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;
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.
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.
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.
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;
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.
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.
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.
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.
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.
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.
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;
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;
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;
- Inflammation, oxidative stress, apoptosis, and autophagy in diabetes mellitus and diabetic kidney disease: the Four Horsemen of the Apocalypse.
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;
- The shedding-derived soluble receptor for advanced glycation endproducts sustains inflammation during acute Pseudomonas aeruginosa lung infection.
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.
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;
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.
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;
- Bazedoxifene Ameliorates Homocysteine-Induced Apoptosis and Accumulation of Advanced Glycation End Products by Reducing Oxidative Stress in MC3T3-E1 Cells.
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).
- Plasma Levels of Pentosidine, Carboxymethyl-Lysine, Soluble Receptor for Advanced Glycation End Products, and Metabolic Syndrome: The Metformin Effect.
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;
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.