Saturday, April 14, 2012

The Panda Paradox

Zoologists classify the panda as a carnivore.
The panda has gut structure, gut function, and gut enzymes like a carnivore.

The panda does not have multiple stomachs, nor an enlarged cecum, nor the gut microbes found in animals that eat diets composed largely of fiber, like cattle and sheep.

A study published in the Proceedings of the National Academies of Science states:  "The giant panda genome codes for all necessary enzymes associated with a carnivorous digestive system but lacks genes for enzymes needed to digest cellulose, the principal component of their bamboo diet."

Source:  Wikimedia

Yet wild giant pandas consume around 20-40 pounds of highly fibrous bamboo stalks and leaves every day.

The San Diego Zoo states that the small Red Panda's diet is 95 percent bamboo.

The Smithsonian National Zoo states that "A wild giant panda’s diet is almost exclusively (99 percent) bamboo."

At the Talk Origins site on human evolution, Douglas Theobald, professor of biochemistry at Brandeis University writes "... even though humans are herbivorous, the small human caecum does not house significant quantities of cellulase-excreting bacteria, and we cannot digest more than but a few grams of cellulose per day."  [Emphasis added]

Leaving aside for the moment the interesting fact that this staunch defender of evolutionary theory describes humans as herbivorous, the panda's ability to digest cellulose is similar to humans.   The gut microbes of pandas digest very little of the fiber the pandas consume; 92 percent of cellulose a panda ingests ends up eliminated in its feces.

If in pandas gut microbes convert only 8 percent of ingested cellulose into short chain fatty acids, this probably means that the panda gets most of its energy from the digestible carbohydrate and protein provided by bamboo leaves and stalks, not from fat.  Does the panda challenge the idea that "the natural diet of mammals is a high-fat diet"?

The pandas provide a striking example of a non-human mammal that has almost none of the genetic or physiological equipment associated with herbivory (only having some dental and grip adaptations), yet it spontaneously lives as an herbivore.

It is believed that the first giant panda ancestor to include some bamboo in it diet was Ailuropoda micrta which existed about 3million years ago.  This species appears to have descended from the primal panda, Ailuaractos Lufengensis, an arctoid with a carnivorous diet. The carnivorous arctoids appear first in the evolutionary record about 46 million years ago. 

The fact that a member of the Carnivora order has adapted spontaneously to a highly specialized and extremely fibrous, low fat, 99% herbivorous diet without apparent major physiological and genetic changes seems to raise some interesting questions for those who believe that modern humans are optimally adapted to some diet consumed by some paleolithic human ancestors.

The panda also seems to challenge another presupposition of paleolithic diet theory, which goes something like this:  Any species that at any time in its evolution adopts a meat-based diet is required thenceforth to always maintain a meat-based diet to sustain health. 

This is clearly not true for the panda; despite having physiological equipment that limits its ability to extract nourishment from plants, it has succeeded in its niche for at least a million years. 

The panda shows us that when individuals of a species encounter an environmental challenge, they do whatever they can do to succeed in the changing environment without any concern about what their ancestors did, or whether they have the optimal physiology for the new habit.  The new feeding strategy may not be optimal, and it doesn’t have to be; it only has to be good enough to allow individuals to survive long enough to reproduce.

Now, why does Professor Theobald say that humans are herbivorous?  Because we humans have descended from a very long line of herbivorous ancestors and have a body displaying more features in common with other herbivores than with carnivores, including plantigrade stance, relatively slow sprints (compared, for example, to canines or felines), color vision, nails (rather than claws), small mouth, fleshy lips, non-shearing teeth, carbohydrate taste receptors (rather than amino acid taste receptors found in cats), non-expandable esophagus, haustrated and long intestines, low potency bile, a vermiform appendix,  and a sense of fear (those at the top of the food chain are not stalked so do not need fear to enhance survival). 

During the last two to four million years, climate changes and migrations put human ancestors in environments where they had to adopt omnivorous diets to survive, despite not being fully adapted to the new foods (meat and animal fat), just as the first panda ancestor to eat bamboo was not fully (physiologically) suited to a bamboo diet.  Nevertheless, just as the bamboo diet was/is good enough for the panda lineage to survive, a meat-based diet was/is good enough for the human lineage to survive in plant-food depleted environment.

That does not mean it will produce the best health.  A diet does not have to protect individuals from heart disease or cancer, or support maximum longevity, to be good enough to support the continuation of the species.  These diseases typically kill people long after they have reached reproductive age. 

