Thursday, March 22, 2012

"Man the Fat Hunter" Paper Defines Paleo Diet As Meat-Based, Plant-Poor

I continue to read comments on my blog, and around the web, suggesting that anyone who believes that paleo diet is meat-based and low in carbohydrates is at least misinformed and at worst stupid.  Supposedly, by the time I had written Farewell To Paleo [which I have updated with references supporting my supposedly subjective evaluation of meat-based diets], some panel of experts had already decided that paleo diet is not necessarily meat-based, nor high in fat, nor low in carbohydrates, and I was well behind the learning curve.  Paleo 3.0 had arrived without my knowing it.

Or so some would like to think.

Perhaps unbeknownst to some people, "paleo diet" is short for "paleolithic diet,"  referring to the diet that humans evolved to eat during the so-called stone age.   The people who originally promoted paleolithic diet as a modern method for supporting health and preventing disease conceived of a modern paleo diet as an attempt to replicate the salient nutritional features of the diet that supported human evolution using foods from the food groups believed to constitute prehistoric paleolithic diets.

Anthropologists, biochemists, and biologists who study the evolution of humans and human nutrition and the recent diets of hunter-gatherers have produced the evidence for the model of paleolithic diet that informs Loren Cordain's works.  Among these people it seems there is a general agreement that prehistoric human diets were meat-based, high in animal protein and fat, and low in plants and carbohydrates.  There are dissenters who have attempted to argue against this notion, such as Richard Wrangham and Katherine Milton, and, in the medical community, perhaps David Jenkins, but these individuals are in the minority.  The majority adheres to some form of the Man The Hunter hypothesis, i.e. that increased carnivory separated the human line from our closest primate relatives; that increased meat-eating coupled with decreased plant-eating drove human evolution.

On February 21, 2012, after several people commenting on this blog had repeatedly tried to convince me that paleo diet is not necessarily meat-based, high in fat, or low in carbohydrates, Paul Jaminet posted the following message on the Facebook page for the Journal of Evolution and Health:

In case you have trouble reading it, it says:

"I'd like to welcome Miki Ben Dor to the journal effort. Miki was the lead author on the excellent recent paper "Man the Fat Hunter"" [Jaminet forgot to hyphenate Ben-Dor's name.]

Does this paper depart from the hypothesis that prehistoric paleo diet was meat-based and assert that humans evolved on random combinations of meat, vegetables, fruits and nuts, so that any combination thereof constitutes a paleo diet?

No.  Here is part of the abstract:

"We show that rather than a matter of preference, H. erectus in the Levant was dependent on both elephants and fat for his survival. The disappearance of elephants from the Levant some 400 kyr ago coincides with the appearance of a new and innovative local cultural complex – the Levantine Acheulo-Yabrudian and, as is evident from teeth recently found in the Acheulo-Yabrudian 400-200 kyr site of Qesem Cave, the replacement of H. erectus by a new hominin. We employ a bio-energetic model to present a hypothesis that the disappearance of the elephants, which created a need to hunt an increased number of smaller and faster animals while maintaining an adequate fat content in the diet, was the evolutionary drive behind the emergence of the lighter, more agile, and cognitively capable hominins."

They believe that H. erectus in the Levant was so dependent on dietary fat (and meat, particularly of elephants) for survival,  that the disappearance of the elephants drove them to hunt smaller animals, and this need to hunt smaller, faster, more agile animals coupled with a presumed physiological need for dietary animal fat provided a selective pressure that favored survival of a lighter, more agile, and smarter hominin, namely H. sapiens.

They expressly argue against the idea that human evolutionary diets could have been plant-based.  For example, they state that human ancestors needed to consume animal fat because they couldn't eat enough plants to meet nutrient requirements:

"The need to consume animal fat is the result of the physiological ceiling on the consumption of protein and plant foods."
Under the heading "The Obligatory Animal Fat Dietary Model" they use the standard argument for an animal fat-based based paleolithic diet using the expensive tissue hypothesis; they think our supposedly small gut coupled with our large brain provide evidence that meat-eating fueled human brain evolution:

"The more compact, the human gut is less efficient at extracting sufficient energy and nutrition from fibrous foods and considerably more dependent on higher-density, higher bio-available foods that require less energy for their digestion per unit of energy/nutrition released. It would therefore appear that it was the human carnivorousness rather than herbivorous nature that most probably energized the process of encephalization throughout most of human history."  [Emphasis added]
(Ben-Dor et al incorrectly state that encephalization took place during human history, when presumably it actually took place in prehistory, i.e. before written records.)

