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.
Monday, November 7, 2011
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
Thursday, June 23, 2011
Review of The Great Cholesterol Con by Malcolm Kendrick
According to the WHO-MONICA project 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. (1) When comparing people within in the same country (more like a controlled study), less LDL is associated with less heart disease. Dr. Kendrick only told us about ONE exception. A subset of men with the lowest educational achievement who drink too much alcohol in Russia. They must be the only ones or he would have told us about the rest of them.
On the other hand, the data in Dr. Kendrick's graph comparing average serum cholesterol and heart disease death rates in 21 countries plus the Australian aborigines amounts to an uncontrolled observational study. The same is true of his graph of saturated fat consumption. Such studies can be useful for generating hypotheses but they can't prove cause and effect of lack of it. There are too many confounding variables (e.g. affluence, quality of healthcare, malnutrition, sanitation, stress levels, smoking rates and alcoholism etc. etc.)
MORE EVIDENCE THAT ELEVATED LDL IS A MAJOR RISK FACTOR FOR CORONARY ARTERY DISEASE
1. People with two copies of the mutation for familial hypercholesterolemia (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. (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.
3. People with very low LDL tend to be protected from CHD. 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 a strong association between serum cholesterol and heart disease. (7,8,9)
5. The fact that HDL is protective and carries LDL away from the arteries 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) Dr. Kendrick says INTERHEART supports his stress theory but as I show in the next section stress can't be the most important cause.
6. Atherosclerosis can be induced in many different animal species including non-human primates by raising serum cholesterol high enough and maintaining it long enough. And atherosclerosis can then be reversed by lowering serum cholesterol low enough and maintaining it long enough. (11) This can't be explained away by stress or some infectious agent. Although adding inflammatory factors can speed up the process, 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). Dr. Kendrick makes a big deal about LDL not being important for elderly people, but 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. Last but not least elevated LDL is essential to the mechanism of atherosclerosis. Apo B lipoproteins (mostly LDL) diffuse into the artery wall. 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. (14,15,16,10)
9. 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 Dr. Kendrick himself. (17,18)
EVIDENCE THAT STRESS IS NOT THE MAIN FACTOR IN CORONARY ARTERY DISEASE
1. Atherosclerosis can be induced in many different animal species including non-human primates by raising serum cholesterol high enough and maintaining it long enough. And atherosclerosis can then be reversed by lowering serum cholesterol low enough and maintaining it long enough. There is no evidence that increased stress followed by decreased stress is involved. (11)
2. Statins reduce heart attacks but there is no evidence that they lower cortisol levels. (19)
3. Fruit and vegetables reduce heart attacks but Dr. Kendrick admits he can see no connection to the HPA-axis. They can however reduce hypertension and oxidized LDL. (20)
4. Dr. Esselstyn's study got better results than Dr. Ornish's study even though Dr. Ornish used stress reduction therapy and Dr. Esselstyn didn't. However Dr. Esselstyn's patients had lower LDL levels. (21,22)
There is no doubt that stress is one of the risk factors for CAD. And there is no doubt that injury to the endothelium and blood clots are part of the mechanism. But unless you are an alcoholic elevated LDL is probably more important.
EVIDENCE THAT EATING GRAIN FED MEAT AND DAIRY RAISES SERUM CHOLESTEROL
Dr. Kendrick says the body can't turn saturated fat into cholesterol. That's correct but that's not the problem. Dietary saturated fat causes LDL receptors in the liver to down regulate causing LDL to build up in the blood. (23)
Dr. Stephen Phinney conducted a normal caloric intake metabolic ward trial with nine healthy lean men, "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." 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. (24)
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. (25)
THE LIMITS OF OBSERVATIONAL STUDIES
Heart disease has several risk factors. Therefore in uncontrolled observational studies we can see a lot of inconsistent results. But associations or lack of associations in an uncontrolled observational study can only suggest, not prove cause and effect or lack of it. The results depend on:
1) CONFOUNDING VARIABLES. These include smoking, hypertension, diabetes, abdominal obesity, stress, sucrose consumption etc. For example, in an uncontrolled study lower saturated fat can be associated with either less heart disease or more heart disease depending on whether people replaced the saturated fat with canola oil or stick margarine with trans fat.
2) THE RANGE OF THE VARIABLE. Studies where the difference between the lowest level of saturated fat and highest level is very great have better resolution than studies with a smaller difference. When the difference is large, the effect of confounding variables is less pronounced. For example, in studies of very high saturated fat diets, even if they are not controlled, the harmful effects of saturated fat override the confounding variables and give consistent positive associations between saturated fat and heart disease.
3) 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. 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 a lower LDL level. The lifetime average cholesterol level is much more relevant than the level when admitted to the hospital.
Dr. Kendrick relies heavily on observational studies to ridicule the conclusions of experimental studies when it's the experimental studies that carry the most weight.
EXPERIMENTAL EVIDENCE OF WHAT SAVES LIVES IN PEOPLE WITH HEART DISEASE
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat 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. (26)
In the 80s, 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. (27)
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." (28)
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. (29)
A meta-analysis 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%. (20)
OBSERVATIONAL EVIDENCE OF DIET AND LONGEVITY
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. They ate 40% 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). Ancel Keys followed this version of the Mediterranean diet and lived to be 100 years old. (29)
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.)
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. Campbell TC, Campbell TM. The China Study. 2005, BenBella Books. 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. Badimon L, Storey RF, Vilahur G. Update on lipids, inflammation and atherothrombosis. Thromb Haemost. 2011 Apr 11;(Suppl. 1).
15. 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.
16. 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
17. Steinberg, Daniel. The Cholesterol Wars. 2007, Academic Press. Page 211.
18. Kendrick, Malcolm. The Great Cholesterol Con. 2007, John Blake Publishing. Page 79.
19. Wani TA, Samad A, Tandon M, Saini GS, Sharma PL, Pillai KK. The effects of rosuvastatin on the serum cortisol, serum lipid, and serum mevalonic acid levels in the healthy Indian male population. AAPS PharmSciTech. 2010 Mar;11(1):425-32. Epub 2010 Mar 19.
20. Crujeiras AB, Parra D, Abete I, Martínez JA. A hypocaloric diet enriched in legumes specifically mitigates lipid peroxidation in obese subjects. Free Radic Res. 2007 Apr;41(4):498-506.
21. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
22. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
23. John M. Dietschy. Dietary Fatty Acids and the Regulation of Plasma Low Density Lipoprotein Cholesterol Concentrations. J. Nutr. February 1, 1998 vol. 128 no. 2 444S-448S.
24. 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.
25. 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.
26. [[ASIN:B00129IJJ2 The Low-Fat Way to Health and Longer Life]]
27. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
28. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
29. 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)
30. Various biographies of Ancel Keys are available on the Internet.
On the other hand, the data in Dr. Kendrick's graph comparing average serum cholesterol and heart disease death rates in 21 countries plus the Australian aborigines amounts to an uncontrolled observational study. The same is true of his graph of saturated fat consumption. Such studies can be useful for generating hypotheses but they can't prove cause and effect of lack of it. There are too many confounding variables (e.g. affluence, quality of healthcare, malnutrition, sanitation, stress levels, smoking rates and alcoholism etc. etc.)
MORE EVIDENCE THAT ELEVATED LDL IS A MAJOR RISK FACTOR FOR CORONARY ARTERY DISEASE
1. People with two copies of the mutation for familial hypercholesterolemia (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. (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.
3. People with very low LDL tend to be protected from CHD. 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 a strong association between serum cholesterol and heart disease. (7,8,9)
5. The fact that HDL is protective and carries LDL away from the arteries 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) Dr. Kendrick says INTERHEART supports his stress theory but as I show in the next section stress can't be the most important cause.
6. Atherosclerosis can be induced in many different animal species including non-human primates by raising serum cholesterol high enough and maintaining it long enough. And atherosclerosis can then be reversed by lowering serum cholesterol low enough and maintaining it long enough. (11) This can't be explained away by stress or some infectious agent. Although adding inflammatory factors can speed up the process, 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). Dr. Kendrick makes a big deal about LDL not being important for elderly people, but 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. Last but not least elevated LDL is essential to the mechanism of atherosclerosis. Apo B lipoproteins (mostly LDL) diffuse into the artery wall. 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. (14,15,16,10)
9. 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 Dr. Kendrick himself. (17,18)
EVIDENCE THAT STRESS IS NOT THE MAIN FACTOR IN CORONARY ARTERY DISEASE
1. Atherosclerosis can be induced in many different animal species including non-human primates by raising serum cholesterol high enough and maintaining it long enough. And atherosclerosis can then be reversed by lowering serum cholesterol low enough and maintaining it long enough. There is no evidence that increased stress followed by decreased stress is involved. (11)
2. Statins reduce heart attacks but there is no evidence that they lower cortisol levels. (19)
3. Fruit and vegetables reduce heart attacks but Dr. Kendrick admits he can see no connection to the HPA-axis. They can however reduce hypertension and oxidized LDL. (20)
4. Dr. Esselstyn's study got better results than Dr. Ornish's study even though Dr. Ornish used stress reduction therapy and Dr. Esselstyn didn't. However Dr. Esselstyn's patients had lower LDL levels. (21,22)
There is no doubt that stress is one of the risk factors for CAD. And there is no doubt that injury to the endothelium and blood clots are part of the mechanism. But unless you are an alcoholic elevated LDL is probably more important.
