Category Archives: Toxins and Toxicity

Do the Elderly Need Paleo More than the Young?

I also do work in economics and one of my favorite economics blogs is Evolving Economics by Jason Collins. He has an interest in biology and Paleo diets and recently linked to an interesting train of thought from evolutionary biologist Michael Rose.

Here is a summary from Peter Turchin, who adopted a Paleo diet this spring after talking to Rose:

We think of people having ‘traits,’ but actually we change quite dramatically as we age. … As an extreme example, consider reproductive ability, something of great interest to evolution. Humans do not reproduce until they reach a fairly advanced age of maturation (puberty). Young adults are not very good mothers or fathers, but they improve with age during their twenties. After that reproductive ability declines and eventually disappears. …

Ability to digest certain foods can also be age-dependent. I have already mentioned the ability to digest lactose, the sugar present in milk. Before we domesticated animals such as cows and sheep, only very young humans had this ability. Natural selection turned this ability off in adults because they never needed it (and it would be wasteful to continue producing the enzyme lactase that aids in the digestion of milk sugar). …

Because abilities to do something at the age of 10, 30, 50, etc. are separate (even if correlated) traits, they evolve relatively independently of each other. When grains became a large part of the diet, the ability of children to digest them (and detoxify the chemical compounds plants put into seeds to protect them against predators such as us) became critical. If you don’t have genes to help you deal with this new diet, you don’t survive to adulthood and don’t leave descendants. In other words, evolution worked very hard to adapt the young to the new diet. On the other hand, the intensity of selection on the old (e.g., 55 years old) was much less – in large part, because most people did not live to the age of 55 until very recently. …

The striking conclusion from this argument is that older people, even those coming from populations that have practiced agriculture for millennia, may suffer adverse health effects from the agricultural diet, despite having no problems when they were younger.

This is an intriguing argument. Several aspects of it are well supported: there has been recent evolution to enable people to cope with toxic diets, and there are substantial changes in how we respond to food as we age.

Recent Genetic Evolution

We know that there has been recent evolution for greater tolerance to evolutionarily novel foods such as wheat. This is (presumably) why peoples with a long history of grain agriculture are less obese and diabetic on “western” diets than people with a long history of eating healthy foods.

The Pacific islanders are a great example. The world’s highest obesity rates are in the Pacific – for instance, in the Kosrae district of Micronesia, 88% of adults are overweight and 59% obese – yet they were notably slim sixty years ago when still eating their traditional diets. [1]

In our book, we note that the traditional diets of Pacific Islanders are almost toxin-free. A logical inference is that because they have for millennia eaten the world’s least toxic diets, Pacific Islanders never needed to evolve (or lost) an ability to cope with toxin-rich diets, and now suffer much more harm from toxic foods than do peoples whose ancestors have eaten toxic diets.

Age-Based Differences in the Biological Response to Unhealthy Food

It’s also the case that we respond to food differently as we age.

It’s not only digestion, such as the age-related decline in lactase enzyme expression, that changes. There are metabolic changes.

The elderly consume far fewer calories than the young; presumably evolution selected for minimal food utilization so that they would not be a burden to those who had to hunt and gather on their behalf. Their contribution was likely cultural, which didn’t require extensive physical activity.

Another change is that the elderly become less likely than the young to store calories in adipose tissue. This has significant consequences.

We know from a broad range of evidence that adipose tissue protects other tissues from damage by lipotoxicity; and that when adipose tissue refuses to store fat, obesogenic diets lead to metabolic syndrome and diabetes. [2] So reduced storage of calories in adipose tissue in the elderly will lead to (a) reduced rates of obesity (as measured by adipose tissue accumulation), but (b) higher rates of metabolic syndrome and diabetes.

This is exactly what we see. Here are obesity rates by age group [3]:

Obesity rates for people over age 65 are lower than for people aged 30-64.

Here are diabetes rates by age group [4]:

Despite their lower obesity rates, the elderly have higher diabetes incidence.

