Dietary fats and the risk of incident Alzheimer disease.
"Persons in the upper fifth of saturated-fat intake had 2.2 times the risk of incident Alzheimer disease compared with persons in the lowest fifth in a multivariable model adjusted for age, sex, race, education, and apolipoprotein E epsilon4 allele status (95% confidence interval, 1.1-4.7)."
http://www.ncbi.nlm.nih.gov/pubmed/12580703
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Food combination and Alzheimer disease risk: a protective diet.
"RESULTS: Two hundred fifty-three subjects developed AD during a follow-up of 3.9 years. We identified a dietary pattern (DP) strongly associated with lower AD risk: compared with subjects in the lowest tertile of adherence to this pattern, the AD hazard ratio (95% confidence interval) for subjects in the highest DP tertile was 0.62 (0.43-0.89) after multivariable adjustment (P for trend = .01). This DP was characterized by higher intakes of salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, and dark and green leafy vegetables and a lower intake of high-fat dairy products, red meat, organ meat, and butter."
http://www.ncbi.nlm.nih.gov/pubmed/20385883
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Alzheimer's disease: the cholesterol connection
"A hallmark of all forms of Alzheimer's Disease (AD) is an abnormal accumulation of B-amyloid protein (AB) in specific brain regions. Both the generation and clearance of AB are regulated by cholesterol. Elevated cholesterol levels increase AB in cellular and most animal models of AD, and drugs that inhibit cholesterol synthesis lower AB in these models...The identification of a variant of the Apolipoprotein E (APOE) gene as a major genetic risk factor for AD is also consistent with a role for cholesterol in the pathogenesis of AD."
http://www2.massgeneral.org/neurology/kovacs/publications/pdf/NN_AD_cholesterol_03.pdf
Since the most effective way to raise cholesterol is by consuming saturated fat, it is not surprising that saturated fat would be associated with increased Alzheimer's disease. BTW, Asian countries that consume a higher percentage of carbohydrates and a lower percentage of saturated fat than Americans have a lower rate of Alzheimer's than Americans. BTW, the apoe4 gene that increases the risk of Alzheimer's disease also raises cholesterol levels.
Saturday, January 12, 2013
Friday, November 9, 2012
Review of The Smarter Science of Slim : Is Paleo a Panacea?
At the very least people need to read other points of view before accepting the author's conclusions. Even if you are persuaded that this is the best diet for you, there are millions of healthy people eating very different kinds of diets who are not overweight.
POINTS OF AGREEMENT
1) The diet recommended by the book is effective for short term weight loss (but there are no long term clinical trails showing it reduces heart disease, cancer or all-cause mortality.)
2) Filling up on high fiber foods helps to control the appetite (but high protein is not required, the Japanese have 1/10 our rate of obesity on a high grain, low fat, moderate protein diet.)
3) Diets high in certain carbohydrates, like sugar and white flour, are not healthy (but Harvard recommends fruits, vegetables, whole grains and beans which are healthy in long term trials.)
4) Interval training is an effective form of exercise (but modern hunter gatherers get a lot of low intensity exercise like walking.)
5) Hunter gatherers have a near absence of heart disease (but they also have 50 to 70 mg/dL LDL levels (1) which are not duplicated in clinical trails of high protein diets. Parasitic infections and fiber are responsible for their low LDL levels and near absence of heart disease. (2))
6) Hunter gatherers have a near absence of cancer (but this is in spite of their high protein diet not because of it.)
POINTS OF DISAGREEMENT
1) THERE ARE NO LONG TERM STUDIES OF THIS DIET AND THE ENDORSEMENTS DON'T REPRESENT WHAT ANY UNIVERSITY RECOMMENDS LONG TERM: The current Harvard School of Public Health website states (Copyright © 2012 The President and Fellows of Harvard College):
"The answer to the question "What should I eat?" is actually pretty simple. But you wouldn't know that from news reports on diet and nutrition studies, whose sole purpose seems to be to confuse people on a daily basis. When it comes down to it, though--when all the evidence is looked at together--the best nutrition advice on what to eat is relatively straightforward: Eat a plant-based diet rich in fruits, vegetables, and whole grains; choose healthy fats, like olive and canola oil; and eat red meat and unhealthy fats, like saturated and trans fats, sparingly. Drink water and other healthy beverages, and limit sugary drinks and salt. Most important of all is keeping calories in check, so you can avoid weight gain, which makes exercise a key partner to a healthy diet." This is basically a Mediterranean diet. See [[ASIN:0743266420 Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating]]. This diet is high in whole grains and relatively low in animal protein, very different from the grain-free, 33% protein diet recommended by Jonathan Bailor.
2) THE VIEWS OF UFFE RAVNSKOV ON LDL DO NOT REPRESENT THE MAJORITY OF DOCTORS AND SCIENTISTS: There is a lot of evidence contradicting Dr. Ravnskov. The following studies are just a few examples.
According to the third report of the National Cholesterol Education Program (NCEP), "Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD." (3)
"Scientists studied nine single nucleotide polymorphisms which influence LDL levels. From homozygous familial hypercholesterolemia (FH) at the high extreme (over 600 mg/dL LDL cholesterol) to hypobeta-lipoproteinemia at the low extreme (less than 15mg/dL LDL cholesterol). Since these SNP's are present from birth, this allowed them to see the effect of low LDL levels maintained over a lifetime. The results show a three times greater benefit for these life long low LDL levels compared taking statins later in life."
The lead scientist stated, "the effect of each of the included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect." "The researchers also conducted a meta-analysis of the "natural" randomized trials by combining non-overlapping data from multiple SNPs involving 326,443 participants. Results of this study indicated that lifetime exposure to lower LDL was associated with a 54% (95% CI, 48-59) relative reduction of CVD for each 38.7 mg/dL (1 mmol/L) lower LDL." (4) There is a clear dose response relationship.
Michael Brown and Joseph Goldstein discovered that the number of functional LDL receptors on the surface of cells, especially liver cells determines the level of LDL in the blood. If the receptors are defective or too few in number, LDL builds up in the blood instead of being taken into the cells. Familial hypercholesterolemia (FH) is caused by the mutation of a single gene that does one thing; make LDL receptors. People with two copies of the mutation for FH have LDL levels 6 to 10 fold above normal and can have a heart attack as early as 18 months of age. People with one copy of the mutation have LDL levels 2 to 4 times above normal and develop clinical symptoms between the ages of 30 and 60. (5) In the era before the statins, FH patients aged 20 to 39 years old were 100 times more likely die of heart disease and 10 times more likely to die from all causes than someone in the general population. (6)
It is claimed by Dr. Ravnskov that Ancel Keys misled us in his Six Countries Study. In 1957 Yerushalmy and Hilleboe took another look at the FAO data that Keys had used. Their primary criticism was that there were other variables more strongly associated with heart disease mortality than TOTAL FAT which had a correlation of .659. (BTW, even though a graph of all 22 countries didn't make a straight line the correlation was strong and significant even for total fat.) It's ironic that Jonathan Bailor chose to cite this study, since the two variables that Yerushalmy and Hilleboe found most strongly associated with heart disease mortality in the 22 countries were ANIMAL PROTEIN first (correlation of .756) and ANIMAL FAT second (.684). (7) It's Dr. Ravnskov, who is not even a scientist, who misled us.
3) THE BOOK CLAIMS WE ARE IN THE MIDST OF A HEART DISEASE EPIDEMIC CAUSED BY OBESITY: In reality the age-adjusted mortality rate for cardiovascular disease peaked in 1963 and has been falling ever since. This is a well established fact.
In the introduction, the book contains a graph showing that the TOTAL NUMBER OF NON FATAL HEART DISEASE INCIDENTS has gone up from 1.4 to 2.2 million (57%). However, the population has grown by 50% during that time period and the percentage of elderly has also increased so it's not surprising that the total number of incidents might also go up. And various factors other than an actual increase in heart disease could account for non fatal incident reports. This seems like a very misleading way to report the evidence.
However the age-adjusted RATE OF DEATH from cardiovascular disease has been falling and at present is less than half of what is was at the peak of the heart disease epidemic in the 1960`s. According to the CDC: "Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56% (Figure 1). Age-adjusted death rates for coronary heart disease (the major form of CVD contributing to mortality) continued to increase into the 1960s, then declined. In 1996, 621,000 fewer deaths occurred from coronary heart disease than would have been expected had the rate remained at its 1963 peak."
A greater than 50% decline in cardiovascular disease is further confirmed by the Framingham Heart Study. (8)
And a study by Ergin et al. in 2004 shows that both the incidence and mortality of cardiovascular disease fell in the United states from 1971 through 1992. (9)
And according to the Atherosclerosis Risk in Communities (ARIC) Study: "Scientists now have information indicating that reductions in the risk factors for coronary heart disease are contributing to the decline in coronary heart disease rates, such as lowering blood cholesterol, blood pressure, and smoking rates (24%, 20%, and 12% reduction in coronary heart disease mortality from each)." The remaining 44% reduction is due to improved care during an acute heart attack.
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The book claims that between 1930 and 1970 heart attacks increased by 1000% in England while meat consumption remained stable. And that a similar increase in heart attacks occurred in the US while animal fat consumption actually fell. However because of vague classifications of heart disease the death rate from all diseases of the heart is a better measure and that only increased about 2.5 times in England.(10)
And in the US, from 1909 until the peak of the heart disease epidemic around 1965, while butter and lard consumption did fall, meat consumption rose from 141 to 148 pounds per capita and dairy products excluding butter rose from 177 to 237. Wheat flour fell from 291 to 147 and potatoes fell from 182 to 94. Percent fat increased from 32.1 to 41.1 percent and carbohydrates fell from 56.2 to 47.0 percent. During this time period meat transitioned from mostly grass-fed with less saturated fat to factory-farmed which contains several times as much saturated fat. This fact was not considered by the study and would make a large increase in animal fat. (11) So as fat climbed and carbohydrates fell the heart disease epidemic gained momentum.
4) THERE ARE SEVERAL REASONS AN EXTREMELY HIGH PROTEIN DIET (33% OF TOTAL CALORIES) MAY BE HARMFUL IN THE LONG RUN:
a) High meat diets increase IGF-1, which is a risk factor of cancer.
"Reducing protein intake from an average of 1.67 g kg '1 of body weight per day to 0.95 g kg '1 of body weight per day for 3 weeks in six volunteers practicing CR resulted in a reduction in serum IGF-1 from 194 ng mL '1 to 152 ng mL '1 ." (12)
"Men with relatively high intakes of total protein (top quintile) and minerals (top quintile of the five minerals combined) had a 25% higher mean plasma level of IGF-I compared with those in the low quintiles simultaneously." (13)
b) In three very large studies (one by AARP and two by Harvard) red meat intake was associated with mortality.
According to the AARP study of over half a million people "Conclusion: Red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality." (14)
Concerning the Harvard studies of over 37,000 men and over 83,000 women, the Harvard School of Public Health says "Replacing one serving of total red meat with one serving of a healthy protein source was associated with a lower mortality risk: 7% for fish, 14% for poultry, 19% for nuts, 10% for legumes, 10% for low-fat dairy products, and 14% for whole grains." (15)
c) Restriction of the amino acid methionine extends life in rodents (and methionine restriction reduces free radical formation) (16)
5) THE BOOK MISLEADS US ABOUT LOW-FAT DIETS: The book uses the Women's Health Initiative to claim that low fat diets are ineffective for weight loss or the prevention of heart disease and cancer. But in that study people were free to replace fat with anything they chose and in this country that's usually sugar, white flour and fried potatoes swimming in trans fat. And there was no significant lowering of LDL. However there are other kinds of low fat diets that are very effective at lowering LDL and reducing heart attacks.
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat, high protein diet and another 50 survivors were told to eat as usual. Total cholesterol fell from 312 mg/dl to 220 mg/dl in the experimental group. That's a reduction of 29%. And over a period of 8 years, 38 patients eating as usual died while only 22 in the experimental group died. (17)
In the 80's Dr. Esselstyn used a 10% fat, high fiber diet plus low dose statins to arrest or reverse heart disease in 18 severely ill heart patients. The average for total cholesterol and LDL was maintained at 145 mg/dl and 82 mg/dl respectively. We know it worked because of before and after coronary angiograms and cardiac PET scans. Some had been given less than a year to live by their referring cardiologist. After 12 years, "Adherent patients have experienced no extension of clinical disease, no coronary events, and no interventions. This finding is all the more compelling when we consider that the original compliant 18 participants experienced 49 coronary events in the 8 years before the study." There was no requirement to count calories or exercise to get these results. Although the sample was small, the results were statistically significant. The percent of reduction in mortality and cardiac events by far outperforms any other study that has ever been done on coronary artery disease patients. (18) Also see [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].
Dr. Ornish also reversed heart disease using a similar diet plus exercise and meditation but no statins. Since then Dr. Ornish has enrolled at least 3800 patients in demonstration projects (to demonstrate savings on surgery) which resulted in over 40 insurance companies including Medicare covering a program in diet and lifestyle for heart disease patients. According to Dr. Ornish, "In brief, we found that almost 80 percent of patients who were eligible for bypass surgery or angioplasty were able to safely avoid it for at least three years." Insurance companies wouldn't pay for something that made a lot of people worse. If any one got worse it had to be a small minority of patients. (19) Also see [[ASIN:0345496310 The Spectrum: A Scientifically Proven Program to Feel Better, Live Longer, Lose Weight, and Gain Health]].
