to take our money while slowly, painfully, and expensively killing us. But our money is not the only thing they rob us of. They rob us of our dignity as well, for their food does more than anything else to rob us of our memories. We allow them to do this because none of their foods require warning labels, like that of cigarettes.

We’ve given this industry our lives and souls by bending to their advertising and buying into their game. We allow them to addict us when we’re infants by dumping sugar and corn syrup solids into the baby food we feed our kids. Then we allow them to continue their assault by buying into advertising schemes every Saturday morning with their cereal commercials. To fully hook us they add sugar to this already sugar laden food simply to make it more palatable.

When an industry does this, how are we supposed to fight the addiction? This makes every American who buys into this behavior a slave to this industry. Slaves make the best captive audience. They have no choice in what they do except to choose their device of demise.

What more do you need than a captive audience to sell your wares to? This is why a Coke at a ballgame costs 3 times more what you can get it for, at the grocery store. At the ballgame, you’re a captive audience. It’s the same when you’re addicted. Every ‘pusher’ knows this and they charge a premium price for it. This is exactly why everyone who remains in this trap makes themselves a slave, captive to the whims of these industries.

The Litigation Game

gallery-thumbnailsYet these industries are tied up with lawsuits in other areas of their agrochemical businesses. For example, Monsanto has fought legal claims of false advertising, as explained again in Wikipedia; “In 1996, the New York Times reported that: “Dennis C. Vacco, the Attorney General of New York, ordered the company to pull ads that said Roundup was “safer than table salt” and “practically nontoxic” to mammals, birds and fish. The company withdrew the spots, but also said that the phrase in question was permissible under E.P.A. guidelines.”

”In 1999, Monsanto was condemned by the UK Advertising Standards Authority (ASA) for making “confusing, misleading, unproven and wrong” claims about its products over the course of a £1 million advertising campaign. The ASA ruled that Monsanto had presented its opinions “as accepted fact” and had published “wrong” and “unproven” scientific claims.[127] Monsanto responded with an apology and claimed it was not intending to deceive and instead “did not take sufficiently into account the difference in culture between the UK and the USA in the way some of this information was presented.”[128][129]

“In 2001, French environmental and consumer rights campaigners brought a case against Monsanto for misleading the public about the environmental impact of its herbicide Roundup, on the basis that glyphosate, Roundup’s main ingredient, is classed as “dangerous for the environment” and “toxic for aquatic organisms” by the European Union. Monsanto’s advertising for Roundup had presented it as biodegradable and as leaving the soil clean after use. In 2007, Monsanto was convicted of false advertising and was fined 15,000 Euros. Monsanto’s French distributor Scotts France was also fined 15,000 Euros. Both defendants were ordered to pay damages of 5,000 Euros to the Brittany Water and Rivers Association and 3,000 euros to the CLCV (Consommation Logement Cadre de vie), one of the two main general consumer associations in France.[130] Monsanto appealed and the court upheld the verdict; Monsanto appealed again to the French Supreme Court, and in 2009 it also upheld the verdict.[131]

“In August 2012, a Brazilian Regional Federal Court ordered Monsanto to pay a $250,000 fine for false advertising. In 2004, advertising that related to the use of GM soya seed, and the herbicide glyphosate used in its cultivation, claimed it was beneficial to the conservation of the environment. The federal prosecutor maintained that Monsanto misrepresented the amount of herbicide required and stated that “there is no scientific certainty that soybeans marketed by Monsanto use less herbicide.” The presiding judge condemned Monsanto and called the advertisement “abusive and misleading propaganda.” The prosecutor held that the goal of the advertising was to prepare the market for the purchase of genetically modified soybean seed (sale of which was then banned) and the herbicide used on it, at a time when the approval of a Brazilian Biosafety Law, enacted in 2005, was being discussed in the country.[132][133]

“In March 2014 the South African Advertising Standards Authority (ASA) upheld a complaint, made by the African Centre for Biosafety, that Monsanto had made “unsubstantiated” claims about genetically modified crops in its radio advertisements, and ordered that these adverts be pulled.[134] In March 2015 after considering further documentation from Monsanto, the ASA reversed its ruling.”

“In 2009, Monsanto came under scrutiny from the U.S. Department of Justice, which began investigating whether the company’s activities in the soybean markets were breaking anti-trust rules.[105][106] In 2010, the Department of Justice created a website through which comments on “Agriculture and Antitrust Enforcement Issues in Our 21st Century Economy” could be submitted; over 15,000 comments were submitted including a letter by 14 State Attorneys General. The comments are publicly available.[107] On November 16, 2012, Monsanto announced that it had received written notification from the U.S. Department of Justice that the Antitrust Division had concluded its inquiry and that the Department of Justice had closed the inquiry without taking any enforcement action.[108][109] Opponents of Monsanto’s seed patenting and licensing practices expressed frustration that the Department of Justice released no information about the results of the inquiry.[110]

“In 2009, Monsanto came under scrutiny from the U.S. Department of Justice, which began investigating whether the company’s activities in the soybean markets were breaking anti-trust rules.[105][106] In 2010, the Department of Justice created a website through which comments on “Agriculture and Antitrust Enforcement Issues in Our 21st Century Economy” could be submitted; over 15,000 comments were submitted including a letter by 14 State Attorneys General. The comments are publicly available.[107] On November 16, 2012, Monsanto announced that it had received written notification from the U.S. Department of Justice that the Antitrust Division had concluded its inquiry and that the Department of Justice had closed the inquiry without taking any enforcement action.[108][109] Opponents of Monsanto’s seed patenting and licensing practices expressed frustration that the Department of Justice released no information about the results of the inquiry.[110]

All of these case are a clear indication of the extent to which Monsanto is willing push the limits. This is how corporate risk/loss assessment works. Sometimes the risk of paying a $15,000 find is worth the theft of a patent. My problem with this is they playing with my health, if I decide to eat their products. The problem is what are their products? Who knows? Who knows who grows the crops for the corn flakes that you ate this morning for breakfast. Do you? I don’t. But I now know it was one of these companies.

Syngenta as well has been accused of making false claims about being involved in suits for false patent infringement. “In 2001, the United States Patent and Trademark Office ruled in favor of Syngenta which had filed a suit against Bayer for patent infringement on a class of neonicotinoid insecticides. The following year Syngenta filed suits against Monsanto and other companies claiming infringement of its U.S. biotechnology patents covering genetically modified corn and cotton. In 2004, it again filed a suit against Monsanto, claiming antitrust violations related to the U.S. biotech corn seed market, and Monsanto countersued. Monsanto and Syngenta settled all litigation in 2008.[49]

I mention this to point out the extent of their influence in the crop seed industry, where they have 15 of their own seed companies that all provide GMO crop  seed for farmers to plant for their crops for food which ends  up on our tables. Syngenta is the second largest corporation in the industry, Monsanto is even larger. (And we haven’t considered Bayer Cropscience, DOW Argrosciences or DuPont Pioneer.) Most of these cases involve patent rights to GMO seed with companies like Monsanto or DuPont Pioneer. It’s not just patent problems; most of these companies like to make out that their products are completely harmless to the environment, when they’ve been proven otherwise.