This difference alone is sufficient to answer the question in our title: Yes, the elderly do need a Paleo (ie healthy) diet more than the young. Diabetes is much more dangerous than adipose tissue accumulation, so the elderly will suffer greater health impairment from an obesogenic (and diabetes-genic) diet than the young.

Is There Data Specifically Testing Rose’s Idea?

Rose’s idea that an evolved tolerance for toxin-rich diets will be specific to reproductively-aged persons with agriculturalist ancestors, is, so far as I know, not easily tested by available empirical evidence.

Studies in western populations alone will not be able to test Rose’s idea, because greater intolerance of toxic diets with higher age could simply be a result of an aging process that is universal in all populations. In order to find a process that recently evolved in agriculturalists, we would have to look at rates of aging or morbidity in different populations, both western and aboriginal, and see how aging rates or disease incidence depend on dietary toxicity:

  • Are Pacific Islanders more likely than westerners on similar diets to develop diabetes at reproductive ages, but equally likely at late ages? Are they more likely to become obese at younger ages than old?
  • Is aging more rapid in traditional peoples than in westerners during reproductive years, but similarly fast during elderly years, if they eat similar diets?

I am not aware of any such studies. Let me know if you are!


[1] Cassels S. Overweight in the Pacific: links between foreign dependence, global food trade, and obesity in the Federated States of Micronesia. Global Health. 2006 Jul 11;2:10.

[2] Unger RH, Scherer PE. Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity. Trends Endocrinol Metab. 2010 Jun;21(6):345-52. Sun K et al. Adipose tissue remodeling and obesity. J Clin Invest. 2011 Jun;121(6):2094-101.

[3] Health, United States, 2008: With Special Feature on the Health of Young Adults. National Center for Health Statistics (US).

[4] 2011 National Diabetes Fact Sheet,

Why Did We Evolve a Taste for Sweetness?

After I did my post on Seth Roberts’s new therapies for circadian rhythm disorders, Seth learned of my experience with scurvy and blogged about a similar experience of his own.

Seth made the important point that food cravings are driven by nutritional deficiencies – a point I heartily agree with, which is why it’s so important for those seeking to lose weight to be well nourished – and asked, “Why do we like sweet foods?” His suggested answer was that the taste for sweetness encouraged Paleo man “to eat more fruit so that we will get enough Vitamin C.”

This led to a fascinating contribution from Tomas in the comment thread:

I have read several books on the Traditional Chinese Medicine and they attributed that increased craving for sweets is in fact signaling some serious nutritious deficiencies. They said that it’s in fact meat or starches or other nutritionally dense foods that will soothe the craving, but sweets are more readily available. The taste of meat is in fact sweet as well.

In my experience this seems (the TCM view) to be true. I always have been very skinny, but eating enormous amounts of sweets. After I switched to a proper, paleo-like diet, the situation changed in many aspects and I no longer have such strong cravings and slowly I am gaining some weight.

Shou-Ching and I have great respect for the empirical claims of Traditional Chinese Medicine, and so I found this a fascinating idea. Is our modern taste for sweets actually derived from a taste that evolved to encourage meat eating?

Human tastes

It is generally agreed that animals evolved the sense of taste to detect nutrients and toxins:

Taste helps animals to decide whether a food is beneficial for them and should be consumed or whether it is dangerous for them and should be rejected. Probably, taste evolved to insure animals choose food appropriate for body needs. [1]

The five basic human tastes are sweet, salty, sour, bitter, and umami. Each taste detects either a nutrient class we need or toxins we should avoid:

  • Sweet – carbohydrate.
  • Salty – electrolytes.
  • Sour – acids.
  • Bitter – toxins.
  • Umami – glutamate and nucleotides.

Electrolytes are essential to life, and toxins best avoided, so the evolution of salty and bitter tastes is easy to understand. The umami taste is mainly a sensor for natural (healthy) protein. The sour taste is interesting, in that it is attractive in small doses but aversive in large. Seth argues that low-dose sourness is desirable because it leads us to seek out fermented foods, which supply probiotic bacteria and their fermentation products such as vitamin K2. If so, it is natural that strong sourness, indicating high bacterial populations, would be aversive.