6) THE CAUSE OF THE OBESITY EPIDEMIC IS NOT SETTLED SCIENCE: Dr. Lustig believes it's the fructose in sugar (especially in soft drinks and fruit juice) and not starch that is causing obesity and metabolic syndrome. Numerous studies in rodents have demonstrated that diets high in fructose induce insulin resistance. And fructose can induce metabolic syndrome in non-human primates as well. And fructose suppresses leptin, the hormone that controls appetite. And sugar is associated with the symptoms of metabolic syndrome in people. Starch does not produce the same effects even if the glycemic index is high. According to a study by Stanhope et al. in 2009 which compared fructose-sweetened to glucose-sweetened beverage consumption for 10 weeks: Only the fructose group had a significant increase in belly fat and markers of altered lipid metabolism including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. And American's consume more calories from sucrose and caloric sweeteners (like HFCS) than any other single food. In 2007 they consumed 629 calories per person per day of caloric sweeteners and this doesn't count the fructose in the fruit juice.
Wherever American fast food restaurants (large portions, high in sugar and salt and low in phytochemicals and fiber) spread around the world, obesity soon follows. And according to this study by the USDA, "The number of fast-food outlets increased from about 30,000 in 1970 to 140,000 in 1980, and fast-food sales increased by about 300%. More recent estimates show that in 2001, there were about 222,000 fast-food locations in the United States, generating sales of more than $125 billion." (20)
7) THE BOOK MISLEADS US ABOUT GRAINS: During the 50's and 60's Greece had the best longevity in the world and they ate more whole grains than Americans. Today Japan has the best longevity in the world and 1/10 as much obesity of Americans but they eat a lot more grain. However both these countries ate much less sugar than Americans. Millions of people including myself eat a diet containing a lot of whole grain and we're not overweight or unhealthy. The books high protein diet may be good for weight loss but there are no long term studies to show it will make people live longer. It is patterned after hunter gatherers, but hunter gatherers are not known for longevity. However cultures that consume more grains than Americans are known for less obesity and longer life.
The author actually claims on page 202 "... the amount of starch in the average Chinese or Indian diet is lower than the amount of starch in the average American diet." However according to the FAO the total calories/day/person from grains, starchy roots and beans consumed in 2007 by China was 1614, by India was 1570 and by the United States was only 964. What was he thinking? Did someone dare him to write this?
There is something called the "Rice Diet" developed by Dr. Kempner from Duke University that is free of added sugar or salt, is low in protein and most of the calories come from rice. According to this study "Treatment of massive obesity with rice/reduction diet program. An analysis of 106 patients with at least a 45-kg weight loss" it's extremely effective for weight loss. (21)
8) THE BOOKS CLAIMS TO REACH OBJECTIVE CONCLUSIONS BASED ON ALL THE EVIDENCE: Although the book says "Yet all too often a popular author selectively cites the scientific evidence, emphasizing only those aspects of the wide-ranging research that support the diet plan he or she is promoting." It seems that is exactly what the author did, perhaps without realizing it. Evidence was selected to make his high protein diet look as good as possible and make alternative diets look as bad as possible including the diet endorsed by Harvard Medical School. The result is a gross distortion of the facts. All the research that looks good for carbohydrate restricted diets is done along with weight loss so that the beneficial effects of calorie restriction are confused with the effects of the diet. But during weight maintenance, when calorie restriction is no longer around to help, it's another story. And when carbohydrate restricted diets are compared to low fat diets generally a 30% fat, low fiber diet with junky carbs is used instead of an optimal low fat diet with lots of fiber.
CONCLUSION: THERE ARE SEVERAL WAYS TO BE HEALTHIER THAN THE AVERAGE AMERICAN
People are different. People who are insulin resistant have a greater problem with carbs. People with fewer LDL receptors have a greater problem with saturated fat. People with the APOE4 allele are more likely to have problems with both. About 10% of people need to avoid gluten. Bottom line, everyone should follow a diet that makes them feel good as well as having some evidence for long term health.
The vast majority of the American people are not eating a Mediterranean diet, an Asian diet or whole foods vegetarian diet so their problems don't prove anything about these healthy diets. The diet the vast majority eat is much higher in animal protein, animal fat and sugar and much lower in fiber and phytonutrients.
Seven choices healthier than the SAD.
1. Vegetarian Adventist men and women live an average of 87 and 89 years, respectively and have a typical cholesterol level in the 180s. They abstain from alcohol and tobacco, exercise regularly and eat nuts, eggs and dairy products.
2. In the 50's and 60's Crete had the best longevity in the world. According to the Seven Countries Study, they ate 37% fat mostly from olive oil, but only 8% saturated fat. The total red meat, poultry and fish consumed per-person, per-week in Crete was only about 371 grams (13 ounces). According to the FAO, in 1961 they ate 1327 calories/person/day from whole grains, mostly wheat and they ate almost no table sugar. Ancel Keys and his wife followed a similar diet and he lived to be 100 years old and she lived to be 97 years old.
3. Japan has the best life expectancy of any country. The average man lives 79.4 years and the average women 86.1 years. They eat more carbs (about 59% versus 49%) and less fat (about 28% versus 38%) than the U.S. They eat more seafood than they do meat.
4. Iceland has the best longevity in Europe. The average man lives 80.1 years and the average women 83.5 years. They eat less carbs and more fat than the U.S. They eat more seafood than they do meat and their meat is grass fed. (In France they also eat grass fed meat.)
5. If you have heart disease, a 10% low-fat diet with low glycemic index, high fiber carbs can save your life. Dr. Ornish' diet is associated with higher levels of telomerase, an enzyme that maintains telomere length which is associated with health and longevity. Skim milk and egg whites are allowed. People without heart disease can eat more fat including wild salmon. Dr. Esselstyn's extremely successful study used a strict vegan diet.
6. If you have metabolic syndrome or can't eat grains, an Eco-Atkins diet with regular meat, that includes 12% or less animal protein and 12% or less saturated fat has been shown to be healthier than the standard American Diet.
7. The real Paleo diet/lifestyle. Modern hunter gatherers have a near absence of modern diseases, but they also have very low levels of LDL which are not duplicated in clinical trails of high protein diets. The HGs eat wild game which contains on average about 1/8th as much saturated fat as factory-farmed meat, with few exceptions they eat over 100 grams of fiber/person/day, they have parasitic infections which lower their LDL and they get a lot of moderate intensity exercise not once a week interval training. And their average life span is 72 years and "Heart attacks and strokes appear rare and do not account for these old-age deaths (see Eaton, Konner, and Shostak 1988), which tend to occur when sleeping." (22) So in spite of escaping chronic disease and hunting accidents and not smoking or eating processed foods they tend to die of old age around 72.
Two bad choices
1) Eat low fat diet with lots of sugar, white flour and salty fried potatoes swimming in trans fat and order large portions when you eat out. That will increase your risk of the obesity, metabolic syndrome and diabetes.
2) Eat a Paleo diet without lots of allium (e.g. onions, leeks, garlic) and cruciferous (e.g. broccoli, Brussels sprouts, cabbage etc.) vegetables and lots of berries to offset the cancer promoting effects of meat.
REFERENCES
1. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
2. Portugal LR, Fernandes LR, Alvarez-Leite JI. Host cholesterol and inflammation as common key regulators of toxoplasmosis and artherosclerosis development. Expert Rev Anti Infect Ther. 2009 Sep;7(7):807-19.
3. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002;106;3143.
4. Ference BA. Late-breaking clinical trials IV. Presented at: the American College of Cardiology 61st Scientific Session & Expo; March 24-27, 2012; Chicago.
5. Brown MS, Goldstein JL. Human mutations affecting the low density lipoprotein pathway. Am J Clin Nutr. 1977 Jun;30(6):975-8.
6. Risk of fatal coronary heart disease in familial hypercholesterolemia. British Medical Journal, 1991;303:893-896.
7. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med. 1957 Jul 15;57(14):2343-54.
8. Sarah Rosner Preis, ScD MPH1,2, Shih-Jen Hwang, PhD1,2, Sean Coady, MA2, Michael J. Pencina, PhD3, Ralph B. D'Agostino Sr, PhD3, Peter J. Savage, MD2, Daniel Levy, MD1,2, and Caroline S. Fox, MD MPH. Trends in All-Cause and Cardiovascular Disease Mortality among Women and Men with and without Diabetes in the Framingham Heart Study, 1950-2005. Circulation. 2009 April 7; 119(13): 1728-1735.
9. Ergin A, Muntner P, Sherwin R, He J. Secular trends in cardiovascular disease mortality, incidence, and case fatality rates in adults in the United States. Am J Med. 2004 Aug 15;117(4):219-27.
10. MAURICE CAMPBELL, O.B.E., D.M., F.R.C.P. DEATH RATE FROM DISEASES OF THE HEART: 1876 TO 1959. British Medical Journal August 31, 1963 page 528-535.
11. Nutrients in United States Food Supply, A Review of Trends, 1909-1913 to 1965
THE AMERICAN JOURLNAL OF CLINICAL NUTRITION. Vol. 20, No. 8, August, 1967, pp. 907-914.
12. Luigi Fontana, Edward P. Weiss, Dennis T. Villareal, Samuel Klein, and John O. Holloszy. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Aging Cell. 2008 October; 7(5): 681-687.
13. Giovannucci E, Pollak M, Liu Y, Platz EA, Majeed N, Rimm EB, Willett WC. Nutritional predictors of insulin-like growth factor I and their relationships to cancer in men. Cancer Epidemiol Biomarkers Prev. 2003 Feb;12(2):84-9.
14. Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 2009 Mar 23;169(6):562-71.
15. An Pan, Qi Sun, Adam M. Bernstein, Matthias B. Schulze, JoAnn E. Manson, Meir J. Stampfer, Walter C. Willett, Frank B. Hu, Red meat consumption and mortality: results from 2 prospective cohort studies, Archives of Internal Medicine, online March 12, 2012
16. Caro P, Gomez J, Sanchez I, Naudi A, Ayala V, López-Torres M, Pamplona R, Barja G.
Forty percent methionine restriction decreases mitochondrial oxygen radical production and leak at complex I during forward electron flow and lowers oxidative damage to proteins and mitochondrial DNA in rat kidney and brain mitochondria. Rejuvenation Res. 2009 Dec;12(6):421-34.
17. Morrison LM. Reduction of mortality rate in coronary atherosclerosis by a low cholesterol-low fat diet. Am Heart J. 1951 Oct;42(4):538-45.
18. Esselstyn CB Jr. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am J Cardiol. 1999 Aug 1;84(3):339-41, A8.
19. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet. 1990 Jul 21;336(8708):129-33.
20. SAHASPORN PAERATAKUL, MBBS, PhD; DAPHNE P. FERDINAND, MN, RN; CATHERINE M. CHAMPAGNE, RD, PhD; DONNA H. RYAN, MD; GEORGE A. BRAY, MD. Fast-food consumption among US adults and children: Dietary and nutrient intake profile.
21. Kempner W, Newborg BC, Peschel RL, Skyler JS. Treatment of massive obesity with rice/reduction diet program. An analysis of 106 patients with at least a 45-kg weight loss. Arch Intern Med. 1975 Dec;135(12):1575-84.
22. MICHAEL GURVEN, HILLARD KAPLAN. Longevity Among Hunter-Gatherers: A Cross-Cultural Examination.
POINTS OF AGREEMENT
1) The diet recommended by the book is effective for short term weight loss (but there are no long term clinical trails showing it reduces heart disease, cancer or all-cause mortality.)
2) Filling up on high fiber foods helps to control the appetite (but high protein is not required, the Japanese have 1/10 our rate of obesity on a high grain, low fat, moderate protein diet.)
3) Diets high in certain carbohydrates, like sugar and white flour, are not healthy (but Harvard recommends fruits, vegetables, whole grains and beans which are healthy in long term trials.)
4) Interval training is an effective form of exercise (but modern hunter gatherers get a lot of low intensity exercise like walking.)
5) Hunter gatherers have a near absence of heart disease (but they also have 50 to 70 mg/dL LDL levels (1) which are not duplicated in clinical trails of high protein diets. Parasitic infections and fiber are responsible for their low LDL levels and near absence of heart disease. (2))
6) Hunter gatherers have a near absence of cancer (but this is in spite of their high protein diet not because of it.)
POINTS OF DISAGREEMENT
1) THERE ARE NO LONG TERM STUDIES OF THIS DIET AND THE ENDORSEMENTS DON'T REPRESENT WHAT ANY UNIVERSITY RECOMMENDS LONG TERM: The current Harvard School of Public Health website states (Copyright © 2012 The President and Fellows of Harvard College):
"The answer to the question "What should I eat?" is actually pretty simple. But you wouldn't know that from news reports on diet and nutrition studies, whose sole purpose seems to be to confuse people on a daily basis. When it comes down to it, though--when all the evidence is looked at together--the best nutrition advice on what to eat is relatively straightforward: Eat a plant-based diet rich in fruits, vegetables, and whole grains; choose healthy fats, like olive and canola oil; and eat red meat and unhealthy fats, like saturated and trans fats, sparingly. Drink water and other healthy beverages, and limit sugary drinks and salt. Most important of all is keeping calories in check, so you can avoid weight gain, which makes exercise a key partner to a healthy diet." This is basically a Mediterranean diet. See [[ASIN:0743266420 Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating]]. This diet is high in whole grains and relatively low in animal protein, very different from the grain-free, 33% protein diet recommended by Jonathan Bailor.
2) THE VIEWS OF UFFE RAVNSKOV ON LDL DO NOT REPRESENT THE MAJORITY OF DOCTORS AND SCIENTISTS: There is a lot of evidence contradicting Dr. Ravnskov. The following studies are just a few examples.
According to the third report of the National Cholesterol Education Program (NCEP), "Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD." (3)
"Scientists studied nine single nucleotide polymorphisms which influence LDL levels. From homozygous familial hypercholesterolemia (FH) at the high extreme (over 600 mg/dL LDL cholesterol) to hypobeta-lipoproteinemia at the low extreme (less than 15mg/dL LDL cholesterol). Since these SNP's are present from birth, this allowed them to see the effect of low LDL levels maintained over a lifetime. The results show a three times greater benefit for these life long low LDL levels compared taking statins later in life."