Under the heading "The physiological ceiling on plant food intake" they argue that plant foods could not have been a significant part of prehistoric diets for all the time-worn reasons given by previous paleo diet theorists:  takes too much time to gather plants, impossible to get adequate calories from raw plants, too many toxins and antinutrients in plants, no control of fire by H. erectus, lack of large cecum in human gut.  

You will find this passage in their paper:

"Similarly, modern hunter-gatherer (HG) groups, despite having access to fire and metal tools, also seem to have a strong preference for carnivorous foods over vegetal foods ([53]:682), a notion also supported by a recent study [75] that emphasizes limited consumption of carbohydrates by present day HG groups.

"Indeed, an analysis of nine HG groups for which detailed dietary information exists ([76]:166) shows that five groups, located in an area abundant in vegetation, consumed only a meager amount of plant foods (17% of calories on average)."[Emphasis added]
This paper also includes a line I think I might have read first in Paul Jaminet's book, The Perfect Health Diet:  "In fact, the natural diet of mammals is a high-fat diet." (Apparently they imagine that no mammal could break this supposed general rule, not even it it was peculiarly dependent on glucose to fuel its extraordinary brain.)

So, there you have it:  These archaeologists and anthropologists, like others before them, believe that humans probably evolved on (and presumably are presently adapted to) a diet consisting largely of meat and fat with "only a meager amount of plant foods" and "limited consumption of carbohydrates."  They apparently believe that because we are mammals, our natural diet is a high-fat diet.

Apparently Ben-Dor et al have not gotten the update on paleo diet from the blogosphere.  Anyone want to send them version 3.1?

Of course those internet experts know more about paleolithic diet than these anthropologists and archaeologists, right?

Just like Denise Minger, who admits having no formal training in statistics or medicine, knows more about statistics than Richard Peto, PhD, the Professor of Medical Statistics and Epidemiology from Oxford University who was elected a Fellow of the Royal Society of London (for the introduction of meta-analyses) in 1989, and was knighted (for services to epidemiology and to cancer prevention) in 1999, and worked on the Cornell-Oxford-China Project, right?

The same way that Anthony Colpo, who has no medical training and has never published any peer-reviewed cardiovascular disease research,  knows more about atherosclerosis than WC Roberts, who has authored several books on cardiovascular disease, has spoken at more than 1,300 medical meetings, serves as editor-in-chief of The American Journal of Cardiology, and with colleagues published more than 1,150 peer-reviewed articles on cardiovascular disease in medical journals, right?

And Gary Taubes, a science writer with no experience in bench obesity or medical research, and no peer-reviewed publications in the field of obesity research, knows more about nutrition and obesity, than, say, George Bray, Ph.D., Boyd Professor and Chief of the Division of Clinical Obesity and Metabolism at Pennington Biomedical Research Center, who over his 40 year career has authored or coauthored more than 1,700 publications, ranging from peer-reviewed articles to reviews, books, book chapters and abstracts, primarily in the field of obesity research.

If you think I am falling for a fallacious argument from authority, you don't understand that fallacy.   As explained at, an argument relying on authority is fallacious only if in the question under consideration, 1) no expertise is necessary or possible, 2) the cited authority is not a recognized expert in the field, 3) the authority is expert, but not disinterested, or 4) the authority is an expert, but his opinion varies markedly from the consensus of experts in his field.  Fallacy Files recommends this procedure for determining whether an argument from authority is fallacious or not:

To sum up these points in a positive manner, before relying upon expert opinion, go through the following checklist:
  • Is this a matter which I can decide without appeal to expert opinion? If the answer is "yes", then do so. If "no", go to the next question:
  • Is this a matter upon which expert opinion is available? If not, then your opinion will be as good as anyone else's. If so, proceed to the next question:
  • Is the authority an expert on the matter? If not, then why listen? If so, go on:
  • Is the authority biased towards one side? If so, the authority may be untrustworthy. At the very least, before accepting the authority's word seek a second, unbiased opinion. That is, go to the last question:
  • Is the authority's opinion representative of expert opinion? If not, then find out what the expert consensus is and rely on that. If so, then you may rationally rely upon the authority's opinion.
If an argument to authority cannot pass these five tests, then it commits the fallacy of appeal to misleading authority.
If you apply these five tests to Denise Minger's authority on the Cornell-Oxford-China Project, or Anthony Colpo's authority on diet and cardiovascular disease, or Gary Taube's authority on diet and obesity (or diet-related diseases), you will see who commits the fallacious appeal to authority. 