EVIDENCE THAT EATING GRAIN FED MEAT AND DAIRY RAISES SERUM CHOLESTEROL
Dr. Kendrick says the body can't turn saturated fat into cholesterol. That's correct but that's not the problem. Dietary saturated fat causes LDL receptors in the liver to down regulate causing LDL to build up in the blood. (23)
Dr. Stephen Phinney conducted a normal caloric intake metabolic ward trial with nine healthy lean men, "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." 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. (24)
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. (25)
THE LIMITS OF OBSERVATIONAL STUDIES
Heart disease has several risk factors. Therefore in uncontrolled observational studies we can see a lot of inconsistent results. But associations or lack of associations in an uncontrolled observational study can only suggest, not prove cause and effect or lack of it. The results depend on:
1) CONFOUNDING VARIABLES. These include smoking, hypertension, diabetes, abdominal obesity, stress, sucrose consumption etc. For example, in an uncontrolled study lower saturated fat can be associated with either less heart disease or more heart disease depending on whether people replaced the saturated fat with canola oil or stick margarine with trans fat.
2) THE RANGE OF THE VARIABLE. Studies where the difference between the lowest level of saturated fat and highest level is very great have better resolution than studies with a smaller difference. When the difference is large, the effect of confounding variables is less pronounced. For example, in studies of very high saturated fat diets, even if they are not controlled, the harmful effects of saturated fat override the confounding variables and give consistent positive associations between saturated fat and heart disease.
3) 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. 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 a lower LDL level. The lifetime average cholesterol level is much more relevant than the level when admitted to the hospital.
Dr. Kendrick relies heavily on observational studies to ridicule the conclusions of experimental studies when it's the experimental studies that carry the most weight.
EXPERIMENTAL EVIDENCE OF WHAT SAVES LIVES IN PEOPLE WITH HEART DISEASE
In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat 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. (26)
In the 80s, 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. (27)
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." (28)
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. (29)
A meta-analysis 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%. (20)
OBSERVATIONAL EVIDENCE OF DIET AND LONGEVITY
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. They ate 40% 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). Ancel Keys followed this version of the Mediterranean diet and lived to be 100 years old. (29)
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.)
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. Campbell TC, Campbell TM. The China Study. 2005, BenBella Books. 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. Badimon L, Storey RF, Vilahur G. Update on lipids, inflammation and atherothrombosis. Thromb Haemost. 2011 Apr 11;(Suppl. 1).
15. 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.
16. 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
17. Steinberg, Daniel. The Cholesterol Wars. 2007, Academic Press. Page 211.
18. Kendrick, Malcolm. The Great Cholesterol Con. 2007, John Blake Publishing. Page 79.
19. Wani TA, Samad A, Tandon M, Saini GS, Sharma PL, Pillai KK. The effects of rosuvastatin on the serum cortisol, serum lipid, and serum mevalonic acid levels in the healthy Indian male population. AAPS PharmSciTech. 2010 Mar;11(1):425-32. Epub 2010 Mar 19.
20. Crujeiras AB, Parra D, Abete I, Martínez JA. A hypocaloric diet enriched in legumes specifically mitigates lipid peroxidation in obese subjects. Free Radic Res. 2007 Apr;41(4):498-506.
21. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
22. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
23. John M. Dietschy. Dietary Fatty Acids and the Regulation of Plasma Low Density Lipoprotein Cholesterol Concentrations. J. Nutr. February 1, 1998 vol. 128 no. 2 444S-448S.
24. 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.
25. 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.
26. [[ASIN:B00129IJJ2 The Low-Fat Way to Health and Longer Life]]
27. [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]]
28. [[ASIN:0804110387 Dr. Dean Ornish's Program for Reversing Heart Disease: The Only System Scientifically Proven to Reverse Heart Disease Without Drugs or Surgery]]
29. 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)
30. Various biographies of Ancel Keys are available on the Internet.
Sunday, June 19, 2011
Coconuts and grain fed meat have different effects on heart disease
In chapter eight of GCBC Mr. Taubes tells us about the Tokelau Island Migration Study. Unfortunately there's always more than one way to interpret an observational study.
But there's another way to interpret the evidence. Coconuts and fish are healthy sources of saturated fat. Studies have shown that coconuts (which are high in lauric acid and polyphenols) improve the HDL:LDL ratio. And fish is high in omega-3 fatty acids. On the other hand, grain fed meat is low in lauric and omega-3 fatty acids and contains no polyphenols. And unlike coconuts, grain fed meat and dairy makes the HDL:LDL ratio worse.
http://www.ncbi.nlm.nih.gov/pubmed/12600847
Studies show that sugar increases triglycerides and decreases HDL and it's associated with metabolic syndrome, so it's bad for heart disease. BUT IF SUGAR WAS THE ONLY PROBLEM THEN PEOPLE WHO GO ON A TRADITIONAL ATKINS DIET SHOULD BE HEART ATTACK PROOF. However, according to the most favorable study that actually measures mortality, high saturated fat diets are no better than the standard American diet and according to the least favorable study diets high in saturated fat from grain fed meat and dairy (similar to what Dr. Atkins recommended) show 81% more heart attacks and 48% more all-cause mortality.
Low-carbohydrate-diet score and the risk of coronary heart disease in women.
http://www.ncbi.nlm.nih.gov/pubmed/17093250
Mediterranean and carbohydrate-restricted diets and mortality among elderly men
http://www.ncbi.nlm.nih.gov/pubmed/20826627
Even in the most favorable study for high saturated fat diets, when low carbohydrate scores were equal the people who ate less animal fat (most likely from grain fed meat and dairy) had significantly less heart disease.
The original diet with no western diseases:
- coconuts
- fish
- breadfruit
- less coconuts but still a lot
- less fish but still a lot
- seven fold increase in sugar
- six fold increase in flour
- canned meat
- frozen foods
- virtually no coconuts or fish
- a lot of meat, bread, potatoes and sugar
But there's another way to interpret the evidence. Coconuts and fish are healthy sources of saturated fat. Studies have shown that coconuts (which are high in lauric acid and polyphenols) improve the HDL:LDL ratio. And fish is high in omega-3 fatty acids. On the other hand, grain fed meat is low in lauric and omega-3 fatty acids and contains no polyphenols. And unlike coconuts, grain fed meat and dairy makes the HDL:LDL ratio worse.
http://www.ncbi.nlm.nih.gov/pubmed/12600847
Studies show that sugar increases triglycerides and decreases HDL and it's associated with metabolic syndrome, so it's bad for heart disease. BUT IF SUGAR WAS THE ONLY PROBLEM THEN PEOPLE WHO GO ON A TRADITIONAL ATKINS DIET SHOULD BE HEART ATTACK PROOF. However, according to the most favorable study that actually measures mortality, high saturated fat diets are no better than the standard American diet and according to the least favorable study diets high in saturated fat from grain fed meat and dairy (similar to what Dr. Atkins recommended) show 81% more heart attacks and 48% more all-cause mortality.
Low-carbohydrate-diet score and the risk of coronary heart disease in women.
http://www.ncbi.nlm.nih.gov/pubmed/17093250
Mediterranean and carbohydrate-restricted diets and mortality among elderly men
http://www.ncbi.nlm.nih.gov/pubmed/20826627
Even in the most favorable study for high saturated fat diets, when low carbohydrate scores were equal the people who ate less animal fat (most likely from grain fed meat and dairy) had significantly less heart disease.
Friday, May 27, 2011
Review of Why We Get Fat : A high saturated fat diet is not needed in order to eat low carb
In studies, the average person who tries the Cordain Paleo diet sees their HDL go up, and both their triglycerides and LDL go down. The average person who tries a high saturated fat Atkins diet sees both their HDL and LDL go up and only their triglycerides go down. And in EVERY long term study of high saturated fat diets in this country, there is more heart disease in the group eating a high amount than the group eating a moderate amount.
Throughout the book, Taubes focuses on reducing carbs, but there is a long list of differences between modern humans and hunter gatherers besides refined carbs and increased insulin: Grain fattened meat with more saturated fat and less CLA and omega-3, vitamin D insufficiency, a sedentary lifestyle, a shortage of phytochemicals from fruit and vegetables, a shortage of omega-3, eating too much salt, smoking and alcohol. And according to Weston Price, organically grown food, minimally processed food, calcium, fat soluble nutrients and whole grains were important reasons for the health of the people he studied. All these things effect Western diseases including heart disease and cancer.
