To: All Paleodieters From: Mary and Sally Reply to Loren Cordain, Part II 7. You cite a study by Artaud to support the assertion that the "highest dietary correlates to CHD in world wide epidemiological studies come from consumption of milk and dairy products." This study was conducted by dieticians (who are trained to dispense fabricated foods) and William E Connor who is an avid supporter of the lipid hypothesis. We note that the study contains no tables of actual food consumption, so we are unable to assess some of their surprising claims, such as the assertion that the French consume much larger amounts of vegetable oil than the Finns. In fact, consumption of vegetable oil is remarkably low in France at 5 pounds per person per year (compared to 18 in the US) with 8 pounds of trans fats (compared to 24 in the US.) As there are many societies that consume dairy products and suffer little or no heart disease (not only France, but also the Masai studied by George Mann and the primitive Swiss studied by Weston Price), we would caution against basing any conclusions about milk on this paper. It should be noted that Switzerland and Austria have the longest lifespan of the western countries, almost the same as Japan, consuming a diet rich in dairy products. The Greeks are slightly behind, on a diet containing lots of rich (and salty) feta cheese. (Goat milk has 25% more fat than cow's milk.) You continue to argue that dairy fats as sources of 12:0, 14:0 and 16:0 are "atherogenic." Our question is this: Why were these fats not atherogenic at the turn of the century when the American diet was just loaded with butter, whole milk and cream? Why are they not atherogenic to the French? Why are they not atherogenic to the Masai? Why are they not atherogenic to peoples in the tropics who consume large amounts of coconut? Why are they not atherogenic to the peoples of Soviet Georgia? Why are they not atherogenic to babies drinking mother's milk, which contains more medium chain fatty acids (12:0 at 2.56 g/32 fl oz, 14:0 at 3.15 g/32 fl oz and 16:0 at 9.05 g/32 fl oz) than stearic acid (2.85 g/32 fl oz)? As we stated earlier, just because these fats raise cholesterol levels in short term metabolic ward studies does not mean that they cause heart disease. You also argue that milk consumption results in an unfavorable Ca:Mg ratio. The Ca:Mg ratio of cow's milk is about 9:1, which is "better" than the ratio of 11:1 found in mother's milk, and very close to serum Ca:Mg ratios of 8:1. Weston Price found that calcium levels in primitive diets were about 4 times higher than the calcium levels in the American diet of his day. Those people who did not consume dairy products got their calcium from preparations made from bone, particularly bone broths, which are a distinguishing feature of traditional diets. Small fish consumed with their bones contain considerably more calcium than milk, and it is safe to assume that insects, consumed with their hard shells, were also an excellent source of calcium. Of course, it is likely that magnesium levels were also higher in the Paleolithic diet. Magnesium is very important for the health of the cardiovascular system--but so is calcium. You give no reference for your assertion that the Ca:Mg ratio in "pre-agricultural" diet was 1:1. The body's mechanism for regulating calcium intake is complex, involving signals from the parathyroid gland when calcium is needed, and the action of special calcium binding proteins in the gut to transport calcium across the intestinal wall. These mechanisms guard against overabsorption of calcium should it be superabundant in the diet. The emphasis in modern diets should be on increasing magnesium from organically grown green vegetables and nuts and grains that have been properly prepared to neutralize phytic acid content (which can block magnesium absorption)--not on decreasing calcium. The theory that the lactose component of milk is a cause of CHD is an interesting one and deserves more study. It is one explanation for the fact that France has a low incidence of CHD with a high consumption of dairy products. In France, dairy products are rarely consumed as milk, but as fermented products such as cheese, yoghurt, butter and sour cream. Alternative explanations are the relatively low fat content in modern milk, leading to a vitamin A deficiency (18), and the addition of additives such as powdered milk containing oxidized cholesterol to reduced fat milks. Any one of these explanations supports our argument that the problem lies not with consumption of milk products per se, but in the abandonment of traditional processing methods (cheese-making, natural yoghurt, natural fermentation to make clabber, etc.) all of which do in fact reduce lactose content. Genetic selection in favor of low-fat-producing cows, use of inappropriate feed, pasteurization (which destroys lactase) and homogenization are other possible explanations. The study you cite regarding copper deficiencies involved rats on copper deficient diets that contained 62% fructose. Feeding powdered lactoalbumin exacerbated the effects of copper deficiency more than casein or egg white--but lactoalbumin was not the cause of copper deficiency. These experiments have little relevance for populations that do not have a high level of fructose consumption and that eat well-mineralized food and properly processed dairy products. Hunter/gatherers and traditional societies got sufficient copper from frequent consumption of liver and other organ meats. 