Of course, the consensus could be wrong.  But, when 50 or more years of research has produced enough evidence in support of a particular hypothesis to produce a wide consensus in a field, such as the lipid hypothesis, then you need really extraordinary evidence to overturn that hypothesis.

I highly doubt that Ben-Dor et al are going to change their view of paleolithic diet because some bloggers have decided that "paleo" includes plant-based diets with only meager amounts of meat and fat.

Just to be clear, I am not in this post agreeing, nor disagreeing, with any of the hypotheses of the Ben-Dor et al paper, so far as they apply to defining paleolithic diet or explaining the emergence of H. sapiens from H. erectus.   Even if their hypothesis about how modern humans emerged is strongly supported by evidence I do not believe that it in any way establishes or strongly supports the idea that a meat-based, high-fat diet with a meager amount of plant foods and limited amount of carbohydrates best supports human health in a modern context.  The direct way to discover the effects of foods on health of modern people in modern nations is to study the effects of various foods on modern people in modern nations, not speculate about how H. sapiens emerged.

In fact, if you believe that Ben-Dor et al have shown that a fat-based carnivorous diet is the best to support human health, I suggest you first subject them to the five tests to see if they are qualified authorities.  I submit that anyone who asserts that a fat-based carnivorous diet is the best to support human health fails the last test, at least, and that anthropologists and archaeologists are not appropriately qualified authorities on diet, nutrition, or health care (test 3). 

A strong theory of evolution of human diet would be able to explain why vegetarian diets are associated with a lower risk of heart disease than omnivorous diets (as another of many possible examples see this), why vegetarians have a lower body mass index than omnivores, why an essentially vegan soy- and gluten-rich diet reduces cholesterol as effectively as a statin drug, and why eating red meat increases the risk of all cause mortality.  Instead of providing an explanation for these painstakingly established scientific findings, some supporters of the hypothesis that humans evolved as carnivores spend their time trying to explain them away because they don't fit their hypothesis. This is not science, it is anti-science.  A scientist molds his hypotheses to accommodate the facts, not the other way around.

By the way, I wonder if Ben-Dor et al have any idea what hunting elephants entails.  The video below shows primitive spear hunting, including hunting of elephants and hippos.  Knowing the high level of intelligence and sensitivity of elephants (and the other animals as well), I find it appalling.

Thankfully we have evolved and found other ways to sustain ourselves in good health. 

Monday, March 19, 2012

Lustig Proposes Regulating Sugar Like Alcohol

 Robert Lustig, M.D., thinks sugar is so dangerous, he wants to use guns to prevent certain people from eating it.  In an editorial in Nature, Lustig and colleagues have expressed their belief that sugar is as toxic as alcohol and argue for regulating sugar consumption by use laws, i.e. guns.

They suggest establishing taxes on sweetened fizzy drinks (soda), other sugar-sweetened beverages (for example, juice, sports drinks and chocolate milk) and sugared cereal, use zoning to control distribution of fast-food outlets and convenience stores, and establish what I will call a 'legal sugar age' at which you can purchase sweetened foods and beverages.  From the editorial:

"States could apply zoning ordinances to control the number of fast-food outlets and convenience stores in low-income communities, and especially around schools, while providing incentives for the establishment of grocery stores and farmer's markets. Another option would be to limit sales during school operation, or to designate an age limit (such as 17) for the purchase of drinks with added sugar, particularly soda. Indeed, parents in South Philadelphia, Pennsylvania, recently took this upon themselves by lining up outside convenience stores and blocking children from entering them after school. Why couldn't a public-health directive do the same?"
Imagine this:

When you go to purchase a soft drink, ice cream, doughnut, or candy bar, you have to produce an I.D..