The lead scientist stated, "the effect of each of the included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect." "The researchers also conducted a meta-analysis of the "natural" randomized trials by combining non-overlapping data from multiple SNPs involving 326,443 participants. Results of this study indicated that lifetime exposure to lower LDL was associated with a 54% (95% CI, 48-59) relative reduction of CVD for each 38.7 mg/dL (1 mmol/L) lower LDL." (4) There is a clear dose response relationship.
Michael Brown and Joseph Goldstein discovered that the number of functional LDL receptors on the surface of cells, especially liver cells determines the level of LDL in the blood. If the receptors are defective or too few in number, LDL builds up in the blood instead of being taken into the cells. Familial hypercholesterolemia (FH) is caused by the mutation of a single gene that does one thing; make LDL receptors. People with two copies of the mutation for FH have LDL levels 6 to 10 fold above normal and can have a heart attack as early as 18 months of age. People with one copy of the mutation have LDL levels 2 to 4 times above normal and develop clinical symptoms between the ages of 30 and 60. (5) In the era before the statins, FH patients aged 20 to 39 years old were 100 times more likely die of heart disease and 10 times more likely to die from all causes than someone in the general population. (6)
It is claimed by Dr. Ravnskov that Ancel Keys misled us in his Six Countries Study. In 1957 Yerushalmy and Hilleboe took another look at the FAO data that Keys had used. Their primary criticism was that there were other variables more strongly associated with heart disease mortality than TOTAL FAT which had a correlation of .659. (BTW, even though a graph of all 22 countries didn't make a straight line the correlation was strong and significant even for total fat.) It's ironic that Jonathan Bailor chose to cite this study, since the two variables that Yerushalmy and Hilleboe found most strongly associated with heart disease mortality in the 22 countries were ANIMAL PROTEIN first (correlation of .756) and ANIMAL FAT second (.684). (7) It's Dr. Ravnskov, who is not even a scientist, who misled us.
3) THE BOOK CLAIMS WE ARE IN THE MIDST OF A HEART DISEASE EPIDEMIC CAUSED BY OBESITY: In reality the age-adjusted mortality rate for cardiovascular disease peaked in 1963 and has been falling ever since. This is a well established fact.
In the introduction, the book contains a graph showing that the TOTAL NUMBER OF NON FATAL HEART DISEASE INCIDENTS has gone up from 1.4 to 2.2 million (57%). However, the population has grown by 50% during that time period and the percentage of elderly has also increased so it's not surprising that the total number of incidents might also go up. And various factors other than an actual increase in heart disease could account for non fatal incident reports. This seems like a very misleading way to report the evidence.
However the age-adjusted RATE OF DEATH from cardiovascular disease has been falling and at present is less than half of what is was at the peak of the heart disease epidemic in the 1960`s. According to the CDC: "Age-adjusted death rates per 100,000 persons (standardized to the 1940 U.S. population) for diseases of the heart (i.e., coronary heart disease, hypertensive heart disease, and rheumatic heart disease) have decreased from a peak of 307.4 in 1950 to 134.6 in 1996, an overall decline of 56% (Figure 1). Age-adjusted death rates for coronary heart disease (the major form of CVD contributing to mortality) continued to increase into the 1960s, then declined. In 1996, 621,000 fewer deaths occurred from coronary heart disease than would have been expected had the rate remained at its 1963 peak."
A greater than 50% decline in cardiovascular disease is further confirmed by the Framingham Heart Study. (8)
And a study by Ergin et al. in 2004 shows that both the incidence and mortality of cardiovascular disease fell in the United states from 1971 through 1992. (9)
And according to the Atherosclerosis Risk in Communities (ARIC) Study: "Scientists now have information indicating that reductions in the risk factors for coronary heart disease are contributing to the decline in coronary heart disease rates, such as lowering blood cholesterol, blood pressure, and smoking rates (24%, 20%, and 12% reduction in coronary heart disease mortality from each)." The remaining 44% reduction is due to improved care during an acute heart attack.
----
The book claims that between 1930 and 1970 heart attacks increased by 1000% in England while meat consumption remained stable. And that a similar increase in heart attacks occurred in the US while animal fat consumption actually fell. However because of vague classifications of heart disease the death rate from all diseases of the heart is a better measure and that only increased about 2.5 times in England.(10)
And in the US, from 1909 until the peak of the heart disease epidemic around 1965, while butter and lard consumption did fall, meat consumption rose from 141 to 148 pounds per capita and dairy products excluding butter rose from 177 to 237. Wheat flour fell from 291 to 147 and potatoes fell from 182 to 94. Percent fat increased from 32.1 to 41.1 percent and carbohydrates fell from 56.2 to 47.0 percent. During this time period meat transitioned from mostly grass-fed with less saturated fat to factory-farmed which contains several times as much saturated fat. This fact was not considered by the study and would make a large increase in animal fat. (11) So as fat climbed and carbohydrates fell the heart disease epidemic gained momentum.
4) THERE ARE SEVERAL REASONS AN EXTREMELY HIGH PROTEIN DIET (33% OF TOTAL CALORIES) MAY BE HARMFUL IN THE LONG RUN:
a) High meat diets increase IGF-1, which is a risk factor of cancer.
"Reducing protein intake from an average of 1.67 g kg '1 of body weight per day to 0.95 g kg '1 of body weight per day for 3 weeks in six volunteers practicing CR resulted in a reduction in serum IGF-1 from 194 ng mL '1 to 152 ng mL '1 ." (12)
"Men with relatively high intakes of total protein (top quintile) and minerals (top quintile of the five minerals combined) had a 25% higher mean plasma level of IGF-I compared with those in the low quintiles simultaneously." (13)
b) In three very large studies (one by AARP and two by Harvard) red meat intake was associated with mortality.
According to the AARP study of over half a million people "Conclusion: Red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality." (14)
Concerning the Harvard studies of over 37,000 men and over 83,000 women, the Harvard School of Public Health says "Replacing one serving of total red meat with one serving of a healthy protein source was associated with a lower mortality risk: 7% for fish, 14% for poultry, 19% for nuts, 10% for legumes, 10% for low-fat dairy products, and 14% for whole grains." (15)
c) Restriction of the amino acid methionine extends life in rodents (and methionine restriction reduces free radical formation) (16)
5) THE BOOK MISLEADS US ABOUT LOW-FAT DIETS: The book uses the Women's Health Initiative to claim that low fat diets are ineffective for weight loss or the prevention of heart disease and cancer. But in that study people were free to replace fat with anything they chose and in this country that's usually sugar, white flour and fried potatoes swimming in trans fat. And there was no significant lowering of LDL. However there are other kinds of low fat diets that are very effective at lowering LDL and reducing heart attacks.
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat, high protein diet and another 50 survivors were told to eat as usual. Total cholesterol fell from 312 mg/dl to 220 mg/dl in the experimental group. That's a reduction of 29%. And over a period of 8 years, 38 patients eating as usual died while only 22 in the experimental group died. (17)
In the 80's Dr. Esselstyn used a 10% fat, high fiber diet plus low dose statins to arrest or reverse heart disease in 18 severely ill heart patients. The average for total cholesterol and LDL was maintained at 145 mg/dl and 82 mg/dl respectively. We know it worked because of before and after coronary angiograms and cardiac PET scans. Some had been given less than a year to live by their referring cardiologist. After 12 years, "Adherent patients have experienced no extension of clinical disease, no coronary events, and no interventions. This finding is all the more compelling when we consider that the original compliant 18 participants experienced 49 coronary events in the 8 years before the study." There was no requirement to count calories or exercise to get these results. Although the sample was small, the results were statistically significant. The percent of reduction in mortality and cardiac events by far outperforms any other study that has ever been done on coronary artery disease patients. (18) Also see [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].
Dr. Ornish also reversed heart disease using a similar diet plus exercise and meditation but no statins. Since then Dr. Ornish has enrolled at least 3800 patients in demonstration projects (to demonstrate savings on surgery) which resulted in over 40 insurance companies including Medicare covering a program in diet and lifestyle for heart disease patients. According to Dr. Ornish, "In brief, we found that almost 80 percent of patients who were eligible for bypass surgery or angioplasty were able to safely avoid it for at least three years." Insurance companies wouldn't pay for something that made a lot of people worse. If any one got worse it had to be a small minority of patients. (19) Also see [[ASIN:0345496310 The Spectrum: A Scientifically Proven Program to Feel Better, Live Longer, Lose Weight, and Gain Health]].
6) THE CAUSE OF THE OBESITY EPIDEMIC IS NOT SETTLED SCIENCE: Dr. Lustig believes it's the fructose in sugar (especially in soft drinks and fruit juice) and not starch that is causing obesity and metabolic syndrome. Numerous studies in rodents have demonstrated that diets high in fructose induce insulin resistance. And fructose can induce metabolic syndrome in non-human primates as well. And fructose suppresses leptin, the hormone that controls appetite. And sugar is associated with the symptoms of metabolic syndrome in people. Starch does not produce the same effects even if the glycemic index is high. According to a study by Stanhope et al. in 2009 which compared fructose-sweetened to glucose-sweetened beverage consumption for 10 weeks: Only the fructose group had a significant increase in belly fat and markers of altered lipid metabolism including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. And American's consume more calories from sucrose and caloric sweeteners (like HFCS) than any other single food. In 2007 they consumed 629 calories per person per day of caloric sweeteners and this doesn't count the fructose in the fruit juice.
Wherever American fast food restaurants (large portions, high in sugar and salt and low in phytochemicals and fiber) spread around the world, obesity soon follows. And according to this study by the USDA, "The number of fast-food outlets increased from about 30,000 in 1970 to 140,000 in 1980, and fast-food sales increased by about 300%. More recent estimates show that in 2001, there were about 222,000 fast-food locations in the United States, generating sales of more than $125 billion." (20)
7) THE BOOK MISLEADS US ABOUT GRAINS: During the 50's and 60's Greece had the best longevity in the world and they ate more whole grains than Americans. Today Japan has the best longevity in the world and 1/10 as much obesity of Americans but they eat a lot more grain. However both these countries ate much less sugar than Americans. Millions of people including myself eat a diet containing a lot of whole grain and we're not overweight or unhealthy. The books high protein diet may be good for weight loss but there are no long term studies to show it will make people live longer. It is patterned after hunter gatherers, but hunter gatherers are not known for longevity. However cultures that consume more grains than Americans are known for less obesity and longer life.
The author actually claims on page 202 "... the amount of starch in the average Chinese or Indian diet is lower than the amount of starch in the average American diet." However according to the FAO the total calories/day/person from grains, starchy roots and beans consumed in 2007 by China was 1614, by India was 1570 and by the United States was only 964. What was he thinking? Did someone dare him to write this?
There is something called the "Rice Diet" developed by Dr. Kempner from Duke University that is free of added sugar or salt, is low in protein and most of the calories come from rice. According to this study "Treatment of massive obesity with rice/reduction diet program. An analysis of 106 patients with at least a 45-kg weight loss" it's extremely effective for weight loss. (21)
8) THE BOOKS CLAIMS TO REACH OBJECTIVE CONCLUSIONS BASED ON ALL THE EVIDENCE: Although the book says "Yet all too often a popular author selectively cites the scientific evidence, emphasizing only those aspects of the wide-ranging research that support the diet plan he or she is promoting." It seems that is exactly what the author did, perhaps without realizing it. Evidence was selected to make his high protein diet look as good as possible and make alternative diets look as bad as possible including the diet endorsed by Harvard Medical School. The result is a gross distortion of the facts. All the research that looks good for carbohydrate restricted diets is done along with weight loss so that the beneficial effects of calorie restriction are confused with the effects of the diet. But during weight maintenance, when calorie restriction is no longer around to help, it's another story. And when carbohydrate restricted diets are compared to low fat diets generally a 30% fat, low fiber diet with junky carbs is used instead of an optimal low fat diet with lots of fiber.
CONCLUSION: THERE ARE SEVERAL WAYS TO BE HEALTHIER THAN THE AVERAGE AMERICAN
People are different. People who are insulin resistant have a greater problem with carbs. People with fewer LDL receptors have a greater problem with saturated fat. People with the APOE4 allele are more likely to have problems with both. About 10% of people need to avoid gluten. Bottom line, everyone should follow a diet that makes them feel good as well as having some evidence for long term health.
The vast majority of the American people are not eating a Mediterranean diet, an Asian diet or whole foods vegetarian diet so their problems don't prove anything about these healthy diets. The diet the vast majority eat is much higher in animal protein, animal fat and sugar and much lower in fiber and phytonutrients.
Seven choices healthier than the SAD.
1. Vegetarian Adventist men and women live an average of 87 and 89 years, respectively and have a typical cholesterol level in the 180s. They abstain from alcohol and tobacco, exercise regularly and eat nuts, eggs and dairy products.
2. In the 50's and 60's Crete had the best longevity in the world. According to the Seven Countries Study, they ate 37% fat mostly from olive oil, but only 8% saturated fat. The total red meat, poultry and fish consumed per-person, per-week in Crete was only about 371 grams (13 ounces). According to the FAO, in 1961 they ate 1327 calories/person/day from whole grains, mostly wheat and they ate almost no table sugar. Ancel Keys and his wife followed a similar diet and he lived to be 100 years old and she lived to be 97 years old.
3. Japan has the best life expectancy of any country. The average man lives 79.4 years and the average women 86.1 years. They eat more carbs (about 59% versus 49%) and less fat (about 28% versus 38%) than the U.S. They eat more seafood than they do meat.
4. Iceland has the best longevity in Europe. The average man lives 80.1 years and the average women 83.5 years. They eat less carbs and more fat than the U.S. They eat more seafood than they do meat and their meat is grass fed. (In France they also eat grass fed meat.)
5. If you have heart disease, a 10% low-fat diet with low glycemic index, high fiber carbs can save your life. Dr. Ornish' diet is associated with higher levels of telomerase, an enzyme that maintains telomere length which is associated with health and longevity. Skim milk and egg whites are allowed. People without heart disease can eat more fat including wild salmon. Dr. Esselstyn's extremely successful study used a strict vegan diet.