EVIDENCE THAT HUNTER GATHERERS ATE MEAT THAT WAS VERY DIFFERENT FROM WHAT MODERN AMERICANS EAT
On page 163 Taubes says, "The idea is that the longer a particular type of food has been part of the human diet, the more beneficial and less harmful it probably is---the better adapted we become to that food. And if some food is new to the human diets, or new in large quantities, it's likely that we haven't yet had time to adapt, and so it's doing us harm."
Yet he lets the reader assume that grain fattened meat is no problem even though it has been a staple in the American diet for less than 100 years (it increased during the same era that sugar and white flour increased.) It contains about 10.2 times as much palmitic, myristic and lauric acid as wild elk and about 5.4 times as much as lean grass fed meat. Stearic acid lowers LDL so it wasn't used in the calculation. And I adjusted for the fact that the t-bone had 22% refuse (leaving only 78 grams meat), the grass fed beef had 34% refuse (leaving only 66 grams of meat) and the elk was all meat. You can check T-bone, grass-fed beef and game meat elk in the USDA food composition database for yourself. Not only does grain fed meat contain more palmitic (16:O), myristic (14:O) and lauric acid (12:O), but it contains a lower percentage of LDL lowering stearic acid (18:O) and very little omega-3 or CLA and don't forget, added hormones and antibiotics. And the blubber of sea mammals that live in the arctic contains a much lower percentage of saturated fat than the fat of land animals.
On page 164 - 65 Taubes says, "The best we can do is what nutritional anthropologists began doing in the mid-1980s---use modern day hunter-gatherer societies as surrogates for our Stone Age ancestors. In 2000, researchers from the United States and Australia published an analysis of 229 hunter gatherer populations that survived deep into the twentieth century to have their diets assessed by anthropologists."
Taubes says this is "the best we can do", then he decides to ignore their findings on saturated fat, because they don't fit his preconceived ideas.
In his latest book, The Paleo Diet: Lose Weight and Get Healthy by Eating the Foods You Were Designed to Eat, published in December 2010, Professor Loren Cordain says that hunter gatherers ate about half the palmitic acid eaten in the modern American diet (this is the main saturated fatty acid that elevates LDL in the American diet.) This is in spite of the fact that they consumed the entire carcass of the animal. This is because they ate wild game (average of .89 grams saturated fat per serving) instead of grain fattened domestic animals (average of 7.04 grams saturated fat per serving). Cordain et al actually gathered the data and did the calculations. Modern HG diets ranged from very low to very high in saturated fat consumption. They were not uniformly high. Because one group can eat a high saturated fat diet proves nothing about people whose ancestors didn't do this. No one with basic knowledge of natural selection and genetics would assume we are all equally adapted to eat a high saturated fat diet. And according to Eaton et al (1988) the average cholesterol of the hunter gatherers they studied was about 124. This can't be achieved on a high diet high in grain fed meat and dairy, unless you have genetic hypocholesterolemia like the Masai.
In metabolic ward trials where all variables are controlled and people live in the ward and eat meals prepared by the research staff, LDL is routinely increased by increasing dietary saturated fat when carbs are at a moderate level as well as when carbs are virtually eliminated. For example, Dr. Stephen Phinney conducted a normal caloric intake metabolic ward trial with nine healthy lean men, "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." These men consumed nothing but meat, fish, eggs, cheese and cream 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.
Humans have always eaten saturated fat, but the average human has never eaten as much as they do now. Then along comes Dr. Atkins and Mr. Taubes who tell us to eat even more. If you are going to recommend a diet for life long consumption by the general public, the burden of proof is on you to show that it's safe. However, every long term study shows that high saturated fat diets are associated with more heart disease than the control. Therefore recommending this kind of diet to the general public seems reckless. Especially since there's no need to eat a lot of saturated fat in order to eat low carb.
HOW SOME BUT NOT ALL SATURATED FAT CONTRIBUTES TO ATHEROSCLEROSIS
Chemicals in the body have a healthy range. When they're too high or too low it makes us sick, whether it's glucose or LDL or something else. As long as you keep them in the healthy range, I guess it doesn't matter how you do it. Your body needs LDL, but if it's too low there is an increased risk of infection and stroke. If it's too high, there's an increased risk of atherosclerosis and heart attack. You could keep meat consumption moderate like the ECo-ATkins. Or you could eat a lot of meat as long as you avoid fatty cuts grain fattened meat like the Cordain Paleo.
Certain dietary saturated fatty acids (16:O, 14:O and 12:O) down regulate LDL receptors on the surface of your cells. This interferes with the cells ability to take in the LDL they need and causes the level of LDL in the blood to go up. In the blood, macrophages absorb oxidized LDL and become foam cells. They continue to grow and eventually rupture depositing plaque inside the artery walls.
People are different. Some have more LDL receptors than others which means that eating the same amount of saturated fat does not elevate their LDL as much. And people with too few LDL receptors have hypercholesterolemia and premature heart disease. Saturated fat is not the only risk factor for heart disease but the fewer LDL receptors a person has the more important it is for them.
According to a study by Nicholls et al in 2006, consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins as well as endothelial function. And according to a meta-analysis of 24 studies by Ip et al in 2009, higher LDL particle number was consistently associated with increased risk for cardiovascular disease, independent of size or density.
There are different kinds of saturated fat. Stearic acid lowers LDL. And the diets of HGs had a higher percentage of stearic acid and a lower percentage of palmitic acid than modern diets. Coconuts are rich in saturated fat, but Pacific Islanders consume the coconut water and coconut fiber which contain chemicals that lower LDL.
WHY UNCONTROLLED STUDIES CAN GIVE INCONSISTENT RESULTS
Heart disease has multiple risk factors. In uncontrolled studies we see a lot of inconsistent results. But associations or lack of associations in an uncontrolled study can only suggest, not prove cause and effect or lack of it. The results depends on:
1) CONFOUNDING VARIABLES. These include genetics of the population, smoking, sedentary lifestyle, hypertension, diabetes, trans fat, high glycemic index carbohydrates etc. For example, in an uncontrolled study lower saturated fat can be associated with either less heart disease or more heart disease depending on whether people replaced the saturated fat with olive oil or stick margarine with trans fat.
2) THE RANGE OF THE VARIABLE. Studies where the difference between the lowest level of saturated fat and highest level is very great have better resolution than studies with a smaller difference. When the difference is large, the effect of confounding variables is less pronounced. For example, in studies of very high saturated fat diets, even if they are not controlled, the harmful effects of saturated fat override the confounding variables and give consistent positive associations between saturated fat and heart disease. This is why the Seven Countries Study with large differences in saturated fat consumption showed a strong association and other studies where everyone was more or less similar didn't.
EVIDENCE THAT EATING LESS SATURATED FAT CAN BE HELPFUL
Since there's more than one risk factor for heart disease, it makes since that interventions to treat heart disease that reduce the most risk factors would be the most effective. And the most effective interventions usually involve eating less saturated fat and lowering LDL. For example:
In China and Japan where they eat less saturated fat and over 50% carbs, they have a low rate of heart disease and they don't have an obesity epidemic. They eat less sugar and white flour. That seems to be all the vast majority of us need to give up.
Dr. Esselstyn used a 10% fat, low glycemic index, high fiber diet plus low dose Statins to reverse heart disease. (See [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].) 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 20 years later. There was no requirement to count calories or exercise to get these results.
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."
The Mediterranean diet which is low in saturated fat is also associated with low rates of heart disease. Statins, exercise or meditation are not necessary to produce this result. (See Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating.) Statins alone or exercise alone or meditation alone can't achieve these results. So it appears that diet is partly, perhaps mostly responsible for the favorable results.
The book makes no mention of Dr. Esselstyn or that heart disease can be reversed consistently on a diet that restricts saturated fat and cholesterol or that taking fish oil with a high complex carbohydrate diet reduces triglycerides better than eating a high fat diet according to a study by Jiménez-Gómez et al in 2010.
All that the book shows conclusively about saturated fat is that it can't be the only cause of heart disease and everybody knows that already. And while high glycemic index carbs are associated with heart disease, low glycemic index, high fiber carbs are associated with reversal of heart disease.
The book uses the false dilemma logical fallacy to make it seem like you only have two choices if you're overweight; follow the USDA recommendations and continue to be part of the obesity epidemic or follow Atkins and lose weight and reduce your risk of heart disease. There are many things wrong with this characterization. First, there are at least two ways of eating low carb that don't require you to eat a lot of saturated fat (Eco-Atkins and the Cordain Paleo). Second, people who are not insulin resistant can effectively reduce blood glucose and insulin, lose weight and reduce the risk of heart disease by reducing high GI carbs and saturated fat, even if they eat 70% carbs. Third, while a few risk factors look good on a high saturated fat diet, many other risk factors are not even measured, and tests show that atherosclerosis is accelerated in the short run and there's more heart disease mortality in the long run. Also, the book uses the straw man logical fallacy to make it seem like the obesity edipemic is the result of eating less saturated fat. However, Americans have not been following the USDA guidelines about the kind of carbs to eat and they have been eating out (with large portions) more than ever, and they are not even close to following the Ornish diet or the Mediterrnaean diet.