“Syngenta was a defendant in a class action lawsuit by the city of Greenville, Illinois concerning the adverse effects of atrazine in human water supplies. The suit was settled for $105 million in May 2012.[50][51][52] A similar case involving six states has been in federal court since 2010.[53][54]

“In the US, Syngenta is facing lawsuits from farmers and shipping companies regarding Viptera genetically modified corn. The plaintiffs in nearly 30 states contend that Syngenta’s introduction of Viptera drove down US grain market prices, leading to financial harm, and that Syngenta acted irresponsibly by doing too little to enable shipping companies to export the grain to approved ports.[55] Before Viptera’s 2010 introduction Syngenta secured all US and NCGA-recommended export approvals, but none from China. China had imported little to no US grain prior to 2010, and at the time was not considered a major partner, but it became a major partner in 2010, when it dramatically increased US grain imports.[56] For three years, China imported U.S. Viptera grain without formal approval. In November 2013, Chinese officials destroyed a U.S. grain shipment containing Viptera grain, started rejecting all US shipments with the GM grain, but continued to accept it from all countries other than the US.[57] That same year, US corn market prices dropped $4 per bushel, causing over $2.9B in losses, with just over half of that loss occurring prior to China’s November rejection.[58] China later approved the GM corn in 2014 but US corn grain market prices have not rebounded.”

The choice is yours

These are the kind of companies that are ultimately providing your food. Do you want them making your drugs also? As you’ve seen, they already do. Do you wonder why the prevalence of these diseases is so rampant? It’s in these industries’ best interest that this cycle continues.

Do you want this kind of industry to be responsible for your food? Or medicine? How about the medicine they make to treat the problems their foods create? We’ve allowed this to take place, right under our noses and we should be ashamed. Doesn’t this sound a lot like a wicked witch luring small children with candy and sweets? Because of our addiction we allow them to continue this behavior.

This addiction has and is costing America more money and lives than any other addiction that we’ve ever experienced. There are 24,000,000 deaths worldwide each year due to ECC, excessive carbohydrate consumption. There were 17.3 million deaths in 2013 alone due to cardiovascular disease. Cancer claims over 4 million each year and Alzheimer’s takes 5 million each year, yet I here no outrage about it. All of these deaths and suffering can be curbed simply by curbing carbohydrate consumption.

It’s time to put an end to this addiction. It’s time for a cure. But to stop the addiction, you first have to de-celebratize it. We have to stop celebrating its addictive qualities and exchange that celebration for the horror for what this addiction really does.

Everybody needs to think about what harm this food does before they put it in their mouth instead of thinking how good it tastes. Unfortunately for my generation and all those that have come along since, we’re stuck in the quagmire of addiction that we have to carry for the rest of our lives. Even most natural causes of death happen due, in part, due to what this food has done to the body over the lifetime of the deceased. An autopsy will likely show some form of arthritis, as this is evidence of inflammation, oxidative stress and cell degradation that these foods cause. If the inflammation, oxidative stress and cell degradation exists in the joints, it has to exist elsewhere in the body and since it exists throughout the body, as that’s where inflammation exists, in the blood. It has to affect everything it comes in contact with. That means it affects your heart, your brain, and every internal organ. How can that not have an effect on your life? It has to, so I have to ask, why is this food still allowed to be sold without a warning about just how dangerous it is? Cigarettes are. Alcohol is. Heroin is illegal and opioids require prescriptions. But not the one substance that minimizes all the damage caused by these other substances collectively, sugar from grains requires no warning for the damage they inflict. Why?

Going back to the problems this industry has had in court, mostly protecting their own patents and falsely claiming that their products are nutritious, when they’re not. Most of the patent problems lie in the resistance their new crop seeds have to their insecticides and pesticides, which have proven to have adverse effects in the human body. Yet they are still allowed to spray their crops with these herbicides and pesticides. My question is, how much of these herbicides and pesticides trickle into our food supply? How confident are you that no chemicals are in what you eat? How confident are you that no enzyme controlling chemicals are not in your biscuits or crackers? How confident are you that your sugar addiction won’t turn into diabetes? How confident are you that you addiction won’t turn into heart disease, or cancer? Whether you worry about it or not, you will experience brain loss. That’s just in the science. You can’t change it without saying good-bye to your addiction. This obviously isn’t easy with a grain industry that feeds the pharmaceutical industry. It’s even more obvious that they’ll never let us know the damage their foods do to everyone who ingests them. That’s up to you to know the dangers of sugar and grains, and now you do.

It’s time to say no to the industry that feeds you,

so you can say no to the industry that drugs you.

Learn to just say no to sugar, grains and drugs!

The Power of Being Thin Is Found By Eating Fat

The Power of Being Thin Is Found By Eating Fat

Most everybody wants to be thin simply to
look good,fat-thin-people-13593846 but the advantages of being thin go a lot further than just looking good. Being thin is not only highly beneficial for your looks but it’s crucial for your health and even more important for your brain’s health. Did you know that the fatter you are, the smaller your brain is? It’s true. That is directly from Dr Perlmutter’s book Grain Brain. Conversely, the thinner you are, the bigger your brain is. Don’t believe me? Look at the research studies and what Dr Perlmutter says in Grain Brain: 

“The dots connecting excessive body fat, obesity, and brain dysfunction are not hard to follow given the information you’ve already learned in this book. Excessive body fat increases not only insulin resistance, but also the production of inflammatory chemicals that play directly into brain degeneration. For this very reason, waist circumference is often a measurement of “health,” as it predicts future health challenges and mortality; the higher your waist circumference, the higher your risk for disease and death.”

danger-obesity-grim-reaper-touches-shoulder-happy-overweight-black-woman-big-cupcake-vector-illustration-health-41031554“It’s well documented that visceral fat is uniquely capable of triggering hormonal actions.  This, in turn, keeps the cascade of of negative effects from visceral fat going. In addition, visceral fat does more than just generate inflammation down the road through a chain of biological events; visceral fat itself becomes inflamed. This kind of fat houses tribes of inflammatory white blood cells. In fact, the hormonal and inflammatory molecules produced by visceral fat get dumped directly into the liver, which, as you can imagine, responds with another round of ammunition (i.e., inflammatory reactions and hormone-disrupting substances). Long story short: More than merely a predator lurking behind a tree, it is an enemy that is armed and dangerous. The number of health conditions now linked to visceral fat is tremendous, from the obvious ones such as obesity and metabolic syndrome to the not-so-obvious—cancer, autoimmune disorders, and brain disease.”

I copied and pasted the information above from Grain Brain for a reason. Obesity is a danger to more than just your body, by filling it with inflammation, it’s shrinking your brain by using these same process that creates plaque. I will show you exactly how obesity shrinks your brain and on the other hand, I’ll show you exactly how being thin can help your brain to grow in size. It all boils down to consumption of carbohydrates, mostly the high starchy carbs that you find in all pastries and breads, pastas, cereals, snack chips and crackers and some vegetables.

According to  Donald W. Miller, Jr., MD, Carbohydrates are the primary cause of weight gain, not fats. (Animals raised for food are fattened with carbohydrates.)” He goes on to say that eating fat is not only healthier than eating carbohydrates, it makes you thinner. “We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active” (Arch Int Med 1992;152:1271—2). It’s true,  I know from experience that eating fat makes you thin. It’s time for a new news alert;

Eating Fat Makes You Thin

Studies have shown that getting back to what our original metabolism likes for a diet and what our bodies are meant to digest means getting back to diet high in fats and low in carbohydrates. Low Carb diets date back to 1923 when the ketogenic diet was first created to help control epileptic seizures in infants. Dr Atkins came out with his low carb diet in 1958,  but it really got its boost when the Paleo diet came out early this century and with Dr Perlmutter’s recommendation for a ketogenic diet for optimal brain growth.

