Tag Archives: dementia

Is Your Dementia Curable or Just Treatable?

Can Your Dementia or Alzheimer’s, Osteoarthritis, IBS/ IBD, Lupus 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 produce 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 your 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 in 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 your 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 hyperglycemia 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. They 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 is 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 the 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, thanks 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-localized 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 a non-invasive treatment against the 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-localized with MG-H1… endochondral 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 died because she bought into this ruse herself. This makes this ruse the most dangerous 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 aging 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 aging and disease processes – vascular complications associated with diabetes renal failure, Alzheimer’s disease, and tumorigenesis 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 killing 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 of Advanced 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 potential 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.

The Glucose Ruse to Feed You Disease, Compliments of the Grain and Pharmaceutical Industries

The Glucose Ruse to Feed You Disease

This is a matter of your health being engineered without your knowledge or consent. The engineering, in this case, is not good. Actually, it’s creating pain where none should exist. Our food supply industry may be the most important industry concerned when it comes to our health. As everyone knows, ‘you are what you eat’, so it’s vital that what you eat won’t make you sick. Unfortunately, for those who still masturbate their taste buds with their addiction to sugar, this couldn’t be further from the truth. It’s those who have fallen for this glucose ruse. Our food supply has been hijacked by the same industry that treats you for the illness their food supplies. Granted the healthcare industry is vital to our health, but I submit that it wouldn’t be as important as it is today if we paid more attention to what we eat. Because I now watch what I eat, I can change the “we” to “you”, meaning “you” have to watch what you eat. (All that means is that you still have an addiction to break, I don’t, I broke mine three years ago.) Because of this addiction, you’ve doomed yourself unwittingly to a lifetime of medications. That is unless you’re one of the .05% who shows no ill effects from glycation. I have yet to meet one of them. If you eat at a restaurant or buy groceries at a grocery store, you’re subject to this addiction. It’s in their food everywhere you look. You actually look for it because you love to eat it. You love their advertising. What’s not to love, it’s full of attractive people selling you what appears to provide health, but in all reality provides nothing but the opposite, as it’s responsible for most all pain, most all disease, all brain damage, all atherosclerosis, all diseases affiliated with inflammation, and this is just for starters.

Monsanto has politically engineered their dominance of your food supply and subsequent health by forcing as many farmers as they can to use Monsanto’s seed companies’ GMO seed to grow their crops. Monsanto has many seed companies. Their control over the seed industry is mirrored by their control over the pharmaceutical industry because they can use the seed companies to influence the profits of their drug companies. , owns 15 crop seed companies all selling GMO seed for their contracted farmers to grow. Five of these companies sell seed for wheat crops. That’s the seed that grows the wheat that’s ground into flour for your bread and crackers. Their contracted farmers have to grow Monsanto’s GMO seed at risk of facing legal action if caught growing anything else. This is how Monsanto controls what goes on your table to eat. This is also how Monsanto forces you into purchasing the Celebrex, made by GD Searle Pharmaceuticals. Searle has been part of Monsanto since 1985. The Celebrex is what your doctor prescribes for your arthritis that’s caused by the glycation set up from the grain diet you’ve been on all your life. After you get arthritis that you will inevitably get from eating their GMO grains, you’ll be begging your doctor for that prescription for the Celebrex. Then you’ll get to deal with the side effects of the Celebrex that it inevitably has and presents to the body. That’s the damage to your body from the drug side of their industry.  The damage from the crop seed side includes crops that are not only GMO seed, they are laden with Roundup, the glyphosate herbicide that works by inhibiting enzymes from doing what they supposed to do by instructing cells how to operate. Even though Monsanto claims that these enzyme inhibitors affect only targeted enzymes, the rise in cancer alone, that the nation has seen since the mid to late 80’s, has told a completely different story. The rise in these disorders is directly caused by an increase in the glycation that occurs in the blood by the high glucose laden grains this company forces their farmers to grow. That means that the food going on your table is engineered to make you need the medications that the pharmaceutical side of Monsanto’s companies sells.

 According to Wikipedia; “In December 1997 Monsanto merged with Pharmacia and Upjohn.[14] The agricultural division became a wholly owned subsidiary of the “new” Pharmacia; Monsanto’s medical research division, which included products such as Celebrex.[61]

GD Searle and Pharmacia are the other side of Monsanto’s multinational chemical companies,  that includes now,  Pfizer and Upjohn, as well. GD Searle was purchased by Monsanto in 1985 two years after Monsanto started dabbling in GMO crops.  In 1993 GD Searle file for a patent for Celebrex, its widely used arthritis drug. I’ll bet you didn’t know that it is Monsanto’s seed companies that force their contracted farmers to grow GMO seed designed to make you need their Celebrex. Is this what you thought you were buying when you bought those corn chips last time? Was this what you thought you were buying when you purchased those pretzels? Whether it was or not, that’s what you got. You also got all the rest of the damage that glycation does to the body, which includes cataracts, atherosclerosis, cancer and dementia as well. You’re also subjecting yourself to the hunger cycle, probably the worst manifestation of a carb diet. The more carbs you eat, the hungrier your get. That’s a cycle that can’t be broken if you don’t stop the fuel that feeds it. Stopping the fuel is the only way to stop the glycation. That means that it’s the only way to stop the inflammation, which means it’s the only way to stop the illness and disorder that glycation is responsible for.

This study done on glycative effects and Alzheimer’s disease was completed in 2005. Glycation of cholesterol into amyloid plaque was researched in this study. It showed that the plaque was responsible for Alzheimer’s disease. Where were the warnings then? It’s now 15 years later and millions of people have died from Alzheimer’s disease. The question I ask is why? Why weren’t we notified of this revelation 14 years ago? It’s been in the archives of PubMed since then. Why the delay? How many more must die before this news of the glycative effects of glucose, is released to the media to inform the public of this devastating news?

5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) attenuates the expression of LPS- and Aβ peptide-induced inflammatory mediators in astroglia

J Biol Chem. 1985 Sep 5;260(19):10629-36.

Glycation of amino groups in protein. Studies on the specificity of modification of RNase by glucose.

Watkins NGThorpe SRBaynes JW.

This study done on the effects of glucose on glycation was done in September 1985. Have you seen or heard of any part of this report prior to today? I haven’t. I had to search for it. The question I have is why wasn’t the public notified of this revelation? Were the research results suppressed so as to hide the truth from the public? I have to wonder.

About this same time, according to Wikipedia; In 1985, Monsanto acquired G. D. Searle & Company, a life sciences company focusing on pharmaceuticals, agriculture and animal health. In 1993, its Searle division filed a patent application for Celebrex,[42][43] which in 1998 became the first selective COX‑2 inhibitor to be approved by the U.S. Food and Drug Administration (FDA).[44] Celebrex became a blockbuster drug and was often mentioned as a key reason for Pfizer‘s acquisition of Monsanto’s pharmaceutical business in 2002.[45]

What wasn’t disclosed publicly was the benefit that the stockholders retained when the merger was finalized. Stockholders of Pharmacia retained 23% of their control in the new Pfizer. You wouldn’t think that would have an influence in what they do to grow their customer base to sell more drugs, would you? Regardless of what you think, it does, and they do care. Monsanto sends this industry most of their customers just from the damage their food does to those who eat it. This industry has grown to accommodate those customers, mostly with their diabetes industry and ever expanding interests in dementia. Inflammation,  cancer and atherosclerosis, just for starters.

Was it coincidence? I have to wonder. Since then Monsanto has made moves to control all of the grain industry in America, by contracting farmers to grow no other seed than their own GMO seed. This forces the farmers who do this, to spray massive amounts of herbicide on those crops. The herbicide they spray is Monsanto’s Roundup, a glyphosate herbicide that works by inhibiting the actions of enzymes. Enzymes are important proteins in the body as they’re cell signaling proteins that instruct cells how to operate. This is important because it’s that instruction that the cells need to not become glycation. Otherwise, without that enzyme, you create inflammation. Inflammation is the foundation of all modern diseases. This is why grains are slowly killing those who eat them, cutting their lives short, to the tune of 2,684 deaths every day, that can be attributed to these killing field grains. These signaling cells are cells like hormones and cytokines that affect your body’s functions. If these aren’t working because of any enzyme inhibitor floating around in your blood, it’s going to lead to glycation and disease. This is the scary part of this story, if you eat bread, crackers, corn chips or anything flour is used in (whether it’s wheat flour or corn flour), your eating this herbicide along with your bread and cornpone.

Did you have any idea that this was being done to you without your consent or knowledge? I didn’t until I did this research. Did you have time to do your research? Why not? If you couldn’t, wouldn’t you think that we need some regulation in the field? The FDA and the USDA are supposed to provide that. With Monsanto’s control of each of those agencies, how much honest regulation do you think could take place? The regulation that does take place, takes place only for the benefit of Monsanto and Pfizer, not the consumer. We end up the lab rats in  this experiment. In my opinion, this is a failed experiment and should be shut down as soon as possible.

