High-Carb Diets Can Be Tough on Bacteria, Too

Sugars are toxic in excess because they are highly reactive. But we don’t normally think of them as toxic to bacteria. Bacteria thrive by eating sugars.

I was reading “TB or Not TB?” at The Scientist and was amused at this anecdote, about efforts to find new ways to kill drug-resistant TB:

Rainer Kalscheuer, now at Heinrich-Heine University in Germany, was searching for genes and proteins that made some TB cells more treatment tolerant than others. After doing a microarray analysis, Kalscheuer wanted to investigate a metabolic intermediate enzyme called GlgE, but Jacobs balked. “I told him a group at Harvard had already shown that glgE was an essential gene that can’t be manipulated,” Jacobs remembers. But Kalscheuer persevered and found out that glgE could be knocked out and studied if grown in the right culture medium.

Note for grammarians: glgE is the gene, GlgE is the protein.

The key to creating viable glgE knockout strains turned out to be trehalose, a cell wall carbohydrate. TB bacteria that lacked glgE died instantly when trehalose was present, but survived if it was removed. The Harvard group had used medium that contained trehalose without realizing it because the carbohydrate, used as a preservative, was an unlisted ingredient.

This is the kind of thing that drives impatient biologists crazy. Experiments are so sensitive to subtle variations, such as an unlisted preservative in the culture medium, that Biology smiles only on those who are exceedingly careful, thoughtful, and patient with tedious troubleshooting. Also, those who don’t put too much faith in the results of their peers!

The next step for Kalscheuer and Jacobs was figuring out the functional relationship between the two proteins. GlgE had been implicated in glycogen metabolism, but the connection with trehalose was unclear. Finally, after a painstaking series of suppressor genetics experiments, they elucidated the biochemical pathway: Glycogen and glucose produce trehalose; an enzyme known as trehalose synthase converts the trehalose into maltose; then, the maltose becomes maltose-1-phosphate, the protein that GlgE converts into glucan. When glgE is knocked out, maltose-1-phosphate accumulates, which kills the tuberculosis bacterium.

Turnabout is fair play. It seems only fitting that bacteria should die from high-carb diet toxicity. Why should humans be the only ones?

Obesity: Often An Infectious Disease

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.


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.


[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.

Saturated Fat REDUCES risk of stroke and heart disease

As readers of the book know, we regard saturated and monounsaturated fats as the only macronutrients that are safe in unlimited doses. Other macronutrients become toxic above certain levels: glucose above 600 calories per day, protein above about 600 calories, and polyunsaturated fats above 100 calories. We recommend that 60% of calories or more be obtained from saturated and monounsaturated fats.

Since eating more saturated and monounsaturated fats is likely to displace toxic nutrients from the diet, in the general population we would expect higher saturated and monounsaturated fat intake to reduce disease rates.

Despite the prejudice the medical profession has long held against saturated fats, there was never real evidence against them. But after many decades of demonization, high quality studies are now showing saturated fat to be health-improving – just as we would expect.

A New Study from Japan

Via Dr. Briffa and Dr. Stephan Guyenet comes word of a new study from Japan.

This study followed 58,453 Japanese adults, aged 40 to 79 at the start of the study, for 14.1 years. [1] The study found that higher saturated fat intake was associated with:

  • A 31% reduction in mortality from stroke
  • An 18% reduction in mortality from cardiovascular disease

It was only earlier this year that a systematic review of the literature found that “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.” [2] In a few decades the reviews will probably have to go further: there will be significant evidence that dietary saturated fat is protective against CHD and CVD.


[1] Yamagishi K et al. Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk Study. Am J Clin Nutr. 2010 Aug 4. [Epub ahead of print] http://pmid.us/20685950.

[2] Siri-Tarino PW et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46. http://pmid.us/20071648.

Happy Birthday, Walter Breuning!

Those who have bought the book know that the world’s oldest man, Walter Breuning of Great Falls, Montana, figures prominently, as he did in this post.

Walter is celebrating his 114th birthday today, Tuesday, September 21. We’d like to offer him our best wishes for a happy day!  May his liver and onions be most tasty!

Sunday’s Great Falls Tribune had a story about Walter’s upcoming birthday. They interviewed some of his fellow residents at The Rainbow in downtown Great Falls:

92-year-old resident Ray Milversted … said he doesn’t mind Breuning living in the Rainbow, but he expressed sympathy for the world’s oldest man, who has visitors “waiting in line and all asking the same questions.”…

Milversted said Breuning is “a nice person” and “not a pain.”

If at 114 I’m still here and my neighbors don’t mind having me around, I’ll consider that quite an accomplishment! Congratulations Walter!