Wikipedia suggests, “we need to evaluate the low-carbohydrate diets over much longer periods of time, controlled studies as long as two years and survey studies as long as two decades.[7][13][14][15]” 

Dr Atkins was the first to promote a low carb diet as early as 1958, yet it seems that the carbohydrate addiction complex had already started its devious work in addicting our society to the ravages of the Wheat Belly saga. Too many members of our congress were sold on the notion that it is better to restrict our consumption fats, thinking that’s what was causing all the problem with obesity and diabetes. In all actuality, it is carbs that cause the fat that causes obesity and diabetes, not fat at all. You can find out how that happens in Carbs, The New Death Sentence. (I have to wonder who persuaded them to come to these conclusions, the grain industry?)

It’s all a matter of how they are digested. To digest carbohydrates, your body has to turn them into fat. This is because your body can’t run on glucose. It runs on fat. The studies showing this include,  Iris Shai, R.D., Ph.D. (July 2008), “Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet.” and New England Journal of Medicine 359 (3): 229–41. doi:10.1056/NEJMoa0708681.PMID 18635428, Low-carbohydrate-Diet Score and the Risk of Coronary Heart Disease an Omen, from The New England Journal of Medicineand the two others listed above ([14][15]). What this means is that when you eat carbohydrates, your body can’t use that as food because it burns fat.

When you eat fat, your body doesn’t have to convert that into anything else, so it can use it. Fats are digested in your small intestine unlike carbs that are digested cellularly with the help of insulin. That means that the glucose that carbs break down to, have to float around in your blood stream until they can enter a cell to be used as glycogen. This is where the problem begins. Anyone who’s been on a diet of carbohydrates for any amount of time has enough glycogen built up in their systems that they don’t need anymore, so the glucose turns into fat to be stored for future use.

The first place your body stores this fat is around your mid section, hence its name, belly fat or visceral fat. This is a dangerous fat to have in your body as this is where diabetes starts, along with a host of cancers and CVDs or heart diseases and most every kind of dementia, including Alzheimer’s Disease, Parkinson’s Disease and Huntington’s Disease.

Human biology hasn’t changed evolutionarily enough to allow humans to continue to eat carbohydrates in the massive amounts that everyone everywhere is eating them. The Paleo Diet  is a recent addition to the low carb diet choice. The ketogenic diet is the ultimate in a low carb diet and has already shown numerous benefits for better health. It’s the recommended diet for Celiac Disease since Celiac Disease is caused by the gluten that’s found in wheat, barley and rye and a few other grains. It’s also the oldest low carb diet, first designed in 1923, to help control seizures. The diet fell out of use when seizure medicines became more prevalent.

It turns out that a ketogenic diet is the healthiest diet that any human can eat and it brings with it, the most natural form of weight loss, possible. It goes back to the way our bodies have  metabolized food for the last 100,000 years. Simply because this diet is based on fat and not carbs, the diet provides much more efficient fuel for our bodies to use. A carbohydrate diet requires refueling every two hours or so and they has a tendency to gum up your body. It does it by creating plaque. That gets into to glycation of proteins and LDL cholesterol, which you can read about in Carbs, How They Cause AGEs

This plaque build up is the foundation of 75% of the deadliest and costliest diseases, known to man, ranging from breast cancer  to Atherosclerosis to 99% of all dementias, making carbohydrates some of the deadliest food that any human can eat. It’s not that this food just makes us fat, it kills us slowly and expensively, with an arm long list of  disorders. For this one reason alone, the power of being thin cannot be overspoken.

Studies have also shown the simple practice of calorie restriction to have multiple beneficial effects for the body, such as extended life. It’s amazing what just going hungry, can do for your body. It not only ramps up your immune system by boosting your anti-oxidants exponentially, it actually helps your brain grow, through a little protein known as BDNF, brain derived neurotrophic factor. This is what makes your brain grow and it doesn’t happen in obese people. This is part of the power of being thin.

The Power of MCTs and Coconut Oil

Calorie restriction on a carbohydrate diet is next to impossible. Yet I do it every day, quite easily and comfortably, while on my MCT ketogenic diet. MCT ketogenic diet is, in my estimation, the easiest low carbohydrate diet to get adjusted to. MCTs (Medium Chain Triglycerides) work differently in your body than LCTs (Long Chain Triglycerides). MCTs are a good way to actually lower your cholesterol because they build up the HDL cholesterol. Coconut oil and Palm kernel oil are optimal for this, as they contain lauric acid  and lauric acid is the foundation of HDL cholesterol, the good cholesterol.

Although curbing your carbs is the best way to lower your LDL cholesterol, adding coconut oil and other saturated fats to your diet will help curb your appetite for carbs, which in turn will cut down your LDL cholesterol and at the same time build up your HDL cholesterol.

Going back to what Dr Miller had included in his paper, “calorie restriction prolongs life as well as helps to make your brain grow.” This is the true power of being thin. It comes easiest from being on a high fat low carb diet.

What kind of fats then, do we need to eat, to be thinner? I mentioned before, MCTs. Medium chain triglycerides are the best, along with olive oil and avocado oil, palm kernel oil is also an excellent source of MCTs but coconut oil is by far the best MCT, in my opinion.

Coconut oil and palm Kernel oil have lauric acid in their chains of triglycerides, which is the foundation of HDL cholesterol. This means that a diet high in coconut oil or palm kernel oil MCTs helps build up HDL cholesterol, which in turn can help lower LDL cholesterol. Lauric acid is at the core of apolipoprotein A1, which in turn is at the core of HDL cholesterol. Studies have shown higher levels of HDL particles in the blood to be very beneficial for one’s health.

I can’t recommend staying away from dairy either. As I said before, all milk fats are MCTs. If you truly are lactose intolerant, then it may be best to limit your intake to nothing more than cheese. Cheese looses its lactose as the cheese hardens, so most cheeses have little to no lactose content in them. Just don’t choose the low fat cheeses.

Butter’s Back

butterFor MCTs, I like milk fats. All milk fats are MCTs. That means that all milk fats can help you lose weight. I’ll bet you didn’t expect that, did you? That means that low fat milk and skim milk actually help make you fatter by taking away the healthy MCTs in milk fat. That also means, butter is back! Wow, how much better can it be? Butter can help you lose weight. What a concept, the more milk fat you eat, the healthier you will be. I love it!!! Cause I love cheese, and cheese is a milk fat.

MCTs are so important, Neuropharmacology just completed a study in June 2013 showing the ability of MCTs to control epileptic seizures. All MCTs are saturated fats. Your body uses saturated fats and would much rather have it fed to it than have to make its own through the ingestion of carbohydrates.

That also means that I can go back to eating bacon. I love bacon. (As a matter of fact, I’ve already gone back to eating bacon. I just enjoyed about 6 slices.) Bacon may not be a medium chain triglyceride, but it’s a saturated fat and I still love it, and I’m not restricted from eating it by my religion, so I eat it and lots of it. I couldn’t do that though, if I ate carbs. That would lead to major problems like hypertensive heart disease.