EVIDENCE THAT EATING TOO MUCH SATURATED FAT CAN BE HARMFUL
Six long term studies show that high saturated 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 no long term studies that show otherwise. All the studies that some people think show otherwise are either short term and only look at risk factors or only compare one moderate level of saturated fat with another moderate level. (It's the high saturated fat that's important, not the high protein.)
First study: "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 epidemiological study; it's the kind of study that can be used to establish cause and effect because confounding variables have been controlled. 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 it 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. The reason she devotes so much effort trying to tear it down, is because the evidence against a high animal fat diet is so compelling.
Second study: "Low carbohydrate-high protein diet and mortality in a cohort of Swedish women" by Lagiou et al published in 2007. "CONCLUSIONS: A diet characterized by low carbohydrate and high protein intake was associated with increased total and particularly cardiovascular mortality amongst women."
Third study: "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.
Fourth study: "Low-carbohydrate-high-protein diet and long-term survival in a general population cohort" by Trichopoulou et al in 2007. "CONCLUSION: Prolonged consumption of diets low in carbohydrates and high in protein is associated with an increase in total mortality."
Fifth study: A study of patients on a high-meat diet by Fleming in 2000 showed a worsening of blood flow after one year with an overall 39.7% progression of coronary artery disease.
Sixth study: People are different. A high-meat Atkins is especially bad for people with the APOE4 allele. In a study by Corella et al in 2010, when saturated fat intake was greater than 10% of total calories in individuals carrying the APOE4 allele, the risk of heart disease was over 300% higher. About 25 to 30 percent of Americans carry this allele. And people with the metabolic syndrome are more likely to carry APOE4 than other people.
Taken together these six studies show that measuring the few risk factors that improve during the weight loss phase does not accurately predict what will actually happen after decades on the maintenance phase. They are giving people a false sense of security.
CONCLUSION : THERE ARE SEVERAL WAYS TO BE HEALTHY
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. The Cordain Paleo diet, the Ornish diet and the Mediterranean diet all have less high GI carbs and less saturated fat than most Americans eat and they are all good for heart disease. The list of foods in the Appendix of WWGE only reduces carbs, while increasing saturated fat. It makes sense that the more risk factors you reduce the better results you will get.
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. They ate 40% 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). Ancel Keys followed the Mediterranean diet and lived to be 100 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 low-fat diet with low glycemic index, high fiber carbs can save your life. This 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.
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. Lower values give even better lipid profiles.
7. The Cordain Paleo diet is good if you have metabolic syndrome or can't eat grains. But unless you eat wild game or lean cuts of grain fed meat you are not likely to get good results for heart disease and cancer (even if you lose weight and lower your blood sugar.)
Two bad choices
1) Reduce saturated at a little bit but eat lots of sugar, white flour, white rice and potatoes and order large portions when you eat out. It will increase your risk of the obesity, metabolic syndrome and diabetes.
2) Eat low carb with fatty cuts of grain fed meat. It won't increase everyone's LDL or give everyone heart disease and cancer, but it will increase the risk for the average American.
Throughout the book, Taubes focuses on reducing carbs, but there is a long list of differences between modern humans and hunter gatherers besides refined carbs and increased insulin: Grain fattened meat with more saturated fat and less CLA and omega-3, vitamin D insufficiency, a sedentary lifestyle, a shortage of phytochemicals from fruit and vegetables, a shortage of omega-3, eating too much salt, smoking and alcohol. And according to Weston Price, organically grown food, minimally processed food, calcium, fat soluble nutrients and whole grains were important reasons for the health of the people he studied. All these things effect Western diseases including heart disease and cancer.
EVIDENCE THAT HUNTER GATHERERS ATE MEAT THAT WAS VERY DIFFERENT FROM WHAT MODERN AMERICANS EAT
On page 163 Taubes says, "The idea is that the longer a particular type of food has been part of the human diet, the more beneficial and less harmful it probably is---the better adapted we become to that food. And if some food is new to the human diets, or new in large quantities, it's likely that we haven't yet had time to adapt, and so it's doing us harm."
Yet he lets the reader assume that grain fattened meat is no problem even though it has been a staple in the American diet for less than 100 years (it increased during the same era that sugar and white flour increased.) It contains about 10.2 times as much palmitic, myristic and lauric acid as wild elk and about 5.4 times as much as lean grass fed meat. Stearic acid lowers LDL so it wasn't used in the calculation. And I adjusted for the fact that the t-bone had 22% refuse (leaving only 78 grams meat), the grass fed beef had 34% refuse (leaving only 66 grams of meat) and the elk was all meat. You can check T-bone, grass-fed beef and game meat elk in the USDA food composition database for yourself. Not only does grain fed meat contain more palmitic (16:O), myristic (14:O) and lauric acid (12:O), but it contains a lower percentage of LDL lowering stearic acid (18:O) and very little omega-3 or CLA and don't forget, added hormones and antibiotics. And the blubber of sea mammals that live in the arctic contains a much lower percentage of saturated fat than the fat of land animals.
On page 164 - 65 Taubes says, "The best we can do is what nutritional anthropologists began doing in the mid-1980s---use modern day hunter-gatherer societies as surrogates for our Stone Age ancestors. In 2000, researchers from the United States and Australia published an analysis of 229 hunter gatherer populations that survived deep into the twentieth century to have their diets assessed by anthropologists."
Taubes says this is "the best we can do", then he decides to ignore their findings on saturated fat, because they don't fit his preconceived ideas.
In his latest book, The Paleo Diet: Lose Weight and Get Healthy by Eating the Foods You Were Designed to Eat, published in December 2010, Professor Loren Cordain says that hunter gatherers ate about half the palmitic acid eaten in the modern American diet (this is the main saturated fatty acid that elevates LDL in the American diet.) This is in spite of the fact that they consumed the entire carcass of the animal. This is because they ate wild game (average of .89 grams saturated fat per serving) instead of grain fattened domestic animals (average of 7.04 grams saturated fat per serving). Cordain et al actually gathered the data and did the calculations. Modern HG diets ranged from very low to very high in saturated fat consumption. They were not uniformly high. Because one group can eat a high saturated fat diet proves nothing about people whose ancestors didn't do this. No one with basic knowledge of natural selection and genetics would assume we are all equally adapted to eat a high saturated fat diet. And according to Eaton et al (1988) the average cholesterol of the hunter gatherers they studied was about 124. This can't be achieved on a high diet high in grain fed meat and dairy, unless you have genetic hypocholesterolemia like the Masai.
In metabolic ward trials where all variables are controlled and people live in the ward and eat meals prepared by the research staff, LDL is routinely increased by increasing dietary saturated fat when carbs are at a moderate level as well as when carbs are virtually eliminated. For example, Dr. Stephen Phinney conducted a normal caloric intake metabolic ward trial with nine healthy lean men, "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." These men consumed nothing but meat, fish, eggs, cheese and cream 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.
Humans have always eaten saturated fat, but the average human has never eaten as much as they do now. Then along comes Dr. Atkins and Mr. Taubes who tell us to eat even more. If you are going to recommend a diet for life long consumption by the general public, the burden of proof is on you to show that it's safe. However, every long term study shows that high saturated fat diets are associated with more heart disease than the control. Therefore recommending this kind of diet to the general public seems reckless. Especially since there's no need to eat a lot of saturated fat in order to eat low carb.
HOW SOME BUT NOT ALL SATURATED FAT CONTRIBUTES TO ATHEROSCLEROSIS
Chemicals in the body have a healthy range. When they're too high or too low it makes us sick, whether it's glucose or LDL or something else. As long as you keep them in the healthy range, I guess it doesn't matter how you do it. Your body needs LDL, but if it's too low there is an increased risk of infection and stroke. If it's too high, there's an increased risk of atherosclerosis and heart attack. You could keep meat consumption moderate like the ECo-ATkins. Or you could eat a lot of meat as long as you avoid fatty cuts grain fattened meat like the Cordain Paleo.
Certain dietary saturated fatty acids (16:O, 14:O and 12:O) down regulate LDL receptors on the surface of your cells. This interferes with the cells ability to take in the LDL they need and causes the level of LDL in the blood to go up. In the blood, macrophages absorb oxidized LDL and become foam cells. They continue to grow and eventually rupture depositing plaque inside the artery walls.
People are different. Some have more LDL receptors than others which means that eating the same amount of saturated fat does not elevate their LDL as much. And people with too few LDL receptors have hypercholesterolemia and premature heart disease. Saturated fat is not the only risk factor for heart disease but the fewer LDL receptors a person has the more important it is for them.
According to a study by Nicholls et al in 2006, consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins as well as endothelial function. And according to a meta-analysis of 24 studies by Ip et al in 2009, higher LDL particle number was consistently associated with increased risk for cardiovascular disease, independent of size or density.
There are different kinds of saturated fat. Stearic acid lowers LDL. And the diets of HGs had a higher percentage of stearic acid and a lower percentage of palmitic acid than modern diets. Coconuts are rich in saturated fat, but Pacific Islanders consume the coconut water and coconut fiber which contain chemicals that lower LDL.