6. If you have metabolic syndrome or can't eat grains, an Eco-Atkins diet with regular meat, that includes 12% or less animal protein and 12% or less saturated fat has been shown to be healthier than the standard American Diet.
7. The real Paleo diet/lifestyle. Modern hunter gatherers have a near absence of modern diseases, but they also have very low levels of LDL which are not duplicated in clinical trails of high protein diets. The HGs eat wild game which contains on average about 1/8th as much saturated fat as factory-farmed meat, with few exceptions they eat over 100 grams of fiber/person/day, they have parasitic infections which lower their LDL and they get a lot of moderate intensity exercise not once a week interval training. And their average life span is 72 years and "Heart attacks and strokes appear rare and do not account for these old-age deaths (see Eaton, Konner, and Shostak 1988), which tend to occur when sleeping." (22) So in spite of escaping chronic disease and hunting accidents and not smoking or eating processed foods they tend to die of old age around 72.
Two bad choices
1) Eat low fat diet with lots of sugar, white flour and salty fried potatoes swimming in trans fat and order large portions when you eat out. That will increase your risk of the obesity, metabolic syndrome and diabetes.
2) Eat a Paleo diet without lots of allium (e.g. onions, leeks, garlic) and cruciferous (e.g. broccoli, Brussels sprouts, cabbage etc.) vegetables and lots of berries to offset the cancer promoting effects of meat.
REFERENCES
1. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
2. Portugal LR, Fernandes LR, Alvarez-Leite JI. Host cholesterol and inflammation as common key regulators of toxoplasmosis and artherosclerosis development. Expert Rev Anti Infect Ther. 2009 Sep;7(7):807-19.
3. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002;106;3143.
4. Ference BA. Late-breaking clinical trials IV. Presented at: the American College of Cardiology 61st Scientific Session & Expo; March 24-27, 2012; Chicago.
5. Brown MS, Goldstein JL. Human mutations affecting the low density lipoprotein pathway. Am J Clin Nutr. 1977 Jun;30(6):975-8.
6. Risk of fatal coronary heart disease in familial hypercholesterolemia. British Medical Journal, 1991;303:893-896.
7. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med. 1957 Jul 15;57(14):2343-54.
8. Sarah Rosner Preis, ScD MPH1,2, Shih-Jen Hwang, PhD1,2, Sean Coady, MA2, Michael J. Pencina, PhD3, Ralph B. D'Agostino Sr, PhD3, Peter J. Savage, MD2, Daniel Levy, MD1,2, and Caroline S. Fox, MD MPH. Trends in All-Cause and Cardiovascular Disease Mortality among Women and Men with and without Diabetes in the Framingham Heart Study, 1950-2005. Circulation. 2009 April 7; 119(13): 1728-1735.
9. Ergin A, Muntner P, Sherwin R, He J. Secular trends in cardiovascular disease mortality, incidence, and case fatality rates in adults in the United States. Am J Med. 2004 Aug 15;117(4):219-27.
10. MAURICE CAMPBELL, O.B.E., D.M., F.R.C.P. DEATH RATE FROM DISEASES OF THE HEART: 1876 TO 1959. British Medical Journal August 31, 1963 page 528-535.
11. Nutrients in United States Food Supply, A Review of Trends, 1909-1913 to 1965
THE AMERICAN JOURLNAL OF CLINICAL NUTRITION. Vol. 20, No. 8, August, 1967, pp. 907-914.
12. Luigi Fontana, Edward P. Weiss, Dennis T. Villareal, Samuel Klein, and John O. Holloszy. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Aging Cell. 2008 October; 7(5): 681-687.
13. Giovannucci E, Pollak M, Liu Y, Platz EA, Majeed N, Rimm EB, Willett WC. Nutritional predictors of insulin-like growth factor I and their relationships to cancer in men. Cancer Epidemiol Biomarkers Prev. 2003 Feb;12(2):84-9.
14. Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 2009 Mar 23;169(6):562-71.
15. An Pan, Qi Sun, Adam M. Bernstein, Matthias B. Schulze, JoAnn E. Manson, Meir J. Stampfer, Walter C. Willett, Frank B. Hu, Red meat consumption and mortality: results from 2 prospective cohort studies, Archives of Internal Medicine, online March 12, 2012
16. Caro P, Gomez J, Sanchez I, Naudi A, Ayala V, López-Torres M, Pamplona R, Barja G.
Forty percent methionine restriction decreases mitochondrial oxygen radical production and leak at complex I during forward electron flow and lowers oxidative damage to proteins and mitochondrial DNA in rat kidney and brain mitochondria. Rejuvenation Res. 2009 Dec;12(6):421-34.
17. Morrison LM. Reduction of mortality rate in coronary atherosclerosis by a low cholesterol-low fat diet. Am Heart J. 1951 Oct;42(4):538-45.
18. Esselstyn CB Jr. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am J Cardiol. 1999 Aug 1;84(3):339-41, A8.
19. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet. 1990 Jul 21;336(8708):129-33.
20. SAHASPORN PAERATAKUL, MBBS, PhD; DAPHNE P. FERDINAND, MN, RN; CATHERINE M. CHAMPAGNE, RD, PhD; DONNA H. RYAN, MD; GEORGE A. BRAY, MD. Fast-food consumption among US adults and children: Dietary and nutrient intake profile.
21. Kempner W, Newborg BC, Peschel RL, Skyler JS. Treatment of massive obesity with rice/reduction diet program. An analysis of 106 patients with at least a 45-kg weight loss. Arch Intern Med. 1975 Dec;135(12):1575-84.
22. MICHAEL GURVEN, HILLARD KAPLAN. Longevity Among Hunter-Gatherers: A Cross-Cultural Examination.
Wednesday, April 25, 2012
During weight maintenance a high saturated fat, high beef diet increased the number of small dense LDL particles.
In a study co-authored by Ronald Krauss, during weight maintenance two low-carb diets (one high and one low in saturated fat) were compared to a high-carb diet that was also high in saturated fat. The values for small dense LDL were 222 nmol/l in the low-carb, high saturated fat diet ; 207 nmol/l in the high-carb diet, high saturated fat diet; and 187 nmol/l in the low-carb, low saturated fat diet.
Mangravite LM, Chiu S, Wojnoonski K, Rawlings RS, Bergeron N, Krauss RM. Changes in atherogenic dyslipidemia induced by carbohydrate restriction in men are dependent on dietary protein source. J Nutr.2011Dec;141(12):2180-5.
http://www.slideshare.net/pronutritionist/beef-low-carb-diet (see slide 6)
What Dr. Krauss said about this study:
"This is one of the surprises that keep life interesting for us for us as researchers and also for the world out there who happens to be looking over our shoulder. In this case, the surprise was that the combination of the high beef diet and the high saturated fat diet caused very serious increases in all of the cholesterol related risk factors we had been measuring, including total particle numbers, small LDL, total LDL cholesterol, inflammation, whatever we looked at, we saw an adverse effect."
http://www.meandmydiabetes.com/2012/04/17/ron-krauss-saturated-fat-red-meat-it-depends
Mangravite LM, Chiu S, Wojnoonski K, Rawlings RS, Bergeron N, Krauss RM. Changes in atherogenic dyslipidemia induced by carbohydrate restriction in men are dependent on dietary protein source. J Nutr.2011Dec;141(12):2180-5.
http://www.slideshare.net/pronutritionist
What Dr. Krauss said about this study:
"This is one of the surprises that keep life interesting for us for us as researchers and also for the world out there who happens to be looking over our shoulder. In this case, the surprise was that the combination of the high beef diet and the high saturated fat diet caused very serious increases in all of the cholesterol related risk factors we had been measuring, including total particle numbers, small LDL, total LDL cholesterol, inflammation, whatever we looked at, we saw an adverse effect."
http://www.meandmydiabetes.com/2012/04/17
Wednesday, April 11, 2012
Lifelong reductions in LDL linked to consistent reduction in CHD risk
Scientists studied nine single nucleotide polymorphisms which influence LDL levels. From homozygous familial hypercholesterolemia at the high extreme (over 600 mg/dL LDL cholesterol) to hypobeta-lipoproteinemia at the low extreme (less than 15mg/dL LDL cholesterol). Since these SNP's are present from birth, this allowed them to see the effect of low LDL levels maintained over a lifetime. The results show a three times greater benefit for these life long low LDL levels compared taking statins later in life. Ference stated, "the effect of each of the included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect."
"The researchers also conducted a meta-analysis of the "natural" randomized trials by combining non-overlapping data from multiple SNPs involving 326,443 participants. Results of this study indicated that lifetime exposure to lower LDL was associated with a 54% (95% CI, 48-59) relative reduction of CVD for each 38.7 mg/dL (1 mmol/L) lower LDL." There is a clear dose response relationship. And no one is suggesting that people that statins all their life, but low animal fat diets can do a lot to improve LDL.
Ference BA. Late-breaking clinical trials IV. Presented at: the American College of Cardiology 61st Scientific Session & Expo; March 24-27, 2012; Chicago
http://www.endocrinetoday.com/view.aspx?rid=95991
Modified 04-20-2012
"The researchers also conducted a meta-analysis of the "natural" randomized trials by combining non-overlapping data from multiple SNPs involving 326,443 participants. Results of this study indicated that lifetime exposure to lower LDL was associated with a 54% (95% CI, 48-59) relative reduction of CVD for each 38.7 mg/dL (1 mmol/L) lower LDL." There is a clear dose response relationship. And no one is suggesting that people that statins all their life, but low animal fat diets can do a lot to improve LDL.
Ference BA. Late-breaking clinical trials IV. Presented at: the American College of Cardiology 61st Scientific Session & Expo; March 24-27, 2012; Chicago
http://www.endocrinetoday.com/view.aspx?rid=95991
Modified 04-20-2012
Monday, November 7, 2011
Review of Ignore the Awkward : Is Dr. Ravnskov also ignoring the awkward?
OBSERVATIONAL EVIDENCE
1. Michael Brown and Joseph Goldstein discovered that the number of functional LDL receptors on the surface of cells, especially liver cells determines the level of LDL in the blood. If the receptors are defective or too few in number, LDL builds up in the blood instead of being taken into the cells. Familial hypercholesterolemia (FH) is caused by the mutation of a single gene that does one thing; make LDL receptors. People with two copies of the mutation for FH have LDL levels 6 to 10 fold above normal and can have a heart attack as early as 18 months of age. People with one copy of the mutation have LDL levels 2 to 4 times above normal and develop clinical symptoms between the ages of 30 and 60. Dr. Ravnskov is in denial about the obvious dose response relationship. (1) In the era before the statins, FH patients aged 20 to 39 years old were 100 times more likely die of heart disease and 10 times more likely to die from all causes than someone in the general population. (2) In a later study, FH patients treated with statins lived just as long as people without FH. (3)
2. Atherosclerotic plaque contains a lot of cholesterol. In 1856 a German pathologist named Rudolf Virchow proposed that lipid accumulation in the artery wall caused atherosclerosis. In 1914 Nikolai Anitschkow also observed cholesterol crystals in advanced plaque in the aorta of cholesterol fed rabbits.
3. People with very low LDL tend to be protected from CHD, with the exception of alcoholics. (Alcohol lowers LDL and damages the endothelium at the same time.) The normal LDL cholesterol range is 50 to 70 mg/dl for modern hunter-gatherers, healthy human newborns, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). (4) And during the 80s, rural Chinese had an average serum cholesterol level of 127 mg/dl. And the men in rural China had a rate of CHD that was only 1/17th that of American men. This was in spite of the fact that close to 80% of them smoked. (5) According to the third report of the National Cholesterol Education Program (NCEP), "Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD." (6)
4. People with an intermediate level of LDL have intermediate levels of heart disease. Virtually 100% of observational studies comparing people within the same country show an association between serum cholesterol and heart disease. (7,8,9)
5. The fact that HDL is protective and does the opposite of LDL is further proof of the harmfulness of elevated LDL. The INTERHEART study looked at 52 different countries and found that the ratio of apo-B (mostly LDL) to apo-A1 (HDL) could account for 50% of the risk of CHD mortality. (10)
EXPERIMENTAL EVIDENCE
6. Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. (11 This can't be explained away by stress, inflammation or some infectious agent. In clinical trials, Dr. Esselstyn's group did better than Dr. Ornish's group even though Dr. Ornish used stress reduction and Dr. Esselstyn didn't. However Dr. Esselstyn's patients had lower LDL. And although adding inflammatory factors like infection can speed up atherosclerosis, oxidized LDL, foam cells and cholesterol crystals inside the artery wall provide their own inflammation. See point eight.
7. In a meta-analysis of 35 randomized trials using diet and/or medication for every 10 percentage points of cholesterol lowering, CHD mortality was reduced by 13% and total mortality by 10% (12). And a meta-analysis of 9 randomized trials shows that when statins are used for secondary prevention in elderly patients they can reduce all-cause mortality by 22% and heart disease mortality by 30%. (13)
8. Lowering LDL can halt and even reverse heart disease in humans. In the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, coronary atherosclerosis was virtually stopped in its tracks when LDL was maintained at 79 mg/dL. (14) And Dr. Esselstyn was able to reverse atherosclerosis by maintaining LDL at 81 mg/dL using a 10% fat, high fiber diet and a low dose statin. (15)
How does LDL cause atherosclerosis?
