Bests & Worsts Reviews from Amazon

"The normal low-density lipoprotein (LDL) cholesterol range is 50 to 70 mg/dl for native hunter-gatherers, healthy human neonates, free-living primates, and other wild mammals (all of whom do not develop atherosclerosis). Randomized trial data suggest atherosclerosis progression and coronary heart disease events are minimized when LDL is lowered to <70 mg/dl. (1). Statins have side effects but these examples of healthy people and animals show those side effects have nothing to do with low cholesterol. In fact people with hypobeta-lipoproteinemia can have LDL as low as 15mg/dL and still live longer than average and be very healthy. MOST DOCTORS AND SCIENTISTS REALIZE THAT LDL-C HAS BEEN PROVEN BEYOND A REASONABLE DOUBT TO BE A MAJOR CAUSE OF HEART DISEASE Scientists studied nine single nucleotide polymorphisms which influence LDL levels. From homozygous familial hypercholesterolemia at the high extreme (over 600 mg/dL LDL cholesterol) to hypobeta-lipoproteinemia at the low extreme (less than 15mg/dL LDL cholesterol). Since these SNPs are present from birth, this allowed them to see the effect of low LDL levels maintained over a lifetime. The results show a three times greater benefit for these life long low LDL levels compared taking statins later in life. Ference stated, "the effect of each of the included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect." "The researchers also conducted a meta-analysis of the "natural" randomized trials by combining non-overlapping data from multiple SNPs involving 326,443 participants. Results of this study indicated that lifetime exposure to lower LDL was associated with a 54% (95% CI, 48-59) relative reduction of CVD for each 38.7 mg/dL (1 mmol/L) lower LDL." There is a clear dose response relationship. And no one is suggesting that people that statins all their life, but low animal fat diets can do a lot to improve LDL. (2) No one claims that LDL is the only factor contributing to heart disease, but it is clearly the most important one. This particular study does more to prove beyond a reasonable doubt that LDL is a very important cause of heart disease than any study I know of. First is looks at the effect of lower LDL over a lifetime rather than during a few months or years. Second it isolates the effect of LDL from other variables as well as a randomized clinical trial with 100% compliance. According to the third report of the National Cholesterol Education Program (NCEP), "Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD." (3) 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. (4) 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. (5) CONTRARY TO THE BOOK'S ASSERTION, BOTH LARGE AND SMALL LDL PARTICLES ARE ATHEROGENIC It's the apo-B particle that is atherogenic whether it is found in small dense LDL, large fluffy LDL or VLDL which is even larger than fluffy LDL. In fact according to one article, "... after accounting for their inverse correlation, both LDL subclasses showed highly significant and independent associations with IMT (carotid intima-media thickness), with a greater difference in IMT per large LDL particle compared with small LDL." (6) HIGH HDL PROBABLY DOES NOT PROTECT US FROM HEART DISEASE New drugs have been developed that raise HDL, but they have proved ineffective at lowering the rate of heart attacks. Also a mendelian randomization study of 116,000 people genetically predisposed to have higher HDL levels showed that they did not have a lower rate of heart disease. (7) ANCEL KEYS AND THE SIX COUNTIES STUDY The authors repeat the libel of Uffe Raviskov as if it were a fact. But they thought he was referring to the Seven Counties Study which was published in 1970. Actually Ravnskov's criticism involved the Six Countries Study which was published in the 1950's. Dr. Ravnskov used a 1957 paper by Yerushalmy and Hilleboe to criticize Keys. Their primary criticism was that there were other variables more strongly associated with heart disease mortality than TOTAL FAT which had a correlation of .659. (BTW, even though a graph of all 22 countries didn't make a straight line the correlation was strong and significant even for total fat.) It's ironic that Dr Ravnskov chose to talk about this study, since the two variables that Yerushalmy and Hilleboe found most strongly associated with heart disease mortality in the 22 countries were ANIMAL PROTEIN first (correlation of .756) and ANIMAL FAT second (.684). The correlations for vegetable fat, vegetable protein and carbohydrate were -0.468, -0.651 -0.562 respectively. The negative correlation meant they appeared to be protective. (8) It's Dr. Ravnskov, who is not even a scientist, who misled us. WHAT ABOUT HOSPITAL ADMISSIONS? How can you explain people being admitted to the hospital for heart disease with relatively low LDL levels? The effect of LDL on heart disease depends on a lifetime of exposure to high levels. If high risk people recently started taking a statin or started eating a low saturated fat diet their LDL would be lower but not necessarily low enough to completely stop the progression of plaque (less than 80 mg/dL LDL is needed to halt or reverse heart disease). And cholesterol tends to go down quite a bit in older people, so someone who has had a heart attack probably had much higher cholesterol when they were younger. And this particular study did not adjust for the other risk factors of heart disease like smoking, hypertension, sedentary lifestyle, diabetes and abdominal obesity. The scientists didn't bother to adjust for other these variables because they weren't trying establish a causal relationship between LDL and heart disease. That has already been done. WHAT ABOUT ABOLUTE VERSUS RELATIVE RISK? Heart disease is the number one cause of death here in the US. It causes roughly 40% of deaths each year or 40/100 absolute risk and 40/100 relative risk over a lifetime . Yet on a daily basis less than one person in 100,000 will die of heart disease. The absolute daily risk is < 1/100,000. Does stating the short term absolute risk make the lifetime risk insignificant? Of course not, that's why short term absolute risk is misleading. It trivializes major issues. Relative risk is similar whether you are looking at a short term study or a