Grass fed beef is always a good source of fats as well as protein. Lamb is always good also as it’s almost always grass fed. I’m sorry vegans, but a vegetarian diet is too carbohydrate laden to be a fully healthy diet, unless you get the bulk of your calories from healthy oils like olive oil, avocado oil, palm kernel oil, and most importantly coconut oil. Simply because carbohydrates are involved in a vegetarian diet, you’re going to be suffering the same consequences as everyone else on a high carbohydrate diet. It may take longer for the disorders to manifest, because your vegan diet is a little healthier than most high carbohydrate diets, but they will, simply because carbohydrates are involved. The science of metabolism doesn’t allow any variation on this rule.

Carbs, not fats create body fat, especially visceral  fat,  the kind that kills.

The secret is to get more of your calories from fat and fewer from carbohydrates. Fat has more calories per gram of usable food anyway, making it a much more efficient fuel. Like proteins, carbohydrates only give you 4 calories per gram of food, but fat gives you 9 calories per gram of food. That’s over twice as many calories for the same weight of the food you put in your body.

That means that you have to eat more than twice as many carbohydrates to get the same amount of calories. It’s no wonder that a carbohydrate diet is so fattening.

A high fat, low carb diet is like than running high octane gas in your car but it’s even better, for your body. What high octane gas does for your car, fat does more for your body. On the other hand, What sugar does for your car, it also does to your body. Only it does it much slower.If you know of anyone who has put sugar in a gas tank, you know what that did top the engine. The same thing happens in your body. It gums it up. Glucose is to akin too glue, to be healthy.

It does it slower because your body doesn’t burn fuel as fast or as hot as your car engine, so it takes it longer to gum up. But when it does, the results are exactly the same, disastrous. That is the curse of being on a carbohydrate diet.

It’s Time For A Cure

Carbs and Cancer go together like love and marriage.

How Carbs Influence Cancer

17601735-cancer-word-cloud-concept-with-great-terms-such-as-disease-chemo-survivor-patient-doctor-and-more
Cancer is responsible for over 8,200,000 deaths every year.

Cancer comes in so many different forms , it makes it very difficult to nail down any one solution for all the different types of cancer. However, playing a major influence in half of the different types of cancer, listed below, is one common thread that permeates our diets everywhere – glucose. It’s woven of three strands – wheat, sugar and grain based foods (flour and sugar). These basic staples that we were all encouraged to eat massive quantities of, is actually what’s killing us. The worst aspect of this whole problem is that we were told to eat them. We were told that they should be the largest portion of our meals and that we eat them on a daily basis. We were told to do this because, (we were told) that it was healthy for us. Why was the truth was never shared? I don’t know. But we do know now, just how dangerous this food staple really is. Cancer is like the carriage to the carbs’ horse. Carbs lead the way and the cancer follows.

I mentioned in Carbs! The Newly Discovered Death Sentence that this is not healthy food, and I intend to prove it, starting with  this page.

Because of the lack of studies done of the effects of wheat in the diet and cancer, it’s not always easy to piece the information together. Many of the studies that were done years ago have been suppressed from public knowledge and are not easy to obtain now. Dr Davis and Dr Perlmutter have already located many of these studies and they can be found in their books, Wheat Belly and Grain Brain. I spent only enough time to decipher sugar and wheat’s influence in half of the various types of cancer listed below. If the CPSC is considering warnings for chemicals that cause cancer, (which they are in California) why isn’t anyone considering warnings for the consumption of these food staples, sugar and flour?

Suffice it to say, there is enough evidence here to prove that this food source should come with the same warning that everything that causes cancer has to bear, like cigarettes, and now, processed meats and fast foods, and chemicals in California. (California’s attorney general, Bill Lockyer, filed suit in August against McDonald’s; Burger King; Frito-Lay, owned by PepsiCo; and six other food companies, saying that they should be forced to put labels on all fries and potato chips sold in California. The proposed warning might say something to this effect: “This product contains a chemical known to the state of California to cause cancer.”)

It’s interesting that California is going after fast food companies for the “cancer causing French fries” when it’s the bread that has as much if not more influence on cancer as trans-fats. I’ll admit, French fries play a definite role in cancer, but if they’d only look at the studies that show how sugar and wheat cause cancer, diabetes, HBP, cardio-vascular disease, digestive disorders, etc they’d soon have labels on everything that flour and sugar were used in. The full list is viewable on the page mentioned above.

This page is going to show how this food actually contributes to the environmental factors that are at the root cause of many cancers.

Cancer – There are over 100 different known cancers that affect humans.[2] causing 8.2 million deaths as of 2012 The great majority of cancers, some 90–95% of cases, are due to environmental factors. The remaining 5–10% are due to inherited genetics.[5] Environmental, as used by cancer researchers, means any cause that is not inherited genetically, such as lifestyle, economic and behavioral factors, and not merely pollution.[28] Common environmental factors that contribute to cancer death include tobacco (25–30%), diet and obesity (30–35%), infections (15–20%), radiation (both ionizing and non-ionizing, up to 10%), stress, lack of physical activity, and environmental pollutants.[5] Diet, physical inactivity, and obesity are related to up to 30–35% of cancer deaths.[5][39  The largest influence in obesity is wheat, sugar and grain based foods.