WHY UNCONTROLLED STUDIES CAN GIVE INCONSISTENT RESULTS
Heart disease has multiple risk factors. In uncontrolled studies we see a lot of inconsistent results. But associations or lack of associations in an uncontrolled study can only suggest, not prove cause and effect or lack of it. The results depends on:
1) CONFOUNDING VARIABLES. These include genetics of the population, smoking, sedentary lifestyle, hypertension, diabetes, trans fat, high glycemic index carbohydrates etc. For example, in an uncontrolled study lower saturated fat can be associated with either less heart disease or more heart disease depending on whether people replaced the saturated fat with olive oil or stick margarine with trans fat.
2) THE RANGE OF THE VARIABLE. Studies where the difference between the lowest level of saturated fat and highest level is very great have better resolution than studies with a smaller difference. When the difference is large, the effect of confounding variables is less pronounced. For example, in studies of very high saturated fat diets, even if they are not controlled, the harmful effects of saturated fat override the confounding variables and give consistent positive associations between saturated fat and heart disease. This is why the Seven Countries Study with large differences in saturated fat consumption showed a strong association and other studies where everyone was more or less similar didn't.
EVIDENCE THAT EATING LESS SATURATED FAT CAN BE HELPFUL
Since there's more than one risk factor for heart disease, it makes since that interventions to treat heart disease that reduce the most risk factors would be the most effective. And the most effective interventions usually involve eating less saturated fat and lowering LDL. For example:
In China and Japan where they eat less saturated fat and over 50% carbs, they have a low rate of heart disease and they don't have an obesity epidemic. They eat less sugar and white flour. That seems to be all the vast majority of us need to give up.
Dr. Esselstyn used a 10% fat, low glycemic index, high fiber diet plus low dose Statins to reverse heart disease. (See [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].) 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 20 years later. There was no requirement to count calories or exercise to get these results.
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."
The Mediterranean diet which is low in saturated fat is also associated with low rates of heart disease. Statins, exercise or meditation are not necessary to produce this result. (See Eat, Drink, and Be Healthy: The Harvard Medical School Guide to Healthy Eating.) Statins alone or exercise alone or meditation alone can't achieve these results. So it appears that diet is partly, perhaps mostly responsible for the favorable results.
The book makes no mention of Dr. Esselstyn or that heart disease can be reversed consistently on a diet that restricts saturated fat and cholesterol or that taking fish oil with a high complex carbohydrate diet reduces triglycerides better than eating a high fat diet according to a study by Jiménez-Gómez et al in 2010.
All that the book shows conclusively about saturated fat is that it can't be the only cause of heart disease and everybody knows that already. And while high glycemic index carbs are associated with heart disease, low glycemic index, high fiber carbs are associated with reversal of heart disease.
The book uses the false dilemma logical fallacy to make it seem like you only have two choices if you're overweight; follow the USDA recommendations and continue to be part of the obesity epidemic or follow Atkins and lose weight and reduce your risk of heart disease. There are many things wrong with this characterization. First, there are at least two ways of eating low carb that don't require you to eat a lot of saturated fat (Eco-Atkins and the Cordain Paleo). Second, people who are not insulin resistant can effectively reduce blood glucose and insulin, lose weight and reduce the risk of heart disease by reducing high GI carbs and saturated fat, even if they eat 70% carbs. Third, while a few risk factors look good on a high saturated fat diet, many other risk factors are not even measured, and tests show that atherosclerosis is accelerated in the short run and there's more heart disease mortality in the long run. Also, the book uses the straw man logical fallacy to make it seem like the obesity edipemic is the result of eating less saturated fat. However, Americans have not been following the USDA guidelines about the kind of carbs to eat and they have been eating out (with large portions) more than ever, and they are not even close to following the Ornish diet or the Mediterrnaean diet.
EVIDENCE THAT EATING TOO MUCH SATURATED FAT CAN BE HARMFUL
Six long term studies show that high saturated 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 no long term studies that show otherwise. All the studies that some people think show otherwise are either short term and only look at risk factors or only compare one moderate level of saturated fat with another moderate level. (It's the high saturated fat that's important, not the high protein.)
First study: "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 epidemiological study; it's the kind of study that can be used to establish cause and effect because confounding variables have been controlled. 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 it 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. The reason she devotes so much effort trying to tear it down, is because the evidence against a high animal fat diet is so compelling.
Second study: "Low carbohydrate-high protein diet and mortality in a cohort of Swedish women" by Lagiou et al published in 2007. "CONCLUSIONS: A diet characterized by low carbohydrate and high protein intake was associated with increased total and particularly cardiovascular mortality amongst women."
Third study: "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.
Fourth study: "Low-carbohydrate-high-protein diet and long-term survival in a general population cohort" by Trichopoulou et al in 2007. "CONCLUSION: Prolonged consumption of diets low in carbohydrates and high in protein is associated with an increase in total mortality."
Fifth study: A study of patients on a high-meat diet by Fleming in 2000 showed a worsening of blood flow after one year with an overall 39.7% progression of coronary artery disease.
Sixth study: People are different. A high-meat Atkins is especially bad for people with the APOE4 allele. In a study by Corella et al in 2010, when saturated fat intake was greater than 10% of total calories in individuals carrying the APOE4 allele, the risk of heart disease was over 300% higher. About 25 to 30 percent of Americans carry this allele. And people with the metabolic syndrome are more likely to carry APOE4 than other people.
Taken together these six studies show that measuring the few risk factors that improve during the weight loss phase does not accurately predict what will actually happen after decades on the maintenance phase. They are giving people a false sense of security.
CONCLUSION : THERE ARE SEVERAL WAYS TO BE HEALTHY
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. The Cordain Paleo diet, the Ornish diet and the Mediterranean diet all have less high GI carbs and less saturated fat than most Americans eat and they are all good for heart disease. The list of foods in the Appendix of WWGE only reduces carbs, while increasing saturated fat. It makes sense that the more risk factors you reduce the better results you will get.
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. They ate 40% 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). Ancel Keys followed the Mediterranean diet and lived to be 100 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 low-fat diet with low glycemic index, high fiber carbs can save your life. This 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.
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. Lower values give even better lipid profiles.
7. The Cordain Paleo diet is good if you have metabolic syndrome or can't eat grains. But unless you eat wild game or lean cuts of grain fed meat you are not likely to get good results for heart disease and cancer (even if you lose weight and lower your blood sugar.)
Two bad choices
1) Reduce saturated at a little bit but eat lots of sugar, white flour, white rice and potatoes and order large portions when you eat out. It will increase your risk of the obesity, metabolic syndrome and diabetes.
2) Eat low carb with fatty cuts of grain fed meat. It won't increase everyone's LDL or give everyone heart disease and cancer, but it will increase the risk for the average American.
Thursday, May 26, 2011
EVIDENCE THAT ELEVATED LDL IS A MAJOR RISK FACTOR FOR CHD
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. (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. 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 carries LDL away from the arteries 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 can speed up the process, 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)
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.
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. (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. 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 carries LDL away from the arteries 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 can speed up the process, 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)
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.
Tuesday, March 1, 2011
Lipid profile of Cordain Paleo diet is superior to high saturated fat Atkins
In studies, the average person who tries the Cordain Paleo diet sees their HDL go up, and both their triglycerides and LDL go down. The average person who tries a high saturated fat Atkins diet sees both their HDL and LDL go up and only their triglycerides go down.
Low fat diets can be effective for weight loss, metabolic syndrome and diabetes IF sugar, white flour, white rice and potatoes replaced with unrefined carbs. And low fat, high complex carbohydrate diets plus fish oil are even better than a high fat diet in reducing triglycerides.
http://www.ncbi.nlm.nih.gov/pubmed/20631323
Low fat diets can be effective for weight loss, metabolic syndrome and diabetes IF sugar, white flour, white rice and potatoes replaced with unrefined carbs. And low fat, high complex carbohydrate diets plus fish oil are even better than a high fat diet in reducing triglycerides.
http://www.ncbi.nlm.nih.gov/pubmed/20631323
Thursday, January 27, 2011
Review of Good Calories Bad Calories
EXTREMELY MISLEADING. NOT A PANACEA FOR WESTERN DISEASES.
IN A NUTSHELL
An Eco-Atkins diet can give you all the advantages of the high-meat Atkins without increasing the risk of heart disease or cancer. In a study by Jenkins et al in 2009, a plant based, low carb diet (26% carbs) produced an extremely good lipid profile, outperforming a low fat diet (25% fat) and the traditional Atkins diet. And in a 26 year study by Fung et al in 2010, an Eco-Atkins diet with only 12% animal protein showed a 43% decrease in all cause mortality compared to a reduced carb diet with 18% animal protein controlled for other variables. (This is not some uncontrolled epidemiological study; it's the kind of study that can be used to establish cause and effect. The high-meat group actually ate slightly less omega-6 and refined carbs so there`s no reason to think something other than grain fed meat caused them to do poorly.)
