Category Archives: Diabetes - Page 3

Wheat Is A Cause of Many Diseases, I: Leaky Gut

Posted by on October 26, 2010 80 comments

I realized last week that I often call wheat the most toxic food, but I haven’t really explained why on the blog. The book has a detailed explanation, which focuses on toxicity effects and on autoimmune processes attacking the gut and thyroid. Here I would like to add to the book’s argument by showing how wheat causes other autoimmune diseases.

There are about 50 diseases which are thought to have an autoimmune basis. Autoimmune diseases are caused by three processes:

  1. Leaky gut and inflammation. A leaky gut lets bacteria and food toxins enter the body. In the body, these precipitate an immune response which creates inflammation and a chance for antibodies to form.
  2.  “Molecular mimicry.” A bacterial protein or food toxin resembles a human protein sufficiently closely that an antibody to the foreign protein may also recognize human proteins, potentially precipitating attacks on self tissue.
  3. Adjuvant activity. Vaccines are produced by bonding an antigen (the target of the hoped-for antibody) to an adjuvant (a molecule that greatly increases the likelihood antibodies will be made – a sort of catalyst). If a “molecular mimic” can bind to an adjuvant, then autoimmune disease becomes much more likely.

Wheat causes many autoimmune diseases because it promotes all three aspects. I’ll look at each aspect in a separate post this week.

Leaky Gut

In a recent comment – it’s nice to have smart readers! – Rich brought up the links between wheat and leaky gut.

Leaky gut is the first step toward autoimmune disease. As a recent review states:

Susceptibility to at least 50 diseases, including celiac disease (CD) and type 1 diabetes (T1D), has been associated with specific HLA class I or class II alleles. A common denominator of these diseases is the presence of several preexisting conditions that lead to an autoimmune process…. In all cases, increased permeability precedes disease and causes an abnormality in antigen delivery that triggers immune events, eventually leading to a multiorgan process and autoimmunity. [1]

Gluten is a complex of proteins found in wheat, rye, oats (PAJ: see comments), barley, and other grains. One part of gluten is a type of protein called prolamins, which are chiefly responsible for gut damage:

It is the gliadin fraction of wheat gluten and similar alcohol-soluble proteins in other grains (collectively known as prolamins) that are associated with the development of intestinal damage. A common feature of the prolamins of wheat, rye, and barley is a high content of glutamine (>30%) and proline (>15%), whereas the nontoxic prolamins of rice and corn have lower glutamine and proline content. [1]

I’m quoting this because it speaks to the differences among grains. Rice and corn do not contain gluten. Corn contains other dangerous toxins, but is not a primary cause of autoimmune disease. Rice is the only grain we consider safe to eat.

From Cholera to the Cause of Leaky Gut

The mechanisms by which wheat causes leaky gut have been intensively studied by Dr. Alessio Fasano’s group. In 1995 Dr. Fasano and colleagues discovered that a toxin released by Vibrio cholerae, the bacterium that causes cholera http://en.wikipedia.org/wiki/Cholera, causes tight junctions to open for a time. [2] This makes the small intestine leaky.

Dr. Fasano and colleagues suspected that the bacterial protein’s action must mimic some natural human protein which controls intestinal permeability. In 2000, they discovered this human protein and named it “zonulin.” [3]

Wheat and Crohn’s Disease

They subsequently showed that gliadin stimulates zonulin release. Gliadin binds to a receptor called CXCR3, and activation of this receptor triggers zonulin release and increased intestinal permeability.

Interestingly, zonulin release was much higher and longer-lasting in Crohn’s disease patients than in healthy patients. [1] Restriction of gluten restores intestinal integrity in Crohn’s disease patients.

So Crohn’s disease patients should absolutely not eat wheat!

Leaky Gut and Type I Diabetes

A leaky small intestine is a feature of many autoimmune diseases, but Crohn’s disease and Type I diabetes are notable for highly permeable small intestines. Patients with both diseases have high serum levels of zonulin. [1]

In a rat model of Type I diabetes, the BioBreeding diabetes prone or “BBDP” line of rats often develops a leaky gut at age 50 to 75 days when eating a (toxic) diet of rat chow. Zonulin levels increase up to 35-fold at this time, but were reduced if the rats were fed a gluten-free diet. Rats with the highest zonulin levels developed Type I diabetes develops 15 to 25 days later. If a compound that blocks the action of zonulin is given to the rats, Type I diabetes incidence is reduced 70%. [1, 4]

This shows how crucial a leaky gut is to onset of autoimmune diseases like Type I diabetes, and also how quickly diseases can develop once the gut is compromised. The longer the gut is leaky, the greater the likelihood that some autoimmune disease will develop.