Juvenile detention centers filled with kids convicted of  buying a soft drink before the age of 17.  (Like our jails filled with people convicted of buying hashish.)

Gangs creating a black market for candies and sodas around grade and secondary schools.  (A predictable effect of market suppression.)

When you want to serve sweets to 'minors' at a birthday party held in a public place (say, a park), you need to get a special license from city hall, and have government "monitors" (i.e. police) present.

How about a SWAT team invading your grandmother's kitchen while she and her friends make Christmas cookies, charging them with endangering minors?

Hold It Granny!  Put that sugar down slowly and hands up!

I probably would have considered this last proposition hyperbole 10 years ago, but since then an organic food buying club and a raw milk dairy have been raided by SWAT teams looking for raw milk products.  Raids on sugar warehouses and baking clubs might not be that far off.

Nothing would please these people more, I guess.

Apparently Lustig et al don't see the crucial difference between parents taking it upon themselves to influence their children's behavior through action based on love, and using laws, backed by the force of police and guns, to regulate everyone's behavior.

If you don't think anyone would create an armed sugar or food police, keep in mind the Bureau of Alcohol, Tobacco, and Firearms (BATF), which sets the precedent. 

I just loathe this fascist mentality.  I think eating too much sugar can cause harm, but it is definitely not as toxic as alcohol, and I will defend to the death the right of individuals to choose to eat as much as they want, and to feed it to their children.

Conspicuously missing from the reports I have seen of their recommendations is any mention of stopping subsidies of the agricultural enterprises that make cheap corn, cane, and beets available for sugar production.  Instead of cutting off support of production, they propose regulating the individual users of sugar.  This is a bit like swatting mosquitos one by one while rewarding the people who create the swamps in which they breed.

In 2010 corn subsidies amounted to more than $3.5 billion, and between 1995 and 2010 they amounted to about $81 billion. [Environmental Working Group]

U.S. cane sugar subsidies amount to about $2 billion annually, and cause economic and environmental damage as well as supporting sugar consumption.  "Large areas of the Florida Everglades have been converted to cane sugar production as a result of sugar protection. That has caused damage from the related land drainage, runoff of chemical fertilizers, and the destruction of natural habitat."  [Cato Institute]

The sugar beet producers received $242 million in subsidies between 2000 and 2005. [Environmental Working Group]

Sugar subsidies cause considerable economic havoc. [The Great Sugar Shaft at the Future of Freedom Foundation]

How about looking for the causes of imbalances, instead of focusing on regulating symptoms?  Here, imbalanced consumption of sugar is largely a result of imbalanced production of sugar, and this is due to subsidies.

Removal of subsidies for corn, cane, and beets would increase the cost of these raw materials, which would increase the cost of sugar, which would lead to a voluntary reduction in use.   It would lead to a reduction of farmland devoted to overproduction of these commodities, and thus a reduction of environmental damage caused by that overproduction.  It would reduce the cost of 'government' and make unnecessary any 'sugar police' or 'sugar czar.'  

Instead Lustig et al propose creating another level of police state, another bureaucracy, another pile of laws.

I would hope that no-one takes him seriously, but unfortunately, some politicians like nothing more than any proposal that gives them another reason to create another law and take more control of more territory, even if it reaches into your kitchen.

Your favorite food could be the next candidate for regulations.  First, they came for the raw milk, and I said nothing.  Then, they came for the sugar, and I said nothing.  Then, they came for the starch, and I said nothing.....

I just say "No!" to sugar regulation and sugar subsidies.

Thursday, March 1, 2012

Arachidonic Acid and Breast, Prostate, and Colon Cancers

Arachidonic acid (AA) is a long-chain polyunsaturated omega-6 fat.  It does not occur in commonly consumed plant tissues, so animal foods supply dietary AA consumed by humans.  According to the National Cancer Institute, the top ten sources of arachidonic acid in U.S. diets include:

1. Chicken and chicken dishes (27%)
2. Eggs and egg dishes (18%)
3. Beef and beef dishes (7%)
4.  Sausage, franks, bacon, and ribs (7%)
5. Other fish and fish mixed dishes (6%)
6.  Burgers (5%)
7.  Cold cuts (3%)
8.  Pork and pork mixed dishes (3%)
9.  Mexican mixed dishes (3%)
10.  Pizza (3%)