We’re only going to look at a few of the 100s of different kinds of cancer.
Of the 12 listed below, we’ll look at 6 of those in detail further below;
  1. Lung cancer – 1.56 million deaths annually, as of 2012
  2. Pancreatic cancer – 330,000 deaths globally
  3. Colorectal (colon) cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.)
  4. Breast cancer – 18.2% of all cancer deaths for men and women together or 283,920 deaths
  5. Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol
  6. Thyroid cancer – in 2010, 36,000 deaths globally up from 24,000 in 1990.[35]Obesity may be associated with a higher incidence of thyroid cancer, but this relationship remains the subject of much debate.[36] 
  7. Ovarian cancer – estimated 15,000 deaths in 2008
  8. Cervical cancer – 266,000 deaths
  9. Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]
  10. Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3]
  11. Kidney cancer –17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  12. Endometrial cancer – caused 76,000 deaths
Let’s take a closer look at some of these types of cancer;
  • Lung cancer – 1.56 million deaths annually, as of 2012, is the most common cause of cancer in the US. The most common cause of lung cancer is smoking which warnings are required on cigarette packs.
  • Breast cancergallery-thumbnails– 18.2% of all cancer deaths for men and women together or 283,920 deaths is the second most common cause of cancer related deaths in women. Risk factors for developing breast cancer include: female sex, obesity, lack of physical exercise, drinking alcohol, hormone replacement therapy during menopauseionizing radiation, early age at first menstruation, having children late or not at all, older age, and family history.[2][4 There is a relationship between diet and breast cancer, including an increased risk with a high fat diet,[44] alcohol intake,[45] and obesity,[46] related to higher cholesterol levels.[47] In breast adipose tissue, overexpression of leptin leads to increased cell proliferation and cancer.[69] Dietary iodine deficiency may also play a role. [48] Don’t forget what increases leptin levels in the system more than anything else. What would happen to breast cancer if you removed wheat, sugar and grains from the diet? Would that decrease the expression leptin and put a hamper of the spread of cancer? A high fat diet, in this case would be a diet that creates a lot of fat. Carbs create fat. Eating fat doesn’t. I’ve never seen a warning about obesity and breast cancer, or that eating grain based foods can cause obesity. There should be.
  • Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]  is the leading cause of cancer death in males worldwide.   The data on the relationship between diet and prostate cancer is poor.[87] In light of this the rate of prostate cancer is linked to the consumption of the Western diet.[87] There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.[87][88] Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed.[87][89] Vitamin supplements appear to have no effect and some may increase the risk.[9][87] High calcium intake has been linked to advanced prostate cancer.[90] Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.[91] Some evidence supports lower rates of prostate cancer with a vegetarian diet.[92] There is some tentative evidence for foods containing lycopene and selenium.[93] Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.[94]  Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.[94]
  • Colorectal cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.) IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors. It is increasingly thought that alterations to enteral (probiotics?) bacteria can contribute to inflammatory gut diseases[20][21]IBD affected individuals have been found to have 30-50 percent reduced biodiversity of commensalism bacteria such as a decrease in Firmicutes (namely lachnosperacieae and Bacteroidetes), what I believe are pro-biotics (but I can’t find a definitive answer to that). Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD affected individuals are more likely to have been prescribed antibiotics in the 2-5 year period before their diagnosis than unaffected individuals.[22]The enteral bacteria can be altered by environmental factors, such as Concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.[23] This tells me that those who are taking headache medication (NSAIDs) often, are themselves open for colorectal cancer and one thing we know about wheat and grain consumption is that it causes headaches, forcing one to use NSAIDs for pain relief.
  • Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol. Liver cancer, also known as hepatic cancer, is a cancer that originates in the liver. Liver tumors are discovered on medical imaging equipment (often by accident) or present themselves symptomatically as an abdominal mass, abdominal painyellow skin, nausea or liver dysfunction. The leading cause of liver cancer is cirrhosis due to either hepatitis B, hepatitis C, or alcohol.[1] Cirrhosis is most commonly caused by alcoholhepatitis Bhepatitis C, and non-alcoholic fatty liver disease.[1][2] Non-alcoholic fatty liver disease(NAFLD) is one of the causes of fatty liver, occurring when fat is deposited (steatosis) in the liver due to causes other than excessive alcohol use. NAFLD is related to insulin resistance and the metabolic syndrome and may respond to treatments originally developed for other insulin-resistant states (e.g.diabetes mellitus type 2) such as weight loss, metformin, and thiazolidinediones.[4] We know that carbohydrate consumption in the form of wheat and grains cause insulin resistance. Doesn’t it make sense then, that the consumption of wheat and grains has a major influence in liver cancer?
  • Kidney cancer – Factors that increase the risk of kidney cancer include smoking, which can double the risk of the disease; regular use of NSAIDs such as ibuprofen and naproxen, which may increase the risk by 51%[9] or may not;[10] obesity; faulty genes; a family history of kidney cancer; having kidney disease that needs dialysis; being infected with hepatitis C; and previous treatment for testicular cancer or cervical cancer. There are also other possible risk factors such as kidney stones [11] and high blood pressure, which are being investigated.[12] 17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  • Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3] and 165,000 deaths occurring in 2012.[4]  Urothelial carcinoma is a prototypical example of a malignancy arising from environmental carcinogenic influences. By far the important cause is cigarette smoking, which contributes to approximately half of the disease burden. Chemical exposures such as those sustained by workers in the petroleum industry, the manufacture of paints and pigments (prototypically aniline dyes), and agrochemicals are known to predispose to urothelial cancer. Interestingly, risk is lowered by increased liquid consumption, presumably as a consequence of increased urine production and thus less “dwell time” on the urothelial surface. Conversely, risk is increased among long-haul truck drivers and others in whom long urine dwell-times are encountered. As with most epithelial cancers, physical irritation has been associated with increased risk of malignant transformation of the urothelium. Thus, urothelial carcinomas are more common in the context of chronic urinary stone disease, chronic catheterization (as in patients with paraplegia or multiple sclerosis), and chronic infections. Some particular examples are listed below:

The one factor that intrigues me the most is the influence of agrochemicals, in the disease. Some of the most treated foods in our diet are wheat, corn, soy and grain based foods. They genetically modify these foods to withstand the rigors of agrochemicals like herbicides and insecticides, both of which contribute to bladder cancer. What is the one food that we were all told to eat the most of? Grains. If this one food were taken out of the diet, would that affect the numbers of people dying from bladder cancer? I think so. (I’m sure Monsanto doesn’t think so.)

Risk factors for pancreatic adenocarcinoma include:[2][3][4][32]

  1. Age, gender, and race; the risk of developing pancreatic cancer increases with age. Most cases occur after age 65,[4] while cases before age 40 are uncommon. The disease is slightly more common in men than women, and in the United States is over 1.5 times more common in African Americans, though incidence in Africa is low.[4]
  2. Cigarette smoking is the best-established avoidable risk factor for pancreatic cancer, approximately doubling risk among long-term smokers, the risk increasing with the number of cigarettes smoked and the years of smoking. The risk declines slowly after smoking cessation, taking some 20 years to return to almost that of non-smokers.[33]
  3. Obesity; a BMI greater than 35 increases relative risk by about half.[3]
  4. Family history; 5–10% of pancreatic cancer cases have an inherited component, where people have a family history of pancreatic cancer.[2] The risk escalates greatly if more than one first-degree relative had the disease, and more modestly if they developed it before the age of 50.[6] Most of the genes involved have not been identified.[2][34] Hereditary pancreatitis gives a greatly increased lifetime risk of pancreatic cancer of 30–40% to the age of 70.[5] Screening for early pancreatic cancer may be offered to individuals with hereditary pancreatitis on a research basis.[35] Some people may choose to have their pancreas surgically removed to prevent cancer developing in the future.[5]
    1. Pancreatic cancer has been associated with the following other rare hereditary syndromes: Peutz–Jeghers syndrome due to mutations in the STK11 tumor suppressor gene (very rare, but a very strong risk factor); dysplastic nevus syndrome (or familial atypical multiple mole and melanoma syndrome, FAMMM-PC) due to mutations in the CDKN2A tumor suppressor gene; autosomal recessiveataxia-telangiectasia and autosomal dominantly inherited mutations in the BRCA2gene and PALB2 gene; hereditary non-polyposis colon cancer (Lynch syndrome); and familial adenomatous polyposis. Pan NETs have been associated with multiple endocrine neoplasia type 1 (MEN1) and von Hippel Lindau syndromes.[2][5][6]
  5. Chronic pancreatitis appears to almost triple risk, and as with diabetes, new-onset pancreatitis may be a symptom of a tumor.[5] The risk of pancreatic cancer in individuals with familial pancreatitis is particularly high.[5][34]
  6. Diabetes mellitus is a risk factor for pancreatic cancer and (as noted in the Signs and symptoms section) new-onset diabetes may also be an early sign of the disease. People who have been diagnosed with Type 2 diabetes for longer than ten years may have a 50% increased risk, as compared with non-diabetics.[5]
  7. Specific types of food (as distinct from obesity) have not been clearly shown to increase the risk of pancreatic cancer.[2] Dietary factors for which there is some evidence of slightly increased risk include processed meatred meat, and meat cooked at very high temperatures (e.g. by frying, broiling or barbecuing).[36][37]

Highlighted areas are all wheat and grain caused conditions that would not exist if this food weren’t in our diet.