But what of the sweet taste? Is it really a sensor for carbohydrates? If so it does a rather poor job. The healthiest carbohydrate source – starch, which is fructose-free – hardly activates this taste, while fructose, a toxin, activates it in spades. If this taste evolved to be a carbohydrate sensor, it should have made us aversive to the carbohydrates it detects, as the bitter taste makes us avoid toxins. But sweet tastes are attractive!

Sweetness activators

It turns out that the sweetness receptors are complex; many things activate them, and they appear to serve multiple functions.

Wikipedia (“Sweetness”) notes:

A great diversity of chemical compounds, such as aldehydes and ketones, are sweet.

Some of the amino acids are mildly sweet: alanine, glycine, and serine are the sweetest. Some other amino acids are perceived as both sweet and bitter.

The sweetness of some amino acids would seem to support Tomas’s assertions that sweetness detect meat: perhaps it is detecting amino acids. But this seems a bit odd: there is another taste, umami, that detects protein. Would we really need two taste receptors for protein? And lean meats don’t taste sweet.

A possible clue is that the sweet tasting amino acids are hydrophobic, while hydrophilic (or polar) amino acids are not sweet.

Proteins that are hydrophobic end up lodging in cell membranes alongside lipids; proteins that are hydrophilic dissolve in water and reside apart from the fat. Glutamate and nucleotides, which are detected by the umami taste, are hydrophilic and water-soluble.

So maybe the umami taste detects proteins that aren’t associated with fat, while the sweet taste detects proteins that are associated with fat.

Indeed, a leading theories of sweetness holds that compounds must be hydrophobic, or fat-associated, in order to invoke the sweetness taste:

B-X theory proposed by Lemont Kier in 1972. While previous researchers had noted that among some groups of compounds, there seemed to be a correlation between hydrophobicity and sweetness, this theory formalized these observations by proposing that to be sweet, a compound must have a third binding site (labeled X) that could interact with a hydrophobic site on the sweetness receptor via London dispersion forces. Wikipedia (“Sweetness”)

The sweet taste seems to work in collaboration with the bitter taste to regulate toxin avoidance. Wikipedia (“Sweetness”) again:

Sweetness appears to have the highest taste recognition threshold, being detectable at around 1 part in 200 of sucrose in solution. By comparison, bitterness appears to have the lowest detection threshold, at about 1 part in 2 million for quinine in solution.[4] In the natural settings that human primate ancestors evolved in, sweetness intensity should indicate energy density, while bitterness tends to indicate toxicity[5][6][7] The high sweetness detection threshold and low bitterness detection threshold would have predisposed our primate ancestors to seek out sweet-tasting (and energy-dense) foods and avoid bitter-tasting foods. Even amongst leaf-eating primates, there is a tendency to prefer immature leaves, which tend to be higher in protein and lower in fibre and poisons than mature leaves.[8]

This makes some sense: we need a certain number of calories per day, and since “the dose makes the poison,” what determines the toxicity of the diet as a whole is not the amount of toxins in a food, but the ratio of toxins to calories. In an evolutionary setting, our ancestors needed to eat foods with a low toxin-to-calorie ratio in order to minimize daily toxin intake.

So if sweetness is an “energy density” detector, it should be especially strongly activated by fatty foods. If it detects fat-associated compounds, then it would do so.

Why not detect fats directly? In natural foods, fats are bound in triglycerides or phospholipids which are chemically inert. So they won’t bond to taste receptors. Free fatty acids will, but these are not present in fresh foods and would probably indicate some kind of degradation of the food. In fact there seems to be a taste receptor for free fatty acids, CD36 [2], but this may be an aversive sensor for decayed food.