This study was complete in September 1985, about the same time Monsanto acquired G.D. Searle Pharmaceuticals. 8 years later they filed for a patent for Celebrex, their arthritis pain killer drug. Celebrex is a Cox 2 NSAID with the following side effects and concerns, according to Searle, and I’m listing all of them;

Contraindications

NSAIDs may be used with caution by people with the following conditions:[6]

Irritable bowel syndrome[6]

  • Persons who are over age 50, and who have a family history of GI (gastrointestinal) problems[6]
  • Persons who have had past GI problems from NSAID use[6]

NSAIDs should usually be avoided by people with the following conditions:[6]

Adverse effects

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly common. Use of NSAIDs increases risk of having a range of gastrointestinal(GI) problems.[16] When NSAIDs are used for pain management after surgery they cause increased risk of kidney problems.[17]

An estimated 10–20% of NSAID patients experience dyspepsia. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding.[18] Over the past decade, deaths associated with gastric bleeding have declined.

NSAIDs, like all drugs, may interact with other medications. For example, concurrent use of NSAIDs and quinolones may increase the risk of quinolones’ adverse central nervous system effects, including seizure.[19][20]

There is argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain. Each drug has a benefit-risk profile [21] and balancing the risk of no treatment with the competing potential risks of various therapies is the clinician’s responsibility.

Combinational risk

If a COX-2 inhibitor is taken, a traditional NSAID (prescription or over-the-counter) should not be taken at the same time.[22][not in citation given] In addition, people on daily aspirin therapy (e.g., for reducing cardiovascular risk) must be careful if they also use other NSAIDs, as these may inhibit the cardio protective effects of aspirin.

Rofecoxib (Vioxx) was shown to produce significantly fewer gastrointestinal adverse drug reactions (ADRs) compared with naproxen.[23] This study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, showed a statistically significant relative risk of cardiovascular events of 1.97 versus placebo[24]—which caused a worldwide withdrawal of rofecoxib in October 2004.

Use of methotrexate together with NSAIDS in rheumatoid arthritis is safe, if adequate monitoring is done.[25]

Cardiovascular

NSAIDs aside from aspirin, both newer selective COX-2 inhibitors and traditional anti-inflammatories, increase the risk of myocardial infarction and stroke.[26][27] They are not recommended in those who have had a previous heart attack as they increase the risk of death and/or recurrent MI.[28]Evidence indicates that naproxen may be the least harmful out of these.[27][29]

NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of heart failure in people without a history of cardiac disease.[29] In people with such a history, use of NSAIDs (aside from low-dose aspirin) was associated with a more than 10-fold increase in heart failure.[30] If this link is proven causal, researchers estimate that NSAIDs would be responsible for up to 20 percent of hospital admissions for congestive heart failure. In people with heart failure, NSAIDs increase mortality risk (hazard ratio) by approximately 1.2–1.3 for naproxen and ibuprofen, 1.7 for rofecoxib and celecoxib, and 2.1 for diclofenac.[31]

On 9 July 2015, the FDA toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAID). Aspirin is an NSAID but is not affected by the new warnings.[32]

Possible erectile dysfunction risk

A 2005 Finnish study linked long term (over 3 months) use of NSAIDs with an increased risk of erectile dysfunction.[33] This study was correlational only, and depended solely on self-reports (questionnaires).

A 2011 publication [34] in the Journal of Urology received widespread publicity.[35] According to this study, men who used NSAIDs regularly were at significantly increased risk of erectile dysfunction. A link between NSAID use and erectile dysfunction still existed after controlling for several conditions. However, the study was observational and not controlled, with low original participation rate, potential participation bias, and other uncontrolled factors. The authors warned against drawing any conclusion regarding cause.[36]

Gastrointestinal

The main adverse drug reactions (ADRs) associated with NSAID use relate to direct and indirect irritation of the gastrointestinal (GI) tract. NSAIDs cause a dual assault on the GI tract: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucus secretion and diminished trophic[clarification needed] effects on epithelial mucosa.

Common gastrointestinal ADRs include:[5]

Clinical NSAID ulcers are related to the systemic effects of NSAID administration. Such damage occurs irrespective of the route of administration of the NSAID (e.g., oral, rectal, or parenteral) and can occur even in patients with achlorhydria.[38]

Ulceration risk increases with therapy duration, and with higher doses. To minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time—a practice that studies show is often not followed. Recent studies show that over 50% of patients who take NSAIDs have sustained some mucosal damage to their small intestine.[39]

There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacinketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates.[5]

Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations that manufacturers claim reduce the incidence of gastrointestinal ADRs. Similarly, some believe that rectal formulations may reduce gastrointestinal ADRs. However, consistent with the systemic mechanism of such ADRs, and in clinical practice, these formulations have not demonstrated a reduced risk of GI ulceration.[5]

Commonly, gastric (but not necessarily intestinal) adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g., omeprazoleesomeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhea). While these techniques may be effective, they are expensive for maintenance therapy.

Inflammatory bowel disease

NSAIDs should be used with caution in individuals with inflammatory bowel disease (e.g., Crohn’s disease or ulcerative colitis) due to their tendency to cause gastric bleeding and form ulceration in the gastric lining. Pain relievers such as paracetamol (also known as acetaminophen) or drugs containing codeine (which slows down bowel activity) are safer medications for pain relief in IBD.[citation needed]

Renal

NSAIDs are also associated with a fairly high incidence of renal adverse drug reactions (ADRs). The mechanism of these renal ADRs is due to changes in renal haemodynamics (kidney blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. This is particularly important in renal failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Prostaglandins serve to dilate the afferent arteriole; by blocking this prostaglandin-mediated effect, particularly in renal failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion pressure).

Common ADRs associated with altered renal function include:[5]

Salt (Sodium) and fluid retention

Hypertension(high blood pressure)

These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II’s vasoconstriction of the efferent arteriole) and a diuretic (which drops plasma volume, and thereby RPF)—the so-called “triple whammy” effect.[40]

In rarer instances NSAIDs may also cause more severe renal conditions:[5]

Interstitial nephritis

Nephrotic syndrome

Acute renal failure

Acute tubular necrosis

Renal papillary necrosis

NSAIDs in combination with excessive use of phenacetinand/or paracetamol (acetaminophen) may lead to analgesic nephropathy.[41]

Photosensitivity

Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs.[42] The 2-arylpropionic acids are the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicamdiclofenac and benzydamine.

Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen has weak absorption, it has been reported as a weak photosensitising agent.[citation needed]

During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and renal ADRs in the fetus. Additionally, they are linked with premature birth[43] and miscarriage.[44][45] Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies.[46] Additionally, Indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal renal blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy, but Leffers et al. released a study in 2010 indicating that there may be associated male infertility in the unborn.[47][48] Doses should be taken as prescribed, due to risk of hepatotoxicity with overdoses.[49]

In France, the country’s health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy.[50]

Allergy/allergy-like hypersensitivity reactions

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, i.e. unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug.[51] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2)Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rashfixed drug eruptionsphotosensitivity reactions, delayed urticaria, and contact dermatitis; or 3) far more severe and potentially life-threatening t-cell mediated delayed systemic reactions such as the DRESS syndromeacute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis. Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites and/or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1)exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals and/or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.[15]

Contraindications

NSAIDs may be used with caution by people with the following conditions:[6]

Irritable bowel syndrome[6]

Persons who are over age 50, and who have a family history of GI (gastrointestinal) problems[6]

Persons who have had past GI problems from NSAID use[6]

NSAIDs should usually be avoided by people with the following conditions:[6]

Peptic ulceror stomach bleeding[6]

Uncontrolledhypertension[6]

Kidney disease[6]

People that suffer with inflammatory bowel disease (Crohn’s disease or ulcerative colitis)[6]

Pasttransient ischemic attack (excluding ibuprofen)[6]

Paststroke (excluding ibuprofen)[6]

Pastmyocardial infarction (excluding ibuprofen)[6]

Coronary artery disease(excluding ibuprofen)[6]

Undergoingcoronary artery bypass surgery[6]

Taking ibuprofen for heart[6]

Congestive heart failure(excluding low-dose ibuprofen)[12]

In third trimester of pregnancy[6]

Persons who have undergonegastric bypass surgery[13][14]

Persons who have a history of allergic or allergic-typeNSAID hypersensitivity reactions, e.g. aspirin-induced asthma[15]

Adverse effects

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly common. Use of NSAIDs increases risk of having a range of gastrointestinal(GI) problems.[16] When NSAIDs are used for pain management after surgery they cause increased risk of kidney problems.[17]

An estimated 10–20% of NSAID patients experience dyspepsia. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding.[18] Over the past decade, deaths associated with gastric bleeding have declined.

NSAIDs, like all drugs, may interact with other medications. For example, concurrent use of NSAIDs and quinolones may increase the risk of quinolones’ adverse central nervous system effects, including seizure.[19][20]

There is argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain. Each drug has a benefit-risk profile [21] and balancing the risk of no treatment with the competing potential risks of various therapies is the clinician’s responsibility.

Combinational risk

If a COX-2 inhibitor is taken, a traditional NSAID (prescription or over-the-counter) should not be taken at the same time.[22][not in citation given] In addition, people on daily aspirin therapy (e.g., for reducing cardiovascular risk) must be careful if they also use other NSAIDs, as these may inhibit the cardioprotective effects of aspirin.

Rofecoxib (Vioxx) was shown to produce significantly fewer gastrointestinal adverse drug reactions (ADRs) compared with naproxen.[23] This study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, showed a statistically significant relative risk of cardiovascular events of 1.97 versus placebo[24]—which caused a worldwide withdrawal of rofecoxib in October 2004.