Since AA is used in muscle cell membranes the AA (20:4 n-6) content (g/100 g edible) of lean flesh from grass-fed cattle may not differ significantly from the meat of corn-concentrate fed  cattle.  One study actually found that the highest AA level occurred in grazed (grass-fed) Scott cattle and the lowest level in Simmental cattle fed concentrate (corn) [1, full text]:

Both lean and fat from animals provides AA; lard may have the highest AA content of any animal fat: 

"The aim of this study was to accurately quantitate the AA content of visible fat and the lean portion of beef, lamb, pork, chicken, duck, and turkey. The visible fat of meat contained a significant quantity of AA, ranging from 20 to 180 mg/100 g fat, whereas the AA content of the lean portion of meat was lower, ranging from 30 to 99 mg/100 g lean meat. Beef and lamb meats contained lower levels of AA in both the visible fat and lean portion than that from the other species. The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat." [2 ]

In the absence of AA intake, an intake of linoleic acid (LA, the omega-6 fat found in plants) up to four percent of calories either has no effect on AA or reduces AA levels, but an intake of twenty percent of calories might stimulate undesirable eicosanoid synthesis temporarily. [3, 4]  In one study, a liquid formula diet supplying twenty percent of calories as linoleic acid significantly reduced platelet aggregation (-25%) and thromboxane formation (-43%). Levels of some prostaglandin metabolites increased during the first 10 days, then declined to a level lower than the pre-experimental values at the end of the 3-week period. [4]  Thus, it appeared that a diet enriched in LA ultimately reduced tissue levels of AA metabolites.

A review of 36 high-quality reports of studies of the effect of dietary LA on AA levels found "Increasing LA by as much as 551% from baseline and reducing LA by as much as 90% from baseline failed to yield compelling evidence supporting the concept that any conversion of dietary LA to downstream metabolites results in tissue enrichment of AA, a notion commonly assumed." [26 full text]  

In contrast, increased dietary intake of AA (i.e. meat and animal fat) increases the production of pro-inflammatory eicosanoids in humans. [5, 6 ]

Probably the body regulates conversion of LA to AA according to need, the same way it regulates conversion of beta-carotene to retinol according to need.  Although it is possible to overdose on retinol (so-called vitamin A), humans can't get an overdose of retinol by route of eating carotenoids because the body will not convert carotenoids to retinol unless it has a retinol deficiency.  Similarly, it appears that the body does not convert LA to AA unless it has a deficiency of AA, but we can get an excess of AA by eating AA directly, just as we can get an excess of retinol by eating retinol directly.  This suggests that human metabolism is not well adapted to diets containing preformed retinol or AA.

 Cells supplied with exogenous AA show increased production of an eicosanoid, PGE2, which in turn decreases production of tumor necrosis factor (TNF), a type of cytokine that induces programmed cell death (apoptosis) in tumor cells. [7]   This becomes relevant to cancer promotion; less TNF means less immune system control over tumor cells.

Research seems to suggest that promotion of AA metabolism promotes breast, prostate, and colon cancer, while inhibition of AA metabolism, even using aspirin or other COX2 inhibitor NSAIDs, reduces occurrence of these, the most common cancers in the United States.

"Epidemiologic evidence suggests the incidence of breast, colon, and lung cancers is inversely related to the use of aspirin and nonsteroidal anti-inflammatory drugs, which are nonspecific inhibitors of COX. COX-1 and COX-2 are enzymes that generate prostaglandins and thromboxanes from free arachidonic acid." [8
Below I have quoted some relevant publications or abstracts (when I don't have access to the full document), showing that scientists doing basic research on the biochemistry involved in cancer growth have identified AA metabolism as a target for cancer prevention and therapy. 

If you search PubMed with "arachidonic acid and (insert name of cancer)" you will find many more like these.