9. Last but not least elevated LDL is essential to the mechanism of atherosclerosis. Apo B lipoproteins (mostly LDL) diffuse into the artery wall that has been damaged by hypertension, smoking, or high blood pressure. They become oxidized and cause inflammation which attracts macrophages. Macrophages devour oxidized LDL and become foam cells which form plaque and produce more inflammatory chemicals. They grow and eventually rupture depositing cholesterol crystals in the plaque. The crystals penetrate the artery wall causing even more inflammation. Elevated LDL also impairs endothelial function, reduces nitric oxide production and promotes platelet aggregation which promotes clotting. There are other factors besides elevated LDL that contribute to heart disease like smoking, hypertension, diabetes, abdominal obesity, stress, inflammation, homocysteine, sedentary lifestyle and excess sucrose but according to the INTERHEART study the ratio of apo-B (mostly LDL) to apo-A1 (HDL) can account for 50% of the risk. (16,17,18,10)
10. People who know the most about the subject agree. Scientists studying atherosclerosis know more about the subject than anyone else and the vast majority think that cholesterol is connected to heart disease. This is according a scientist who supports the cholesterol hypothesis as well as a leading cholesterol skeptic. (19,20)
SUMMARY OF ANSWERS TO OBJECTIONS
11. Dr. Ravnskov wants you to trust him and ignore people who know more about the subject than he does. However, in the introduction he tells us that "high cholesterol is good; the higher the better." This statement is so ridiculous that you shouldn't take anything else he says seriously. Why? Every chemical in the body has a healthy range. Too high or too low causes disease. Your body needs glucose. It's a natural energy source, if you don't eat it your body will make it, but that doesn't mean that more is always better. If it's too high you have diabetes. If it's too low, you go into a coma and die. Your body needs LDL but that doesn't mean that more is always better. Too high or too low causes disease.
12. In Chapter 3, Dr. Ravnskov was not thinking clearly when he tells us that people with familial hypercholesterolemia (FH) live just as long as others. In the study he cites to make this claim it clearly says that the FH patients were taking statins. 3)
13. Uncontrolled observational studies are good for generating hypotheses but can't prove anything by themselves. However Dr. Ravnskov uses this kind of study to ridicule conclusions based on experimental studies when it's the experimental studies that can actually prove something.
14. CANCER - The book leads us to believe that low serum cholesterol causes cancer, but there is abundant observational as well as experimental evidence that contradicts this conclusion. Calorie restriction lowers serum cholesterol and reduces the risk of cancer and heart disease at the same time. Meta-analysis of statin trials show no increase in the overall risk of cancer even after 5 to 10 years of use. Countries with lower serum cholesterol like China have lower rates of prostate, breast and colon cancer than the U.S. Hunter gatherers with their low LDL levels are known for the near-absence of cancer. In clinical trials, the cholesterol lowering Ornish diet slows the growth of prostate cancer. And finally people with stable low cholesterol levels don't have higher cancer rates, just people whose cholesterol level has fallen recently. (21,22,23) The evidence not only proves that low LDL does not cause cancer, it strongly suggests that lifelong high LDL increases the risk of cancer. If it is discovered in the future that long term use of statins causes cancer in humans, it definitely won't be due to low LDL.
15. THE ELDERLY - Dr. Ravnskov claims that "old people with high cholesterol live the longest" based on associations in observational studies. He also claims "Cholesterol-lowering is only able to lower mortality in young and middle-aged men with heart disease." He is misinformed. A meta-analysis of 9 randomized trials shows that when statins are used for secondary prevention in elderly patients they can reduce all-cause mortality by 22% and heart disease mortality by 30%. (13) As he points out himself, associations in observational studies can be very misleading, it's the experimental evidence that carries the most weight and that clearly shows that people of all ages with heart disease live longer when they reduce LDL. Furthermore elderly people have higher cholesterol than young people and they also have more heart attacks than young people.
16. The reason that there's a stronger correlation between atherosclerosis and age than between atherosclerosis and serum cholesterol is because it takes a long time for elevated LDL to do its damage. To see the association all the autopsies would need to be performed on people of the same age.
17. In uncontrolled observational studies when comparing different countries, LDL and heart attacks are not always associated (France has higher LDL and fewer heart attacks than the United States). But HDL is also important and in France people have higher levels of HDL. And within France, people with higher LDL are still more likely to get heart disease. And according to the MONICA study of 21 countries including France, in men aged 55 to 64 years, 10-year population changes in serum cholesterol level alone explained 35% of the variance of change in fatal and nonfatal coronary events. (24)
18. When talking about statins, Dr. Ravnskov focuses on the absolute reduction which can be as little as 1% in short term studies of healthy people. He uses this to ridicule the effectiveness of medication. However in studies of elderly patients with heart disease you would expect the absolute risk reduction to approach the relative risk reduction of 30% if the study ran long enough.
19. Eating fish or taking fish oil with a high complex carbohydrate diet reduces triglycerides better than eating a high fat diet. (25)
20. STATIN SIDE EFFECTS - 10mg simvastatin is so safe it is sold over the counter in the UK. High dose statins on the other hand should probably only be prescribed to patients who have tried a low first and been screened for elevated liver enzymes etc. And statins deplete CoQ10 so anyone taking a statin should also take CoQ10. Should we believe every side effect is caused by low LDL? There are millions of people with LDL levels lower than the levels of people on high dose statins who are not known for muscle weakness or poor memory or liver problems. For example, the Masai don't seem to be suffering from muscle weakness or birth defects. And wild mammals with 50 to 70 mg/dL LDL are known for their excellent health. Almost all prescription drugs are dangerous if taken by the wrong person. But they can be life saving when taken by the right person. For people who don't want to take statins there are several alternative ways to lower LDL that are not likely to cause side effects.
SOME LIMITS OF UNCONTROLLED OBSERVATIONAL STUDIES (Observational studies are good for coming up with hypotheses, but experimental studies are good for proving cause and effect plus they carry more weight.)
1) ASSOCIATION DOES NOT PROVE CAUSATION: All knowledge of cause and effect starts with observing an association but not all associations indicate cause and effect. Low LDL and cancer are associated, but an observational study can't tell you which one is cause and which one is effect or if they're both caused by something else. Associations or lack of associations in an uncontrolled observational study can only suggest a hypothesis, not prove cause and effect or lack of it.
2) CONFOUNDING VARIABLES: Smoking, hypertension, diabetes, abdominal obesity, stress, excess sucrose consumption, alcoholism etc. are all risk factors for heart disease. Therefore, a study could show that elevated LDL was not associated with heart disease in people with low LDL who were also alcoholics and smoked and had hypertension because these variables add up to a greater risk than elevated LDL alone.
3) SOME VARIABLES EFFECT OTHER VARIABLES: For example, studies of saturated fat consumption are also measuring the effects of what people eat more of when they eat less saturated fat. For example, less saturated fat can be associated with a less heart disease if people replace it with something better like canola oil based margarine in the Lyon Diet-Heart Study. Less saturated fat can be associated with the same rate of heart disease if people replace it with something equally bad like sugar and white flour (like the MRFIT study). Less saturated fat can even be associated with or a higher rate of heart disease if people replace it with something worse like stick margarine that's high in trans fat.
4) LUMPING TOGETHER VARIABLES WITH DIFFERENT EFFECTS: Studies can fail to distinguish between saturated fat that makes the HDL:LDL ratio worse (like grain fed meat) and saturated fat that makes the HDL:LDL ratio better (like coconuts). A study could also assume that all meats contain a similar amount of saturated fat when grain fed meat can contain over 5 times more than grass fed meat.
5) PAST VERSUS PRESENT. Before statins or the link between saturated fat and heart disease was discovered, people with chest pain or survivors of heart attacks did not reduce saturated fat or take medication to lower cholesterol. When their LDL was measured it was likely to represent their lifetime average. Now LDL is routinely measured every time someone gets a complete physical, and dietary changes or prescription medication is recommended to high risk individuals long before they have a heart attack. Atherosclerosis is slowed and the heart attack is delayed for several years and occurs with lower saturated fat consumption and/or a lower LDL level. Today the LDL level of a heart patient admitted to the hospital is very unlikely to represent their lifetime average.
EXPERIMENTAL EVIDENCE THAT SATURATED FAT RAISES SERUM CHOLESTEROL
A meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol. (26)
The book tells us that metabolic ward studies of saturated fat don't count because the negative outcome might have been due to trans fat in hydrogenated vegetable oil instead of saturated fat. However, Dr. Stephen Phinney conducted a metabolic ward trial, during weight maintenance not weight loss like so many other studies, with nine healthy lean men. These men consumed nothing but meat, fish, eggs, cheese and cream (no hydrogenated vegetable oil) for 35 days. Their carbohydrate intake was less than 20 grams a day. Their blood cholesterol went up from 159 to 208 on average in 35 days. That is a 31% increase. The average adult in this country has a cholesterol level of 199. A 31% increase would give 261. The high risk category is anything over 240. (27)
These studies report the average for large groups, but there can be exceptions to the rule without making the conclusion about the average false. For example Jeanne Louise Calment smoked most of her life and lived to be 122 years old, but the average smoker's life is shortened by 10 years.
You might ask, what about hunter gatherers who eat a lot of meat and have low cholesterol levels? It turns out that wild elk, moose or whale meat are so low in palmitic acid that they could be part of an Ornish diet. For example whale meat contains about 1/75 as much as T-bone from feedlot meat. You can verify this for yourself by searching the USDA National Nutrient Database.
What about the Inuit? Some people claim their diet contains 75% saturated fat because of all the whale blubber they eat. It turns out that the animal food with the highest percentage of saturated fat is cream which contains 57%, so the claim of 75% is impossible for any group eating exclusively animal food. Compared to beef tallow, whale blubber contains much less saturated fat and much more MUFA and PUFA. In the fact the ratio of palmitic acid (which is the main saturated fatty acid in meat that raises LDL) to PUFA (which lowers LDL) is over 14 times greater in beef tallow. (36)
But hunter gatherers don't eat dairy. What about the Masai? Eighty two percent of their plant food additives contain potentially cholesterol lowering saponins and phenolics. (28) And they eat raw blood which exposes them to parasites which also lowers cholesterol. When Westerners eat a lot of animal fat and they're not losing weight their TC goes up drastically. So without statin-like chemicals and parasites in their food, the serum cholesterol of the Masai would be much higher. And their low serum cholesterol along with their low rate of CHD is further support for the lipid hypothesis.
What about Pacific Islanders? Don't they eat a lot of saturated fat and have a low rate of heart disease? Coconuts are different than feedlot meat. They contain mostly lauric acid instead of palmitic acid. And they don't raise LDL as much. And they improve the LDL/HDL ratio (29) while feedlot meat makes it worse.
According to a meta-analysis of 24 studies by Ip et al in 2009, LDL particle number was a better predictor of risk for cardiovascular disease than LDL subfractions. (30)
VERY HIGH ANIMAL FAT DIETS AND HEART DISEASE AND CANCER
These long term observational studies show that very high animal fat diets are associated with more heart disease, cancer and/or all-cause mortality than the control. This may not seem like very many, but there are only a few studies that focus on very high animal fat diets.
"Low-carbohydrate diets and all-cause and cause-specific mortality" by Fung et al published in 2010. A high-meat diet with about 20% saturated fat had 43% greater all-cause mortality and than an Eco-Atkins diet with 12% saturated fat. This was not an uncontrolled study; even though it's observational it's carefully controlled for the relevant variables. The high-meat group ate the same or less trans fat, omega-6 and refined carbs so there's no reason to think something other than the meat caused them to do poorly. This study is as good as any observational study gets, in spite of what Denise Minger says. She is nihilistic about any evidence against animal fat. To her, every study has a flaw and nothing is ever certain. But when it comes to uncontrolled observational studies of other cultures (evidence that's much weaker than the evidence she finds fault with), she accepts it without critical thinking. (34)
"Mediterranean and carbohydrate-restricted diets and mortality among elderly men" by Sjogren et al published in 2010. The low carb, high meat group had 48% greater all-cause mortality and 81% greater heart disease mortality than the group eating a Mediterranean Diet. (37)
Eating low carb with lots of fatty cuts of grain fed meat won't increase everyone's LDL or give everyone heart disease and cancer, but it may increase the risk for the average person.
EXPERIMENTAL EVIDENCE OF DIETS THAT SAVE LIVES IN PEOPLE WITH HEART DISEASE
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat, high protein diet and another 50 survivors were told to eat as usual. Total cholesterol fell from 312 mg/dl to 220 mg/dl in the experimental group. That's a reduction of 29%. And over a period of 8 years, 38 patients eating as usual died while only 22 in the experimental group died. (31)
In the 1980s, Dr. Esselstyn used a 10% fat, high fiber diet plus low dose statins to reverse heart disease in 17 men and one woman. The average for total cholesterol and LDL was maintained at 145 mg/dl and 82 mg/dl respectively. We know it worked because of before and after coronary angiograms and cardiac PET scans. People given less than a year to live are alive and healthier over 23 years later. During that time no patient died of coronary artery disease, but one died of an arrhythmia. (15)
Dr. Ornish also reversed heart disease using a similar diet plus exercise and meditation but no statins. Since then Dr. Ornish has enrolled at least 3800 patients in demonstration projects (to demonstrate savings on surgery) which resulted in over 40 insurance companies including Medicare covering a program in diet and lifestyle for heart disease patients. According to Dr. Ornish, "In brief, we found that almost 80 percent of patients who were eligible for bypass surgery or angioplasty were able to safely avoid it for at least three years." (32)
In the Lyon Diet-Heart Study of heart attack survivors there was a 76% reduction in major cardiovascular events in the group eating a Mediterranean diet where they replaced saturated fat with canola based margarine. (33)
Low carb can be healthy if you do it right. If you have metabolic syndrome or can't eat grains, a low carb diet with regular meat, that includes 12% or less animal protein and 12% or less saturated fat has been shown to be healthier than the standard American Diet. Less animal fat gives even better lipid profiles. (34)
According to observational evidence, in the 50's and 60's Crete had the best longevity in the world. They ate 40% fat mostly from olive oil, but only 8% saturated fat. The total red meat, poultry and fish consumed in Crete was only about 2 ounces/person/day. Ancel Keys followed this version of the Mediterranean diet and lived to be 100 years old. (35)
Statins can lower LDL 50%. According to Dr. Ornish on average a 10% fat, high fiber diet can lower LDL by 40%. And according to [[ASIN:0307339114 Cholesterol Down: Ten Simple Steps to Lower Your Cholesterol in Four Weeks--Without Prescription Drugs]] there is a combination of specific foods and fibers, like apples and Metamucil that can lower LDL by 30%.
