Category Archives: Obesity - Page 5

Why We Get Fat: Food Toxins

Posted by on January 20, 2011 88 comments

Erich asked about the link between omega-6 fats and obesity. It’s a good question and also a good way to introduce the first step of the Perfect Health Diet weight loss program:  removal of toxic foods from the diet.

Vegetable Oils With Fructose or Alcohol

These toxic foods are particularly dangerous in combination. We discuss this mix of toxins in the book (pp 56-59).

If you feed lab animals high doses of polyunsaturated fat (either omega-6 or omega-3 will do) along with high doses of either fructose or alcohol, then fatty liver disease develops along with metabolic syndrome. Metabolic syndrome is a major risk factor for obesity, and it’s not very difficult to induce obesity on these diets.

Both sugar and vegetable oils are individually risks for obesity:

  • Stephan did a nice post a few years back, “Vegetable Oil and Weight Gain,” discussing a couple of studies showing that both rats and humans get fatter the more polyunsaturated fat they eat.
  • Dr. Richard Johnson and colleagues did a review of the evidence for sugar (fructose) as a cause of obesity in the American Journal of Clinical Nutrition a few years ago. [1]

What the animal studies show us is that when fructose and vegetable oils are consumed together, they multiply each other’s obesity-inducing effects.

Here are a few pictures illustrating the correlation between polyunsaturated fat consumption, fructose consumption, and obesity.

Here is the Johnson et al chart showing historical fructose consumption in the UK and US [1]:

Here is Stephan’s chart showing historical polyunsaturated fat consumption in the US:

And here are obesity rates in the US:

Cereal Grains

It’s a common observation that the toxic grains, especially wheat, can produce a potbelly or “beer belly.” Rice doesn’t seem to do that.

There is epidemiological evidence for this effect. Here, for instance, is obesity prevalence by country from the World Health Organization Global Infobase:

Note the low obesity prevalence in the rice eating countries of China, India, Japan, Indonesia, and southeast Asia; and in sub-Saharan Africa, where a diversity of starch sources are eaten, including manioc/cassava, sorghum, millet, rice, maize, and wheat. The highest obesity prevalence is found in wheat-eating countries.

This correlation persists within countries. In the China Study, the correlation of wheat consumption with BMI was 56%, whereas the correlation of total calorie intake with BMI was only 13%. (Since total calorie intake is correlated with muscle mass, total calorie intake may be completely uncorrelated with fat mass. It’s not how much you eat, but how much wheat!)

Similar outcomes occur in mice. I can’t find any mouse studies comparing wheat to rice, but I did find one comparing wheat to rye [4]. Wheat was far more obesity-inducing than rye:

Body fat percentage was 20.2% in the wheat group, 13.7% in the rye group; fasting insulin was 126 pM in the wheat group, 90 pM in the rye group; and fasting cholesterol, triglycerides, and free fatty acids were higher in the wheat group.

In short:  wheat made mice fatter, more insulin resistant, and more dyslipidemic than rye.

Just for fun here’s a picture comparing fat tissue in the rye (left) versus wheat (right) fed mice:

I believe that rice would have done even better than rye, but I was unable to find a paper directly comparing rice vs wheat or rye.

Why We Get Fat

This brings me to a point of difference with Gary Taubes. Although glucose is toxic in high doses, the body has an extensive machinery for disposing of excess glucose. As we discussed in our last post, all tissues of the body participate in glucose disposal. Dietary glucose is not likely to do much damage unless the body’s glucose-disposal machinery has been damaged by other toxins first.

Obesity is caused not by carb calories per se, but by natural plant toxins. Plants, not carbs, make you fat!

It’s possible, by the way, that differing toxicities among grains could be responsible for epidemiological evidence favoring “whole grains” over “refined grains.” In America, products made with refined grains are usually 100% wheat; but products made with whole grains are often of mixed origin (“7 grain bread”). Since wheat is the most obesity-inducing grain, dilution of wheat content may be masking the toxicity of whole grains.

Conclusion

Certain toxic foods seem to be very effective at causing obesity:  vegetable oils, fructose, and wheat. Along with malnourishment (for instance, by choline deficiency) and infectious disease, food toxins are why we get fat.

