Tag Archives: Irritable bowel syndrome

Is Your Diabetes Curable or Just Treatable?

Can Your Diabetes be Cured or Just Treated?

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

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

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

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

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

From PMC and PubMed,

Evidence of your carb intake and Diabetes

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

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

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

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

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

  • Issues in Nutrition:Carbohydrates.

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

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

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

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

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

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

OBJECTIVE:

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

RESEARCH DESIGN AND METHODS:

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

RESULTS:

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

CONCLUSIONS:

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

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

  • [Composition of macronutrients in the diabetic diet].

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

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

BACKGROUND:

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

OBJECTIVE:

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

METHODS:

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

RESULTS:

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

CONCLUSION:

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

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

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

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

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

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.