Both high-meat Atkins and Eco-Atkins are good at producing short term weight loss and blood sugar control. But a long term study of patients on a high-meat diet by Fleming in 2000 showed a worsening of blood flow after one year with an overall 39.7% progression of coronary artery disease. And a study that lasted over 10 years by Sjogren et al in 2010 showed that elderly men eating a Mediterranean diet were 37% less likely to die of heart disease, while elderly men eating a high meat, carbohydrate restricted diet were 44% more likely to die of heart disease.
This book leaves many readers strongly convinced that meat and full fat dairy are the best replacements for refined carbs. But the evidence is mostly based on stories of individuals which tell us nothing about the average person; uncontrolled observational studies of other cultures with many confounding variables (such as genetic differences, calorie restriction, cholesterol lowering saponins, grass fed meat high in CLA and omega-3, absence of alcohol and tobacco, greater vitamin D, organic produce, higher exercise levels etc.); and clinical trials where people practicing low carb were also practicing calorie restriction which is totally misleading about the maintenance phase and about the long term risk of heart disease and cancer. A study in 2009 by Miller et al that compared three diets (Atkins, South Beach and Ornish) during weight maintenance showed Atkins produced less favorable results for lipids and flow-mediated vasodilatation than the other two.
People are different. In a study by Corella et al in 2010, when saturated fat intake was greater than 10% of calories in individuals carrying the APOE4 allele, the risk of heart disease was over 300% higher. About 25 to 30 percent of Americans carry this allele. But cholesterol skeptics have convinced many Americans with the APOE4 allele to try a high animal fat diet and it's giving them heart disease.
Taken together these six studies show that weight loss, fluffy LDL etc. are not protecting people from heart disease. The incomplete risk profile in studies used to promote a high-meat Atkins diet fail to accurately predict what will actually happen decades in the future. They are giving people a false sense of security.
Some people think Denise Minger's blog proves a high-meat diet is safe. But the Tuoli data that Denise makes a big deal about, can't tell us anything about health because it doesn't represent the way the people were eating all year long. The people are nomadic and eat different foods at different times of year and they were feasting to impress the visitors. And the Tuoli culture has confounding variables just like the examples in GCBC. And the fact that the protein deficient rural Chinese benefited from a small amount of animal protein doesn't mean that Americans who are already eating ten times as much animal protein as the rural Chinese need even more. There are places in China as well as the rest for world where high wheat consumption is not associated with heart disease. Denise' analysis does not distinguish between low glycemic index forms of wheat (like pasta cooked al dente) and high glycemic index forms of wheat (like white bread.)
WATCH OUT FOR CONFIRMATION BIAS
According to Wikipedia, "Confirmation bias refers to a type of selective thinking whereby one tends to notice and to look for what confirms one's beliefs, and to ignore, not look for, or undervalue the relevance of what contradicts one's beliefs."
For example, Mr. Taubes is nihilistic about any evidence against animal fat. To him, every study has a flaw, nothing is ever certain. But when it comes to uncontrolled observational studies of other cultures (evidence that's much weaker than the evidence he finds fault with), he accepts it without critical thinking.
"Confirmation biases contribute to overconfidence in personal beliefs and can maintain or strengthen beliefs in the face of contrary evidence. Hence they can lead to disastrous decisions, especially in organizational, military, political and social contexts."
"Individuals have to constantly remind themselves of this tendency and actively seek out data contrary to their beliefs." Since this isn't easy, most of the time we're stuck with bias. Nobody can be completely free of bias but we can make an effort. But we should always be biased in favor of studies published in peer reviewed journals over opinions published in books or on web sites. (Peer review attempts to find obvious errors and correct biased interpretations that go beyond the data.) And we should always value long term studies that measure disease more than short term studies that only measure risk factors.
For example, if Mr. Taubes had submitted his book to peer review, someone would have pointed out that the Masai are not a good argument for eating a high animal fat diet since they eat cholesterol lowering saponins and are believed to have genetic hypocholesterolemia.
FULL REVIEW
POINTS OF AGREEMENT
1) I agree that low carb is effective for diabetes and weight loss (but so are low fat, high fiber diets.)
2) I agree that high glycemic index carbs should be included in the long list of risk factors for heart disease (but animal fat is as least as bad and probably worse.)
3) I agree that total cholesterol below 150 is associated with a greater risk of stroke, but only for people with untreated hypertension or who smoke or drink alcohol or caffeine.
POINTS OF DISAGREEMENT
1) MISLEADING ABOUT THE DIET OF HUNTER GATHERERS : On page 69 of GCBC, Mr. Taubes cites a study by Loren Cordain et al that says hunter-gatherers ate 28% to 58% total fat. Taubes uses this study as evidence that all humans are adapted to a high saturated fat diet. But when you look at the details, Taubes completely misrepresents what Cordain believes. Here's what Cordain says about saturated fat, "The typical Paleolithic diet compared with the average modern American diet contained 2 to 3 times more fiber [from fruits and vegetables], 1.5 to 2.0 times more polyunsaturated and monounsaturated fats, 4 times more omega-3 fats, but 60% to 70% less saturated fat." This is in spite of the fact that they consumed the entire carcass of the animal. This is because they ate wild game (average of .89 grams saturated fat per serving) instead of grain fattened domestic animals (average of 7.04 grams saturated fat per serving). Grass fed meat also contains more CLA and omega-3 fatty acids which are associated with a reduced risk of heart disease and cancer.
2) MISLEADING ABOUT HEALTHY CARBS: Beans have a low glycemic index and if eaten on a regular basis their fiber and resistant starch (depending on the variety) can lower fasting blood sugar, insulin, triglycerides and improve the HDL/total cholesterol ratio. Oats and barley contain beta glucan and resistant starch which can lower fasting blood sugar, insulin and improve the HDL/total cholesterol ratio. Insoluble fiber like wheat bran is very important for digestive health. For the small percentage of people with celiac disease (1%) or gluten sensitivity (3 - 15%) there are many grains without gluten. Cultures where people live the longest eat more whole grains, beans and yams than the average American.
Most people handle low glycemic index, high fiber carbs just fine (these include fruit, non-starchy vegetables, peas, beans, whole grain pasta cooked al dente, rolled oats, corn on the cob, brown rice, sprouted grain bread, yams etc.) They don't cause the metabolic syndrome or increase the number of small dense LDL particles. The American public has never tried replacing saturated animal fat, sugar, white flour and baking potatoes with low glycemic index, high fiber carbs, nuts, olive or canola oil and fish. And the average American is eating out more often (sometimes twice a day instead of twice a week) and getting bigger portions than we would at home. Therefore the obesity epidemic proves nothing about beans and peas and whole grains and yams.
On page 454 GCBC says "By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume the leaner we will be." If there is even one exception then there is something wrong with the hypothesis. In rural China during the 80s, they ate 75.8% carbs (but they're healthy carbs) and more calories than Americans and they had extremely low rates of obesity, diabetes and heart disease. These facts about China are not in dispute. By ignoring them GCBC misleads us about the complexities of physiology and the fact that some people do best on low carb while many others do best on low fat.
3) MISLEADING ABOUT DIABETES : Following the diet recommended by the American Diabetes Association reduced HbA1c by 0.4 percentage points, but eating an ultra low fat diet with low glycemic index, high fiber carbs reduced HbA1c by 3 times that amount. This is a greater effect than taking a diabetic medication. (See [[ASIN:1594868107 Dr. Neal Barnard's Program for Reversing Diabetes: The Scientifically Proven System for Reversing Diabetes without Drugs]].) So both low fat and low carb diets lower blood sugar and improve insulin resistance compared to the standard American diet.
Excess insulin is just one factor in a long list of things that affect Western diseases. Excess calories, excess IGF1, vitamin D insufficiency (See [[ASIN:B002B55DTA Vitamin D Prescription: The Healing Power of the Sun & How It Can Save Your Life]]), a sedentary lifestyle, a shortage of phytochemicals from fruit and vegetables, a shortage of omega-3, eating too much salt, excess alcohol and smoking all have huge effects on Western diseases. And according to Weston Price free range meat and dairy, organically grown food, minimally processed food, calcium and fat soluble nutrients and whole grains were important reasons for the health of the people he studied. Since just eating less carbs can't correct all these problems, even the beneficial Eco-Atkins is not a panacea for Western disease.
4) MISLEADING ABOUT HEART DISEASE : Dr. Esselstyn used a 10% fat, low glycemic index, high fiber diet to reverse heart disease. (See [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].) 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 20 years later. Done right, the 10% fat, low glycemic index, high fiber diets reduce small dense LDL particles, inflammation, homocysteine, insulin resistance, blood sugar and increase nitric oxide which dilates arteries like nitroglycerin. There is no requirement to count calories or exercise to get these results.
Dr. Ornish also reversed heart disease using similar diet plus exercise and meditation. 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."