The discordance hypothesis favored by some Paleolithic diet advocates states that diseases arise as a consequence of an individual adopting a diet, lifestyle, or habitat sufficiently different from the diet, lifestyle, or habitat of its ancestors to create a discordance with the genetic heritage of its species.

The wild giant panda seems to have a diet substantially discordant with its genetic constitution.  Yet the panda doesn’t suffer from a host of diet-induced diseases.

Pandas in captivity eat a diet perhaps more discordant with the ancestral panda diet. According to this report of captive giant panda diets in five Chinese facilities:

“Each facility feeds a steamed grain mixture comprising 13–56% of the diet on an as-fed basis, animal products (milk, eggs, and/or meat; 8–25% of the diet), and bamboo (17–82% of the diet). Seasonally available fruits and/or vegetables are sometimes included (0–29% of the diet).”

This mixed and cooked diet deviates from the 100% raw, 99% bamboo diet of wild giant pandas, and includes foods never eaten by wild pandas during the past 3 million years (grains).  The San Diego Zoo  reports:

“At the San Diego Zoo, pandas are offered bamboo, carrots, yams, and special leaf eater biscuits made of grain and packed with all the vitamins and minerals pandas need.”

It seems the San Diego veterinarians have settled on a vegan diet for the panda.  The pandas apparently do quite well on this non-ancestral diet, at least in terms of longevity.  According to the SanDiego Zoo, wild pandas live only 14-20 years, but pandas in zoos live 30 years, 50 to 100 percent longer.  Apparently, a panda can live much longer when eating an evolutionarily novel diet including steamed grains than when eating only the raw foods eaten by its wild ancestors.  This experiment apparently trumps the discordance hypothesis.

Consider that the panda has been isolated to a bamboo forest, and eating a bamboo-based diet, for perhaps one million years, yet this sustained selective pressure to adapt to a bamboo diet has had relatively little impact on its basic anatomy and physiology. Today’s panda still does not have an herbivorous body form despite such a long period of evolution on the 99% bamboo diet, but the diet works good enough for the panda (perhaps as good as it gets in the current niche) to pass the bamboo habit to the next generation.

In contrast, the past two million years of human evolution occurred under much more varied ecological conditions. During human ancestral evolution, the variability of the ice age climate and human mobility led to wide variability of plant-animal ratios in ancestral diets, and this combined with intertribal marriages tended to minimize selective pressures for any specific physiological adaptations to meat-eating and supported retention of the basically herbivorous primate physiology. 

The panda seems to challenge the idea that our genes, or the diets of our remote ancestors, determine the optimal diet for present-day humans.  Apparently neither ancestral diets, nor genes, nor physiological equipment will necessarily make a meat-based diet a perpetual requirement, or the optimum choice, for any given species, let alone one (such as humans) with an extensively herbivorous ancestry and numerous adaptations to herbivory. 

I think the panda shows us quite clearly that if we want to know how to prevent degenerative diseases and maximize healthy longevity, we will want to gather knowledge from the experience and experiments (natural and controlled) of present day humans, rather than assume that we will get the best results by eating only the foods consumed by our remote ancestors.

Post Script

This post was inspired by similar, but less dramatic examples of non-human animals adapting to non-ancestral foods/diets in some Plant Positive videos, for example:

Primitive Nutrition 60:  Ketosis Is Natural. Natural Is Good. Part III

"Polar bears in captivity are not fed a diet like they would consume in the wild.  They are actually fed fruits and vegetables.  But this isn’t their natural diet!  Surely this is a form of animal abuse, right?"

"Actually, polar bears in captivity live considerably longer.  But shouldn't an evolutionarily novel diet destroy their health?  This is yet another example of how Paleologic is no substitute for experiment and observation."

From Polar Bears International:

"In the wild, polar bears live an average 15 to 18 years, although biologists have tagged a few bears in their early 30s. In captivity, they may live until their mid- to late 30s. Debby, a zoo bear in Canada, lived to be 42."

 Thus, an evolutionarily novel diet supports a doubling of lifespan in polar bears.

Thanks to Plant Positive for giving inspiration and sharing suggestions for this post.

Monday, April 9, 2012

Harvard Meat Study

On Monday, March 12, 2012, the Archives of Internal Medicine published online "Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies," a study done by researchers from the Harvard School of Public Health.  This study found that eating even one serving daily of red meat increased total mortality and risk of mortality from cardiovascular disease and cancer.