7. Regarding xanthine oxidase, an enzyme found all over the human body and widely spread in animal products including milk, you might want to check a web site on the subject (http://www.bath.ac.uk/Departments/Biosciweb/roger2.htm) describing research examining the possibility that IgM anti-XO antibodies have a protective role in controlling free radicals and other reactive oxygen species. A study by White, et al, which found that high cholesterol induced release of xanthine oxidase in non-milk drinking rabbits, is a further indication that XO plays a protective role. (19) As we have given many examples of healthy populations that consume dairy products (usually fermented dairy products), we do not agree that foods derived from milk "wreak havoc in human health." But we do feel that modern commercial milk--pasteurized, fat-depleted and adulterated with additives--is best avoided. Referring to Mann's 1972 study of the Masai, you state that "...autopsies done on 50 Masai men (milk drinking populations) have revealed extensive atherosclerotic lesions in coronary artery cross sections...[noting that]...earlier reports of freedom from atherosclerosis in the Masai were shown to be incorrect." We find this statement rather curious. In 1993, George Mann quoted this same reference, which was Mann's own work, in the first chapter of his book Coronary Heart Disease: The Dietary Sense and Nonsense (GV Mann, ed, Janus Publishing Co, London, 1993). Mann said "...and our autopsies of 50 adult males showed little evidence of atheroma...[and also stated that]...these animal fat eaters show neither hypercholesteremia, nor atheroma, nor heart attacks." Two other references you cite for their protein research (i.e., 13 and 14, Wolfe and Giovanetti, 1991 and 1992) happened to have referred to Mann's findings with the Masai (as Mann had reported in 1964) as showing "...undetectable coronary heart disease...and...undetectable arteriosclerotic heart diseases..." Thus, we are doubly perplexed by your statement, and we are inclined to accept Mann's 1993 description of his own earlier work. 8. We discussed SFA content of pre-agricultural man earlier. As we stated, the slightly higher PUFA content of the Eskimo diet is not typical of other pre-industrial societies. Most of the fat in the Eskimo diet comes from marine mammals, not fish, which is rich in monounsaturated fatty acids and also provides moderate amounts of saturates. 9. Regarding the supposed calciuric effects of salt, Whiting et al found that calcium excretion with sodium chloride or phosphate could not be detected. (20) If salt causes osteoporosis, why do the Orientals, who consume very high levels of salt, have low levels of osteoporosis? Human skeletons of Huguenot women ages fifteen to eighty-nine recently exhumed in London showed no bone loss among the elderly. The English diet at the time was rich in salt, principally from salted meat and fish. (21) 10. Your thesis is that we have not done any adapting to any of the post agricultural diets, and that all of our modern ills are due to the fact that we are not eating like the hunter=gatherers. But we were not eating like the hunter-gatherers a hundred years ago and we were not suffering from all of the modern day chronic ailments, so obviously there are some other variables to account for the increase in degenerative disease. What we are all trying to determine is what these variables are. We think it is important to keep in mind that it is virtually impossible to determine the overall health status (including infant mortality, length of life, etc.) of Paleolithic man, particularly as he was subject to the vagaries of the hunt, periodic famine, drought, etc., although the fossil record indicates that the hunter/gatherer was in general well formed, well muscled and had good bone mineralization. We have better data about some Neolithic groups, principally from the pioneering work of Weston Price who found 14 societies in which virtually all members of the tribe or village were well formed, robust and enjoyed freedom from degenerative disease including tooth decay. The particulars of these diets varied considerably. Some contained milk products, some did not. Some contained grains and other plant foods; others were almost devoid of plant foods. Some were based on fish; others on animals of the hunt. Some contained much raw food and others consisted mostly of food that was cooked. The underlying characteristics of these healthy diets are summarized as follows: 1. The diets of healthy primitive and nonindustrialized peoples contain no refined or denatured foods such as refined sugar or corn syrup; white flour; canned foods; pasteurized, homogenized, skim or low-fat milk; refined or hydrogenated vegetable oils; protein powders; artificial vitamins or toxic additives and colorings. 2. All traditional cultures consume some sort of animal protein and fat from fish and other seafood; water and land fowl; land animals; eggs; milk and milk products; reptiles; and insects. 3. Primitive diets contain at least four times the calcium and other minerals and TEN times the fat soluble vitamins from animal fats (vitamin A, vitamin D and the Price Factor) as the average American diet. 4. In all traditional cultures, some animal products are eaten raw. 5. Primitive and traditional diets have a high food enzyme content from raw dairy products, raw meat and fish; raw honey; tropical fruits; cold-pressed oils; wine and unpasteurized beer; and naturally preserved, lacto-fermented vegetables, fruits, beverages, meats and condiments. 