Breast Cancer

"Arachidonic acid (AA) and its metabolites play critical role in the development of breast cancer, but the mechanisms through which AA promotes mammary tumorigenesis and progression are poorly understood." [9]

Arachidonic metabolism by LOX enzymes is involved in lymph node metastasis of breast cancer.  [10 full text ]

"Arachidonic acid, a dietary cis-polyunsaturated fatty acid, stimulates adhesion and migration of human cancer cells on the extracellular matrix by activation of intracellular signaling pathways."[11 full text ]

"In our previous work, we utilized a highly metastatic human [breast] cancer cell line, MDA-MB-435, and demonstrated that arachidonic acid induced cellular adhesion to collagen type IV in an integrin-dependent manner requiring the activation of multiple signal transduction proteins." [12 full text ]

"The estrogen independent MDA-MB-435 cell line has the advantage that it metastasizes consistently to the lungs and forms quantifiable secondary nodules when injected into the mammary fat pads. With these breast cancer cells, the stimulating effects of polyunsaturated omega-6 fatty acids on both primary tumor growth and metastasis were demonstrated; in contrast, the long-chain omega-3 fatty acids were inhibitory. The model can also be adapted to examine dietary fatty acids, and inhibitors of their metabolism, as experimental adjuvant therapy after surgical excision of the primary tumors. ..The results obtained by these several approaches have demonstrated distinct roles for the cyclooxygenase and lipoxygenase-mediated products of omega-6 fatty acid metabolism, and suggest new approaches to experimental breast cancer therapy. " [13 ]

"15(S)-Lipoxygenase-2 Mediates Arachidonic Acid-stimulated Adhesion of Human Breast Carcinoma Cells through the Activation of TAK1, MKK6, and p38 MAPK....The cis-polyunsaturated fatty acid arachidonic acid and its many metabolites are important mediators of cell signaling with roles in inflammation, platelet aggregation, tissue development, and carcinogenesis (15). The cis-polyunsaturated fatty acids have been implicated in a number of in vivo and in vitro rodent studies that link fat intake and cellular fatty acid levels with carcinogenesis, tumor development, and metastasis (68)."  [14 full text ]

Prostate Cancer

"The target of arachidonic acid pathway is a new anticancer strategy for human prostate cancer." [15 ]

"Herein we provide evidence that fatty acids (FA) can trigger androgen synthesis within steroid starved prostate cancer (CaP) tumor cells..... We propose that this characterized arachidonic acid induced steroidogenesis mechanism significantly contributes to the activation of AR in CRPC progression and therefore recommend that fatty acid pathways be targeted therapeutically in progressing CaP." [16]

"The arachidonic acid pathway incorporates phospholipase, cyclooxygenase, lipoxygenase and epoxygenase enzymes. This pathway has been shown to have a major role in the development and progression of a number of cancers, including prostate cancer. We discuss the current status of research of this pathway in the area of prostate cancer, ranging from preclinical in vitro studies to human clinical trials....Evolving data suggest a significant role for some areas of the arachidonic acid pathway in prostate cancer. Inhibiting 1 or a number of these enzymes in combination may hold promise for future prostate cancer treatment." [17]

Colorectal Cancer

"Arachidonic acid metabolism through cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P-450 epoxygenase (EPOX) pathways leads to the generation of biologically active eicosanoids, including prostanoids, leukotrienes, hydroxyeicosatetraenoic acid, epoxyeicosatrienoic acid and hydroperoxyeicosatetraenoic acids. Eicosanoid expression levels vary during tumor development and progression of a range of malignancies, including colorectal cancer. The actions of these autocoids are also directly influenced by diet, as demonstrated by recent evidence for omega-3 fatty acids in colorectal cancer (CRC) prevention and/or treatment. Eicosanoids regulate CRC development and progression, while inhibition of these pathways has generally been shown to inhibit tumor growth/progression. A progressive sequence of colorectal cancer development has been identified, ranging from normal colon, to colitis, dysplasia, and carcinoma. ...Finally, novel approaches targeting these arachidonic acid-derived eicosanoids (using pharmacological or natural agents) for chemoprevention and/or treatment of colorectal cancer are outlined. "  [18]

Dietary Regulation of AA Metabolism

In the January 9, 1892 issue of Scientific American, an article stated that some members of the French  Society For The Advancement of Science believed already that "Reclus, the French Geographer, has proved that cancer is most frequent among those branches of the human race where carnivorous habits prevail."  This was before the widespread practice of raising animals on corn-based concentrated feed, suggesting that if diets rich in animal foods do increase the risk of cancer, they do so by components that occur in those foods regardless of the animal's diet, such as arachidonic acid.