lifetime study. That's why relative risk is the normal way of reporting risk. THE BOOK MISLEADS US ABOUT LOW-FAT DIETS The book claims that low fat diets are ineffective for weight loss or the prevention of heart disease and cancer. But in the studies cited people were free to replace fat with anything they chose and in this country that's usually sugar, white flour and fried potatoes swimming in trans fat. And there was no significant lowering of LDL. However there are other kinds of low fat diets that are very effective at lowering LDL and reducing heart attacks. In the 1950s, Dr. Morrison put 50 heart attack survivors on a 15% fat, high protein diet and another 50 survivors were told to eat as usual. Total cholesterol fell from 312 mg/dl to 220 mg/dl in the experimental group. That's a reduction of 29%. And over a period of 8 years, 38 patients eating as usual died while only 22 in the experimental group died. (9) In the 80's Dr. Esselstyn used a 10% fat, high fiber diet plus low dose statins to arrest or reverse heart disease in 18 severely ill heart patients. The average for total cholesterol and LDL was maintained at 145 mg/dl and 82 mg/dl respectively. We know it worked because of before and after coronary angiograms and cardiac PET scans. Some had been given less than a year to live by their referring cardiologist. After 12 years, "Adherent patients have experienced no extension of clinical disease, no coronary events, and no interventions. This finding is all the more compelling when we consider that the original compliant 18 participants experienced 49 coronary events in the 8 years before the study." There was no requirement to count calories or exercise to get these results. Although the sample was small, the results were statistically significant. The percent of reduction in mortality and cardiac events by far outperforms any other study that has ever been done on coronary artery disease patients. (10) Also see Prevent and Reverse Heart Disease: The Revolutionary, Scientifically Proven, Nutrition-Based Cure. Dr. Ornish also reversed heart disease using a similar diet plus exercise and meditation but no statins. Since then Dr. Ornish has enrolled at least 3800 patients in demonstration projects (to demonstrate savings on surgery) which resulted in over 40 insurance companies including Medicare covering a program in diet and lifestyle for heart disease patients. According to Dr. Ornish, "In brief, we found that almost 80 percent of patients who were eligible for bypass surgery or angioplasty were able to safely avoid it for at least three years." Insurance companies wouldn't pay for something that made a lot of people worse. If any one got worse it had to be a small minority of patients. (11) Also see The Spectrum: A Scientifically Proven Program to Feel Better, Live Longer, Lose Weight, and Gain Health. OBSERVATIONAL EVIDENCE OF DIET AND LONGEVITY The book claims that low cholesterol shortens your life and that a serum cholesterol over 200 is ideal, but this is based on uncontrolled observational studies. This fails to adjust for the fact that cancer and other chronic diseases lower cholesterol. 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 are the longest lived group that has ever been studied. 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 better longevity than the US. They ate 37% fat mostly from olive oil, but only 8% saturated fat. The total red meat, poultry and fish consumed per-person, per-day in Crete was only about 2 ounces. Ancel Keys followed a version of the Mediterranean diet and lived to be 100 years old. 3. According to The Okinawa Program on page 23, the Okinawa centenarians have an average cholesterol of about 170. And contrary to an internet myth that's based on young people, it says on page 71 that the centenarians eat about 2 ounces/person/day of fish and 1 ounce/person/day of meat, poultry and eggs while Americans eat very little fish and close to 10 ounces/person/day of meat, poultry and eggs. (See 4. 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 reduce all-cause mortality. (12) 5. The studies I cited clearly show that lowering LDL with diet and/or medication in heart patients reduces all-cause mortality. Bottom line, everyone should follow a diet that makes them feel good as well as having some evidence for long term health. But any heart patient who trusts books written by cholesterol skeptics greatly increases their risk of heart attack and all-cause mortality. PS The in the 1950's the majority of doctors and scientists were cholesterol skeptics. But today they are only a small albeit vocal minority. REFERENCES 1. O'Keefe JH Jr, Cordain L, Harris WH, Moe RM, Vogel R. Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal. J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6. 2. Ference BA, Yoo W, Alesh I, Mahajan N, Mirowska KK, Mewada A, Kahn J, Afonso L, Williams KA Sr, Flack JM. Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: a mendelian randomization analysis. J Am Coll Cardiol. 2012 Dec 25;60(25):2631-9. doi: 10.1016/j.jacc.2012.09.017. Epub 2012 Oct 17. 3. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report. Circulation 2002;106;3143. 4. Brown MS, Goldstein JL. Human mutations affecting the low density lipoprotein pathway. Am J Clin Nutr. 1977 Jun;30(6):975-8. 5. Risk of fatal coronary heart disease in familial hypercholesterolemia. British Medical Journal, 1991;303:893-896. 6. Mora S, Szklo M, Otvos JD, Greenland P, Psaty BM, Goff DC Jr, O'Leary DH, Saad MF, Tsai MY, Sharrett AR. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA).Atherosclerosis. 2007 May;192(1):211-7. 7. Sekar Kathiresan et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet. 2012 August 11; 380(9841): 572-580. 8. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med. 1957 Jul 15;57(14):2343-54. 9. Morrison LM. Reduction of mortality rate in coronary atherosclerosis by a low cholesterol-low fat diet. Am Heart J. 1951 Oct;42(4):538-45. 10. Esselstyn CB Jr. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease (an overdue requiem for palliative cardiology). Am J Cardiol. 1999 Aug 1;84(3):339-41, A8. 11. Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet. 1990 Jul 21;336(8708):129-33. 12. 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.