Dietary studies where people probably replaced animal fat with sugar and white flour like MRFIT and the Women's Health Initiative --- or replaced sugar and white flour with animal fat like a traditional Atkin's diet --- generally produce no reduction in heart disease mortality.
----
Just like a defense lawyer Dr. Ravnskov is advocating for his position and not even trying to be objective. People need to hear both sides. The book makes no mention of Dr. Morrison, Dr. Esselstyn, Dr. Ornish, the Mediterranean diet or the Eco-Atkins diet and it belittles or ignores other research that can save lives. Except for the warning about high dose statins, the book has little value. For heart patients young and old, trusting Dr. Ravnskov greatly increases the risk of heart attack and all cause mortality.
REFERENCES
1. Brown MS, Goldstein JL. Human mutations affecting the low density lipoprotein pathway. Am J Clin Nutr. 1977 Jun;30(6):975-8.
2. Risk of fatal coronary heart disease in familial hypercholesterolemia. British Medical Journal, 1991;303:893-896.
3. Neil HA, Hawkins MM, Durrington PN, Betteridge DJ, Capps NE, Humphries SE; Simon Broome Familial Hyperlipidaemia Register Group and Scientific Steering Committee. Non-coronary heart disease mortality and risk of fatal cancer in patients with treated heterozygous familial hypercholesterolaemia: a prospective registry study. Atherosclerosis. 2005 Apr;179(2):293-7.
4. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
5. [[ASIN:B0041D843M The China Study: The Most Comprehensive Study of Nutrition Ever Conducted And the Startling Implications for Diet, We]] Pages 78-79.
6. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002;106;3143.
7. Wilson PW, Garrison RJ, Castelli WP, Feinleib M, McNamara PM, Kannel WB. Prevalence of coronary heart disease in the Framingham Offspring Study: role of lipoprotein cholesterols. Am J Cardiol. 1980 Oct;46(4):649-54.
8. Menotti A, Keys A, Kromhout D, Blackburn H, Aravanis C, Bloemberg B, Buzina R, Dontas A, Fidanza F. Giampaoli S, et al. Inter-cohort differences in coronary heart disease mortality in the 25-year follow-up of the seven countries study. Eur J Epidemiol. 1993 Sep;9(5):527-36.
9. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 1986 Nov 28;256(20):2823-8.
10. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004 Sep 11-17;364(9438):937-52.
11. Malinow MR. Atherosclerosis. Regression in nonhuman primates. Circ Res. 1980 Mar;46(3):311-20.
12. A. Lawrence Gould, PhD; Jacques E. Rossouw, MD; Nancy C. Santanello, MD, MSc; Joseph F. Heyse, PhD; Curt D. Furberg, MD Cholesterol Reduction Yields Clinical Benefit. Circulation. 1995;91:2274-2282.
13. Afilalo J, Duque G, Steele R, Jukema JW, de Craen AJ, Eisenberg MJ. Statins for secondary prevention in elderly patients: a hierarchical bayesian meta-analysis. J Am Coll Cardiol. 2008 Jan 1;51(1):37-45.
14. Nissen SE, Tuzcu EM, Schoenhagen P, Brown BG, Ganz P, Vogel RA, Crowe T, Howard G, Cooper CJ, Brodie B, Grines CL, DeMaria AN; REVERSAL Investigators. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004 Mar 3;291(9):1071-80.
15. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
16. Badimon L, Storey RF, Vilahur G. Update on lipids, inflammation and atherothrombosis. Thromb Haemost. 2011 Apr 11;(Suppl. 1).
17. Abela GS. Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation. J Clin Lipidol. 2010 May-Jun;4(3):156-64.
18. Miller M, Beach V, Sorkin JD, Mangano C, Dobmeier C, Novacic D, Rhyne J, Vogel RA. Comparative effects of three popular diets on lipids, endothelial function, and C-reactive protein during weight maintenance. J Am Diet Assoc. 2009 Apr;109(4):713-7
19. Steinberg, Daniel. The Cholesterol Wars. 2007, Academic Press. Page 211.
20. Kendrick, Malcolm. The Great Cholesterol Con. 2007, John Blake Publishing. Page 79.
21. Iribarren C, Reed DM, Chen R, Yano K, Dwyer JH. Low serum cholesterol and mortality. Which is the cause and which is the effect? Circulation. 1995 Nov 1;92(9):2396-403
22. Jacobs EJ, Newton CC, Thun MJ, Gapstur SM. Long-term use of cholesterol-lowering drugs and cancer incidence in a large United States cohort. Cancer Res. 2011 Mar 1;71(5):1763-71.
23. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23.
24. Kuulasmaa K, Tunstall-Pedoe H, Dobson A, et al, for the WHO-MONICA project. Estimation of the contribution of changes in classic risk factors to trends in coronary event rates across WHO-MONICA Project populations. Lancet. 2000;355:675-687.
25. Jiménez-Gómez Y, Marín C, Peérez-Martínez P, Hartwich J, Malczewska-Malec M, Golabek I, Kiec-Wilk B, Cruz-Teno C, Rodríguez F, Gómez P, Gómez-Luna MJ, Defoort C, Gibney MJ, Pérez-Jiménez F, Roche HM, López-Miranda J. A low-fat, high-complex carbohydrate diet supplemented with long-chain (n-3) fatty acids alters the postprandial lipoprotein profile in patients with metabolic syndrome. J Nutr. 2010 Sep;140(9):1595-601.
26. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-7.
27. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism. 1983 Aug;32(8):757-68.
28. Johns T, Mahunnah RL, Sanaya P, Chapman L, Ticktin T. Saponins and phenolic content in plant dietary additives of a traditional subsistence community, the Batemi of Ngorongoro District, Tanzania. J Ethnopharmacol. 1999 Jul;66(1):1-10.
29. Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601.
30. Ip S, Lichtenstein AH, Chung M, Lau J, Balk EM. Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern Med. 2009 Apr 7;150(7):474-84.
31. [[ASIN:B00129IJJ2 The Low-Fat Way to Health and Longer Life]]
32. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
33. De Lorgeril M, Salen P, Martin JL, Mamelle N, Monjaud I, Touboul P, Delaye J. Effect of a mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease. Insights into the cardioprotective effect of certain nutriments. J Am Coll Cardiol. 1996 Nov 1;28(5):1103-8. (Lyon Diet-Heart Study)
34. Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB. Low-carbohydrate diets and all-cause and cause-specific mortality: two cohort studies. Ann Intern Med. 2010 Sep 7;153(5):289-98.
35. Various biographies of Ancel Keys are available on the Internet.
36. Smith, Heather. Fatty acid variation in beluga (Delphinapterus leucas) blubber: implications for estimating diet using fatty acids. Doctoral dissertation at University of Washington Graduate School.
37. Sjögren P, Becker W, Warensjö E, Olsson E, Byberg L, Gustafsson IB, Karlström B, Cederholm T. Mediterranean and carbohydrate-restricted diets and mortality among elderly men: a cohort study in Sweden. Am J Clin Nutr. 2010 Oct;92(4):967-74.
1. Michael Brown and Joseph Goldstein discovered that the number of functional LDL receptors on the surface of cells, especially liver cells determines the level of LDL in the blood. If the receptors are defective or too few in number, LDL builds up in the blood instead of being taken into the cells. Familial hypercholesterolemia (FH) is caused by the mutation of a single gene that does one thing; make LDL receptors. People with two copies of the mutation for FH have LDL levels 6 to 10 fold above normal and can have a heart attack as early as 18 months of age. People with one copy of the mutation have LDL levels 2 to 4 times above normal and develop clinical symptoms between the ages of 30 and 60. Dr. Ravnskov is in denial about the obvious dose response relationship. (1) In the era before the statins, FH patients aged 20 to 39 years old were 100 times more likely die of heart disease and 10 times more likely to die from all causes than someone in the general population. (2) In a later study, FH patients treated with statins lived just as long as people without FH. (3)
2. Atherosclerotic plaque contains a lot of cholesterol. In 1856 a German pathologist named Rudolf Virchow proposed that lipid accumulation in the artery wall caused atherosclerosis. In 1914 Nikolai Anitschkow also observed cholesterol crystals in advanced plaque in the aorta of cholesterol fed rabbits.
3. People with very low LDL tend to be protected from CHD, with the exception of alcoholics. (Alcohol lowers LDL and damages the endothelium at the same time.) The normal LDL cholesterol range is 50 to 70 mg/dl for modern hunter-gatherers, healthy human newborns, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). (4) And during the 80s, rural Chinese had an average serum cholesterol level of 127 mg/dl. And the men in rural China had a rate of CHD that was only 1/17th that of American men. This was in spite of the fact that close to 80% of them smoked. (5) According to the third report of the National Cholesterol Education Program (NCEP), "Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD." (6)
4. People with an intermediate level of LDL have intermediate levels of heart disease. Virtually 100% of observational studies comparing people within the same country show an association between serum cholesterol and heart disease. (7,8,9)
5. The fact that HDL is protective and does the opposite of LDL is further proof of the harmfulness of elevated LDL. The INTERHEART study looked at 52 different countries and found that the ratio of apo-B (mostly LDL) to apo-A1 (HDL) could account for 50% of the risk of CHD mortality. (10)
EXPERIMENTAL EVIDENCE
6. Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. (11 This can't be explained away by stress, inflammation or some infectious agent. In clinical trials, Dr. Esselstyn's group did better than Dr. Ornish's group even though Dr. Ornish used stress reduction and Dr. Esselstyn didn't. However Dr. Esselstyn's patients had lower LDL. And although adding inflammatory factors like infection can speed up atherosclerosis, oxidized LDL, foam cells and cholesterol crystals inside the artery wall provide their own inflammation. See point eight.
7. In a meta-analysis of 35 randomized trials using diet and/or medication for every 10 percentage points of cholesterol lowering, CHD mortality was reduced by 13% and total mortality by 10% (12). And a meta-analysis of 9 randomized trials shows that when statins are used for secondary prevention in elderly patients they can reduce all-cause mortality by 22% and heart disease mortality by 30%. (13)
8. Lowering LDL can halt and even reverse heart disease in humans. In the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, coronary atherosclerosis was virtually stopped in its tracks when LDL was maintained at 79 mg/dL. (14) And Dr. Esselstyn was able to reverse atherosclerosis by maintaining LDL at 81 mg/dL using a 10% fat, high fiber diet and a low dose statin. (15)
How does LDL cause atherosclerosis?
9. Last but not least elevated LDL is essential to the mechanism of atherosclerosis. Apo B lipoproteins (mostly LDL) diffuse into the artery wall that has been damaged by hypertension, smoking, or high blood pressure. They become oxidized and cause inflammation which attracts macrophages. Macrophages devour oxidized LDL and become foam cells which form plaque and produce more inflammatory chemicals. They grow and eventually rupture depositing cholesterol crystals in the plaque. The crystals penetrate the artery wall causing even more inflammation. Elevated LDL also impairs endothelial function, reduces nitric oxide production and promotes platelet aggregation which promotes clotting. There are other factors besides elevated LDL that contribute to heart disease like smoking, hypertension, diabetes, abdominal obesity, stress, inflammation, homocysteine, sedentary lifestyle and excess sucrose but according to the INTERHEART study the ratio of apo-B (mostly LDL) to apo-A1 (HDL) can account for 50% of the risk. (16,17,18,10)
10. People who know the most about the subject agree. Scientists studying atherosclerosis know more about the subject than anyone else and the vast majority think that cholesterol is connected to heart disease. This is according a scientist who supports the cholesterol hypothesis as well as a leading cholesterol skeptic. (19,20)
SUMMARY OF ANSWERS TO OBJECTIONS
11. Dr. Ravnskov wants you to trust him and ignore people who know more about the subject than he does. However, in the introduction he tells us that "high cholesterol is good; the higher the better." This statement is so ridiculous that you shouldn't take anything else he says seriously. Why? Every chemical in the body has a healthy range. Too high or too low causes disease. Your body needs glucose. It's a natural energy source, if you don't eat it your body will make it, but that doesn't mean that more is always better. If it's too high you have diabetes. If it's too low, you go into a coma and die. Your body needs LDL but that doesn't mean that more is always better. Too high or too low causes disease.
12. In Chapter 3, Dr. Ravnskov was not thinking clearly when he tells us that people with familial hypercholesterolemia (FH) live just as long as others. In the study he cites to make this claim it clearly says that the FH patients were taking statins. 3)
13. Uncontrolled observational studies are good for generating hypotheses but can't prove anything by themselves. However Dr. Ravnskov uses this kind of study to ridicule conclusions based on experimental studies when it's the experimental studies that can actually prove something.
14. CANCER - The book leads us to believe that low serum cholesterol causes cancer, but there is abundant observational as well as experimental evidence that contradicts this conclusion. Calorie restriction lowers serum cholesterol and reduces the risk of cancer and heart disease at the same time. Meta-analysis of statin trials show no increase in the overall risk of cancer even after 5 to 10 years of use. Countries with lower serum cholesterol like China have lower rates of prostate, breast and colon cancer than the U.S. Hunter gatherers with their low LDL levels are known for the near-absence of cancer. In clinical trials, the cholesterol lowering Ornish diet slows the growth of prostate cancer. And finally people with stable low cholesterol levels don't have higher cancer rates, just people whose cholesterol level has fallen recently. (21,22,23) The evidence not only proves that low LDL does not cause cancer, it strongly suggests that lifelong high LDL increases the risk of cancer. If it is discovered in the future that long term use of statins causes cancer in humans, it definitely won't be due to low LDL.