More than 110 years later, scientists still find cancer risks elevated by consumption of various types of red meat [e.g. 20 full text] or poultry and eggs [e.g. 21].  Some data also suggests that fish oils may promote cancer metastases more potently than safflower oil:

"Rats were kept on either a low-fat diet or on a fish oil (omega-3 PUFAs) or safflower oil (omega-6 PUFAs) diet for 3 weeks before the administration of colon cancer cells to the portal vein, until they were sacrificed at 1 or 3 weeks after tumor transplantation. At 1 week after transplantation, the fish oil diet had induced 7-fold more metastases (in terms of number and size) than had the low-fat diet, whereas the safflower oil diet had not affected the number and total volume of metastases. At 3 weeks after tumor transplantation, the fish oil diet and the safflower oil diet had induced, respectively, 10- and 4-fold more metastases (number) and over 1000- and 500-fold more metastases (size) than were found in the livers of rats on the low-fat diet."[22 full text]
"PUFAs are incorporated into the membranes of both cancer cells and normal cells, altering their physical and functional properties (30, 39), which may interfere seriously with immunological surveillance against cancer cells. Furthermore, n-3 PUFA supplementation decreases cytokine production (40) and MHC class II expression on the cell surface of antigen-presenting macrophages (41, 42), thus interfering with the immune response (43, 44)."[22 full text]
In this study, "Fish oil and safflower oil were kept at 4°C under nitrogen to avoid autooxidation of PUFAs. Vitamin E levels in the food were kept at a minimum of 35 mg/kg of
the low-fat diet [5% (v/w) soybean oil] and at 75 mg/kg of the n-3 and n-6 PUFA diets [20% (v/w) fish oil or safflower oil. respectively] to avoid vitamin E deficiency."  Thus the ill effect of the oils in this study were not likely due to oxidation of the PUFAs.

As the amount of animal flesh, fat, and eggs in the diet increases, so does the intake of AA, which could promote AA metabolism; the more AA present in cells, the more substrate for the COX (cycloxygenase), LOX (lipoxygenase), and EPOX (expoygenase) enzymes that metabolize AA; this would result in chronic increases in PGE2 and chronic reductions in production of TNF.  As noted above [22 full text], omega-3 PUFA supplementation also interferes with immune responses involved in controlling cancer. 

This provides a couple of possible mechanisms by which a diet rich in animal flesh or eggs could support cancer development.  Briefly, chronically eating more food rich in AA would result in greater production of PGE2, which would chronically decrease production of TNF, which could reduce the control that the body has over tumor cell lines.  Eating food rich in n-3 fats (fish oils) would also depress cytokine production and MHC class II expression on the cell surface of antigen-presenting macrophages, also reducing the effectiveness of immune-system control of malignant cells.

Cancerous tumors start as single cells, and progress to detectable tumors by cell-division over the course of six to ten years.  Dr. John McDougall M.D. explains:

"The doublings remain undetectable until the cancer reaches a size of 1 mm (period-size), which now contains a million cells, after about 6 years of growth. After 10 years of growth, the tumor is 1 cm in diameter (eraser-size) and contains one billion cells. At this point in its natural history the doublings become very apparent: one billion cancer cells divide into a mass containing two billion cells, and with the next doubling there are 4 billion cancer cells inside the patient’s body. Thus, cancer is undetectable by the patient and his physician for the first two-thirds of its natural history, and this leads to confusion." [23]
Recognizing that tumors start as single malignant cells, we can appreciate how only a seemingly minor depression of immune function, e.g. a small chronic decrease in TNF production, or other alteration in the cell's environment could favor the survival of just one malignant cell, allowing it to divide to produce two, then four, then eight cells, and so on, for years, until one has a detectable tumor.