Interestingly, color also affects sweetness:

The color of food can affect sweetness perception. Adding more red color to a drink increases its sweetness with darker colored solutions being rated 2–10% higher than lighter ones even though it had 1% less sucrose concentration.[26] Wikipedia (“Sweetness”)

So red meats are sweetest. Richard Nikoley would approve.

Summary and A Puzzle

A plausible inference would be:

1.      The sweet taste evolved primarily to encourage the eating of fatty, energy-dense meats; and of essential fat-associated micronutrients such as choline and inositol.

2.      The sweetness of fruit may result from plants having evolved a way to hijack the sweetness receptors, and animal food preferences, for their own purposes.

This still leaves a few puzzles. Why, Seth asks, do we tend to neglect sweet tastes when we are hungry, but after dinner is done crave sweet desserts?

Here’s something to consider. Fats are a special macronutrient. We have unlimited storage space for fats, in our adipose tissue, but very limited storage space for other calories. Once we’re full, of course we should lose our appetite for calories we cannot store. But for fats, why not get a little extra in case food is scarce in days to come? There’s always room for a little more fat.

Implications for Binge Eaters

Correct me if I’m wrong, but when people go on an eating binge, they go for sweets.

Presumably, they have a craving for the sweet taste – which, evolutionarily, may be a craving for fatty meats and fat-associated micronutrients.

But if they’ve imbibed the anti-fat propaganda of recent decades and are afraid to eat fat, binge eaters must follow their taste buds to sugars – which unfortunately fail to satisfy any of the micronutrient deficiencies the sweet craving is designed to redress.

Perhaps, then, a good fatty steak, preferably accompanied by some liver and cream sauce, would be the best cure for binge eating. It would satisfy the craving, but also satisfy the underlying nutritional need that generated the craving.

Implications for Weight Loss

If, as I believe, the key to weight loss and curing obesity is eliminating appetite, then it’s important to eliminate any deficiencies of fat-associated micronutrients. Micronutrient deficiencies trigger food cravings, and deficiencies of fat-associated micronutrients will trigger a craving for sweets.

In the modern world, we know how a craving for sweets is likely to be satisfied – by eating sugary, nutrient-poor foods. Unfortunately these foods do not contain the fat-associated nutrients (such as choline) whose deficiency is probably driving the craving. So the craving persists unabated no matter how many sugars are eaten.

Persistent food cravings despite an excess of caloric intake is probably a necessary (though not sufficient) condition for obesity to develop. Unsatisfied cravings probably make weight loss extremely difficult.

What of Vitamin C?

Vitamin C – ascorbic acid – is an acid so it directly activates the sour taste.

So perhaps the sour taste evolved to help us get vitamin C. This would actually complement Seth’s idea that the sour taste encourages us to eat fermented foods. Fermented foods are high in vitamin C.

I had a fairly severe case of scurvy and don’t recall being attracted to sweet flavors. Instead, I was ravenously hungry. My appetite generally, not craving for any particular taste, was promoted. If anything, I was less attracted to sweet tastes. So I think it’s plausible that vitamin C deficiencies may lead to a general appetite upregulation, or to cravings for sour foods, rather than a craving for sweets.


Our evolved taste receptors can tell us a lot about what our bodies need. Food cravings are a pretty good sign of an unsatisfied nutrient deficiency.

But sometimes, it’s less than obvious what a craving signifies. Our modern food environment is so different from the Paleolithic: We have many industrially produced foods designed to fool our Paleolithic taste buds into eating nutritionally unsatisfying calories.

Humans evolved, not in the forests where fruit was available, but in open woodlands where tubers and other tasteless starch sources were abundant but fruit rare. In this context, our cravings for sweet foods may have been directing us to eat animal fats.

It may be that the cravings for sweets often experienced by binge eaters and the obese are really a craving for animal fats. If you feel drawn to sugar, perhaps you should ask yourself: Steak or salmon?


[1] Bachmanov AA, Beauchamp GK. Taste receptor genes. Annu Rev Nutr. 2007;27:389-414.