6. Seeds, grains and nuts are soaked, sprouted, fermented or naturally leavened before being consumed. 7. Only about 4% of calories come from polyunsaturated oils naturally occurring in grains, pulses, nuts, fish, animal fats and vegetables (compared to modern diets with values as high as 30% from polyunsaturates.) The balance of fat calories comes from monounsaturated and saturated fats. (An exception is the Eskimos with higher total fat from polyunsaturates.) 8. Traditional diets contain nearly equal amounts of omega-6 and omega-3 essential fatty acids. 9. All primitive diets contain some salt. 10. Primitive and traditional cultures use make use of animal bones, principally by preparation and consumption of mineral- and gelatin-rich bone broths. 11. Traditional cultures make provisions for the health of future generations by providing special nutrient-rich foods for parents-to-be, pregnant women and growing children; by proper spacing of children; and by teaching the principles of right diet to the young. In summary, we feel that the debate over dairy products, saturated fat and salt is misplaced. The conquest of degenerative diseases need not entail deleting nutritious and delicious foods like cheese, butter, sauces, gravies, salt and whole grains from our diet. Rather it requires more wisdom in our application of technology to the entire chain of food production, including the cultivation of plant foods so that they will be rich in vitamins and minerals; humane and natural animal husbandry; the delivery of fresh foods to the marketplace through a well-maintained infrastructure and appropriate packaging (rather than sterilization, pasteurization, additives and irradiation); a return to traditional preservation and preparation techniques including lacto-fermentation and the making of broth; and the elimination of refined, devitalized and denatured foods including modern vegetable oils, trans fats, sugar and white flour, soft drinks, most canned foods and protein powders. Rather than "lean meat, occasional organ meats and wild fruits and vegetables," (and we wonder how we would obtain those wild fruits and vegetables and still have time to participate in the paleodebate) may we suggest a varied and interesting diet that includes juicy well-marbled steaks served with Bernaise or a nice reduction sauce, sauteed liver with onions, traditional (but not genetically engineered) cultivars of organic vegetables (lightly steamed and dressed with butter or in salads with dressings composed of raw vinegar, extra virgin olive oil and cold pressed flax oil), and a variety of delicious fruits served with old-fashioned cream. References 1. Divi and George, Proceedings of the ISSX, 1996 2. W. C. Willett et al, Intake of trans fatty acids and risk of coronary heart diseases among women. Lancet 1993; 341:581-585; F.B Hu et al, Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997; 337:1491-1499 3. Harumi Okuyama, et al, Prog Lipid Res, Vol 35, No 4, pp 409-457 1997 4. Tatu A Meittinen, et al, JAMA Oct 18, 1985 vol 254, No 15, pp 2097 - 2102; and Timo Strandberg, et al, JAMA September 4, 1991 vol 266, No 9 pp 1225 - 1229 5. Loren Cordain et al, Abstract presented at the International Conference on the Return of N-3 Fatty Acids Into the food Supply: I. Land-Based Animal Food Products. Natcher Conference Center, NIH, Bethesda, MD 1997. 6. Trautwein et all, British Journal of Nutrition 77:605-620, 1997 7. M. G Enig, "Health and Nutritional Benefits From Coconut Oil and Its Advantages Over Competing Oils," 1995 Indian Coconut Journal 26:2-10 8. J.K.G. Kramer et al, Lipids, Vol 17, No 5, 1982, pp 372-382 9. David F. Horrobin, "The regulation of prostaglandin biosynthesis by manipulation of essential fatty acid metabolism," Reviews in Pure and Applied Pharmacological Sciences, Vol 4, pp 339 - 383, Freund Publishing House, 1983. 10. Russell L Smith, "Diet, Blood Cholesterol and Coronary Heart Disease: A Critical Review of the Literature," 1991, Vol 2, pp 3-18 to 3-100. 11. ìAmericans: Then and Now,î Price-Pottenger Nutrition Foundation Health Journal, Vol 20, No 4, 1996 12. P Khosla and K. C. Hayes, Dietary trans-monounsaturated fatty acids negatively impact plasma lipids in humans: critical review of the evidence. J Am Coll Nutr 1996; 15:325-339 13. B. A. Clevidence et al, Plasma lipoprotein (a) levels in men and women consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty acids. Arterioscler Thromb Vasc Biol 1997; 17:1657-1661 14. David J. A. Jenkins et al, Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34:362-366 15. O. Rasmussen et al, Differential effects of saturated and monounsaturated fat on blood glucose and insulin responses in subjects with non-insulin- dependent diabetes mellitus. Am J Clin Nutr 1996; 63:249-253 16. Okuyama, op cit. 17. M. G. Enig et al, "Comparisons of Fatty Acid Profiles Used in NHANES II Data Base and Data Available in the Literature." Abstract #2509, FASEB 73rd Annual Meeting; and M. G. Enig "Trans Fatty Acids in Diets and Data Bases." 1996, Cereal Foods World 41:58-63 18. Sally Fallon, "Vitamin A Vagary" Price-Pottenger Nutrition Foundation Health Journal, Vol 19, No 2, 1995 19. White et al, Proceed Nat Acad Sci 1996:93:8745-8749 20. Whiting et al, Am J Clin Nutr 1997:65:1465-72 21. B Lees et al, "Differences in proximal femur bone density over two centuries," Lancet, March 1993, 341:673-675.