The first step in any weight loss effort, therefore, ought to be removal of these toxic foods from the diet. Removing these toxins may not cure obesity; but without this step a cure is unlikely.

References

[1] Johnson RJ et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007 Oct;86(4):899-906. http://pmid.us/17921363.

[2] Andersson U et al. Metabolic effects of whole grain wheat and whole grain rye in the C57BL/6J mouse. Nutrition. 2010 Feb;26(2):230-9. http://pmid.us/19647415.

How Does a Cell Avoid Obesity?

Posted by on January 18, 2011 53 comments

I am optimistic that everyone can acquire an attractive and healthy body composition, including women of a certain age. I’ll discuss what I think is the best strategy for that in future blog posts. First, some ground work.

Obesity and weight regulation is a complicated subject, and I have to confess upfront that I am not thoroughly conversant with the literature. I still learn new things every time I delve into the journals. Occasionally, I will I write posts (like today’s) that look into journal articles and molecular pathways related to obesity. This helps me explore ideas and learn. Hopefully you’ll have some fun following along.

A good starting point for an investigation into obesity would seem to be the issue of how weight regulation works in a healthy person. How does our body keep itself at its ideal weight?

Now all the problems our body has to solve, had to be solved about 2 billion years earlier by the first eukaryotic cells. Formed by the merger of fat-eating mitochondria with glucose-eating bacteria, single-celled eukaryotes had to regulate their various metabolic pathways to keep themselves from becoming too fatty or too lean (and to control the urge of mitochondria to eat their hosts!). Then, when multi-cellular organisms developed, these cellular-level mechanisms were the building blocks available for organism-level weight regulation.

So we can simplify the subject a bit by looking at individual cells. And here CarbSane gets a huge “hat tip” for finding a fascinating paper that neatly summarizes how an individual human muscle cell controls its fat and glucose levels.

Obese Cells on High-Carb Diets

The paper dates from 2004, looks at muscle cells, and has the latinate title of “Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity.” [1]

We can (loosely) translate “de novo lipogenesis” as “fat creation from glucose,” “lipotoxicity” as “too much fat” and “glucolipotoxicity” as “too much glucose in a cell that has too much fat.” So the paper is examining cells that are:

  1. fat;
  2. eating a high-carb diet; and
  3. disposing of excess glucose by converting it to fat.

Sounds familiar! How do these cells control their weight?

Cells Follow the Same Strategy as the Body

Glucose can be toxic and it feeds bacteria, so excess glucose is removed from the body as quickly as possible. First, it’s stored as liver and muscle glycogen; beyond that it is mostly converted to fat by de novo lipogenesis.

The main organs which do that conversion are the liver and adipose tissue, but this paper points out that muscle cells do it too:

The recent recognition that de novo lipogenesis might have relevance for lipid homeostasis in skeletal muscle stems from the realization that Sterol regulatory element binding protein-1c (SREBP-1c), a member of the family of transcription factors that regulate the expression of genes involved in lipid storage in liver and adipose tissue, is also present in skeletal muscle at a level close to that observed in the liver,41,42 … [M]ost fascinating are the very recent demonstrations that glucose alone (in the absence of insulin) can stimulate de novo lipogenesis in skeletal muscle cells….

[I]t is clear that de novo lipogenesis, although low in skeletal muscle, can be markedly stimulated in muscle cells, particularly under conditions of high glucose (and/or high insulin) concentrations. [1]

So muscle cells convert glucose to fat just as liver cells do. Indeed, they convert glucose to fat even without any insulin stimulation, just to get rid of it – but they dispose of glucose most aggressively when stimulated by insulin.

The likely reason for this is to help the body avoid glucose toxicity:

Extrapolated to conditions of postprandial elevation in blood glucose and insulin (particularly after a high-carbohydrate meal), de novo lipogenesis in skeletal muscle, like in the liver, could also contribute to blood glucose homeostasis by disposing some of the excess circulating glucose as muscle triglycerides, particularly if the glycogen stores are full. In other words, de novo lipogenesis in myocytes may provide another sink for glucose disposal through skeletal muscles. [1]

Insulin gets the muscle cells to take in more glucose and do more of this glucose-to-fat conversion. So insulin is a glucose disposal hormone. Muscle cells respond to it as an act of charity to the rest of the body.