In humans, the relationships between these diseases are much the same as in rats. Crohn’s disease and Type I diabetes are co-morbid: the prevalence of Crohn’s among Type I diabetics is 6- to 9-fold higher than in the general population. Meanwhile, newborn children exposed to wheat at 3 months of age or earlier, when the gut is immature, are 4- to 5-fold more likely to develop Type I diabetes. [4]

Conclusion

Leaky gut is a prerequisite for development of autoimmune disease. Wheat seems to create a transient, mild leaky gut in nearly everyone, but in Crohn’s disease the gut becomes chronically and severely leaky in response to wheat consumption.

In rats, this leaky gut can lead to development of autoimmune diseases like Type I diabetes in as little as a few weeks.

If you eat wheat, it’s probably only a matter of time before you develop some disease or other. All of the autoimmune diseases, from rheumatoid arthritis to Hashimoto’s to lupus, are made more likely by wheat consumption. Why not switch to rice or other “safe starches” and save yourself some trouble?

Related Posts

Other posts in this series:

  1. Why Wheat Is A Concealed Cause of Many Diseases, II: Auto-Antibody Generation. Oct 28, 2010.
  2. Why Wheat Is A Concealed Cause of Many Diseases, III: Adjuvant Activity Nov 1, 2010.

References

[1] Visser J et al. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Ann N Y Acad Sci. 2009 May;1165:195-205. http://pmid.us/19538307.

[2] Fasano A et al. Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization, in vitro. J Clin Invest. 1995 Aug;96(2):710-20. http://pmid.us/7635964.

[3] Wang W et al. Human zonulin, a potential modulator of intestinal tight junctions. J Cell Sci. 2000 Dec;113 Pt 24:4435-40. http://pmid.us/11082037.

[4] Watts T et al. Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats. Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2916-21. http://pmid.us/15710870.

Obesity: Often An Infectious Disease

Posted by on September 22, 2010 36 comments

In the book we attribute obesity mainly to food toxins and malnutrition. Both are well attested as causes of obesity in animals:

  • The easiest way to induce obesity in animals is to feed them a carb toxin and a fat toxin – e.g. wheat, fructose, or alcohol with polyunsaturated fats or hydrogenated trans-fats.
  • Obesity in animals can also be induced by nutrient deficiencies, as in the “methionine-choline deficient diet.”

These causes also seem to be active in humans:

  • Intake of fructose and polyunsaturated fats is strongly associated with obesity in humans.
  • Famine studies show that those who experience a period of severe malnourishment are more likely to become obese.

However, in general we attribute diseases to three causes: food toxins, malnutrition, and infections. This suggests we should look also for infectious causes of obesity.

Adenoviruses Can Cause Obesity in Humans

The study of “infectoobesity,” or pathogen-induced obesity, got underway with the discovery of four viruses that could induce obesity in animals. These four viruses — canine distemper virus, Rous-associated virus type 7, Borna disease virus, scrapie agent – were not able to infect humans. However, in chickens, mice, sheep, goat, dogs, rats and hamsters, these viruses infect the central nervous system and induce obesity through effects on the brain and nerves. [1,2]

But then an avian adenovirus, SMAM-1, was found that infects humans and induces obesity in chickens. SMAM-1 works by a different mechanism; it acts directly on fat cells. [2]

Subsequently 3 human adenoviruses, AD-36, AD-37, and AD-5, have been found that act directly on human fat cells and are associated with human obesity. [2] A group led by Dr. Nikhil Dhurandhar of Wayne State University in Michigan showed that AD-36 can induce obesity when given to chickens, mice, and marmosets. [1]

AD-36 Can Spread By Contact

In Dr. Dhurandhar’s chicken experiments, the virus spread fairly easily. Chickens that shared a cage with an infected bird showed signs of the virus in their blood within 12 hours, suggesting that the virus can be spread by nose or mouth secretions. [3]

To Get Really Fat, You Need an Adenovirus Infection

A new study [4] has given us new information about the prevalence and effects of AD-36 in humans. The study found that 22% of obese children (that is, children in the top 5 percentiles of BMI), but only 7% of non-obese, have AD-36 antibodies. Moreover, among the obese children, those who were AD-36-antibody-positive were much fatter than the other obese children. It seems the top 0.1% of children in BMI are probably overwhelmingly made up of AD-36-infected children.