15. THE ELDERLY - Dr. Ravnskov claims that "old people with high cholesterol live the longest" based on associations in observational studies. He also claims "Cholesterol-lowering is only able to lower mortality in young and middle-aged men with heart disease." He is misinformed. A meta-analysis of 9 randomized trials shows that when statins are used for secondary prevention in elderly patients they can reduce all-cause mortality by 22% and heart disease mortality by 30%. (13) As he points out himself, associations in observational studies can be very misleading, it's the experimental evidence that carries the most weight and that clearly shows that people of all ages with heart disease live longer when they reduce LDL. Furthermore elderly people have higher cholesterol than young people and they also have more heart attacks than young people.
16. The reason that there's a stronger correlation between atherosclerosis and age than between atherosclerosis and serum cholesterol is because it takes a long time for elevated LDL to do its damage. To see the association all the autopsies would need to be performed on people of the same age.
17. In uncontrolled observational studies when comparing different countries, LDL and heart attacks are not always associated (France has higher LDL and fewer heart attacks than the United States). But HDL is also important and in France people have higher levels of HDL. And within France, people with higher LDL are still more likely to get heart disease. And according to the MONICA study of 21 countries including France, in men aged 55 to 64 years, 10-year population changes in serum cholesterol level alone explained 35% of the variance of change in fatal and nonfatal coronary events. (24)
18. When talking about statins, Dr. Ravnskov focuses on the absolute reduction which can be as little as 1% in short term studies of healthy people. He uses this to ridicule the effectiveness of medication. However in studies of elderly patients with heart disease you would expect the absolute risk reduction to approach the relative risk reduction of 30% if the study ran long enough.
19. Eating fish or taking fish oil with a high complex carbohydrate diet reduces triglycerides better than eating a high fat diet. (25)
20. STATIN SIDE EFFECTS - 10mg simvastatin is so safe it is sold over the counter in the UK. High dose statins on the other hand should probably only be prescribed to patients who have tried a low first and been screened for elevated liver enzymes etc. And statins deplete CoQ10 so anyone taking a statin should also take CoQ10. Should we believe every side effect is caused by low LDL? There are millions of people with LDL levels lower than the levels of people on high dose statins who are not known for muscle weakness or poor memory or liver problems. For example, the Masai don't seem to be suffering from muscle weakness or birth defects. And wild mammals with 50 to 70 mg/dL LDL are known for their excellent health. Almost all prescription drugs are dangerous if taken by the wrong person. But they can be life saving when taken by the right person. For people who don't want to take statins there are several alternative ways to lower LDL that are not likely to cause side effects.
SOME LIMITS OF UNCONTROLLED OBSERVATIONAL STUDIES (Observational studies are good for coming up with hypotheses, but experimental studies are good for proving cause and effect plus they carry more weight.)
1) ASSOCIATION DOES NOT PROVE CAUSATION: All knowledge of cause and effect starts with observing an association but not all associations indicate cause and effect. Low LDL and cancer are associated, but an observational study can't tell you which one is cause and which one is effect or if they're both caused by something else. Associations or lack of associations in an uncontrolled observational study can only suggest a hypothesis, not prove cause and effect or lack of it.
2) CONFOUNDING VARIABLES: Smoking, hypertension, diabetes, abdominal obesity, stress, excess sucrose consumption, alcoholism etc. are all risk factors for heart disease. Therefore, a study could show that elevated LDL was not associated with heart disease in people with low LDL who were also alcoholics and smoked and had hypertension because these variables add up to a greater risk than elevated LDL alone.
3) SOME VARIABLES EFFECT OTHER VARIABLES: For example, studies of saturated fat consumption are also measuring the effects of what people eat more of when they eat less saturated fat. For example, less saturated fat can be associated with a less heart disease if people replace it with something better like canola oil based margarine in the Lyon Diet-Heart Study. Less saturated fat can be associated with the same rate of heart disease if people replace it with something equally bad like sugar and white flour (like the MRFIT study). Less saturated fat can even be associated with or a higher rate of heart disease if people replace it with something worse like stick margarine that's high in trans fat.
4) LUMPING TOGETHER VARIABLES WITH DIFFERENT EFFECTS: Studies can fail to distinguish between saturated fat that makes the HDL:LDL ratio worse (like grain fed meat) and saturated fat that makes the HDL:LDL ratio better (like coconuts). A study could also assume that all meats contain a similar amount of saturated fat when grain fed meat can contain over 5 times more than grass fed meat.
5) PAST VERSUS PRESENT. Before statins or the link between saturated fat and heart disease was discovered, people with chest pain or survivors of heart attacks did not reduce saturated fat or take medication to lower cholesterol. When their LDL was measured it was likely to represent their lifetime average. Now LDL is routinely measured every time someone gets a complete physical, and dietary changes or prescription medication is recommended to high risk individuals long before they have a heart attack. Atherosclerosis is slowed and the heart attack is delayed for several years and occurs with lower saturated fat consumption and/or a lower LDL level. Today the LDL level of a heart patient admitted to the hospital is very unlikely to represent their lifetime average.
EXPERIMENTAL EVIDENCE THAT SATURATED FAT RAISES SERUM CHOLESTEROL
A meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol. (26)
The book tells us that metabolic ward studies of saturated fat don't count because the negative outcome might have been due to trans fat in hydrogenated vegetable oil instead of saturated fat. However, Dr. Stephen Phinney conducted a metabolic ward trial, during weight maintenance not weight loss like so many other studies, with nine healthy lean men. These men consumed nothing but meat, fish, eggs, cheese and cream (no hydrogenated vegetable oil) for 35 days. Their carbohydrate intake was less than 20 grams a day. Their blood cholesterol went up from 159 to 208 on average in 35 days. That is a 31% increase. The average adult in this country has a cholesterol level of 199. A 31% increase would give 261. The high risk category is anything over 240. (27)
These studies report the average for large groups, but there can be exceptions to the rule without making the conclusion about the average false. For example Jeanne Louise Calment smoked most of her life and lived to be 122 years old, but the average smoker's life is shortened by 10 years.
You might ask, what about hunter gatherers who eat a lot of meat and have low cholesterol levels? It turns out that wild elk, moose or whale meat are so low in palmitic acid that they could be part of an Ornish diet. For example whale meat contains about 1/75 as much as T-bone from feedlot meat. You can verify this for yourself by searching the USDA National Nutrient Database.
What about the Inuit? Some people claim their diet contains 75% saturated fat because of all the whale blubber they eat. It turns out that the animal food with the highest percentage of saturated fat is cream which contains 57%, so the claim of 75% is impossible for any group eating exclusively animal food. Compared to beef tallow, whale blubber contains much less saturated fat and much more MUFA and PUFA. In the fact the ratio of palmitic acid (which is the main saturated fatty acid in meat that raises LDL) to PUFA (which lowers LDL) is over 14 times greater in beef tallow. (36)
But hunter gatherers don't eat dairy. What about the Masai? Eighty two percent of their plant food additives contain potentially cholesterol lowering saponins and phenolics. (28) And they eat raw blood which exposes them to parasites which also lowers cholesterol. When Westerners eat a lot of animal fat and they're not losing weight their TC goes up drastically. So without statin-like chemicals and parasites in their food, the serum cholesterol of the Masai would be much higher. And their low serum cholesterol along with their low rate of CHD is further support for the lipid hypothesis.
What about Pacific Islanders? Don't they eat a lot of saturated fat and have a low rate of heart disease? Coconuts are different than feedlot meat. They contain mostly lauric acid instead of palmitic acid. And they don't raise LDL as much. And they improve the LDL/HDL ratio (29) while feedlot meat makes it worse.
According to a meta-analysis of 24 studies by Ip et al in 2009, LDL particle number was a better predictor of risk for cardiovascular disease than LDL subfractions. (30)
VERY HIGH ANIMAL FAT DIETS AND HEART DISEASE AND CANCER
These long term observational studies show that very high animal fat diets are associated with more heart disease, cancer and/or all-cause mortality than the control. This may not seem like very many, but there are only a few studies that focus on very high animal fat diets.
"Low-carbohydrate diets and all-cause and cause-specific mortality" by Fung et al published in 2010. A high-meat diet with about 20% saturated fat had 43% greater all-cause mortality and than an Eco-Atkins diet with 12% saturated fat. This was not an uncontrolled study; even though it's observational it's carefully controlled for the relevant variables. The high-meat group ate the same or less trans fat, omega-6 and refined carbs so there's no reason to think something other than the meat caused them to do poorly. This study is as good as any observational study gets, in spite of what Denise Minger says. She is nihilistic about any evidence against animal fat. To her, every study has a flaw and nothing is ever certain. But when it comes to uncontrolled observational studies of other cultures (evidence that's much weaker than the evidence she finds fault with), she accepts it without critical thinking. (34)
"Mediterranean and carbohydrate-restricted diets and mortality among elderly men" by Sjogren et al published in 2010. The low carb, high meat group had 48% greater all-cause mortality and 81% greater heart disease mortality than the group eating a Mediterranean Diet. (37)
Eating low carb with lots of fatty cuts of grain fed meat won't increase everyone's LDL or give everyone heart disease and cancer, but it may increase the risk for the average person.
EXPERIMENTAL EVIDENCE OF DIETS THAT SAVE LIVES IN PEOPLE WITH HEART DISEASE
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat, high protein diet and another 50 survivors were told to eat as usual. Total cholesterol fell from 312 mg/dl to 220 mg/dl in the experimental group. That's a reduction of 29%. And over a period of 8 years, 38 patients eating as usual died while only 22 in the experimental group died. (31)
In the 1980s, Dr. Esselstyn used a 10% fat, high fiber diet plus low dose statins to reverse heart disease in 17 men and one woman. The average for total cholesterol and LDL was maintained at 145 mg/dl and 82 mg/dl respectively. We know it worked because of before and after coronary angiograms and cardiac PET scans. People given less than a year to live are alive and healthier over 23 years later. During that time no patient died of coronary artery disease, but one died of an arrhythmia. (15)
Dr. Ornish also reversed heart disease using a similar diet plus exercise and meditation but no statins. Since then Dr. Ornish has enrolled at least 3800 patients in demonstration projects (to demonstrate savings on surgery) which resulted in over 40 insurance companies including Medicare covering a program in diet and lifestyle for heart disease patients. According to Dr. Ornish, "In brief, we found that almost 80 percent of patients who were eligible for bypass surgery or angioplasty were able to safely avoid it for at least three years." (32)
In the Lyon Diet-Heart Study of heart attack survivors there was a 76% reduction in major cardiovascular events in the group eating a Mediterranean diet where they replaced saturated fat with canola based margarine. (33)
Low carb can be healthy if you do it right. If you have metabolic syndrome or can't eat grains, a low carb diet with regular meat, that includes 12% or less animal protein and 12% or less saturated fat has been shown to be healthier than the standard American Diet. Less animal fat gives even better lipid profiles. (34)
According to observational evidence, in the 50's and 60's Crete had the best longevity in the world. They ate 40% fat mostly from olive oil, but only 8% saturated fat. The total red meat, poultry and fish consumed in Crete was only about 2 ounces/person/day. Ancel Keys followed this version of the Mediterranean diet and lived to be 100 years old. (35)
Statins can lower LDL 50%. According to Dr. Ornish on average a 10% fat, high fiber diet can lower LDL by 40%. And according to [[ASIN:0307339114 Cholesterol Down: Ten Simple Steps to Lower Your Cholesterol in Four Weeks--Without Prescription Drugs]] there is a combination of specific foods and fibers, like apples and Metamucil that can lower LDL by 30%.
Dietary studies where people probably replaced animal fat with sugar and white flour like MRFIT and the Women's Health Initiative --- or replaced sugar and white flour with animal fat like a traditional Atkin's diet --- generally produce no reduction in heart disease mortality.
----
Just like a defense lawyer Dr. Ravnskov is advocating for his position and not even trying to be objective. People need to hear both sides. The book makes no mention of Dr. Morrison, Dr. Esselstyn, Dr. Ornish, the Mediterranean diet or the Eco-Atkins diet and it belittles or ignores other research that can save lives. Except for the warning about high dose statins, the book has little value. For heart patients young and old, trusting Dr. Ravnskov greatly increases the risk of heart attack and all cause mortality.
REFERENCES
1. Brown MS, Goldstein JL. Human mutations affecting the low density lipoprotein pathway. Am J Clin Nutr. 1977 Jun;30(6):975-8.
2. Risk of fatal coronary heart disease in familial hypercholesterolemia. British Medical Journal, 1991;303:893-896.
3. Neil HA, Hawkins MM, Durrington PN, Betteridge DJ, Capps NE, Humphries SE; Simon Broome Familial Hyperlipidaemia Register Group and Scientific Steering Committee. Non-coronary heart disease mortality and risk of fatal cancer in patients with treated heterozygous familial hypercholesterolaemia: a prospective registry study. Atherosclerosis. 2005 Apr;179(2):293-7.
4. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
5. [[ASIN:B0041D843M The China Study: The Most Comprehensive Study of Nutrition Ever Conducted And the Startling Implications for Diet, We]] Pages 78-79.
6. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002;106;3143.
7. Wilson PW, Garrison RJ, Castelli WP, Feinleib M, McNamara PM, Kannel WB. Prevalence of coronary heart disease in the Framingham Offspring Study: role of lipoprotein cholesterols. Am J Cardiol. 1980 Oct;46(4):649-54.
8. Menotti A, Keys A, Kromhout D, Blackburn H, Aravanis C, Bloemberg B, Buzina R, Dontas A, Fidanza F. Giampaoli S, et al. Inter-cohort differences in coronary heart disease mortality in the 25-year follow-up of the seven countries study. Eur J Epidemiol. 1993 Sep;9(5):527-36.
9. Stamler J, Wentworth D, Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 1986 Nov 28;256(20):2823-8.
10. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004 Sep 11-17;364(9438):937-52.