But if muscle cells are storing fat that they manufacture from glucose, they risk becoming obese. How do they get rid of excess fat?

That gets us to the other latinate phrase in the title, “lipid oxidation,” also known as fat burning, and a key hormone, leptin. The authors write:

It is now well established that the adipocyte-derived hormone leptin, which is well known for its central role in body weight regulation in part via its control over thermogenesis, 52–55 also plays an important role in blood glucose homeostasis and in the protection of insulin-sensitive tissues against excessive ectopic lipid storage by regulating the partitioning of fatty acid away from storage towards oxidation. 56–58 [1]

Leptin is released by adipose cells in proportion to the amount of fat they are storing. High leptin levels mean “I’m obese, help me lose weight”; low leptin levels mean “I’m skinny, please don’t waste any fat, we may need it.”

Leptin helps the body regulate its weight, by two mechanisms: 

  1. Leptin promotes fatty acid oxidation, or the burning of fats.
  2. Leptin triggers thermogenesis, “creation of heat,” which warms the body and causes it to lose energy.

In short, leptin causes the body – and individual muscle cells – to transform fat into waste heat, thereby slimming down the cells and the body.

What happens if you stimulate normal muscle cells with both leptin and insulin?  This situation occurs in a healthy person with too much fat (leading to high leptin) who has eaten a high-carb meal and has lots of extra blood glucose to get rid of (leading to high insulin). The insulin triggers the glucose-to-fat conversion pathway, the leptin triggers thermogenesis – but the effect is compounded because the insulin amplifies leptin activity:

[W]e found that leptin could directly stimulate thermogenesis in skeletal muscle via ObRb,62 and that this thermogenic effect of leptin, which requires PI3K activity (since it is inhibited by wortmannin), is potentiated by insulin, a potent activator of PI3K. [1]

This makes sense: the body really wants to get rid of the excess glucose, which is toxic, but high leptin means it’s already fat and doesn’t want to get fattier. So if you’ve got too much fat and too much glucose, you really, really want to turn up the waste heat generator.

So eating some carbs, by increasing after-meal insulin, will actually tend to increase fat oxidation and waste heat generation. That is, it will lead to more calories out, at least for a few hours after a meal. Whereas a zero-carb diet, by keeping insulin low after meals, might tend to tamp down postprandial waste heat generation.

If you read CarbSane’s post, you’ll see that this is what got her excited. (Maybe it would also excite Matt Stone, advocate of the carb-overfeeding-raises-body-temperature thesis.)

We shouldn’t jump to the conclusion that eating lots of carbs is good for weight loss, since carbs may also increase appetite and calories in, or have other effects such as generating a transient glucotoxicity. But we should keep this thought in the backs of our minds: Not every response to dietary carbs works against weight loss.

The paper notes that it’s not only leptin that stimulates thermogenesis. Other hormones – including adiponectin, which is also released by adipose cells, stimulate the same thermogenic pathways.

One can also entertain the interesting possibility that, in skeletal muscle, this substrate cycling is also activated in response to other hormones and neurotransmitters (eg, adiponectin, catecholamines) particularly since adiponectin, as well as adrenergic agonists, can also stimulate AMPK activity, glucose utilization and fatty acid oxidation in skeletal muscle or adipose tissue.61,66–69 This substrate cycling between de novo lipogenesis and lipid oxidation could therefore constitute a thermogenic effector in skeletal muscle. [1]

Adiponectin is a favorite hormone of Dr. Kenneth Tourgeman of the blog Nephropal. High adiponectin levels are associated with good health; obesity is associated with low levels of adiponectin. Adiponectin, among other effects, increases insulin sensitivity – thus it would tend to promote thermogenesis not only by its own action, but also indirectly by enhancing insulin amplification of leptin-induced thermogenesis.

What If The Cell Became Hormone Resistant?