If 90 – 95% of all cases of cancer are due to lifestyle and behavioral factors, what does that say about our eating habits? Our eating habits are the most influential factor in anyone’s lifestyle. The old adage, “you are what you eat”, is more valid here, than anywhere else.

Our individual diets are what separate us from each other more than almost anything else, as that’s what distinguishes us from each other. In every diet, there exists one common thread throughout the world, and that’s grains, wheat in the western hemisphere and rice in the eastern hemisphere. They’re in every diet of every ethnicity. This is the one common thread that affects everyone on the planet. It does so simply because it’s in every diet on the planet, in some fashion or another.

As evidenced above, there are 6 types of cancer on this page, alone, in which wheat and grains play a part. If you eat food that causes cancer and you’ll more than likely, contract cancer.

What if this one factor was removed from the equation of cancer? What if wheat and grains were removed from our diets? What would happen if you took out that one factor in the equation of cancer, out of the equation? Would you still come still come up with the same result?

I contend that it would change the whole equation enough that the end result of cancer would inevitably be changed. This begs the question, if we removed wheat and grains from the diet, would that be a start for a cure for cancer?

I understand why a warning label is on every pack of cigarettes, one should be, we know that smoking causes lung cancer. If they put out warnings for something that may cause cancer, like processed meats and ‘fast foods’, why can’t they put out a warning for something that clearly causes cancer, sugar and wheat based products?

Hopefully, the day will come soon.

Next, we’ll take a closer look at cardiovascular diseases and grains influence there.

A thousand thanks to Wikipedia, I would have never been able to compile this without their help. 85% of this page came directly from Wkikpedia.

 

Curbing Carbs for Diabetes Control

Curbing Carbs for Diabetes Control

As carbs are the major influence in type 2 diabetes, this post deals entirely with type 2 diabetes.health-care-diabetes-info-text-23318754

Diabetes is due to either the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced.[5] There are three main types of diabetes mellitus:

  • Type 1 DM results from the pancreas’s failure to produce enough insulin. This form was previously referred to as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile diabetes”. The cause is unknown.[3]It’s thought that glucose may trigger an auto-immune response that tells the pancreas to not produce insulin, but this was only theory when I last checked.
  • Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[3] As the disease progresses a lack of insulin may also develop.[6] This form was previously referred to as “non insulin-dependent diabetes mellitus” (NIDDM) or “adult-onset diabetes”. The primary cause is excessive body weight and not enough exercise.[3]
  • Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood-sugar levels.[3]

Only because of the extra glucose in the blood stream, is type 2 diabetes called diabetes called diabetes. In all actuality,  is the result of carbohydrate overload, and should be called carbolism. I call it carbolism, simply because of its addictive nature, and how it acts upon the body in the same that alcohol does. Alcohol is, after all, a carbohydrate. As this post is only concerned with type 2 diabetes, gestational diabetes isn’t even looked at in this article.

As described on the Carbs, The Newly Found Death Sentence;

  • Diabetic Lancet Device In Hand Stock Photo
    Is Diabetes Your Goal?

    Type 2 diabetes is caused primarily by carrying extra fat on the body and carbs play a major part in that. Carbs cause diabetes because of their need for insulin to be turned into fat so the body can use it. This is the beginning of a downhill spiral that forces the body to make adjustments that it would never have to do, if it were on a diet of protein and fats instead of carbohydrates. Because carbs have to be broken down to their most basic sugar, glucose to be used as a fuel, the glucose flows through your blood stream before it can be metabolized on a cellular level, to be used for that fuel. Glucose needs insulin, to be turned into fat to be digested, to use for energy. Glucose cannot enter the cell without insulin to turn it into fat. The problem is, most of the glucose, after it gets turned into fat, it gets stored as fat in any one of the multitude of fat cells on your body. This takes place in the visceral fat (fat around the internal organs) first and foremost, where it’s the most dangerous. The more carbs you eat, the more insulin your body needs to metabolize those carbs and with a body full of sugar (carbs), you need a lot of insulin to turn all those sugars into fat. After processing a diet full of high carbohydrate food over your lifetime, your body starts to have problems, manufacturing enough insulin, so you can continue to digest the carbs you continue to eat. Because your insulin production can’t keep up with your carb intake, the sugar doesn’t get turned into fat and stays in your blood stream as sugar. It begins to build up in your blood system and you become diabetic. Hence the name insulin dependent diabetes or type two diabetes. Remove the carbs, remove the excess blood glucose. If you remove the glucose from the equation, you remove the diabetes. If you take away the carbs, you take away the obesity and excess glucose. Can it really be that simple? Duh!

Insulin induces HMG-CoA reductase activity, whereas glucagon diminishes HMG-CoA reductase activity.[42] While glucagon production is stimulated by dietary protein ingestion, insulin production is stimulated by dietary carbohydrate ingestion. The rise of insulin is, in general, determined by the digestion of carbohydrates into glucose and subsequent increase in serum glucose levels. In non-diabetics, glucagon levels are very low when insulin levels are high; however, those who have become diabetic no longer suppress glucagon output after eating.”

I would have used a better choice of words, when describing “the digestion of carbohydrates into glucose”, I would have said, “breakdown of carbohydrates into glucose”, as the glucose at this point isn’t digested. It’s just broken down. It doesn’t get digested. Not until it can find a little hormone known as insulin, can it get digested. If it can’t find any insulin, it continues to float around in your blood stream as glucose, looking for something to attach to.

This is why this disorder is called type 2 diabetes and it has little to do with type 1 diabetes except that it allows glucose to continue to flow in you blood with being turned into fat  Type 1 diabetes is an auto-immune disease that shuts down the manufacture of insulin by the pancreas by destroying the cells where insulin is produced.

The fact that carbs are the major cause of type 2 diabetes, should be a warning to all who continue to eat this food. But what should alarm everyone, is what the excess glucose does, that carbs put into your system, because it’s this excess glucose that’s so deadly.

Glucose and cholesterol are the basic building blocks of plaque buildup in your system and it’s this plaque, that kills.

Cholesterol is formed by lipids (fat) clinging  around protein cells called apolipoproteins. They come basically in two forms that make up high density and low density particles, the foundation of cholesterol in your blood. You can read about that on the page about The Foundation of LDL Cholesterol; apolipoprotein B.

It’s excess fat in our bodies that form excess cholesterol in our bodies by providing the fat to be formed into cholesterol, and it’s this excess cholesterol in the form of LDL particles that drives fuel necessary to manifest any one of a multitude of illnesses, disorders, and diseases.

When you combine these two destructive forces of glucose and fat in the body, it’s like two weather systems colliding. Havoc ensues. 

Plaque is by far the worst manifestation of diabetes and a carbohydrate diet. It happens when glucose molecules combine with fat, cholesterol or protein molecules, before they can be utilized by your cells, and displays the true destructive force of glucose on your body.

According to Wikipedia, there are seven different kinds of plaque, AmyloidAtheromaDental plaqueMucoid plaquePleural plaqueSenile plaquesViral plaque. We’re going to look at only 4 of these though.