The researchers carefully controlled for intakes of total energy, whole grains, fruits, and vegetables; age; body mass index; race (white or nonwhite); smoking status; alcohol intake; physical activity level; multivitamin use; aspirin use; family history of diabetes mellitus, myocardial infarction, or cancer; and baseline history of diabetes mellitus, hypertension, or hypercholesterolemia. In women, they also adjusted the data for postmenopausal status and menopausal hormone use.

Some in the cattle industry have questioned the validity of the food frequency questionnaires used in this type of study (here).  The authors of the study responded:

"However, all the questionnaires used in this study have been validated against multiple-day food records—at least 14 days during a year—and have been found to be acceptable in terms of validation and reproducibility.
"Second, although there [are individual] day-to-day variations in food consumption, people are generally eating in a pattern that can be captured by the questionnaire. We were interested in between-person variation[s], and we were comparing people who eat a high amount of red meat to those who eat a low amount of red meat. Because we repeated the measurements every four years, the cumulative average used in the analysis represents a long-term dietary pattern. That is a strength of this study, because many other studies may have only a single measure at baseline.
"Last, but most importantly, the measurement error generally tends to attenuate the association, and if we corrected the measurement error using some statistical methods, the associations were much stronger!"  [emphasis added]

Some have responded to this by claiming that "correlation doesn't equal causation" (as if the Harvard researchers don't realize this), or that the results only apply to consumption of conventional meat, not grass-finished.

Such a response ignores two important facts:

1) This study is only one among hundreds finding an association between red meat consumption and increased mortality from heart disease and cancer. 

2) Basic research has shown that these hazards arise from components that occur in meat from grass-fed animals at levels equal to or greater than levels found in meat from grain-fed animals.  

The following provide examples of the large number of studies finding positive associations between consumption of red meat and adverse health outcomes:

Meat consumption and colorectal cancer risk: Dose-response meta-analysis of epidemiological studies

Meat consumption and risk of colorectal cancer:  A meta-analysis of prospective studies 

Processed meat consumption and stomach cancer risk meta-analysis

Meat consumption and the risk of type 2 diabetes meta-analysis

Meat consumption and prostate cancer risk

Thus, this new study is not some isolated, rare, unusual finding.  It resonates with a large body of corroborating epidemiological evidence finding a positive association between red meat consumption and risk of or mortality from disease.  It adds to that growing body of evidence. 

Of course, "correlation does not prove causation," so some scientists have taken the next step required, doing research to find out if there are any plausible mechanisms by which consumption of meat could increase the risk of mortality. 

So far, researchers have found that a number of components of red meat have biological effects providing plausible mechanisms by which diets rich in meat could increase the risk of chronic diseases and mortality.  The suspect components include animal protein, cholesterol, arachidonic acid, heme iron, and Neu5Cg sialic acid, all of which naturally occur in red meat.  Further, the concentration of these components of meat is not markedly affected by feeding or pharmaceutical strategy used in raising the animals; meat from grass-fattened animals has practically the same amount of these components as meat from grain-fattened animals.

Animal Protein

Animal protein typically forms a larger proportion of lean grass-fed than conventional fatty meat, and promotes increases in IGF-1 levels, which appears involved in promotion of breast, colon, and prostate cancers.

High animal protein intake raises serum IGF-1 levels. [Full text]

IGF-1 has roles in growth promotion and carcinogenesis. [Abstract]

Elevated IGF-1 levels were associated with a 49% increased risk of prostate cancer and a 65% increased risk of premenopausal breast cancer.  [Abstract]

Elevated IGF-1 levels are associated with increased risk of prostate cancer, lung cancer, colorectal cancer, and premenopausal breast cancer. [Abstract]  

Dietary Cholesterol

Starting with a zero cholesterol diet, adding small increments of dietary cholesterol raises serum cholesterol levels, in a dose-response fashion.[Full text]

Elevated serum cholesterol increases the risk for cardiovascular disease. [National Cholesterol Education Program]

Elevated serum cholesterol increases risk of ischemic stroke in the general Japanese population.[Abstract]

Mice fed a high fat, high cholesterol diet and showing elevated serum cholesterol have increased mammary tumor growth and metastases compared to controls. [Abstract]

Emerging evidence indicates that oxidized cholesterol plays an important role in the angiogenesis process that supports tumor growth. [Abstract]  

The more unnecessary LDL cholesterol in the blood, the more likely there will be oxidized cholesterol in the blood.