As a thought experiment, we can imagine what would happen if our healthy muscle cell became metabolically damaged – if it became resistant to some of these hormones.

If it became leptin resistant, then it would no longer dispose of excess fat via thermogenesis. The fat would collect and the cell would become obese.

If the cell remained leptin resistant but insulin sensitive, it would gradually kill itself through obesity. So leptin resistance would naturally lead to insulin resistance as the cell protects itself against lipotoxicity.

Once the cell becomes insulin resistant, then it no longer disposes of excess glucose by fat conversion. Glucose levels might become elevated. This corresponds to the condition in the body as a whole that we call metabolic syndrome or prediabetes.

High glucose levels, of course, lead to glucotoxicity or poisoning by excess glucose. The pancreatic beta cells, which produce insulin, are especially subject to glucose poisoning. Thus, prediabetes in the body, continued long enough, leads to loss of these cells and diabetes.

We can imagine two kinds of diabetes:

  • If the insulin resistance developed as a consequence of leptin resistance, then we’d have an obese diabetic.
  • If the insulin resistance developed without leptin resistance, then we’d have a skinny diabetic.

Conclusion

I like this paper a lot because it gives us a look at the key hormonal pathways involved in obesity, but in a very simple model – a single muscle cell.

It suggests that possible causes of obesity are leptin resistance and adiponectin deficiency, and that if we want to fix obesity, we may wish to look for a diet which increases leptin sensivity and/or adiponectin level.

References

[1] Dulloo AG et al. Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity. Int J Obes Relat Metab Disord. 2004 Dec;28 Suppl 4:S29-37.  http://pmid.us/15592483.

Water Weight: Does It Change When Changing Diets? Does It Matter?

Posted by on January 14, 2011 54 comments

We’re now up to the final topic in the series reviewing experiences on the diet. Our final topic is the issue of weight gain and loss. This will take a few posts to explore. Next week will be “fat loss week.” This week, let’s look at the question of water weight.

Overweight people who come to the Perfect Health Diet from a high-carb diet seem to lose weight from the beginning. Here is a recent comment from Robert:

I started PHD a few weeks ago, after finding the blog, and then reading the book. I have only positive experiences to report…. I had been overweight in the past, and lost weight by low-calorie dieting on processed foods, along with strength training. After a while I would revert to some degree of overeating, and have to diet again. I’m mildly overweight now but I have been losing 2 lbs. per week on the PHD. Keep in mind this is before any calorie counting. I keep telling myself I will plug things in to Fitday, but so far my hunger is autoregulating itself and the weight is coming off.

However, some of our readers who came from very low-carb diets experienced immediate weight gains. One commenter on Amazon seemed to think this experience would be universal:

[I]f you are coming to the diet from a zero-carb or very-low-carb regimen, you can count on an immediate and substantial weight gain if you suddenly adopt the recommended intake of “400 carb calories [100 grams] per day of starchy tubers, rice, fruit, and berries.” (K. Hix)

Commenter Maggy reported a gain of 5 pounds in her first week:

Following your advice, I added back a bit of “safe starch” last week, and decreased protein intake, keeping sat fat and MCF pretty high. Well, I got on the scale today and have managed to put on 5 pounds! I’m trying to figure out what is going on and what I need to tweak. I do need to lose a good 20-30 lbs, and while I don’t want to compromise health, I also don’t want to put back on what I managed to lose doing a VLC diet.

Is this an adjustment period I need to get through? Maybe I’m one of those broken metabolism folks who has to stick with VLC?

Commenter Bill also experienced a quick gain of a few pounds, and wondered if it could be due to water weight:

After experimenting with adding modest amounts of “safe starches” to my much lower-carb routine, I have noticed a modest weight gain of 3-5 lbs. I wonder if it’s merely glycogen and water repletion.

Beth Mazur of WeightMaven.org agreed:

I also wouldn’t be surprised about weight gain. Presumably these folks are normally running on fairly low glycogen stores. Add some starchy carbs back, and the resulting water weight gain could be a handful of pounds presumably.

That’s an interesting question, so I thought I’d look into the matter.