Use of methotrexate together with NSAIDS in rheumatoid arthritis is safe, if adequate monitoring is done.[25]

Cardiovascular

NSAIDs aside from aspirin, both newer selective COX-2 inhibitors and traditional anti-inflammatories, increase the risk of myocardial infarction and stroke.[26][27] They are not recommended in those who have had a previous heart attack as they increase the risk of death and/or recurrent MI.[28]Evidence indicates that naproxen may be the least harmful out of these.[27][29]

NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of heart failure in people without a history of cardiac disease.[29] In people with such a history, use of NSAIDs (aside from low-dose aspirin) was associated with a more than 10-fold increase in heart failure.[30] If this link is proven causal, researchers estimate that NSAIDs would be responsible for up to 20 percent of hospital admissions for congestive heart failure. In people with heart failure, NSAIDs increase mortality risk (hazard ratio) by approximately 1.2–1.3 for naproxen and ibuprofen, 1.7 for rofecoxib and celecoxib, and 2.1 for diclofenac.[31]

On 9 July 2015, the FDA toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAID). Aspirin is an NSAID but is not affected by the new warnings.[32]

Possible erectile dysfunction risk

A 2005 Finnish study linked long term (over 3 months) use of NSAIDs with an increased risk of erectile dysfunction.[33] This study was correlational only, and depended solely on self-reports (questionnaires).

A 2011 publication[34] in the Journal of Urology received widespread publicity.[35] According to this study, men who used NSAIDs regularly were at significantly increased risk of erectile dysfunction. A link between NSAID use and erectile dysfunction still existed after controlling for several conditions. However, the study was observational and not controlled, with low original participation rate, potential participation bias, and other uncontrolled factors. The authors warned against drawing any conclusion regarding cause.[36]

Gastrointestinal

The main adverse drug reactions (ADRs) associated with NSAID use relate to direct and indirect irritation of the gastrointestinal (GI) tract. NSAIDs cause a dual assault on the GI tract: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucus secretion and diminished trophic[clarification needed] effects on epithelial mucosa.

Common gastrointestinal ADRs include:[5]

Nausea/vomiting

Dyspepsia

Gastric ulceration/bleeding[37]

Diarrhea

Clinical NSAID ulcers are related to the systemic effects of NSAID administration. Such damage occurs irrespective of the route of administration of the NSAID (e.g., oral, rectal, or parenteral) and can occur even in patients with achlorhydria.[38]

Ulceration risk increases with therapy duration, and with higher doses. To minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time—a practice that studies show is often not followed. Recent studies show that over 50% of patients who take NSAIDs have sustained some mucosal damage to their small intestine.[39]

There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacinketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates.[5]

Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations that manufacturers claim reduce the incidence of gastrointestinal ADRs. Similarly, some believe that rectal formulations may reduce gastrointestinal ADRs. However, consistent with the systemic mechanism of such ADRs, and in clinical practice, these formulations have not demonstrated a reduced risk of GI ulceration.[5]

Commonly, gastric (but not necessarily intestinal) adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g., omeprazoleesomeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhea). While these techniques may be effective, they are expensive for maintenance therapy.

Inflammatory bowel disease

NSAIDs should be used with caution in individuals with inflammatory bowel disease (e.g., Crohn’s disease or ulcerative colitis) due to their tendency to cause gastric bleeding and form ulceration in the gastric lining. Pain relievers such as paracetamol (also known as acetaminophen) or drugs containing codeine (which slows down bowel activity) are safer medications for pain relief in IBD.[citation needed]

Renal

NSAIDs are also associated with a fairly high incidence of renal adverse drug reactions (ADRs). The mechanism of these renal ADRs is due to changes in renal haemodynamics (kidney blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. This is particularly important in renal failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Prostaglandins serve to dilate the afferent arteriole; by blocking this prostaglandin-mediated effect, particularly in renal failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion pressure).

Common ADRs associated with altered renal function include:[5]

Salt (Sodium) and fluid retention

Hypertension(high blood pressure)

These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II’s vasoconstriction of the efferent arteriole) and a diuretic (which drops plasma volume, and thereby RPF)—the so-called “triple whammy” effect.[40]

In rarer instances NSAIDs may also cause more severe renal conditions:[5]

Interstitial nephritis

Nephrotic syndrome

Acute renal failure

Acute tubular necrosis

Renal papillary necrosis

NSAIDs in combination with excessive use of phenacetinand/or paracetamol (acetaminophen) may lead to analgesic nephropathy.[41]

Photosensitivity]

Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs.[42] The 2-arylpropionic acids are the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicamdiclofenac and benzydamine.

Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen has weak absorption, it has been reported as a weak photosensitising agent.[citation needed]

During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and renal ADRs in the fetus. Additionally, they are linked with premature birth[43] and miscarriage.[44][45] Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies.[46] Additionally, Indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal renal blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy, but Leffers et al. released a study in 2010 indicating that there may be associated male infertility in the unborn.[47][48] Doses should be taken as prescribed, due to risk of hepatotoxicity with overdoses.[49]

In France, the country’s health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy.[50]

Allergy/allergy-like hypersensitivity reactions

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, i.e. unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug.[51] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2)Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rashfixed drug eruptionsphotosensitivity reactions, delayed urticaria, and contact dermatitis; or 3) far more severe and potentially life-threatening t-cell mediated delayed systemic reactions such as the DRESS syndromeacute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis. Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites and/or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1)exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals and/or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.[15]

Other

Common adverse drug reactions (ADR), other than listed above, include: raised liver enzymesheadachedizziness.[5]Uncommon ADRs include: hyperkalaemia, confusion, bronchospasm, rash.[5] Rapid and severe swelling of the face and/or body. Ibuprofen may also rarely cause irritable bowel syndrome symptoms. NSAIDs are also implicated in some cases of Stevens–Johnson syndrome.

Most NSAIDs penetrate poorly into the central nervous system(CNS). However, the COX enzymes are expressed constitutively in some areas of the CNS, meaning that even limited penetration may cause adverse effects such as somnolence and dizziness.

In very rare cases, ibuprofen can cause aseptic meningitis.[52]

As with other drugs, allergies to NSAIDs might exist. While many allergies are specific to one NSAID, up to 1 in 5 people may have unpredictable cross-reactive allergic responses to other NSAIDs as well.[53]

Drug interactions

NSAIDs reduce renal blood flow and thereby decrease the efficacy of diuretics, and inhibit the elimination of lithium and methotrexate.[54]

NSAIDs cause hypocoagulability, which may be serious when combined with other drugs that also decrease blood clotting, such as warfarin.[54]

NSAIDs may aggravate hypertension (high blood pressure) and thereby antagonize the effect of antihypertensives,[54] such as ACE Inhibitors.[55]

NSAIDs may interfere and reduce efficiency of SSRIantidepressants.[56][57]

Various widely used nonsteroidal anti-inflammatory drugs (NSAIDs) enhance endocannabinoid signaling by blocking the anandamide-degrading membrane enzyme fatty acid amide hydrolase (FAAH).[58]

How’s that for a warning label?  Did it have enough side effects for you? Think you might need more meds after taking this one? That label was 4094 words long. How many of those do you read? How do you know what you’re doing to your body if you don’t know what you’re putting into it? Do you think it coincidence that Monsanto started their GMO seed about the same time that glycation started being researched? Since much of this kind of research is funded by the industry it affects, I wouldn’t doubt that Monsanto had a hand in this research. This would allow them to immediately file these studies on glycation so that doctors and other scientists couldn’t find them to review. Yet each and every one of these 17,000+ studies have been vetted and examined by the NIH and PubMed. What I want to know is, why weren’t warnings about the glycative affects of glucose revealed at that time? Did Monsanto have anything to do with it?

The above list is the warning label for the adverse effects of Celebrex. Do you take Celebrex? Have you read the above warnings? Use of this drug can only lead to the use of more and more drugs. What do you think that would do for the profits for Monsanto? Do you still think this is coincidence? From renal failure, to the increased risk of myocardial infarction and stroke,[26][27] this drug brings on more drug use, simply so people can get away from their pain, pain caused by consumption of Monsanto’s grains. To me this is completely an unsustainable cycle. It’s a cycle of death and disease, leaving only, people in pain. Where is the sense in keeping this addiction?

Celebrex isn’t the only drug that leads to this interdependent drug abuse orchestrated by Monsanto, Pfizer, Bayer and Syngenta. There is a profitable reason that this cycle continues. Boatloads of investors depend on it. Too bad they don’t know what it’s doing to the society that they have to life in and with.

I propose that we tell Monsanto how we feel about this, not with our voices, but with our mouths in what we eat. Quit eating grains. They’re responsible for nearly all the pain you experience (with the exception of physical injuries).Grains and the glycation they bring, bring also all inflammation that influences all diseases. Stop buying bread, crackers, cookies, anything that flour is used in, stop using it, forever. That’s the only way you can start to free yourself from the addiction. You have to stop buying their junk food. Their junk food is making you sick. It’s making you sicker by the day. Stop it, you have the power to stop it and by stopping it, it gives you power, far more power than what you ever could have imagined you would have.