11. Malinow MR. Atherosclerosis. Regression in nonhuman primates. Circ Res. 1980 Mar;46(3):311-20.
12. A. Lawrence Gould, PhD; Jacques E. Rossouw, MD; Nancy C. Santanello, MD, MSc; Joseph F. Heyse, PhD; Curt D. Furberg, MD Cholesterol Reduction Yields Clinical Benefit. Circulation. 1995;91:2274-2282.
13. Afilalo J, Duque G, Steele R, Jukema JW, de Craen AJ, Eisenberg MJ. Statins for secondary prevention in elderly patients: a hierarchical bayesian meta-analysis. J Am Coll Cardiol. 2008 Jan 1;51(1):37-45.
14. Nissen SE, Tuzcu EM, Schoenhagen P, Brown BG, Ganz P, Vogel RA, Crowe T, Howard G, Cooper CJ, Brodie B, Grines CL, DeMaria AN; REVERSAL Investigators. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004 Mar 3;291(9):1071-80.
15. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
16. Badimon L, Storey RF, Vilahur G. Update on lipids, inflammation and atherothrombosis. Thromb Haemost. 2011 Apr 11;(Suppl. 1).
17. Abela GS. Cholesterol crystals piercing the arterial plaque and intima trigger local and systemic inflammation. J Clin Lipidol. 2010 May-Jun;4(3):156-64.
18. Miller M, Beach V, Sorkin JD, Mangano C, Dobmeier C, Novacic D, Rhyne J, Vogel RA. Comparative effects of three popular diets on lipids, endothelial function, and C-reactive protein during weight maintenance. J Am Diet Assoc. 2009 Apr;109(4):713-7
19. Steinberg, Daniel. The Cholesterol Wars. 2007, Academic Press. Page 211.
20. Kendrick, Malcolm. The Great Cholesterol Con. 2007, John Blake Publishing. Page 79.
21. Iribarren C, Reed DM, Chen R, Yano K, Dwyer JH. Low serum cholesterol and mortality. Which is the cause and which is the effect? Circulation. 1995 Nov 1;92(9):2396-403
22. Jacobs EJ, Newton CC, Thun MJ, Gapstur SM. Long-term use of cholesterol-lowering drugs and cancer incidence in a large United States cohort. Cancer Res. 2011 Mar 1;71(5):1763-71.
23. Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO, Crutchfield L, Yglecias L, Carroll PR, Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008 Dec;72(6):1319-23.
24. Kuulasmaa K, Tunstall-Pedoe H, Dobson A, et al, for the WHO-MONICA project. Estimation of the contribution of changes in classic risk factors to trends in coronary event rates across WHO-MONICA Project populations. Lancet. 2000;355:675-687.
25. Jiménez-Gómez Y, Marín C, Peérez-Martínez P, Hartwich J, Malczewska-Malec M, Golabek I, Kiec-Wilk B, Cruz-Teno C, Rodríguez F, Gómez P, Gómez-Luna MJ, Defoort C, Gibney MJ, Pérez-Jiménez F, Roche HM, López-Miranda J. A low-fat, high-complex carbohydrate diet supplemented with long-chain (n-3) fatty acids alters the postprandial lipoprotein profile in patients with metabolic syndrome. J Nutr. 2010 Sep;140(9):1595-601.
26. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-7.
27. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism. 1983 Aug;32(8):757-68.
28. Johns T, Mahunnah RL, Sanaya P, Chapman L, Ticktin T. Saponins and phenolic content in plant dietary additives of a traditional subsistence community, the Batemi of Ngorongoro District, Tanzania. J Ethnopharmacol. 1999 Jul;66(1):1-10.
29. Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601.
30. Ip S, Lichtenstein AH, Chung M, Lau J, Balk EM. Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes. Ann Intern Med. 2009 Apr 7;150(7):474-84.
31. [[ASIN:B00129IJJ2 The Low-Fat Way to Health and Longer Life]]
32. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
33. De Lorgeril M, Salen P, Martin JL, Mamelle N, Monjaud I, Touboul P, Delaye J. Effect of a mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease. Insights into the cardioprotective effect of certain nutriments. J Am Coll Cardiol. 1996 Nov 1;28(5):1103-8. (Lyon Diet-Heart Study)
34. Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB. Low-carbohydrate diets and all-cause and cause-specific mortality: two cohort studies. Ann Intern Med. 2010 Sep 7;153(5):289-98.
35. Various biographies of Ancel Keys are available on the Internet.
36. Smith, Heather. Fatty acid variation in beluga (Delphinapterus leucas) blubber: implications for estimating diet using fatty acids. Doctoral dissertation at University of Washington Graduate School.
37. Sjögren P, Becker W, Warensjö E, Olsson E, Byberg L, Gustafsson IB, Karlström B, Cederholm T. Mediterranean and carbohydrate-restricted diets and mortality among elderly men: a cohort study in Sweden. Am J Clin Nutr. 2010 Oct;92(4):967-74.
Tuesday, August 30, 2011
Myth #2. Studies have proven that saturated fat does not cause heart disease.
An uncontrolled observational study that measures saturated fat consumption and heart disease mortality can be very misleading. Even a diet experiment that reduces saturated fat but doesn't tell people what to eat more of when they reduce saturated fat has the same problem. Replacing it with stick margarine should increase heart attacks. Replacing it with sugar and white flour (which is just as bad) shouldn't make any difference. Replacing it with canola oil based margarine should reduce heart attacks like it did in the Lyon Diet-Heart Study. Replacing it with fruits, vegetables, beans and whole grains should also reduce heart attacks like it did for the rural Chinese during the 80's and like it did for Dr. Ornish and Dr. Esselstyn's clinical trials.
There's also the problem that different kinds of saturated fat have different effects. Wild game has a higher percentage of stearic acid which lowers LDL, lauric acid from coconuts improves the LDL/HDL ratio and palmitic acid from feedlot meat raises LDL and and makes the LDL/HDL ratio worse. Also meat can have vastly different palmitic acid content depending on whether it is wild game, grass-fed or produced in a feedlot. Also there are confounding variables like smoking, exercise, alcohol, pre-existing health conditions etc. etc.
So there are several observational studies that show an association with heart disease mortality and several that don't. And there are several experimental studies that show an association and others that don't. This isn't surprising. However, in experiments when saturated fat is replaced by polyunsaturated fat with a good balance of omega-3 to omega-6, heart disease is consistently reduced. (1) And in experiments when saturated fat is replaced with fruits, vegetables, whole grains and beans, heart disease is consistently reduced in about 80% of the people.
Is animal fat ever the best replacement for refined carbs? In spite of the claims of non-scientists modern HGs did not eat a diet high in palmitic acid (because wild game is low in palmitic acid). And high palmitic acid diets like the traditional Atkins don't produce the same low LDL levels or the same low rate of heart disease. See myth #1.
REFERENCES
1. Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr. 2010 Dec;104(11):1586-600.
There's also the problem that different kinds of saturated fat have different effects. Wild game has a higher percentage of stearic acid which lowers LDL, lauric acid from coconuts improves the LDL/HDL ratio and palmitic acid from feedlot meat raises LDL and and makes the LDL/HDL ratio worse. Also meat can have vastly different palmitic acid content depending on whether it is wild game, grass-fed or produced in a feedlot. Also there are confounding variables like smoking, exercise, alcohol, pre-existing health conditions etc. etc.
So there are several observational studies that show an association with heart disease mortality and several that don't. And there are several experimental studies that show an association and others that don't. This isn't surprising. However, in experiments when saturated fat is replaced by polyunsaturated fat with a good balance of omega-3 to omega-6, heart disease is consistently reduced. (1) And in experiments when saturated fat is replaced with fruits, vegetables, whole grains and beans, heart disease is consistently reduced in about 80% of the people.
Is animal fat ever the best replacement for refined carbs? In spite of the claims of non-scientists modern HGs did not eat a diet high in palmitic acid (because wild game is low in palmitic acid). And high palmitic acid diets like the traditional Atkins don't produce the same low LDL levels or the same low rate of heart disease. See myth #1.
REFERENCES
1. Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr. 2010 Dec;104(11):1586-600.
Thursday, August 25, 2011
Myth #1. Modern hunter gatherers prove we are all adapted to eat a lot of animal fat
HGs ate wild game, not feedlot meat. If you look up wild elk, moose or whale meat in the USDA National Nutrient Database, you will find that their palmitic acid content (represented as 16:0 under saturated fat in the database) is so low they could be part of an Ornish diet. (1) Even though HGs ate the whole carcass, the average palmitic acid consumption was only about 1/2 that of Americans according to Professor Loren Cordain in his book The Paleo Diet. In fact whale meat contains about 1/75 the amount of palmitic acid found in a comparable portion of T-bone from a feedlot steer. It's also an objective fact that their serum cholesterol is in the 100 to 150 range and their LDL is in the 50 to 70mg/dL range. (2)
In metabolic ward studies when the AVERAGE American eats a high animal fat diet, their serum cholesterol goes up a lot. Dr. Stephen Phinney conducted a metabolic ward trial with nine healthy lean men during weight maintenance, not weight loss. These men consumed nothing but meat, fish, eggs, cheese and cream (no hydrogenated vegetable oil) for 35 days. Their carbohydrate intake was less than 20 grams a day. Their blood cholesterol went up from 159 to 208 on average in 35 days. (3) That is a 31% increase. The average adult in this country has a cholesterol level of 199. A 31% increase would give 261. The high risk category is anything over 240.
A meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol. (4)
The Masai (they are not hunter gatherers and they eat a lot of dairy) seem to contradict this, but 82% of their food additives contain potentially cholesterol lowering saponins or phenolics. (5) If their food wasn't full of statin-like chemicals their serum cholesterol would be high also.
Like the Masai, Pacific Islanders actually did eat a lot of saturated fat, but it was from coconuts. These are high in lauric acid and polyphenols instead of palmitic acid and don't raise serum cholesterol as much. They also improve the LDL/HDL ratio while feedlot meat makes it worse. (6,7)
Finally the very low LDL levels of modern HGs have not been duplicated in clinical trials of Paleo diets even when people eat only lean meat. However various parasitic infections which are common among HGs can lower LDL. In fact the parasitic infection, schistosomiasis, has been shown to lower LDL and reverse atherosclerosis in mice. (8)
REFERENCES
1. The USDA National Nutrient Database: http://www.nal.usda.gov/fnic/foodcomp/search
2. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
3. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism. 1983 Aug;32(8):757-68.4. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-7.
5. Johns T, Mahunnah RL, Sanaya P, Chapman L, Ticktin T. Saponins and phenolic content in plant dietary additives of a traditional subsistence community, the Batemi of Ngorongoro District, Tanzania. J Ethnopharmacol. 1999 Jul;66(1):1-10.
6. Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601.
7. Beauchesne-Rondeau E, Gascon A, Bergeron J, Jacques H. Plasma lipids and lipoproteins in hypercholesterolemic men fed a lipid-lowering diet containing lean beef, lean fish, or poultry. Am J Clin Nutr. 2003 Mar;77(3):587-93.
8. Doenhoff MJ, Stanley RG, Griffiths K, Jackson CL. An anti-atherogenic effect of Schistosoma mansoni infections in mice associated with a parasite-induced lowering of blood total cholesterol. Parasitology. 2002 Nov;125(Pt 5):415-21. http://www.ncbi.nlm.nih.gov/pubmed/12458825
In metabolic ward studies when the AVERAGE American eats a high animal fat diet, their serum cholesterol goes up a lot. Dr. Stephen Phinney conducted a metabolic ward trial with nine healthy lean men during weight maintenance, not weight loss. These men consumed nothing but meat, fish, eggs, cheese and cream (no hydrogenated vegetable oil) for 35 days. Their carbohydrate intake was less than 20 grams a day. Their blood cholesterol went up from 159 to 208 on average in 35 days. (3) That is a 31% increase. The average adult in this country has a cholesterol level of 199. A 31% increase would give 261. The high risk category is anything over 240.
A meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol. (4)
The Masai (they are not hunter gatherers and they eat a lot of dairy) seem to contradict this, but 82% of their food additives contain potentially cholesterol lowering saponins or phenolics. (5) If their food wasn't full of statin-like chemicals their serum cholesterol would be high also.
Like the Masai, Pacific Islanders actually did eat a lot of saturated fat, but it was from coconuts. These are high in lauric acid and polyphenols instead of palmitic acid and don't raise serum cholesterol as much. They also improve the LDL/HDL ratio while feedlot meat makes it worse. (6,7)
Finally the very low LDL levels of modern HGs have not been duplicated in clinical trials of Paleo diets even when people eat only lean meat. However various parasitic infections which are common among HGs can lower LDL. In fact the parasitic infection, schistosomiasis, has been shown to lower LDL and reverse atherosclerosis in mice. (8)
REFERENCES
1. The USDA National Nutrient Database: http://www.nal.usda.gov/fnic/foodcomp/search
2. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.
3. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism. 1983 Aug;32(8):757-68.4. Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-7.
5. Johns T, Mahunnah RL, Sanaya P, Chapman L, Ticktin T. Saponins and phenolic content in plant dietary additives of a traditional subsistence community, the Batemi of Ngorongoro District, Tanzania. J Ethnopharmacol. 1999 Jul;66(1):1-10.
6. Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601.
7. Beauchesne-Rondeau E, Gascon A, Bergeron J, Jacques H. Plasma lipids and lipoproteins in hypercholesterolemic men fed a lipid-lowering diet containing lean beef, lean fish, or poultry. Am J Clin Nutr. 2003 Mar;77(3):587-93.
8. Doenhoff MJ, Stanley RG, Griffiths K, Jackson CL. An anti-atherogenic effect of Schistosoma mansoni infections in mice associated with a parasite-induced lowering of blood total cholesterol. Parasitology. 2002 Nov;125(Pt 5):415-21. http://www.ncbi.nlm.nih.gov/pubmed/12458825
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