Background: Glycogen, Glycoproteins, and Water Weight

Sugars are hydrophilic. If you put some water next to some sugar, the sugar will soak it up. As a result, a person’s water weight depends in part on the weight of sugars in the body. More sugars, more water, more weight.

It’s commonly stated that each gram of glycogen is associated with four grams of water; let’s take that as a general ratio for organic sugars.

A typical adult has around 500 grams of glycogen, roughly one-third in the liver and two-thirds in muscle. With associated water, this would add about 2.5 kg or 5 pounds to body weight.

But there are also several pounds of glucose in glycoproteins throughout the body:

  • Mucus in the digestive tract and airways may be as much as 80% sugar by dry weight.
  • The glycocalyx, a protective polysaccharide coat around cells, is primarily composed of sugars.
  • Hyaluronan, glucosamine, and other compounds that enable joints to move freely have much of their weight as sugar-water associations.

These sugar-containing molecules with their associated water add a lot of weight to the body. Glycogen we’ve said accounts for as much as 5 pounds; mucus probably accounts for several pounds at least; and other glycoproteins must add at least a few pounds more.

Are Glycogen and Glycoproteins Lost on a Low-Carb Diet?

It’s commonly asserted that much of these sugar-containing molecules, and their associated water, are lost on a low-carb diet. From a review of Gary Taubes’ Why We Get Fat, linked today by CarbSane:

[B]etween 5-10lbs of weight are lost on a low-carb diet due to the mobilization of the water stored with glycogen …

I argued in my “zero-carb dangers” series that a danger of zero-carb dieting was that the body would downregulate production of glycoproteins; and that reduced production of these might be quite dangerous.

For instance, reduced production of mucus in the digestive tract might increase the risk of gastrointestinal cancers, bowel diseases, and entry of infectious pathogens through the gut.

If it’s true that low-carb diets reduce water weight by 5 to 10 pounds, there must be a substantial loss of sugar-containing molecules. This is hardly likely to be healthy. Glycoproteins are essential for good health. Indeed, the evolution of glycoproteins was a prerequisite for the evolution of multicellular life!

So I would find this kind of water-weight loss quite alarming.

Let’s look for some data to see if it actually happens.

From High-Carb Diet to Fasting

In our earlier post on fasting for migraines, commenter js290 linked to a very nice post by Ned Kock, in which he talked about the components of weight loss during starvation. Ned posted this picture, taken from a textbook [1]:

Over 30 days of fasting, almost half the weight lost is from fat and almost half from water; small amounts of protein and sugar are lost.

In the first few days, water loss dominates. In the first 48 hours, 3.4 kg are lost, of which roughly 0.35 kg are glycogen, 0.1 kg protein, 0.3 kg fat, and 2.65 kg water.

So in the first two days of fasting, fully 5.8 pounds of water are lost. That’s remarkable.

Presumably, if this person had been returned to his normal diet, that weight would have been regained in a few days.

If the water loss was triggered by a loss of carbohydrate (in glycogen and glycoproteins), then a very low-carb diet might have had the same effect as the fast.

From High-Carb to Low-Carb Diets

There are some metabolic ward studies looking at what happens when people adopt low-carb diets. Here’s one that looked at an Atkins-style diet. [2]

The subjects entered the metabolic ward but continued to eat their normal diet on days 1 through 7, to provide a baseline. Then they adopted an Atkins-style diet for 2 weeks. Carbohydrate was reduced to 21 g (80 calories) per day, and they could eat as much fat and protein as they wished.

The results:

During the low-carbohydrate diet, mean body weight decreased by 2.02 kg from 114.43 kg (last day of the usual diet) to 112.41 kg (last day of the low-carbohydrate diet) …

During the low-carbohydrate diet, mean body water decreased from 46.30 kg to 45.94 kg. Body water decreased in 6 patients, increased in 3 patients, and did not change in 1 patient. After subtraction of body water, mean body weight decreased from 68.13 kg to 66.48 kg. [2]

In other words, water weight hardly changed. The weight loss was accounted for by fat loss, which was understandable because the subjects reduced their calorie intake by 946 calories per day. [2]

So in this study, water weight loss averaged only 360 g (0.8 lb), and some patients actually gained water weight on the low-carb diet!