According to the BJM (British Medical Journal) on Cox 2 inhibitors such as Celebrex,  Selective COX 2 inhibitors are associated with a moderate increase in the risk of vascular events, as are high dose regimens of ibuprofen and diclofenac, but high dose naproxen is not associated with such an excess. How often do you need to take an Advil for your headache? Were you aware of what that painkiller does to your kidneys and liver or how much it increased your odds of having a heart attack? Why weren’t you made aware of that when it was sold to you? Maybe it was. Every drug commercial is primarily a dissertation of the adverse effects and precautions and contraindications each drug has. They all have to include this in all advertising. You’d think that that would dissuade anyone from buying into what has turned out to be nothing more than a perception of health. What drug use leads to is really not relief but continued drug use. It’s called ongoing treatment. Every hospital takes part in it. This is the effect of a society on carbohydrates….a society on drugs.

In all, there were 11,833 studies on PubMed, on the effects of glucose glycating proteins, hemoglobin, and cholesterol dating back to March, 1984. {There were 17628 studies done on PMC.) 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 and advice that it was the AGEs that were hindering my recovery. Again, I have to thank you, Dr Perlmutter.

With having the evidence for over 30 years, why hasn’t the public been told about glycation or the AGEs they create prior to Dr Perlmutter’s book, Grain Brain? 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? Was someone trying to hide something? My guess is yes.

This is Monsanto’s path to power and freedom. Their freedom is to wreak whatever havoc they can on your health by masturbating your taste buds with their glucose laden products, so you’ll be buying their pharmaceuticals in the near future. By near, I mean, it only takes a couple days before you’re indebted (addicted). If you want true power and freedom, you can have it in two weeks. That’s how long it takes to break the addiction. Or you can do it with a fast in 3 days.

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 be 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 a 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 it 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 your 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 overexpress 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 makes 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 anymore 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 divestiture of Monsanto. (Maybe it was the lawsuits that were starting to pile up, that they didn’t appreciate.) I wonder how many lawsuits 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 Advanced Glycation 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 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;

·        Glycation induced 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 have 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 July 15, 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 alarminsAlarmins 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 the 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 carboxymethyl-lysine (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 of 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 promote 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, chemoresistance 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 the 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 defense 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 an 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 of 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. Its 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 an 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 to heal 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 lifespan 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 dodecyl sulfate-polyacrylamide gel electrophoresis did not demonstrate a covalent cross-link between nonenzymatically glycated fibronectins. These results present further evidence 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 of this study is marked as July 29, 1968. That means that his damage was discovered in 1968, 48 years ago.

The association between elevated levels of glycated hemoglobins and diabetes mellitus has been known for twenty years [92]. Since then the determination of glycated hemoglobins has become a valuable tool for the objective assessment of long-term glycemia in diabetic patients. The marked clinical interest in reliable measurements of glycated hemoglobins has stimulated the development and perfection of the necessary methodology. Limitations of the techniques have led to investigations 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 hemoglobin by reactants other than glucose or the existence of labile hemoglobin adducts. With ideal methodology, these features would have gone unnoticed. Furthermore, the determination of glycated hemoglobin in large populations of diabetic patients has lead to the discovery of new, clinically silent mutant hemoglobins. Today, the routine determination of glycated hemoglobins in diabetic patients probably represents the broadest screening for mutant hemoglobins. The experience with glycated hemoglobins 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 oxidize, in the presence of trace amounts of a 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 aging 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 were 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 polymerization (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 polymerization 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 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, a 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 is known about its consequences on membrane. The 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 a positive association of membrane modifications with erythrocyte sedimentation rate, fragility, peroxidation whereas a 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 the 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 lifespan. 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 known 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.

An external file that holds a picture, illustration, etc. Object name is 12940_2014_781_Fig6_HTML.jpg
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 has 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 shown 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 out of the archives. Is someone trying to hide something? In whose best interest would it be to hide this information? The grain industry? My guess is yes.

Consider this; due to the pain cycles this food is responsible for, you can blame the opioid crisis on Monsanto and their amplification of glycation as it’s the pain that’s ramped up by the glycation, done to the crop, right before harvest. Whether intentional or not, it multiplies the profits of the pharmaceutical industry. All because you buy into it.

From every form 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

Sugar; America’s Worst Addiction,

Confessions of a Reformed Carboholic

Sugar, I love it. I grew up loving it. Because I grew up loving it, I’m now addicted to it. It’s an addiction that was forced upon me by our food industry, telling my mother that she had to make refined and whole grains the most prevalent food in my diet. She fed me this food, supposedly, to keep me healthy. Aren’t whole grains supposed to make you healthy? That was 60 years ago. I’m paying the price for that now, with my arthritis. I was paying the price for it just 30 months ago, by carrying 30 lbs more than what I carry right now and being borderline diabetic and in pain all the time. I’m about to debunk this myth that whole grains are healthy. There is a price to be paid for eating a (starchy) carbohydrate diet and you’re paying it with every sandwich you eat, every corn chip you munch, and every noodle you eat.

My sisters are paying the price for it now, also. They are both obese and diabetic. My father has always exercised to keep his weight down. He’s was always able to burn off the excess glucose, until he was about 35. Even though he’s always jogged every day, since I was in 7th grade, he couldn’t run away from this. After being borderline diabetic he couldn’t change his downhill spiral. He’s now taking an anti-diabetes drug which has several side effects that are initially so small that they aren’t noticed but after time, start to inflict other harm to the body, due to the effects of the chemical changes caused by the medication. His carb diet is starting to lead him down the same path as my mother, who passed away 4 months ago. My mother, in trying to be the best mother and wife she could be, went along with what the FDA, the USDA and the ADA told her because she wanted to do what was right for her family. Guidelines from the ADA telling her that grains needed to be at the base of her all of her meals was what drove her to do this to our family. This is what doomed us to our current list of ailments, ailments like obesity and diabetes, arthritis, cancer, stomach ailments galore, and now, side effects from treatment for those ailments. It all comes along with a carbohydrate diet because all carbs break down into glucose. Even yet, MyPlate.gov suggests that whole grains be a part of a healthy diet. The evidence I’m going to show you is completely contrary to this notion.

Because sugar addiction is America’s biggest addiction, that makes it, its worst addiction. It’s an addiction that everybody grew up with and into. It’s an addiction that’s been with us for as long as we’ve been eating it. It’s an addiction that’s become far worse than it’s ever been since we’ve been eating it over its 10,000-year history. It’s an addiction that’s built scores of empires, and then tore them all down. This addiction is far worse than any other addiction that plagues America. Whether it be today, yesterday or tomorrow, this addiction is the worst that Man has ever faced or may ever face. This is simply due to its propensity to expand its influence across the whole world. It’s also driven by the greed of those condemned to this addiction. Their desire to feed their own addiction drives them to impose this addiction on the rest of the world, simply so they can make an extra buck. This addiction is at the root of almost every known form of dementia, heart disease, diabetes and everything that comes along with that, like cancers, cardiovascular diseases. The list is endless because sugar’s worst instigator of inflammation, AGEs, or glycation is at the base of an arm-long list of disorders.

All of these disorders can be curbed simply by curbing carbohydrate consumption but addiction keeps this from happening. That’s why fighting this addiction, in particular, is so important. It’s life-saving at its simplest, just remove contaminating factors from the food source and the diseases cannot manifest themselves. The contaminating factor in this case? You guessed it, sugar. Sugar addiction is leading our society to the brink of destruction because of the nature of its addiction and what it does to the body. Its continued use only leads to discomfort and death. It’s only redeeming factor is that it tastes good and satiates quickly. This is what makes it so deadly, though.

That’s sad. I have to live with it too. I can’t have what I love, what I’ve been addicted to. I have to say no, to stay healthy. So do you. I know that’s exactly the opposite of what you’ve been told, but what you were told is wrong. For us, it’s dead wrong. It should have never been pushed upon us to eat it in the quantities that it was. But pushed upon us it was. And we bought it. We bought into it big time and we’re paying for it now. This is evidenced by the proliferation of Alzheimer’s disease. How many lives does it have to take, before people wake up? How many families does it have to destroy, before people wake up?

Carbolism Should Be Treated Like Alcoholism

We need clinics for sugar addiction and they should be financed by the food industrial complex that imposed this diet on the people who now suffer the consequences of it. The administration of the clinic though should be done by trained medical professionals, because this is an addiction and should be treated as such.

Is this something that should be investigated? Should an industry be held accountable for the ruse that’s been pulled on the American people, and now the world? The ruse is that this is healthy food when it’s really not. Why are they still allowed to claim that it’s healthy? It’s clearly not, and it’s clearly at the root of almost all of the deadliest diseases, that we’re actively fighting right now. Diseases like Atherosclerosis, Endocarditis and Hypertensive heart disease. That’s just the CVD’s. We haven’t even covered the cancers or diseases of inflammation. Those lists are much longer.

Can anyone tell me why this is still allowed to be advertised like it is today? It starts with what’s put in baby food for starches and fillers and sweeteners. These fillers satiate babies quickly often putting them right to sleep after a short burst of energy. This is the first indication of sugar addiction and it starts at a young age. This is done for a purpose. That purpose is to addict you to its lure, so you’ll buy into it when you’re an adult.

It continues with your introduction to breakfast cereals and the load of sugars they carry when you see them advertised with the Saturday morning cartoons. I can remember for commercials for Sugar Pops, Sugar Frosted Flakes, and Captain Crunch. It starts young, real young and continues through your youth with candy and soda, and into your adult years with bread and baked goods (cakes, crackers, cookies).