Plants provide many compounds that inhibit the COX (cycloxygenase), LOX (lipoxygenase), and EPOX (epoxygenase) enzymes that metabolize AA to PGE2 and other compounds :

"In this review, we present evidence that numerous agents identified from fruits and vegetables can interfere with several cell-signaling pathways. The agents include curcumin (turmeric), resveratrol (red grapes, peanuts and berries), genistein (soybean), diallyl sulfide (allium), S-allyl cysteine (allium), allicin (garlic), lycopene (tomato), capsaicin (red chilli), diosgenin (fenugreek), 6-gingerol (ginger), ellagic acid (pomegranate), ursolic acid (apple, pears, prunes), silymarin (milk thistle), anethol (anise, camphor, and fennel), catechins (green tea), eugenol (cloves), indole-3-carbinol (cruciferous vegetables), limonene (citrus fruits), beta carotene (carrots), and dietary fiber. For instance, the cell-signaling pathways inhibited by curcumin alone include NF-kappaB, AP-1, STAT3, Akt, Bcl-2, Bcl-X(L), caspases, PARP, IKK, EGFR, HER2, JNK, MAPK, COX2, and 5-LOX. The active principle identified in fruit and vegetables and the molecular targets modulated may be the basis for how these dietary agents not only prevent but also treat cancer and other diseases. This work reaffirms what Hippocrates said 25 centuries ago, let food be thy medicine and medicine be thy food." [24 ]

Since plants provide no AA (nor long chain omega-3 fats) but many COX2, LOX, and EPOX inhibitors, we could consider them among the "novel approaches" for preventing overproduction of the arachidonic acid-derived eicosanoids and thus "for chemoprevention and/or treatment of" cancer suggested by  [18].

We can expect that diets high in plants and low in or absent animal products would reduce the risk or even stem the growth of cancers, the latter of which has some confirmation by research I discussed here.

Other diseases linked to metabolites of AA include:

  • Inflammatory bowel disease [25 full text]
  • Alzheimer's disease [26]
  • Ischemic heart disease [27 full text]
  • Psoriasis and dermatitis [28, 29]
  • Rheumatoid arthritis [e.g. 30]
  • Osteoarthritis [31, 32, , 36] "Our results demonstrated that AA enhanced superoxide production in RA and OA cells..."[32]
  • Migraine headaches [33]
  • Dysmenorrhea (menstrual pain) and endometriosis [34]
  •  Cystic disease of the breast [35]
  • Osteoporosis [37]
That's just a quickly composed list.  The AA cascade drives inflammation, and chronic inflammation causes tissue damage and malfunction.

In Chinese medicine, we call inflammation pathological 'heat' (a term no less scientific than 'inflammation' which literally means 'in flames'), and land-animal meats and fats are considered common dietary promoters of conditions involving pathological heat, while many plant foods and herbs are considered 'cooling' by which we mean that they reduce or eliminate pathological heat.

Chinese physicians came to this information through logical deductions based on the yin-yang theory, combined with self-experimentation and extensive clinical experience and collaboration.  Plants have relatively yin (i.e. more water-like) characteristics like high water content, relative immobility, relative insentience, silence, low temperature, and dominance by the blue-green color spectrum, while animals generally exhibit relatively yang (i.e. more fire-like) characteristics like lower water content, mobility, greater sentience, loud sounds, inherent warmth, and dominance by the red-yellow color spectrum.

Further, the green parts of plants spend daylight hours in direct hot and drying (yang) sunlight, to which they must adapt by countermeasures that cool and moisten, so the green parts of plants must have cooling and moistening properties to survive; but animals live by burning up (oxidizing) foods, the way a fire burns up (oxidizes) fuel, so animal tissues must have fire-like oxidizing and heating properties in order to survive.

Since animals generally are more like fire (with some exceptions), and plants generally more like water, yin-yang theory predicts that many foods from animals will probably generate more heat and dryness in varying degrees (relative to plants), while many foods from plants will generally reduce heat and generate moisture.  Chinese medicine applies yin-yang theory empirically and flexibly, not dogmatically, and recognizes, for example, that some animal foods have many relatively yin characteristics (e.g. milk, mussels) while some plant foods have yang characteristics (e.g. garlic, cinnamon, chili peppers).  Thus, yin-yang theory also predicts that if a plant or animal food has atypical characteristics, like chili peppers or cinnamon bark (both red, dry, and hot), it will have corresponding effects (e.g. cinnamon will have a warming effect).  Chinese physicians tested this hypothesis with self-experimentation and then clinical application, eventually producing the current Chinese materia medica which categorizes items (mineral, vegetable, and animal) according to thermal and other effects.

The information in this article indicates that Western science supports this point of view, providing some partial biochemical explanations for the traditional Chinese medical view, i.e. arachidonic acid as a promoter of inflammation, and various anti-inflammatory plant compounds as inhibitors of inflammation.