Metabolic Benefits?

It may not be all bad news. AD-36 promotes proliferation of fat cells. Thus, while it promotes obesity, it may also help prevent diabetes. By creating a bigger pool of fat cells to help clear excess glucose from the blood, toxicity from hyperglycemia is reduced, at least for a time.

In Dr. Dhurandhar’s experiments, the extra fat cells showed metabolic effects consistent with enhanced glucose clearance. Infected chickens had lower serum cholesterol and lower triglyceride levels. [3] So infected chickens are fatter, but in some respects healthier.

Pathogens May Be The Source of Disease Diversity

Close readers of our book may have noticed that a combination of carb and fat toxins is, we believe, the most common cause of metabolic syndrome, diabetes, and obesity.

Yet there are thin diabetics and obese non-diabetics. How is it that the same cause can produce different diseases?

One thing the adenovirus work is telling us is that the nature of one’s chronic infections may determine how bad diets translate into disease. Toxic and malnourishing diets make disease inevitable, but which disease depends on which pathogens happen to be around to exploit the bad diet and weakened immunity.

Lessons for the Non-Obese

I certainly wouldn’t avoid contact with obese people for fear of contracting AD-36. These pathogens are everywhere and infection is inevitable. Most elderly probably have hundreds of chronic infections.

The key to health is not avoiding germs, but maintaining a powerful immune system that prevents pathogens from causing disease. That means a healthy diet, good nutrition, and immune-enhancing practices like fasting and ketogenic diet days.

Conclusion

It appears that:

  • It’s possible to become obese from food toxins and malnutrition alone;
  • Some – it’s not yet clear what fraction – obese people do become obese from food toxins and malnutrition alone;
  • But to become really obese, or to become obese really young, you may need a viral infection to help the obesity along.

In the book, we focus on elimination of food toxins and malnutrition as weight-loss steps. The Perfect Health Diet, controlled to 2,000 calories per day, is a weight loss diet for the obese as well as a healing diet for the metabolic derangements that underly obesity.

What the evidence for adenoviruses in obesity is telling us is that the obese may need to take another dietary step as well:  autophagy-promoting steps like fasting. Autophagy is a primary immune mechanism against viruses, so fasting enhances viral immunity.

As always, we recommend that fasts include substantial amounts of coconut oil to help the liver make ketones and relieve the burden on the liver and the risks of glucose deficiency.

References

[1] van Ginneken V et al. “Infectobesity”: viral infections (especially with human adenovirus-36: Ad-36) may be a cause of obesity. Med Hypotheses. 2009 Apr;72(4):383-8. http://pmid.us/19138827.

[2] Atkinson RL. Viruses as an etiology of obesity. Mayo Clin Proc. 2007 Oct;82(10):1192-8. http://pmid.us/17908526.

[3] Dhurandhar NV et al. Transmissibility of adenovirus-induced adiposity in a chicken model. Int J Obes Relat Metab Disord. 2001 Jul;25(7):990-6. http://pmid.us/11443497.

[4] Gabbert C et al. Adenovirus 36 and Obesity in Children and Adolescents. Pediatrics. 2010 Sep 20. [Epub ahead of print] http://pmid.us/20855385. See also http://ucsdnews.ucsd.edu/newsrel/health/09-20ViralInfection.asp.

Drugs: Often Unsafe at any Dose

Posted by on September 18, 2010 17 comments

If you have impaired health, go see a doctor.  Use them first for diagnosis; doctors can do lots of tests to help clarify your condition, and they have tremendous clinical experience and great insight into many conditions. But be wary of their drugs. Do your own independent and critical evaluation of any drug recommendation.