It’s been forced upon us. Nobody has had a choice in this addiction and that is what makes it so lethal. That also makes it profitable for the Pharmaceutical industry. This is what scares me. The Pharmaceutical industry used to be owned by the same industry the provided the crop seed for the farmers that grew the grain that provided the flour to bake all of those loaves of bread that causing so much disease.

The Perfect Ruse

It’s almost the perfect scam. Sell crop seed to farmers that have been genetically modified to accept enzyme inhibiting chemicals, so that it feeds your customer base, food that will require them, in the future to purchase medications from your other companies. How convenient we’ve made it for this industry to take our money. We should be ashamed.

We would be ashamed if we knew that this was done intentionally, especially if it was done for nothing more than profit. That is why this is something that should be investigated. Regardless of how long it takes, we need to know who is responsible. This is a lesson that cannot be lost, like every other study done on these concerns, we cannot allow this to be swept under the rug. Even if they’re no longer around, we need to hold their companies’ accountable. This is the only way we can prevent this from happening in the future.

For 1,000s of years, we’ve been treating the symptoms of the diseases and disorders that carbohydrate digestion cause. Because of our addiction to it, we’ve never looked at the prospect of eliminating the cause completely. When a whole society is addicted to a staple that they’ve eaten their whole lives, how does one tell the truth about something that is so important to everyone on the planet? How does one tell everyone that what they’re eating is killing them slowly, expensively, painfully, and worst of all, undignified because of all the lost memories from brain damage? How does one tell a whole society that a staple that they’ve lived on for close to 10,000 years has been, and continues to be, the one food that creates more disease and illness than any other one food in their diet? How does a world break their addiction, when the addicted are the majority of the world and only 5% of that population can recognize their addiction?

Dr. Perlmutter is trying to tell the people and continues to do so. I honestly feel that he thinks as I do, that if we don’t dispel the consumption of these foods, our society is doomed. From what I’ve learned since I’ve broken the addiction, I see a collapse, due to out of control emotions, due to the wild glucose swings in the blood, making people under the control of a carbohydrate diet, under the control of those who impose this diet on the American public. It’s in their interest to keep America addicted and the best way they can do this is to tell you that it’s healthy and what you need to keep your body healthy. Only those who want to buy their pharmaceuticals, from them in the future, are ones who should buy their food products now, because, they eventually will.

By following what little advice I offer, to curb your carbs dramatically and as completely as possible, you can dramatically slow down if not eliminate many of the disorders and diseases within these pages. If it can’t eliminate your disease, it will reduce the expression of your disorder. If it doesn’t cure you, it will definitely extend your life. My goal is to extend it a minimum of 20 years. I would like to see everyone live to be 100 years old, or more. I know this diet lifestyle can do that (depending on your age and degree of addiction of course). To know this yourself, though, you have to change your diet.

 

 

A Display of Dependence You Don’t Need


Carbs and Dementia

Carbs and Dementia

It’s well documented how much of a pandemic
obesity has become, worldwide. It’s becoming evident that this pandemic of obesity is leading directly into a pandemic of brain damage and dementia. Obesity, after all, leads directly to dementia. Don’t believe me? I’ll show you how and why this disease
acts like it has a mind of it’s own, controlling you to do what it wants.

It’s in the way it influences your hormones, as it uses them to control you, without you even suspecting it.

Dementia is, after all, type 3 diabetes.

If you’re type 2 diabetic now and you don’t change your eating habits, you stand a 100% chance of becoming type 3 diabetic. I can say this confidently because you don’t have to be type 2 diabetic, to get type 3 diabetes, dementia. This is shown in the number of Alzheimer’s patients now in existence. That population is growing exponentially while the diabetic population just multiplies in numbers. Diabetes just has a tendency to hasten the arrival of type 3 diabetes.

If we’re to going stop this epidemic of dementia that’s starting to cripple our population. We need to take drastic measures and the sooner we do so, the better our chance of survival. We have to slow the progression, where it starts, in what we eat. Thus, the reason for this post.

Alzheimer’s Disease

In most cases type 3 diabetes manifests itself in the disorder of Alzheimer’s disease. I know that not everyone who has Alzheimer’s disease has had type 2 diabetes, yet everyone who is type 2 diabetic will lose brain function. That science can’t be changed. The only thing that can stop that runaway train is to stop feeding it.  You must stop feeding carbohydrates into the fat factory that’s responsible for it. Carbs are the only thing that can generate fat inside your body. It’s this body fat, where the visceral fat lies that generates all the hormones and adipokines that dictate what this fat is going to do to your body. And it does plenty, all in the form of damage, damage to every system in your body as well as your brain. The more fat you have, the more damage it does to your body.

Fat creates hormones and adipokines that wreak havoc in your body.

The very first thing fat does, is to generate more fat through the use of the hormones that it produces, mainly leptin, along with Apelin and Chemerin, and it uses 100’s of other adipokines to wreak havoc throughout your entire body, including your brain. These hormones block receptors in the brain that influence behavior. They force us to continue to feed fuel to the cycle unknowingly. I call this our fat factory. This is called also addiction and this is how the addiction of the fat factory works.

By blocking receptor neurons in the brain, the neuropeptides that signal our bodies to stop eating, can’t do their job and tell us to stop eating. This is truly being controlled by your hormones. The pity of this cycle is, the larger you are, the more you experience it. It’s a cycle that feeds itself and it’s science you can’t change, without turning off the spigot.

It seems that this fat has become a self-feeding disease, of its own. I’ve noticed that the worse you have the disease, the harder it is to kick. But it’s also even more crucial to kick at that point because it’s already at the point of no return. Unless drastic measures are taken, a life of forgetfulness and lost memories is right around the corner, if it isn’t happening already? When was the last time you lost your keys or couldn’t remember someone’s name?

Fat, another organ

Even though obesity, excess fat,  is considered to be a disease by many, fat is considered by many professionals to be another internal organ. It’s an organ with its own mind, a mind to keep growing. It’s also one of the few organs that can grow in size, and when it does, it multiplies the hormones’ and adipokines‘ effects on our bodies. And it modifies it exponentially, which isn’t pretty.

Dictionary.com defines an organ as; Biology. a grouping of tissues into a distinct structure, as a heart or kidney in animals or a leaf or stamen in plants, that performs specialized task.”  

By strict definition, fat follows that description. It is a group of tissues in a distinct structure, that performs a specialized task. In this case, it performs many tasks, so many that it’s mind-boggling. This one organ creates more cytokines and hormones than any other organ in the body. That means that fat is one organ in our bodies, that either controls us or that we control it. When I talk about controlling us, I’m talking about control of our hormones which in turn controls our emotions. It also means that this one organ is responsible for more illness and disease than anything else in our entire bodies.

This is exactly why it’s so bad, the worst of these adipokines are cell signaling proteins that trigger hosts of illnesses and diseases. These diseases range from multiple cancers to multiple CVDs, which we’ll talk about later. The fat creates the bad cytokines that muck up your system. They create the adipokines that instruct your cells to turn into amyloid plaque. Amyloids are the foundation of an arm-long list of disorders, many cancers including breast cancer, colorectal cancer, stomach cancer, pancreatic cancer, liver cancer, and on and on. This isn’t even mentioning the mental disorders that come with amyloids. That list is even longer. The devastating effects that these hormones and adipokines have on your body, because of fat in your body, are truly astounding.

Body Fat production depends on Glucose

Now I know that glucose not only creates fat, the fat it creates, creates in turn, hormones and adipokines that trigger the inflammation and cell degradation associated with cancer and CVDs and worse of all brain loss. This fat factory is wasting away your brains and taking with it all of your mental faculties and dignity.

But it’s not only the fat factory that’s destroying our brains. It’s the gliadin that you eat every time you eat gluten. Your body can have this auto-immune response to gliadin, by sending out anti-gliadin antibodies that have the ability to attach themselves to Purkinje cells in your cerebellum as explained by Dr. Davis;. “The antigliadin antibodies triggered by gluten can bind to Purkinje cells of the brain, cells unique to the cerebellum. Brain tissue such as Purkinje cells do not have the capacity to regenerate: Once damaged, cerebellar Purkinje cells are gone . . . forever.” Doesn’t that say brain damage?

Only by taking abrupt action immediately, are you going to interrupt the production of these hormones that the fat factory is producing. And it’s producing these hormones so it can continue to enlarge itself in a vicious cycle. The only  way to stop this cycle at this point is to stop the fuel that feeds it, carbohydrates.

I’m sorry, but there’s no way around it. Not even you can change science. Unless you shut off the spigot of inflammation that you’re pouring into your body, every time you eat carbs, you’re going to feed the the fat that feeds the inflammation that causes all the disorders and disease listed in Carbs, The New Death Sentence, (15 of them, for starters).

A search for Obesity and brain size at NIH’s PMC site brought up over 1200 studies done on obesity and brain size. One in particular that I looked at, showed the influence leptin has on the brain and it’s ability to regulate energy in the body. Leptin is one of the hundreds of hormones and adipokines (cell signaling proteins), that’s manufactured in your body fat.

According to the study on Obesity and Dementia; “Within the brain, leptin regulates energy intake” “Leptin inhibits the expression of orexigenic neuropeptides and stimulates the expression of anorexigenic neuropeptides, which results in inhibition of energy intake (Jequier, 2002).”