The book leads us to believe that lowering cholesterol may reduce heart disease but not increase longevity and that cholesterol levels don't matter in elderly people. But a meta-analysis by Afilalo et al. shows Statins reduce all-cause mortality 22% in elderly heart disease patients.
On page 454 GCBC says "Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes." The initial studies by Dr. Esselstyn and Dr. Ornish that reversed heart disease on a low fat, high carb, high fiber diet are over 20 years old and something he knew about (because he debated Dr. Ornish in 2002) but chose not to mention!
5) MISLEADING ABOUT CANCER : The book leads us to believe that low cholesterol causes cancer. But calorie restriction lowers cholesterol and reduces the risk of cancer and heart disease at the same time. The latest meta-analysis of statin use, based on 26 randomized trials and 170,000 patients, shows they are not associated with higher cancer rates. Countries with low cholesterol have lower rates of prostate, breast and colon cancer than the U.S. In clinical trials, ultra low fat diets slow cancer growth. So why would low cholesterol levels in this country be associated with cancer? Because cancer and other chronic diseases cause lower cholesterol, not the other way around.
Complete protein is the main thing that raises IGF1 which increases the risk of cancer (whey seems to be the only exception). Cancer patients who eat low fat and low meat have much higher survival rates. GCBC tells us people can be healthy eating 100% meat, but fruit, vegetables, whole grains and beans contain phytonutrients that act like low dose chemotherapy. (See [[ASIN:0756628679 Foods to Fight Cancer: Essential foods to help prevent cancer]].) Even Sally Fallon, cofounder of the Weston Price Foundation, in her book Nourishing Traditions admits "... meatless diets often prove beneficial in the treatment of cancer ..." although she does not believe that meat increases the risk of getting cancer.
However in the Fung et al study mentioned earlier, people eating a version of reduced carb with 18% animal protein were 32% more likely to die of cancer than the Eco-Atkins group eating 12% animal protein. In other studies, red meat is associated with an increased risk gastric and colon cancer; saturated fat is associated with an increased risk of breast cancer and dairy is associated with an increased risk of prostate cancer. And in animal studies, cancer rates increase rapidly when complete protein is more than 10% to 12%.
According to the World Health Organization, modern adult humans only require about 0.38 g/lb per day of protein with a protein digestibility-corrected amino acid score (PDCAAS) value of 1.0 to be healthy and maintain nitrogen balance. And the average American eats about 50% more than this. (Pregnant women, children, adolescents, elderly people with congestive heart failure and people recovering from an infection or injury need extra protein.)
6) MISLEADING ABOUT PHYSICAL EXERCISE: Just walking 30 minutes a day reduces the risk of heart disease, cancer, diabetes, hypertension, and Alzheimer's. (See [[ASIN:0345496310 The Spectrum: A Scientifically Proven Program to Feel Better, Live Longer, Lose Weight, and Gain Health]].) Conductors in double-decker buses have about half the rate of heart disease as the drivers who sit all day long. And exercise benefits your health whether you lose weight or not.
CONCLUSION : THERE ARE SEVERAL WAYS TO BE HEALTHY
People are different but medical research can only tell us what is likely to be true for the average person in a carefully defined group using statistical analysis. Some people do best with low fat or Mediterranean and others with Eco-Atkins. Most people with heart disease do well on the diet of Dr. Ornish or Dr. Esselstyn. But there's no evidence that a diet high in grain fed meat is good for anybody in the long run.
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. They ate 40% 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). Ancel Keys followed the Mediterranean diet and lived to be 100 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 low-fat diet with low glycemic index, high fiber carbs can save your life. This 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
6. An Eco-Atkins diet with regular meat, that includes 12% or less animal protein and 12% or less saturated animal fat has been shown to be healthier than the standard American Diet. Lower values give even better lipid profiles.
7. Eat like a hunter gatherer. But unless you have the right genes, eat grass fed meat and copy most of their protective behaviors you are not likely to get good results for heart disease and cancer (even if you lose weight and lower your blood sugar.)
Two bad choices
1) Follow the USDA pyramid version of low fat and eat lots of sugar, white flour, white rice and potatoes. It will increase your risk of the metabolic syndrome and diabetes.
2) Eat low carb with grain fed meat. It will increase your risk of heart disease and cancer.
IN A NUTSHELL
An Eco-Atkins diet can give you all the advantages of the high-meat Atkins without increasing the risk of heart disease or cancer. In a study by Jenkins et al in 2009, a plant based, low carb diet (26% carbs) produced an extremely good lipid profile, outperforming a low fat diet (25% fat) and the traditional Atkins diet. And in a 26 year study by Fung et al in 2010, an Eco-Atkins diet with only 12% animal protein showed a 43% decrease in all cause mortality compared to a reduced carb diet with 18% animal protein controlled for other variables. (This is not some uncontrolled epidemiological study; it's the kind of study that can be used to establish cause and effect. The high-meat group actually ate slightly less omega-6 and refined carbs so there`s no reason to think something other than grain fed meat caused them to do poorly.)
Both high-meat Atkins and Eco-Atkins are good at producing short term weight loss and blood sugar control. But a long term study of patients on a high-meat diet by Fleming in 2000 showed a worsening of blood flow after one year with an overall 39.7% progression of coronary artery disease. And a study that lasted over 10 years by Sjogren et al in 2010 showed that elderly men eating a Mediterranean diet were 37% less likely to die of heart disease, while elderly men eating a high meat, carbohydrate restricted diet were 44% more likely to die of heart disease.
This book leaves many readers strongly convinced that meat and full fat dairy are the best replacements for refined carbs. But the evidence is mostly based on stories of individuals which tell us nothing about the average person; uncontrolled observational studies of other cultures with many confounding variables (such as genetic differences, calorie restriction, cholesterol lowering saponins, grass fed meat high in CLA and omega-3, absence of alcohol and tobacco, greater vitamin D, organic produce, higher exercise levels etc.); and clinical trials where people practicing low carb were also practicing calorie restriction which is totally misleading about the maintenance phase and about the long term risk of heart disease and cancer. A study in 2009 by Miller et al that compared three diets (Atkins, South Beach and Ornish) during weight maintenance showed Atkins produced less favorable results for lipids and flow-mediated vasodilatation than the other two.
People are different. In a study by Corella et al in 2010, when saturated fat intake was greater than 10% of calories in individuals carrying the APOE4 allele, the risk of heart disease was over 300% higher. About 25 to 30 percent of Americans carry this allele. But cholesterol skeptics have convinced many Americans with the APOE4 allele to try a high animal fat diet and it's giving them heart disease.
Taken together these six studies show that weight loss, fluffy LDL etc. are not protecting people from heart disease. The incomplete risk profile in studies used to promote a high-meat Atkins diet fail to accurately predict what will actually happen decades in the future. They are giving people a false sense of security.
Some people think Denise Minger's blog proves a high-meat diet is safe. But the Tuoli data that Denise makes a big deal about, can't tell us anything about health because it doesn't represent the way the people were eating all year long. The people are nomadic and eat different foods at different times of year and they were feasting to impress the visitors. And the Tuoli culture has confounding variables just like the examples in GCBC. And the fact that the protein deficient rural Chinese benefited from a small amount of animal protein doesn't mean that Americans who are already eating ten times as much animal protein as the rural Chinese need even more. There are places in China as well as the rest for world where high wheat consumption is not associated with heart disease. Denise' analysis does not distinguish between low glycemic index forms of wheat (like pasta cooked al dente) and high glycemic index forms of wheat (like white bread.)
WATCH OUT FOR CONFIRMATION BIAS
According to Wikipedia, "Confirmation bias refers to a type of selective thinking whereby one tends to notice and to look for what confirms one's beliefs, and to ignore, not look for, or undervalue the relevance of what contradicts one's beliefs."
For example, Mr. Taubes is nihilistic about any evidence against animal fat. To him, every study has a flaw, nothing is ever certain. But when it comes to uncontrolled observational studies of other cultures (evidence that's much weaker than the evidence he finds fault with), he accepts it without critical thinking.
"Confirmation biases contribute to overconfidence in personal beliefs and can maintain or strengthen beliefs in the face of contrary evidence. Hence they can lead to disastrous decisions, especially in organizational, military, political and social contexts."
"Individuals have to constantly remind themselves of this tendency and actively seek out data contrary to their beliefs." Since this isn't easy, most of the time we're stuck with bias. Nobody can be completely free of bias but we can make an effort. But we should always be biased in favor of studies published in peer reviewed journals over opinions published in books or on web sites. (Peer review attempts to find obvious errors and correct biased interpretations that go beyond the data.) And we should always value long term studies that measure disease more than short term studies that only measure risk factors.
For example, if Mr. Taubes had submitted his book to peer review, someone would have pointed out that the Masai are not a good argument for eating a high animal fat diet since they eat cholesterol lowering saponins and are believed to have genetic hypocholesterolemia.
FULL REVIEW
POINTS OF AGREEMENT
1) I agree that low carb is effective for diabetes and weight loss (but so are low fat, high fiber diets.)