The most helpful drugs are of two kinds:

  • Bio-identical replacements for deficient human compounds. Think insulin for diabetes, or thyroid hormone for hypothyroidism.
  • Antibiotics for conditions in which the causal pathogen is known or strongly suspected. The trouble here is that in many chronic diseases, the pathogens which cause the disease are not known. Choosing the wrong antibiotics may do more harm than good.

Most other drugs are designed to ameliorate some disease symptom, at the cost of introducing new health problems elsewhere. Over time, these negative effects often prove far more damaging than the drug’s benefits.

I explained why a few posts ago:

Much pharmacological research in recent decades has been devoted to “targeting” individual proteins or genes, and seeing if these interventions produce beneficial results in some disease or other….

The human body is the result of a long evolutionary history. Our ancestral genome reached its current size, about 20,000 genes, prior to the Cambrian explosion. For over 500 million years, the thrust of evolution has been to make the gene-protein network as sophisticated as possible, as densely networked with subtle interactions between as many molecules as possible. Every gene has an important role to play in that network, and directly influences perhaps a hundred partners. Thus, targeting a single gene will not only deprive the body of that gene’s function; it will also deprive that gene’s hundred partners of the benefits of its interactions, and thus impair their function, which will have ramifications upon their partners, until the whole genome has been affected. Thus, all interventions in the human body have systemic effects. It is not possible to confine effects to a single “target.”…

If the human body is a highly-optimized densely-networked system, then we must be skeptical toward the “black-box” school of medicine – especially in its new, reductionist, human-gene-targeting form. If evolution has optimized the human gene network to maximize human health, then targeting human genes and proteins is sure to sabotage health, probably in unexpected and insidious ways.

Then, responding to my very next post, Joe D gave us some neat information indicating that the drugs used to treat depression may increase mortality by 30%.

Now Jenny Ruhl, the excellent author of Blood Sugar 101 and proprietor of Diabetes Update, points out that some diabetes drugs are backfiring spectacularly, inducing crippling bone failures and cancer:

A long term study of  Actos [PAJ: pioglitazone] discovered that there is a clear dose and time-related increase in bladder cancer among those who take it.…

Today’s newer generation of drugs target specific genes and cell receptors. The TZD drugs, Actos and Avandia, target the PPAR-gamma transcription factor which regulates genes that affect how lipids are stored….

PPAR-gamma, for example, transforms the bone stem cells that should turn into new bone into new fat cells. This is why after a decade on the drug many people start experiencing broken bones in their arms and legs (the areas where PPAR-gamma is most active) and why once bones begin to break there is no cure. A decade of rebuilding has been subverted and the weakened structure of the bone cannot be fixed.

Jenny observes that the drug approval process, which evaluates for safety over short time periods and efficacy against a specific disease, doesn’t evaluate long-term safety issues:

And this points to the huge problem with the drug regulation process. There is no requirement–none, zilch–that a company applying for permission to market a new drug investigate what OTHER physiological processes are affected by the drugs’s mechanism. All the drug company has to show is that it achieves what they are selling it to do. In the case of Actos and Avandia, that means causing a very modest drop in A1c–about .5%….

Many of these life-ruining side effects happen so slowly they don’t show up for five to ten years–and then it takes a lot of work to link the side effect to the drug….

That is why evidence a that a drug is raising the incidence of cancer rarely appears until a drug is almost at the end of its 14 year patent period. It has taken more than 12 years to notice the link between bladder cancer and Actos. It took nine years after its approval for anyone to notice the signal suggesting that Diovan raises cancer incidence by about 8%.

And that’s why it won’t be until another nine years or more that the public will learn that any drug that inhibits DPP-4 is turning off an immune system mechanism essential to fighting melanoma, prostate cancer, ovarian cancer and lung cancer. Details HERE.

Visit Jenny’s blog to see why Metformin is the only diabetes drug known to be safe, and her recommended changes to the drug approval process. In my view, Jenny’s proposed changes would radically downsize the pharmaceutical industry. Few drugs would pass her filter.

Conclusion

The most powerful and effective way to improve health is through diet and nutrition. Put off drugs until you’ve fixed your diet, and there’s a good chance you won’t need drugs at all.