That explains why those on a diet high in carbs (which is the only thing that can make people fat), run out of energy so much, and need to refuel every two hours or so. It’s the leptin expressing itself in the brain that inhibits the signals that tell us if we have energy or not and if we need to eat or not. And this is where the problem multiplies. Since leptin is formed in the fat around our body, it tells our brain that our body it needs more (fat) by blocking these signals. So what do we do? We eat more, to feed that need. This is leptin resistance, the leptin blocking those receptors in our brain that tells us that we don’t need to eat and have enough energy. It’s this leptin resistance that gives fat a mind of its own and allows it to work within us without our permission. That to me is an unadulterated robbery of our senses and emotions.

If you don’t have the ability to fight your hormones (leptin in this case) and resist this basic expression of survival, hunger, you’re doomed to everything listed in Carbs, The New Death Sentence. That is what makes carbs so addictive and dangerous and why their continuance must be curbed.

“It is known that adipokines, secretory products of adipose tissue such as leptin, interact directly with specific nuclei in certain areas of the brain such as the hippocampus. This results in regulation of not only feeding behavior but also neurodegeneration, synaptic plasticity, neurogenesis and memory consolidation (Doherty, 2011).” Are you starting to get the picture? Leptin isn’t your friend.

The Dangers of Leptin

Wikipedia says that the first adipokine, leptin was discovered in 1994 and since then 100’s have been discovered. Isn’t that disturbing? The fat that we make from glucose manufacturers hosts of hormones that are wreaking havoc on our bodies.

That means with the carbs we eat, we’re making fat, a fat that grows hormones that have cell signaling proteins that control hunger, energy expenditure and fat oxidation, blood pressure, glucose uptake and insulin resistance just to begin with. I didn’t even make it halfway through all the cell signaling proteins that were listed. The others that I did check all triggered a disorder or inflammation somewhere in the body. Many of them are associated with more than half of the known cancers, a multitude of heart diseases and every form of dementia known to man.

Leptin only plays a small part in the assault that our hormones throw at us. Adiponectin plays just as important role. As does Apelinchemerin, and 6 other hormones that they’ve found so far. And they finding more. All these hormones are adipokines and are manufactured in adipose tissue or fat. The other six adipokines listed on Wikipedia that I didn’t list here are all associated with inflammation and the oxidative stress that’s associated almost all cancers, most heart diseases and all brain damage that’s not caused by concussions and blunt force trauma.

If leptin plays a part in neurodegeneration, synaptic plasticity, neurogenesis and memory consolidation, doesn’t it make sense that it’s the creation of leptin that we need to control, to stem its influence in our bodies. If we’re to control the amount of leptin in our bodies, and leptin is made in adipose tissue (fat), then we need to control the amount of fat in our bodies. The only thing that controls the amount of fat that goes into our bodies is the amount of glucose that we feed it. We know that the glucose is controlled by the number of carbs we put in our bodies, so it’s easy to understand why we need to curb the carbs.

You can’t change the science. Glucose in the body creates fat. Fat creates leptin. The more leptin you have in your body, the more resistant you become to it and the more it needs to feed itself. It’s a cycle that keeps feeding itself again and again and again until you’re hungry 10 minutes right after you finished a big meal. I can remember times after a big spaghetti dinner when I was foraging through the cabinets and refrigerator, looking for something else to eat, on a full stomach. When I think about that now, I think, how sick could I have been to be expressing that kind of behavior? Then I think, I was a kid then, I was only eating what was fed to me. Here’s the scary part, I was eating exactly what the ADA was telling me I should eat. That’s exactly what you’re doing right now, following the dietary guidelines that you grew up with. How could they have gotten it so wrong?

Fortunately. I can only remember those times now, as I don’t get hungry much anymore. (Another advantage of being thin, and on a ketogenic diet.) Leptin doesn’t control anything in my body. I don’t have that much leptin in my body to control my urges and my energy. With a body fat ratio of 16 %, my body isn’t ever going to make enough leptin to create any problems in my body, provided that I don’t feed it what it wants, carbohydrates. This is what makes it so easy now to fast.

The Benefit of Adiponectin

This is where Adiponectin plays its role. “Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation.[3]

It’s adiponectin that not only dictates how glucose is turned into fat, it controls how the fat is burned in the body, and this is where it gets really interesting. Higher levels of adiponectin in the body allow the body to generate more energy from a smaller amount of fat, making adiponectin crucial for maximum energy output with minimal intake of food. That is why Dr. Miller says that people on low carb diets have more energy.

Since adiponectin is made in adipose tissue like all other adipokines, one would think that having a lot of fat would create a lot of adiponectin, when actually, we create just as much of it if not more when we don’t have the fat stores in our bodies. Our bodies use fat in our bones to create adiponectin. Actually, Levels of the hormone are inversely correlated with body fat percentage in adults [5]  “Contrary to expectations, despite being produced in adipose tissue, adiponectin was found to be decreased in obesity.[3][5][15]

“The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes,[5] obesity, atherosclerosis,[3] non-alcoholic fatty liver disease (NAFLD) and an independent risk factor for metabolic syndrome.[9] 

So, how do we increase this hormone? Since levels of the hormone are inversely correlated with body fat percentage, the more fat we have the less adiponectin we have in our systems. This in itself, leads to more obesity, more diabetes and everything that comes along with that.

Again According to Wikipedia;

Weight reduction significantly increases circulating levels.[11]” “A low level of adiponectin is an independent risk factor for developing:

That means to avoid low levels of adiponectin in your body, weight loss is crucial. This places more importance on calorie restriction. But there’s good news for those carboholics who have trouble restricting their calories,   “…omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have shown increased plasma adiponectin.[28] Curcumin, capsaicin, gingerol, and catechins have also been found to increase adiponectin expression.[29]

The most optimum way of reducing calorie intake is fasting. Most every religious practice have some form of fasting within is practice, with the exception of Christianity. When Christians get together, it’s usually in the form of a potluck meal. Christians love to eat. But even Jesus fasted for 40 days and nights. Is it any wonder that Jesus was so smart?

Fasting not only affects your hormones, it has multiple, other effects on the body that are all wondrous. Fasting brings with it, important benefits to the health of your brain.

  • It increases BDNF in your brain. This is what enables your brain to grow.
  • It’s ramps up the expression of Nrf2 in your genes and that can boost your anti-oxidants exponentially. ramping up your immune system and keeping your healthier than any medicine can.

So, it not only boosts brain growth, it boosts anti-oxidant production which keeps you healthier by being better able to fight off illness and disease.

Fasting conjures up images of starvation, though. This may be true is you are one of those unfortunate individuals who is still stuck on a carbohydrate diet. On a carbohydrate diet, fasting is next to impossible. At the least, it’s very difficult and involves a massive amount of discomfort.

The best way to avoid this discomfort
is to convert your diet to a low carb diet,

preferably a diet without any carbs.

This is where a fat tax might be a good idea. Tax carbohydrates by the amount of fat they create, which is influenced directly by their place on the glycemic index. This would force the population to cut back on their intake of this dangerous food. It might also help to pay for all the medical needs that carboholics are going to need if they continue to consume these killing field grains.

We as a population have to do something to correct this aberration to our diet. This food is killing us painfully, expensively and indiscriminately. As a society, we can’t allow this to continue unabated, as it has, for the last 60 years.

It’s Time For A Cure,

Curb Your Carbs

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 bloodstream, 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 bloodstream 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 bloodstream 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 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 bloodstream 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 your 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 to 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 signaling 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 cardiovascular 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 a 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 number of carbohydrates you ingest every day. The result is exponentially worse than you would ever want to believe.

So, how do you stop 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, The Newly Discovered Death Sentence

The Newly Discovered Death Sentence of Starches & Carbohydrates

Baguette With Cereals Stock PhotoI know you’ve been told that you need your carbs, that they’re healthy for you and that they must make up a major part of your diet. How long have they been at the bottom of our food pyramid, telling us,
they should make up the largest portion of our meals? How long have we been heeding this messagePopcorn Stock Photo? I’ve been doing it all my life. Haven’t you?

But what if what you’ve been told was wrong?

What if we don’t need them in the quantities we’ve been told to eat them? gallery-thumbnailsCan you eat too many of them? Who doesn’t? It’s easy to do. That’s due to their addictive nature. We’ll get deeper into that, later.

What if you don’t need carbohydrates at all?
Can you live without them?
Can you live without them and still be healthy?

The question I would rather ask, if you can be healthier without them, wouldn’t you want to be?

danger-overeating-grim-reaper-touches-obese-man-eating-big-burger-vector-illustration-41031546==========health-care-diabetes-info-text-23318754

ABSOLUTELY!

I can tell you right now, you can actually live healthier without them. I can tell you that you can live much easier without them. I can tell you that I live with less pain without them and you too can live with less pain without them. I can tell you that you’ll have fewer headaches without them, I don’t have headaches anymore. I can tell you that you that you won’t have intestinal problems anymore and i can tell you that you can save your brain and make it smarter, without them. Does this mean that you were lied to in the past, when you were told that they had to be the largest portion of your diet? to eat them in excess? Examine the evidence, analyze and assess the information, then you be the judge.

You Do Not Need Carbohydrates. 

At least, you don’t need them in the amounts that people everywhere are eating them. By everywhere, I mean everywhere. No place can be found where carbs are not a major part of the diet. To narrow down the problem with carbs, this post and entire site, in general, deals entirely with the high starchy carbs you find in all cereal grains, primarily wheat, barley, and rye because of the gluten that comes with it. But that’s only part of it, which we’ll talk about later in greater detail, because when you ingest gluten, you also eat gliadin. This is the part of wheat that can cause brain damage. That’s something else that we’ll talk about later, in greater detail when we look at how carbs have the capacity to shrink your brain.