By far the worst of the plaques caused by digesting wheat and gluten is amyloid plaque, because of all the diseases it has a role in. According to Wikipedia;

  1. Amyloids are insoluble fibrous protein aggregates sharing specific structural traits. They are insoluble and arise from at least 18 inappropriately folded versions of proteins and polypeptides present naturally in the body.[1] These misfolded structures alter their proper configuration such that they erroneously interact with one another or other cell components forming insoluble fibrils. They have been associated with the pathology of more than 20 serious human diseases in that abnormal accumulation of amyloid fibrils in organs may lead to amyloidosis, and may play a role in various neurodegenerative disorders.[2]” The list of diseases caused by amyloid plaque is quite extensive, ranging from Alzheimer’s disease to Diabetes, Parkinson’s and Huntington’s diseases and more. the list on Wikipedia is 21 diseases and disorders or conditions associated with amyloid plaque. In my opinion, amyloid plaque is caused by the digestion of gluten from any source, whether it be wheat, barley or rye. Wikipedia says; “Studies have shown that amyloid deposition is associated with mitochondrial dysfunction and a resulting generation of reactive oxygen species (ROS), which can initiate a signalling pathway leading to apoptosis.[46]” In short amyloid plaque is caused by oxidative stress and cell death, both of which are caused by consumption of gluten and other high starch foods.
  2. Atheromatous Plaques are basically plaques from fats and is the type of plaque that clogs up your artery walls. This is the type of plaque that causes atherosclerosis and leads to heart and cardio vascular disease.
  3. Dental plaque is caused by the excessive amount of sugar on the teeth, creating bacteria, causing decay. (Remember, carbs = sugar.)
  4. Senile plaques (also known as neuritic plaques, senile druse and brain druse) are extracellular deposits of amyloid beta in the grey matter of the brain.[1][2]” 

They cause Alzheimer’s disease and dementia, and play a role in most every other cognitive disorder due to the way this plaque gums of the neurons in your brain.

This is why Type 3 diabetes is considered dementia or brain damage and this is the major reason you don’t want to play around with type 2 diabetes, the next step is loss of your senses, and you won’t even know it, as you won’t realize it as it happens.

Sugar and fat are what cause the plaque buildup

You need both glucose and lipids flowing through your body to create plaque. The glucose attaches itself to a lipid (fat) molecule that has yet to be utilized for energy, and glycates that lipid molecule. The lipids in this case are LDL cholesterol. Low density lipoproteins particles.

Because they float around in such loose form, they’re easily attacked by any free flowing glucose in the system. This is the doom of maintaining  a high amount of glucose in the body.

This is the beginning of plaque. Multiply this by the amount of carbohydrates your ingest everyday. The result is exponentially worse than you would ever want to believe.

So, how do you stop the diabetes? It’s actually a simple decision, stop eating foods that contain wheat. The problem is that following through on this decision, is it’s the hardest thing you’ll ever have to achieve. The biggest problem is that the worse your addiction is, the harder it is to break the addiction, but also, the more important it is to break the addiction. This could be the worst concern with carbohydrate addiction, there are different degrees of addiction, unlike that of heroin, cocaine and alcohol. This problem manifests itself when trying to cut back as the greater your addiction is, the harder it will be to eliminate this food from your diet. But, it’s essential that you eliminate it, because if you don’t, the world of hurt described on Carbs, The Newly Found Death Sentence, will follow you until you either die or quit eating that which causes it.

The easiest path to this goal is explained at Carbs, How To Cut Back.

Carbs, How They Create A.G.E.s. Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

How Carbs Create A.G.E.s. Your ticket to Alzheimer’s Disease, Cancer, Heart Disease and more

AGES are the single, most influential, factor in what ages us and
are responsible for a majority of the illness and disease that we live with today. Dr Perlmutter explains it much better in his book Grain Brain in chapter 4, starting on page 99, about Advanced Glycation End-productS.

According to Wikipedia;

“In human nutrition and biology, advanced glycation end products, known as AGEs, are substances that can be a factor in the development or worsening of many degenerative diseases, such as diabetes, atherosclerosis, chronic renal failure, and Alzheimer’s disease.[1]

Before we continue on with this post, a disclaimer: all paragraphs that are blocked in quotations marks, are all copied directly from Wikipedia, Grain Brain or Wheat Belly. I did this on numerous passages on this post for the purpose of expediency. I apologize; my time is too limited to deconstruct everything I use from those indispensable sources. With that said, it’s time to get started;

Wikipedia goes on to say,

“These harmful compounds can affect nearly every type of cell and molecule in the body and are thought to be one factor in aging and in some age-related chronic diseases. They are also believed to play a causative role in the blood-vessel complications of diabetes mellitus. AGEs are seen as speeding up oxidative damage to cells and in altering their normal behavior.”

The questions this conjures, is, what ever could cause these damaging substances? They’re a normal part of aging but what amplifies their behavior is a part of our diet that’s been with us forever, carbohydrates, plain and simple. I understand why this is hard for you to accept, so we’ll go through all of the effects they cause and look at what wheat and gluten play in each part.

AGEs have a range of pathological effects, such as:[25][26]

Oxidative stress is caused by “Glycation (sometimes called non-enzymatic glycosylation) is the result of typically covalent bonding of a protein or lipid molecule with a sugar molecule, such as fructose or glucose, without the controlling action of an enzyme.”

“Some AGEs are benign, but others are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as cardiovascular diseases (the endothelium, fibrinogen, and collagen are damaged), Alzheimer’s disease (amyloid proteins are side-products of the reactions progressing to AGEs),[8][9] cancer (acrylamide and other side-products are released), peripheral neuropathy (the myelin is attacked), and other sensory losses such as deafness (due to demyelination). This range of diseases is the result of the very basic level at which glycations interfere with molecular and cellular functioning throughout the body and the release of highly oxidizing side-products such as hydrogen peroxide.”

Of all the causes and effects, listed above, the two we’re going to look at are oxidative stress and cytokines. The primary reason I want to examine these factors is because, these two are responsible for what makes many carboholics look 70, when they’re actually only 55. So, let’s break down each part; we’ll start with cytokines. If you haven’t checked out what Wikipedia has to say about these destroyers of life, you should do so now, right now.

“Cytokines are a broad and loose category of small proteins that are important in cell signaling. They are released by cells and affect the behavior of other cells. Cytokines are produced by a broad range of cells, including immune cells like macrophages, B lymphocytes, T lymphocytes and mast cells, as well as endothelial cells, fibroblasts, and various stromal cells; a given cytokine may be produced by more than one type of cell.[1][2][3]

“They act through receptors, and are especially important in the immune system; cytokines modulate the balance between humoral and cell-based immune responses, and they regulate the maturation, growth, and responsiveness of particular cell populations. Some cytokines enhance or inhibit the action of other cytokines in complex ways.[3]

“They are different from hormones, which are also important cell signaling molecules, in that hormones circulate in much lower concentrations and hormones tend to be made by specific kinds of cells.”

“They are important in health and disease, specifically in host responses to infection, immune responses, inflammation, trauma, sepsis, cancer, and reproduction.”