Individuals with elevated serum cholesterol found to have a 35% increased prostate cancer risk.[Abstract]

Cholesterol-depletion of breast and prostate cancer cell lines induces apoptosis  whereas cholesterol-enrichment via elevated serum cholesterol (due to diet) supports tumor growth and progression.[Abstract, Full Text]

Elevated LDL positively correlates with increased risk of advanced stage colon cancer.[Abstract]

Patients with colon adenomas, the precursors of colon cancer, have elevated LDL.[Abstract]

Patients with distant metastases of colorectal cancer have significantly elevated serum cholesterol levels compared to those without metastases. "Elevated serum lipid levels may facilitate the development of distant metastasis in CRC [colorectal cancer] patients."[Abstract

Heme Iron, Arachidonic Acid, HCAs, PHAs, and Neu5Gc

Heme iron, a form of iron found at the highest levels in red meats. I discussed some of the evidence linking iron intake and levels to inflammatory diseases (including heart disease and cancer) in this post.

Arachidonic acid, which occurs in meat from grass-fed animals at levels equal to or greater than found in meat from grain-fed animals, and is involved in cancer promotion, which I discussed in this post.

Neu5Gc, a type of sialic acid produced by non-human mammals but not by humans, which enters humans through consumption of mammalian meat and milk, is incorporated into epithelial and endothelial tissues, incites an auto-immune response and inflammation in those tissues, and has been found concentrated in malignant tumors (full text).  

Of interest, this paper on Neu5Gc includes the following passage:

"Although earlier studies claimed the absence of Neu5Gc from normal human tissues, we showed thatit is also present in smaller amounts in normal human epithelial and endothelial cells in vivo (Tangvoranuntakul et al. 2003). Furthermore, we recently demonstrated that mice with a human-likedefect in the CMAH gene had no detectable Neu5Gc (Hedlund et al. 2007), effectively ruling out an alternate mammalian pathway for synthesis. This paradox is explained by our finding that humans can metabolically incorporate Neu5Gc via oral intake (Tangvoranuntakul et al. 2003). We have therefore suggested that the well-known epidemiological association of human cancers with consumption of red meat and milk (which happen to be the richest dietary sources of Neu5Gc) (Rose et al. 1986; Norat et al. 2002; Lewin et al. 2006) might be related to this unusual metabolic accumulation. Here, we have demonstrated another required component for this hypothesis – circulating antibodies that can recognize Neu5Gc on human tissues and can potentially generate chronic inflammation. To our knowledge, this is the first example wherein a nonhuman molecule becomes metabolically and covalently incorporated onto human cell surfaces, even in the face of an immune response against it. Further studies are needed to firmly establish a link between Neu5Gc expression in tumors and anti-Neu5Gc in the pathogenesis of carcinomas."[emphasis added]
This passage illustrates that the epidemiological association of human cancers with consumption of red meat and milk is "well-known" among scientists and that they have moved beyond questioning the association (since it is scientifically well established) to elucidating the mechanisms responsible for this association, in this case Neu5Gc, the first nonhuman molecule proven to become part of human cell surfaces despite an immune response against it.

I first learned about Neu5Gc from this video by Plant Positive:

Cooking meat at high temperatures, particularly over open flames, produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) which are carcinogenic.   These will form in meat cooked at high temperatures regardless of how the source animal was fed.    The National Cancer Institute says "numerous epidemiologic studies have used detailed questionnaires to examine participants’ meat consumption and meat cooking methods to estimate HCA and PAH exposures. Researchers found that high consumption of well-done, fried, or barbecued meats was associated with increased risks of colorectal (14), pancreatic (15, 16), and prostate (17, 18) cancer."

Protein, cholesterol, iron, arachidonic acid, and Neu5Gc all occur naturally in meat, and HCAs and PAHs form in meat cooked at high temperatures, regardless of the feeding or pharmaceutical strategy used to raise the animals from which the meat is taken.  

The studies I cited above only provide a small sampling of the laboratory data providing evidence of plausible mechanisms by which an excessive consumption of meat could increase one's risk of mortality.  Epidemiological research generated both the lipid hypothesis and the hypothesis that red meat increases mortality risk, but we now have much stronger data to support these hypotheses. 

We have evidence for specific mechanisms by which these naturally occuring substances can initiate (HCAs or PAHs) or promote (protein, cholesterol, iron, arachidonic acid, and Neu5Gc) fatal diseases, so only someone ignoring or ignorant of the above data could argue that the association of increased risks of mortality from cancer and heart disease apply only to people eating meat from grain-fed or drug-treated animals, or that the epidemiological associations have no plausible physiological basis.