But we should start with why you should limit your carbohydrate intake to as little as possible. For starters,  to ensure yourself better health, lower weight and most importantly, less illness and disease throughout your life. Secondly, to reduce your pain levels by reducing inflammation. Thirdly,  to reduce headaches of any nature. and fourthly, to get better sleep. The full gamut of benefits is really much greater and is covered on the benefits posts of a Life Without Carbs and My Life Without Carbs.

Because your body can’t burn carbohydrates (sugars), it has to turn them into fat, so they can use for fuel. Your body burns fat, not carbs. It actually likes fat so much, it would much rather have it spoon fed to it rather than make its own. The problem with using carbs to supply your fat, is that the fat it turns into, is not a good fat. Because carbs need insulin to be turned into fat, the insulin instructs that fat to go to storage, so all of it gets stored, instead of being used, and this is where the problem begins. It’s the consumption of this starchy food that leads to the massive amounts of weight gain that everyone who eats it, experiences. But then, most of you already know this. It’s just impossible to quit eating it, because of its addictive nature.

Fat Woman Stock Photo
A Simple Decision Can Change Your Health Forever
diet-lady-with-red-apple-100175663
Stop Eating Bread
Time for a disclaimer;

Not all people are subject to this weight gain from cereal grains, only about 90% of us are. That means, about 10% of the population have no intolerances to wheat, gluten or any of the components that come with it. That also means that for 90% of us, we do have an intolerance to it. That means, for 90% of us, we express an allergic reaction to it. The problem with that is, the allergic reaction we experience is weight gain, and this ‘expansion‘ happens, whether it’s wanted or not. Anyone of us who has any kind of an intolerance to wheat, gluten or any other components of this grain will express this ‘expansion’, when we eat it.

Whether you want to accept it or not, carbs are dangerous.

I know you probably don’t want to accept this but bear with me, it’s necessary for you to know what you’re putting in your body and what’s it’s doing to you. Even the smallest amount causes your body distress. This is why we shouldn’t be eating this food, to begin with, remember, (bread = carbs = disease = death);

For the short list, Carbs are responsible for;
  1. Primary Cause of type 2 diabetes 
  2. Primary Cause of Celiac Disease 
  3. Primary Cause of headaches
  4. Primary Cause of Peripheral Neuropathy
  5. Primary Cause of dementia and brain damage (type 3 diabetes)
  6. Primary Cause of heart disease
  7. Contribute to a multitude of gastrointestinal disorders
  8. Are the major contributor to more than half of all cancers
  9. Are the primary cause of LDL particles (“bad” cholesterol)
  10. Primary Cause of Epileptic Seizures
  11. Primary Contributor to Arthritis 
  12. Addictive Nature Making Them as 
  13. Deadly as Heroin, Cocaine, Tobacco and Alcohol.
  14. Primary Thief of Emotional Control
  15. Primary Cause of Of Tooth Decay
  16. Primary Cause of cause of aging
This can be validated by reading Wheat Belly and Grain Brain. Both of these publications will fully explain what these carbs do to you as well as how they do it. (Which is also covered in the rest of the posts on this site) Let’s take a closer look, right now, at the above manifestations that can and do occur from ingesting this food.
  • Type 2 diabetes is caused primarily by obesity and carbs play a
    Diabetic Lancet Device In Hand Stock Photo
    Is Diabetes Your Goal?

    major role in obesity. 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 bloodstream 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 bloodstream 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 diabetes. If you take away the carbs, you take away the obesity and excess glucose. Can it really be that simple? Duh!