“A key focus of interest has been that cytokines in one of these two sub-sets tend to inhibit the effects of those in the other. Dysregulation of this tendency is under intensive study for its possible role in the pathogenesis of autoimmune disorders.”

“Several inflammatory cytokines are induced by oxidative stress.[7][8] The fact that cytokines themselves trigger the release of other cytokines[9][10][11] and also lead to increased oxidative stress makes them important in chronic inflammation, as well as other immunoresponses, such as fever and acute phase proteins of the liver.”

If all this is the responsibility of cytokines, and cytokines are caused by oxidative stress, what does the oxidative stress play in this equation.

“Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage.”

“In humans, oxidative stress is thought to be involved in the development of Asperger syndrome,[2] ADHD,[3] cancer,[4] Parkinson’s disease,[5] Lafora disease,[6] Alzheimer’s disease,[7][8] atherosclerosis,[9] heart failure,[10] myocardial infarction,[11][12] fragile X syndrome,[13] Sickle Cell Disease,[14] lichen planus,[15] vitiligo,[16] autism,[17] infection,[18] and chronic fatigue syndrome.[19] However, reactive oxygen species can be beneficial, as they are used by the immune system as a way to attack and kill pathogens.[20] Short-term oxidative stress may also be important in prevention of aging by induction of a process named mitohormesis.[21]” 

If oxidative stress is bad for you in the long term and good for you in the short term, what about the short term benefits? We’ll come back beck to look at the short benefits of oxidative stress, after we look at what it does to you in the long run.

To summarize the above paragraphs from Wikipedia, long term oxidative can be deadly, but short term oxidative stress is beneficial.

The short term benefits of oxidative stress come mostly from exercise, but also from “curcumin from turmeric, green tea extract, silymarin (milk thistle), bacopa extract, DHA, sulforaphane (contained in broccoli), and ashwagandha”.

“Short-term oxidative stress may also be important in prevention of aging by induction of a process named mitohormesis.[21]” Short term oxidative stress also helps build up Nrf2 in your brain which can supercharge your production of antioxidants. “Activation of Nrf2 results in the induction of many cytoprotective proteins.”

“One of the areas where the concept of hormesis has been explored extensively with respect to its applicability is aging.[12][13] Since the basic survival capacity of any biological system depends on its homeodynamic (homeostatic) ability, biogerontologists proposed that exposing cells and organisms to mild stress should result in the adaptive or hormetic response with various biological benefits. This idea has now gathered a large body of supportive evidence showing that repetitive mild stress exposure has anti-aging effects.[14][15] Exercise is a paradigm for hormesis in this respect.[15] Some of the mild stresses used for such studies on the application of hormesis in aging research and interventions are heat shock, irradiation, prooxidants, hypergravity and food restriction.[14][15][16]Some other natural and synthetic molecules, such as celasterols from medicinal herbs and curcumin from the spice turmeric have also been found to have hormetic beneficial effects.[17] Such compounds which bring about their health beneficial effects by stimulating or by modulating stress response pathways in cells have been termed “hormetins”.[14] Hormetic interventions have also been proposed at the clinical level,[18] with a variety of stimuli, challenges and stressful actions, that aim to increase the dynamical complexity of the biological systems in humans.[19]

Exercise is the best way to induce mitohormesis. but it can be found in curcumin also, which can be found in turmeric, an important spice used extensively on the Indian subcontinent. This one little compound is so important in the proliferation of your antioxidants, that some drug companies, are trying to copy it with their own chemical versions, like, Tecfidera, oltipraz, Bardoxolone methyl, to name a few. It’s that important.

Calorie restriction is another way to build up your anti-oxidants. This will build up more anti-oxidants in you than what you  could ever drink. We’ll talk more about that later.

Effects in aging

“One of the areas where the concept of hormesis has been explored extensively with respect to its applicability is aging.[12][13] Since the basic survival capacity of any biological system depends on its homeostatic ability, biogerontologists proposed that exposing cells and organisms to mild stress should result in the adaptive or hormetic response with various biological benefits. This idea has now gathered a large body of supportive evidence showing that repetitive mild stress exposure has anti-aging effects.[14][15] Exercise is a paradigm for hormesis in this respect.[15] Some of the mild stresses used for such studies on the application of hormesis in aging research and interventions are heat shock, irradiation, prooxidants, hypergravity and food restriction.[14][15][16] Some other natural and synthetic molecules, such as medicinal herbs and curcumin from the spice turmeric have also been found to have hormetic beneficial effects.[17] Such compounds which bring about their healthy beneficial effects by stimulating or by modulating stress response pathways in cells have been termed “hormetins”.[14] Hormetic interventions have also been proposed at the clinical level,[18] with a variety of stimuli, challenges and stressful actions, that aim to increase the dynamical complexity of the biological systems in humans.[19]

“Epidemiological data suggest that individuals with a low calorie intake may have a reduced risk of stroke and neurodegenerative disorders. There is a strong correlation between per capita food consumption and risk for Alzheimer’s disease and stroke. Data from population-based case control studies showed that individuals with the lowest daily calorie intakes had the lowest risk of Alzheimer’s disease and Parkinson’s disease.”

Because “calorie restriction has been demonstrated in a variety of laboratory models to induce Nrf2 activation”, it’s as important as the exercise. Nrf2 is a basic leucine zipper (bZIP) protein that regulates the expression of antioxidant proteins that protect against oxidative damage triggered by injury and inflammation.[2]

When calories are reduced in the diets of lab animals, they not only live longer, but also become remarkably resistant to the development of several cancers.” This is according to Dr Perlmutter, in Grain Brain. Calorie restriction is close to impossible when you are a carboholic, on a carbohydrate diet. Every two hours or so you need another infusion of glucose into your system, to keep you going. Your hunger cycles force you into this repetitive behavior. You really have little choice in it because of the drop in your sugar levels. A carboholic cannot stand the rigors and stress of fasting as easy as someone who’s been on a keto diet for of any length of time. This is one of the biggest reasons that I remain on my MCT keto diet

What else builds up Nrf2 in your brain? A diet high in fats, omega 3 fats in particular. MCT’s are the best. MCTs like coconut oil, and a diet low in carbohydrates. Why? To me, it’s simple, fats won’t glycate other fats. Glycation occurs when glucose mixes with lipoproteins (cholesterol). It’s sugars that glycate cholesterol. If, it’s the glycation of cholesterol that leads to most illness and diseases, and building up Nrf2 in your brain can help protect you from that glycation, why wouldn’t you want to build it up?

Dr. Perlmutter, says it better, in Grain Brain, of page 127 in chapter 5, where he explain the effect of antioxidant protection, and how we can generate more antioxidants, with our diet, than what we can ever ingest through drinking antioxidant beverages. He says, ”Several natural compounds that turn on antioxidant and detoxification pathways through activation of the Nrf2 system have been identified”, which we talked about above.

To summarize,

With all of these deadly consequences AGES offer, why do people still continue to eat carbs and continue to suffer the effects of dealing with the long term effects of these things?

Short term effects are really beneficial, like increasing your auto immune system by ramping up your antioxidant production, protecting from all of the above diseases. If abstaining from carbs can bring you some of the short term effects, again, I have to ask myself, why do people still continue to eat carbs and continue to suffer the the long term effects of these things?

But then, I know the answer, Addiction which is a good reason to visit Why the addiction is so hard to break.