[2] Laugerette F et al. CD36 involvement in orosensory detection of dietary lipids, spontaneous fat preference, and digestive secretions. J Clin Invest. 2005 Nov;115(11):3177-84.

Why We Get Fat: Food Toxins

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.


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.


[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.

[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.

Why Wheat Is A Concealed Cause of Many Diseases, III: Adjuvant Activity

We’ve been looking into how wheat can cause autoimmune diseases other than the “classic” wheat-associated diseases, celiac disease and Hashimoto’s thyroiditis.

The first post in the series discussed how wheat can cause a leaky, permeable gut that lets toxins and bacteria into the body. The second post discussed how wheat can itself generate a variety of auto-antibodies that attack nerves, brain, connective tissue and joints.

Now, we want to look at how wheat can create diseases by binding to other molecules and causing the body to form antibodies to them. Wheat can thereby cause allergies against foods as well as autoimmune attacks on self molecules.

Adjuvant Activity of Wheat Germ Agglutinin

Immunologically speaking, an “adjuvant” is a molecule that when bound to another molecule makes it much more immunogenic. Adjuvants such as aluminum salts are used in vaccines to make the immune system produce antibodies more readily against the target protein. This lowers the vaccine dose needed for immunity.

Wheat germ agglutinin (WGA) is a wheat lectin. (It is not part of gluten.) WGA can act as an adjuvant, causing the body to generate antibodies against proteins that, in isolation, the body would not form antibodies against. 

For instance, antibodies against the egg protein ovalbumin are not generated if it enters the body alone, but are generated if it is accompanied by WGA. [1]

So don’t eat toast with your eggs! If you have a leaky gut, the wheat might give you an egg allergy.

Haptenization Activity of Wheat Gliadin

A similar process that helps create auto-antibodies is “haptenization.” The immune system forms antibodies more readily against large molecules than small ones. (This helps avoid autoimmunity, since small molecules are more likely to have similar human peers.)

When two small molecules bind together, so they look like one big one, the immune system is more likely to form antibodies against the large complex. These antibodies may then react against one of the molecules individually, even if it is not paired up. If the targeted molecule is human, then the antibody is an auto-antibody.

One reason wheat gliadin is so disruptive to the body is that it binds strongly to sugars. The average molecule of wheat gliadin is bound to 1 to 2 molecules of glucose and 2 molecules of sialic acid, another sugar. [2] Since a lot of human molecules have sialic acid residues, gliadin can bind to them.

One of the sialic acid-containing molecules gliadin binds to is called GM1 ganglioside. This molecule is found on the intestinal brush border, but it is also found in nerves. When wheat binds to GM1 ganglioside on the intestinal surface, it induces the formation of auto-antibodies that attack the ganglioside in nerves. In 65% of patients with gluten sensitivity and peripheral nerve damage, anti-ganglioside antibodies are found. [2]


Wheat could be a concealed cause of many food allergies, through WGA’s adjuvant activity. If so, then many food allergies may gradually disappear after wheat is given up.

Wheat proteins can also bind to an extraordinarily large number of human proteins, in part by binding to sialic acid or other carbohydrate residues of glycoproteins or glycolipids, and has a chance to induce antibody formation against many of those proteins.

The bewildering array of ways in which wheat can trigger attacks on human tissue makes it impossible to identify all the wheat-caused diseases.  The only thing we can say for sure is that if you have a disease, it’s a good idea to give up wheat. You may give up your illness at the same time.

Related Posts

Other posts in this series:

  1. Wheat Is A Cause of Many Diseases, I: Leaky Gut Oct 26, 2010.
  2. Why Wheat Is A Concealed Cause of Many Diseases, II: Auto-Antibody Generation Oct 28, 2010.


[1] Lavelle EC et al. The identification of plant lectins with mucosal adjuvant activity. Immunology. 2001 Jan;102(1):77-86.

[2] Alaedini A, Latov N. Transglutaminase-independent binding of gliadin to intestinal brush border membrane and GM1 ganglioside. J Neuroimmunol. 2006 Aug;177(1-2):167-72.