  • They cause headaches Dr. Perlmutter, in his book, Grain Brain, takes 12 pages to explain how headaches are caused by carbohydrates, wheat and gluten in particular. As Dr. Perlmutter is a board-certified neurologist and a nutritionist, I trust him. Wouldn’t you? Shouldn’t you?
  • Peripheral Neuropathy  Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Wikipedia says, It is important to recognize that glucose levels in the blood may spike to nerve-damaging levels after eating, even though fasting blood sugar levels and average blood glucose levels may still remain below normal levels (currently they typically are considered below 100 mg/dL for fasting blood plasma and 6.0% for HGBA1c, the test commonly used to measure average blood glucose levels over an extended period). Studies have shown that many of the cases of peripheral small fiber neuropathy with typical symptoms of tingling, pain, and loss of sensation in the feet and hands are due to glucose intolerance before a diagnosis of diabetes or pre-diabetes. Such damage often is reversible, particularly in the early stages, with changes in diet, exercise, and weight loss.”  According to Dr. Davis, “A common cause of peripheral neuropathy is diabetes. High blood sugars occurring repeatedly over several years damage the nerves in the legs, causing reduced sensation (thus allowing a diabetic to step on a thumbtack without knowing it), diminished control over blood pressure and heart rate, and sluggish emptying of the stomach (diabetic gastroparesis), among other manifestations of a nervous system gone haywire.” He goes on to say, “Of 35 gluten-sensitive patients with peripheral neuropathy who were tested positive for the antigliadin antibody, the twenty-five participants on a wheat- and gluten-free diet improved over one year, while the ten control participants who did not remove wheat and gluten deteriorated.” and ” Formal studies of nerve conduction gluten-consuming group were also performed, demonstrating improved nerve conduction in the wheat- and gluten-free group, and deterioration in the wheat- and gluten-consuming group.”
  • Celiac disease Celiac disease is caused by a reaction to gliadin, a prolamin (gluten protein) found in wheat, and similar proteins found in the crops of the tribe Triticeae (which includes other common grains such as barley and rye).[3]  Gluten—which is Latin for “glue”—is a protein composite that acts as an adhesive material, binding flour together to make bread products, including crackers, baked goods, pasta and pizza dough. It’s this dough that likes to gum things up. Remember the last time you pigged out on pizza? Remember the indigestion? You think, that came from the sauce? Think again.
  • Dementia and Brain Damage   Wheat is associated with dementia and brain dysfunction, triggering an immune stock-photo-44379182-alzheimer-s-word-cloudresponse that infiltrates memory and mind. Dr. William Davis explains it best in his best seller, Wheat Belly, “In one particularly disturbing Mayo Clinic study of thirteen patients with the recent diagnosis of celiac disease, dementia was also diagnosed. Of those thirteen, frontal lobe biopsy (yes, brain biopsy) or postmortem examination of the brain failed to identify any other pathology beyond that associated with wheat gluten exposure. Prior to death or biopsy, the most common symptoms were memory loss, the inability to perform simple arithmetic, confusion, and change in personality. Of the thirteen, nine died due to progressive impairment of brain function.” Yes, you read that right: fatal dementia from wheat ingestion. Dr Perlmutter explains it in more detail in Grain Brain. If you want to join all the other seniors who are all losing their minds to Alzheimer’s disease or dementia of any sort, all you have to do is to continue to eat your bread, pasta, crackers, pancakes, donuts, tortillas and other wheat products and you’ll be right there with everyone else. When was the last 36717144-a-depress-senior-person-with-wood-backgroundtime you misplaced your keys or forgot something? But look on the bright side of it, if you want to keep eating your donuts, you can, as long as you don’t mind that you won’t get to bathe yourself after a while, because you’ll soon have it done for you. I talk more about why this happens.
  • Heart disease (cardiovascular disease) has too many risk factors to list here, because there are many kinds of cardiovascular disease, but one of the biggest of concern, is the excess sugar in the blood (diabetes), as well obesity (excess weight the body need to supply blood to), as well as the high blood pressure and the  high Heart With Stethoscope And Money Stock Photoamount of plaque in the blood due to the glycation of cholesterol thanks to the extra sugar in the blood.  It is estimated that 90% of Heart disease is preventable.[3]  All the causes listed here are caused by eating wheat. Life Insurance agents have to ask 4 times the standard premium to submit an application for a policy on anyone who had both diabetes and high blood pressure, because of the high underwriting risk. If they want a policy, they have to pay 4 times the standard premium because of their condition. And the condition is preventable. What’s keeping you from declaring your independence?
  • Gastrointestinal disorders by gumming up your digestive system with the gluten that comes with all wheat, especially the high gluten bread and pizza dough. All this glue sticks to the walls of your intestines blocking the digestion of other foods as well as itself. Everyone I know who loves to consume their daily pastries, pasta, biscuits, rolls and crackers, already know about the cramps that build up in their stomachs, due to the amount of undigested food that can’t get through the glue to get digested. This gluten, that’s in wheat, barley, spelt, rye and almost every other variant of wheat, is the substance that causes all the damage to your digestive tract. This glue plays a major role in acid indigestion, acid reflux, heartburn, constipation, nausea, and even general stomach upset.  With 10 different disorders of the digestive tract, gluten plays a gumming role in each one of them. You know the gas and bloating you get, sometimes after a meal? Guess what? Yeah, the major cause of that can be tracked to starchy carbs. And it’s not even included in the above list. I can’t help but wonder why people continue to eat this pseudo-food. I keep finding OTC medicine, that I’ve been purchasing over the years, just to combat; excess gas and bloating, acid indigestion, acid reflux, nausea, constipation, diarrhea, worse yet ulcers. All of these manifestations could be curbed with the reduction of wheat and grains in our diets. That gurgling you just heard from your stomach, was that your stomach telling you to get your act together, and stop the carb intake?
  • Cancer gets its assist from the excess sugar that’s continuously circulating in your blood. It keeps your ph levels in an acidic range which is an invitation to illness and disease. Acidosis is not something you want to have to deal with, with all the problems that it can produce. “Healthy human-arterial blood pH varies between 7.35 and 7.45. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.[1]Cancer loves it when your blood ph levels go into acidosis from the amount of sugar, carbs dump into your blood. This is what leaves your body open for attack, from a multitude of illnesses and diseases, cancer only being one of them. A more complicated explanation of how carbs cause cancer is in the post about the Diseases Caused By Plaque. Again, if cancer gets an assist from carbs, doesn’t it make sense that if you took away the carbs, you’d, at the least, hamper the disease’s, progression, if not stop it altogether. Can it be that simple? Can you give me a reason not try it and find out?
  • Epilepsy Illness Means Poor Health And AfflictionsEpileptic seizures A peculiar syndrome of temporal lobe seizures unresponsive to seizure medications and triggered by
    calcium deposition in a part of the temporal lobe called the hippocampus (responsible for forming new memories) has been associated with both celiac disease and gluten sensitivity (positive antigliadin antibodies and HLA markers without intestinal disease).
  • Old Man With Walking Stick Showing Aged 3d Character Stock PhotoArthritis is a disease of inflammation, which is aggravated by wheat more than anything else, because of the amount of sugar it dumps into the bloodstream. Few other sources of sugar are higher than bread and wheat products. Not even table sugar itself. Arthritis is caused by inflammation. Inflammation is influenced by the amount of glucose in your blood, which is influenced by the number of carbs you eat. Again, can it be that simple? Remove the carbs and you can ease, if not eliminate, it’s influence on Arthritis.
  • Addiction According to Dr. Davis, “There is no doubt: For some people, wheat is addictive.” It has to do with the effect it has on our neurotransmitters and neuropeptides,Phrase "addicted To Sugar" Made Of Red Sugary Candies Stock Photo primarily Serotonin and Endorphins. “Endorphins (“endogenous morphine”) are endogenous opioid neuropeptides.” They’re the feel-good neuropeptides. This is the same neuropeptide that’s activated by alcohol, tobacco, heroin, cocaine, marijuana and all other substances of an addictive nature, that give you the ‘morphine‘ feeling. When was the last time, you had to have something to eat? What was it, you hungered for? How long was it before you had eaten the previous time? How long can you go without eating? I often go 18 hours a day eating enough for 1 snack, because of my keto diet. Can you?
  • Emotional Distress and Disorder takes place every time you ingest this food, in any form, it’s ingested, this is directly due to the to the fluctuations in your blood glucose, caused by the consumption of wheat and grain foods. Blood sugars go up, moods rise. blood sugars go down, moods depress. It’s that simple. The point I want to bring up, is it’s the rise and fall of your blood sugars that have the biggest impact on your emotional status and hence your emotional health. This in itself leads to behavior that, many times, should never occur in the first place. And it would never occur in the first place, if it weren’t for the abundance of this food in our diet. Behavior like violence, propagated by anger and antagonism. Both of these emotions are influenced as much, if not more than anything else, by the foods we eat. I submit that these fluctuations in emotional levels, are due to the changes in blood glucose, in all who eat this food, and all have been influenced by it. If you remove the wheat and grains, you remove the influence. If you remove the influence, you can easier retain your senses. It’s that simple. Behavior driven by fear, is quite possibly the biggest danger our society faces, and this food source is a major cause of driving this behavior, because of it’s palatable nature. Sugar tastes good. People love to ear it. Mass consumption of it alters the emotional status of everyone who eats it, when their blood sugars fluctuate. It’s these fluctuations that cause a large majority of the abhorrent behavior that pervades society everywhere. It’s these fluctuations combined with the influence of mass media that are driving most of the terrorism in the world today. This theft of your emotional control, is what makes you a slave to corporate influence and subject to their desires, not your desires. How long do you want to keep your mental faculties?
  • They Rob You Of Your Teeth Ask any archaeologist, The appearance of rotten teeth marked the beginning of the agricultural age in our ancient history. It moved us from being hunter-gatherers to farmers. Even though this transition was one of the first moves into civilization, It also served to introduce our bodies to the ravages of carbohydrate nutrition. Fortunately, for our ancestor’s sake, it wasn’t as dangerous then, as it is, now. It hadn’t been genetically modified.  The wheat that was grown at that time was unmodified einkorn. It didn’t rob us of our senses, then, because it didn’t fluctuate blood sugars to the extent, that all wheat and grain products it does today. Whatever was eaten had 100 times the fiber in it to slow down the absorption of sugars into the system, fluctuating the blood glucose, in the massive ways they do today. Hence, they didn’t cause the diseases, then, that it causes today. I submit, that it this sudden fluctuation in sugars, that is causing 88% of all illnesses and diseases, that we have to deal with in our modern society. That, in itself, makes us victims of our own advancement, going back to the start of civilization. But, that’s only looking at the past, at the reason why we’re ingesting this food that ruins our teeth. Now, for why it does that. Most of you already know why. It can be summed up in one word, sugar. Sugar rots teeth. Not meat, not cheese, not eggs, not fat, nothing that we consume rots teeth like carbohydrates do. The gluten that we love so much, makes it stick to our teeth, and this is where it begins to do its damage. The sugars work there way into the enamel of your teeth and the decay begins. You brush it away, you floss it away, and you do the best you very can, to keep your teeth as clean as possible. And when you make it to your 75 birthday, you pat yourself on the back, for still having all of your teeth. Or, do you? Have there been times when you couldn’t brush and floss? Do you brush every time you take a sip of a sweet drink or a drink of alcohol? All the sugar contained in those liquids, swirls around your mouth for hours and hours, working on decaying your teeth. Remove the sugar, remove the decay. It’s that simple.
  • Carbs are the root cause of aging due to the AGEs that they cause. This factor is at the root of so many disorders and diseases, that it deserves a blog of its own. Read it here

With all of these ailments, illnesses, diseases, disorders, afflictions, and discomfort being caused by these carbs,cropped-time-cure-clock-prevent-disease-sickness-illness-medical-r-words-face-to-illustrate-fundraising-research-to-find-52768147.jpg

The questions I keep asking myself,

Who in their right mind would ever agree to submit themselves to this torture, by eating them?

Those who don’t know that they do!

Most of us know that sugar is bad for us, but what too many don’t want to fully recognize, is that carbs are sugar. With bread being the most popular carb we eat, every time we eat bread, we know that we’re eating carbs, but we don’t want to equate those carbs with sugar, while in all actuality they are. If Sugar Kills, Carbs Kill.

We know that Sugar Kills, but we don’t want to listen to that song because of our addiction to it.

All of the manifestations listed above have been documented in several publications, but they’ve seldom been presented for review and examination, to the medical community. Not until Dr’s Davis’ and Perlmutter’s books, Wheat Belly and  Grain Brain, came forth to warn us about the atrocities this supposedly nutritious food has been doing to us, did we even know we were eating something that is so poisonous (at least to the 90% of us, who are allergic to it).

This, in my estimation, is the biggest problem. Most people are allergic to it. I estimate that more than 90% of the population have some sort of intolerance to wheat, gluten or the gliadin that’s in the wheat. That says, that more than 90% of the people are allergic to bread, pasta, crackers, cereals like Wheaties, Wheat Germ, or Special K (to name just a few), any breaded chicken, shrimp, veal, all breaded fried appetizers, all pastries, all nutrition bars, all cereal bars, anything that has any percentage of wheat or wheat substance in it. The list is too long, even for the length of this post. The question this begs, is why is this food still advertised as being healthy?

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If 90% of the population, (as I speculate) are allergic to wheat, that explains the claim that I made at the beginning of this post,

You Do Not Need Carbohydrates.

If you’re one of the 90% who is allergic to them, you’d be much better off without them. With as many problems as this food brings with it, it makes absolutely no sense to continue eating it except to feed your addiction. So this brings us to our next problem, getting off of our addiction to them.

The question is then, how do we stop eating them? How do we get this food that’s been such an important part of our diet since time immemorial, out of our diet? For that, you’ll have to continue on to Carbs, how to cut back.”

If anybody feels that any of these conclusions are nothing more than opinion, my challenge to you is, prove me wrong. I invite you to research any and all statements, facts, data of any sort, or links, that I’ve provided in these posts, to invalidate anything. I’ll even go to the extent to challenge anyone to prove me wrong, in any of my statements. It will generate a good civil discussion, and that’s something I can look forward to, anytime.

My sincere wish, is that everyone who reads these pages verifies and validates what they read. Only then will they know that the information contained within this site is 100% valid. Maybe then, all who read this, will change their behavior and in turn, change the behavior of the whole world.

My challenge to you, is to give a low carb diet a try, for 2 months. If you don’t see any benefit after just 2 months, of abstinence, go back to your high carb diet. But please, prepare yourself to suffer the consequences. You must have given it an honest try, and not cheated at all, for this to work. Any deviation, will not let your body go into ketosis and that’s what’s important.  You have to look at it like your life depends on it, because, it does.

If You Like Bread, You’re As Well As Dead,

Unless Your Change Your Eating Habits

Don’t Fall For Their Ruse