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.
Friday, May 27, 2011
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)
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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)
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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)
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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.
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19. Steinberg, Daniel. The Cholesterol Wars. 2007, Academic Press. Page 211.
20. Kendrick, Malcolm. The Great Cholesterol Con. 2007, John Blake Publishing. Page 79.
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