So it looks like going from a high-carb diet to a low-carb diet needn’t lead to much loss of water weight.

From Low-Carb Diet to Fasting

I looked for some papers on what happens when a low-carb dieter starts a fast. I found this:

In her book ‘Living on Light’, Jasmuheen tries to animate people worldwide to follow her drastic nutrition rules in order to boost their quality of life. Several deaths have been reported as a fatal consequence. A doctor of chemistry who believably claimed to have been ‘living on light’ for 2 years, except for the daily intake of up to 1.5 l of fluid containing no or almost no calories was interested in a scientific study on this phenomenon.

The 54-year-old man was subjected to a rigorous 10-day isolation study with complete absence of nutrition. During the study he obtained an unlimited amount of tea and mineral water but had no caloric intake….

[The man experienced] a mean weight loss of 0.26 kg/d … [3]

If his weight loss of 260 g/day consisted of 130 g protein and 130 g fat – a plausible mix – then he was expending about 1700 calories per day. This is very plausible, and leaves little room for water weight loss.

So when a low-carb dieter starts a fast, he may lose hardly any water weight at all!

Summary and My Own Experience

These studies are inconsistent. If going from a high-carb diet to a low-carb diet doesn’t produce water weight loss, and going from a low-carb diet to fasting doesn’t, then why would going from a high-carb diet to fasting?

I confess I was surprised by the level of water loss reported by Ned’s source. I fast moderately often, and I lose typically around 1 pound during a 36 hour fast. Shou-Ching’s experience is similar. That doesn’t leave much room for water weight loss.

But clearly, some people do experience large losses of water weight when they adopt a low-carb diet or a fast, and then regain it upon carb re-feeding.

I think we have to conclude that the phenomenon of water weight loss on low-carb diets, and water weight gain on carb re-feeding, is variable across persons. In some persons it happens, and in others it doesn’t.

Conclusion

I think those sugars serve important functional purposes. Glycoproteins are essential for health. Glycogen is a desirable reserve that helps the liver manage blood glucose and muscles exert force.

Maggy asked if she was metabolically broken because she gained 5 pounds in a week by adding carbs back in. Now, a lot can happen in a week, including significant changes in fat and protein mass, and water weight changes due to changes in sodium levels. Low-carb diets tend to lead to salt loss, so that may have been a factor.

But if the weight gain was entirely due to restoration of sugar and water levels, then I’m reluctantly led to the conclusion that Maggy may indeed be “metabolically broken.” The brokenness is not in the gain of bodily sugars when she eats the carbs; it’s in the loss of these important sugars on her very low-carb diet!

If it’s unhealthy to lose those sugars, and if a metabolically healthy person can sustain the body’s sugar and water levels through a fast, then the loss of sugars on either a low-carb diet or fast suggests a damaged metabolism.

As much as Maggy wishes to lose weight, it is important to lose weight from adipose cells, not from water and glycoproteins. Her rapid ~5 lb weight gain upon shifting from a very low-carb diet to the Perfect Health Diet might have been a very good thing.

UPDATE:

CarbSane has begun a series on water weight, and has interesting numbers on water weight in adipose tissue and lean tissue, and how water weight varies between obese and lean persons. This post introduced several papers, and a follow-up contributes an interesting analysis and suggests that movement of fatty acids between adipose and lean tissue may be involved in water weight changes.

I didn’t know that extracellular water weight in tissues was so variable. Thank you CarbSane! 

References

[1] Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics. Cited by Ned Kock, “The amounts of water, carbohydrates, fat, and protein lost during a 30-day fast,” http://healthcorrelator.blogspot.com/2010/10/amounts-of-water-carbohydrates-fat-and.html.

[2] Boden G et al. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005 Mar 15;142(6):403-11. http://pmid.us/15767618. Full text: http://www.annals.org/content/142/6/403.full.pdf.

[3] Heusser P et al. Nutrition with ‘light and water’? In strict isolation for 10 days without food – a critical case study. Forsch Komplementmed. 2008 Aug;15(4):203-9. http://pmid.us/18787329.

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.