2) I agree that high glycemic index carbs should be included in the long list of risk factors for heart disease (but animal fat is as least as bad and probably worse.)
3) I agree that total cholesterol below 150 is associated with a greater risk of stroke, but only for people with untreated hypertension or who smoke or drink alcohol or caffeine.
POINTS OF DISAGREEMENT
1) MISLEADING ABOUT THE DIET OF HUNTER GATHERERS : On page 69 of GCBC, Mr. Taubes cites a study by Loren Cordain et al that says hunter-gatherers ate 28% to 58% total fat. Taubes uses this study as evidence that all humans are adapted to a high saturated fat diet. But when you look at the details, Taubes completely misrepresents what Cordain believes. Here's what Cordain says about saturated fat, "The typical Paleolithic diet compared with the average modern American diet contained 2 to 3 times more fiber [from fruits and vegetables], 1.5 to 2.0 times more polyunsaturated and monounsaturated fats, 4 times more omega-3 fats, but 60% to 70% less saturated fat." This is in spite of the fact that they consumed the entire carcass of the animal. This is because they ate wild game (average of .89 grams saturated fat per serving) instead of grain fattened domestic animals (average of 7.04 grams saturated fat per serving). Grass fed meat also contains more CLA and omega-3 fatty acids which are associated with a reduced risk of heart disease and cancer.
2) MISLEADING ABOUT HEALTHY CARBS: Beans have a low glycemic index and if eaten on a regular basis their fiber and resistant starch (depending on the variety) can lower fasting blood sugar, insulin, triglycerides and improve the HDL/total cholesterol ratio. Oats and barley contain beta glucan and resistant starch which can lower fasting blood sugar, insulin and improve the HDL/total cholesterol ratio. Insoluble fiber like wheat bran is very important for digestive health. For the small percentage of people with celiac disease (1%) or gluten sensitivity (3 - 15%) there are many grains without gluten. Cultures where people live the longest eat more whole grains, beans and yams than the average American.
Most people handle low glycemic index, high fiber carbs just fine (these include fruit, non-starchy vegetables, peas, beans, whole grain pasta cooked al dente, rolled oats, corn on the cob, brown rice, sprouted grain bread, yams etc.) They don't cause the metabolic syndrome or increase the number of small dense LDL particles. The American public has never tried replacing saturated animal fat, sugar, white flour and baking potatoes with low glycemic index, high fiber carbs, nuts, olive or canola oil and fish. And the average American is eating out more often (sometimes twice a day instead of twice a week) and getting bigger portions than we would at home. Therefore the obesity epidemic proves nothing about beans and peas and whole grains and yams.
On page 454 GCBC says "By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume the leaner we will be." If there is even one exception then there is something wrong with the hypothesis. In rural China during the 80s, they ate 75.8% carbs (but they're healthy carbs) and more calories than Americans and they had extremely low rates of obesity, diabetes and heart disease. These facts about China are not in dispute. By ignoring them GCBC misleads us about the complexities of physiology and the fact that some people do best on low carb while many others do best on low fat.
3) MISLEADING ABOUT DIABETES : Following the diet recommended by the American Diabetes Association reduced HbA1c by 0.4 percentage points, but eating an ultra low fat diet with low glycemic index, high fiber carbs reduced HbA1c by 3 times that amount. This is a greater effect than taking a diabetic medication. (See [[ASIN:1594868107 Dr. Neal Barnard's Program for Reversing Diabetes: The Scientifically Proven System for Reversing Diabetes without Drugs]].) So both low fat and low carb diets lower blood sugar and improve insulin resistance compared to the standard American diet.
Excess insulin is just one factor in a long list of things that affect Western diseases. Excess calories, excess IGF1, vitamin D insufficiency (See [[ASIN:B002B55DTA Vitamin D Prescription: The Healing Power of the Sun & How It Can Save Your Life]]), a sedentary lifestyle, a shortage of phytochemicals from fruit and vegetables, a shortage of omega-3, eating too much salt, excess alcohol and smoking all have huge effects on Western diseases. And according to Weston Price free range meat and dairy, organically grown food, minimally processed food, calcium and fat soluble nutrients and whole grains were important reasons for the health of the people he studied. Since just eating less carbs can't correct all these problems, even the beneficial Eco-Atkins is not a panacea for Western disease.
4) MISLEADING ABOUT HEART DISEASE : Dr. Esselstyn used a 10% fat, low glycemic index, high fiber diet to reverse heart disease. (See [[ASIN:1583333002 Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure]].) 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 20 years later. Done right, the 10% fat, low glycemic index, high fiber diets reduce small dense LDL particles, inflammation, homocysteine, insulin resistance, blood sugar and increase nitric oxide which dilates arteries like nitroglycerin. There is no requirement to count calories or exercise to get these results.
Dr. Ornish also reversed heart disease using similar diet plus exercise and meditation. 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."
The book leads us to believe that lowering cholesterol may reduce heart disease but not increase longevity and that cholesterol levels don't matter in elderly people. But a meta-analysis by Afilalo et al. shows Statins reduce all-cause mortality 22% in elderly heart disease patients.
On page 454 GCBC says "Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes." The initial studies by Dr. Esselstyn and Dr. Ornish that reversed heart disease on a low fat, high carb, high fiber diet are over 20 years old and something he knew about (because he debated Dr. Ornish in 2002) but chose not to mention!
5) MISLEADING ABOUT CANCER : The book leads us to believe that low cholesterol causes cancer. But calorie restriction lowers cholesterol and reduces the risk of cancer and heart disease at the same time. The latest meta-analysis of statin use, based on 26 randomized trials and 170,000 patients, shows they are not associated with higher cancer rates. Countries with low cholesterol have lower rates of prostate, breast and colon cancer than the U.S. In clinical trials, ultra low fat diets slow cancer growth. So why would low cholesterol levels in this country be associated with cancer? Because cancer and other chronic diseases cause lower cholesterol, not the other way around.
Complete protein is the main thing that raises IGF1 which increases the risk of cancer (whey seems to be the only exception). Cancer patients who eat low fat and low meat have much higher survival rates. GCBC tells us people can be healthy eating 100% meat, but fruit, vegetables, whole grains and beans contain phytonutrients that act like low dose chemotherapy. (See [[ASIN:0756628679 Foods to Fight Cancer: Essential foods to help prevent cancer]].) Even Sally Fallon, cofounder of the Weston Price Foundation, in her book Nourishing Traditions admits "... meatless diets often prove beneficial in the treatment of cancer ..." although she does not believe that meat increases the risk of getting cancer.
However in the Fung et al study mentioned earlier, people eating a version of reduced carb with 18% animal protein were 32% more likely to die of cancer than the Eco-Atkins group eating 12% animal protein. In other studies, red meat is associated with an increased risk gastric and colon cancer; saturated fat is associated with an increased risk of breast cancer and dairy is associated with an increased risk of prostate cancer. And in animal studies, cancer rates increase rapidly when complete protein is more than 10% to 12%.
According to the World Health Organization, modern adult humans only require about 0.38 g/lb per day of protein with a protein digestibility-corrected amino acid score (PDCAAS) value of 1.0 to be healthy and maintain nitrogen balance. And the average American eats about 50% more than this. (Pregnant women, children, adolescents, elderly people with congestive heart failure and people recovering from an infection or injury need extra protein.)
6) MISLEADING ABOUT PHYSICAL EXERCISE: Just walking 30 minutes a day reduces the risk of heart disease, cancer, diabetes, hypertension, and Alzheimer's. (See [[ASIN:0345496310 The Spectrum: A Scientifically Proven Program to Feel Better, Live Longer, Lose Weight, and Gain Health]].) Conductors in double-decker buses have about half the rate of heart disease as the drivers who sit all day long. And exercise benefits your health whether you lose weight or not.
CONCLUSION : THERE ARE SEVERAL WAYS TO BE HEALTHY
People are different but medical research can only tell us what is likely to be true for the average person in a carefully defined group using statistical analysis. Some people do best with low fat or Mediterranean and others with Eco-Atkins. Most people with heart disease do well on the diet of Dr. Ornish or Dr. Esselstyn. But there's no evidence that a diet high in grain fed meat is good for anybody in the long run.
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. They ate 40% 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). Ancel Keys followed the Mediterranean diet and lived to be 100 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 low-fat diet with low glycemic index, high fiber carbs can save your life. This 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
6. An Eco-Atkins diet with regular meat, that includes 12% or less animal protein and 12% or less saturated animal fat has been shown to be healthier than the standard American Diet. Lower values give even better lipid profiles.
7. Eat like a hunter gatherer. But unless you have the right genes, eat grass fed meat and copy most of their protective behaviors you are not likely to get good results for heart disease and cancer (even if you lose weight and lower your blood sugar.)
Two bad choices
1) Follow the USDA pyramid version of low fat and eat lots of sugar, white flour, white rice and potatoes. It will increase your risk of the metabolic syndrome and diabetes.
2) Eat low carb with grain fed meat. It will increase your risk of heart disease and cancer.
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