Thursday, March 29, 2007

European Heart Journal on "Low Fat/Low Cholesterol"

I came across this article from the European Heart Journal with evidence from clinical trials about the so called heart healthy diet. It can be found on line at http://www.omen.com/corr.html. I reduced the text size of the 'Reference' section not because that information is less important rather to save some space. In fact the #1 principal to defend against junk science (as found in "The Junk Science Self-Defense Manual" by Anthony Colpo) is to 'Check the research yourself!'.

Here's a quote from that publication.

"I’ve lost count of the number of times I’ve checked studies that were cited in support of a specific stance, and found they either did not support that stance or even contradicted it!

A striking example of this phenomenon can be found in a joint statement by the American Heart Association and the NIH's National Heart, Lung, and Blood Institute entitled The Cholesterol Facts, where one finds the following claim: "The results of the Framingham study indicate that a 1% reduction…of cholesterol [corresponds to a] 2% reduction in CHD risk"[1].

Incredibly, one of the papers cited in support of the above statement was a thirty-year follow-up report from Framingham that flatly contradicts any claim that cholesterol reduction is beneficial. This report found that those whose cholesterol levels decreased during the study experienced an increase in both total and cardiovascular mortality! To quote the Framingham researchers themselves: "There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years…". So don’t be satisfied with the fact that someone has posted a bunch of scientific-looking citations at the end of their article. Check those citations for yourself! Doing so will often paint a very different picture to the one the original author wants you to see!"

Well enough intro - on to the article that prompted this post.

The low fat/low cholesterol diet is ineffective
Reprinted with permission from: European Heart Journal (1997) 18, 18-22
L.A. Corr, Guy's and St. Thomas' Hospitals, London, U.K. M.F. Oliver, National Heart and Lung Institute, London, U.K.
Correspondence: Dr. Laura A. Corr, MB, BS, MRCP, PhD, FESC,Consultant Cardiologist, Guys and St. Thomas' Hospitals, St. Thomas Street, London SE1 9RT
Ask almost member of the general public about a diet which would reduce their chance of heart disease and the reply is the same: "a low fat diet". On closer questioning, this means a diet with a reduction in cholesterol and saturated 'animal' fats, i.e. less meat, butter, milk and cheese. Most national and international recommendations for the prevention of heart disease, whether for primary prevention of or for patients who have developed the clinical manifestations of coronary heart disease, have made dietary restriction of total and saturated fats and of cholesterol the primary advice and often the sine qua non in relation to all other forms of management. To this extent they are to be congratulated that the message seems to be so universally accepted. Unfortunately, the available trials provide little support for such recommendations and it may be that far more valuable messages for the dietary and non-dietary prevention of coronary heart disease are getting lost in the immoderate support of the low fat diet.

The origin of the 'low fat' diet

The international bodies which developed the current recommendations based them on the best available evidence[1-3]. Numerous epidemiological surveys confirmed beyond doubt the seminal observation of Keys in the Seven Countries Study of a positive correlation between intake of dietary fat and the prevalence of coronary heart disease[4] although recently a cohort study of more than 43,000 men followed for 6 years has shown that this is not independent of fiber intake[5] or risk factors. The prevalence of coronary heart disease has been shown to be correlated with the level of serum total and low density lipoprotein cholesterol (LDL) as well as inversely with high density lipoprotein. As a consequence of these studies, it was assumed that the reverse would hold true: reduction in dietary total and especially saturated fat would lead to a fall in serum cholesterol and a reduction in the incidence of coronary heart disease. The evidence from clinical trials does not support this hypothesis.

The evidence from clinical trials

It can be argued that it is virtually impossible to design and conduct an adequate dietary trial. The alteration of any one component of a diet will lead to alterations in others and often to further changes in lifestyle so it is extremely difficult to determine which, if any, of these produce an effect. Dietary trials cannot generally be blinded and changes in the diet of the 'control' population are frequently seen: they may be so marked as to render the study irrevocably flawed. It is also recognized that adherence to dietary advice over many years by large population samples, as for most people in real life, is poor and that the stricter the diet, the worse the compliance. Nonetheless, the evidence for a reduction in saturated fat from dietary trials for both primary and secondary prevention merits closer scrutiny.

Trials of low fat diets in primary prevention

There have been six randomized, controlled trials with the long-term follow-up designed to modify the development of coronary heart disease in healthy subjects [6-11]. Remarkably, no primary prevention trial of sufficient size or sensitivity to examine the effect of a low total and saturated fat diet alone has ever been conducted. All six primary prevention trials involved alteration of one or more other risk factors such as cigarette smoking, blood pressure and exercise.

Of the three smallest trials(approximately 300-600 subjects per group), two suggested a significant reduction in coronary events. In the Oslo Study[7], men at high risk were given dietary advice aimed at reducing saturated fat intake and modestly increasing polyunsaturated fat intake, and counseled to stop smoking. General advice was given to increase fish, whale meat, vegetable and fruit intake. Over 5 years the mean difference in serum cholesterol between the two groups was relatively large for a dietary trial - 13% and tobacco consumption was lower in the intervention group. There were fewer coronary events in the control group (P<0.028)Trials of low fat diets in secondary prevention
There have been two trials of the effect of a low saturated fat diet alone in patients with coronary heart disease. The MRC study[13] followed 252 men randomized to a very low fat diet or no change in diet over three years: the low fat diet was poorly tolerated but achieved a 10% reduction in cholesterol. There was no difference in the rate of reinfarction or death and the researchers concluded that the low fat has no place in the treatment of myocardial infarction. An Australian trial of 458 men substituted polyunsaturated margarine for butter and found a slightly lower 5 year survival in the intervention group (3.3% deaths per year) than in the control group (2.4% deaths per year) although multivariate analysis showed that none of the dietary factors was significantly related to survival[14]. Following the negative results of these trials, no further studies of a low saturated fat diet alone have been conducted.

Should we be recommending diet at all?

The overwhelming importance of coronary heart disease in terms of morbidity, mortality and economic cost in the Western world made dietary advice, which was perceived to be cheap and safe, very attractive to Governments and their Health Departments. Vast sums of money have been invested in nutritional programs, dietary advice and nurse counseling to promote low saturated fat, low cholesterol diet--yet the trials to date for both primary and secondary prevention suggest that these diets do not work. However, this does not mean that all dietary interventions are futile. Other trials of secondary prevention have to a greater or lesser extent tried to alter the quality of the dietary fat intake and other components in patients with coronary heart disease, rather than restrict the quantity of saturated and total fat, and the results are more encouraging.

Trials of diets not dependent on fat reduction

Vegetable oil supplements were used in four of these trials[15-18]. In the LA Veterans Administration study, increasing ingestion of corn, safflower, soyabean and cottonseed oils significantly reduced total cardiovascular events after eight years[15]. The study by Rose et al, found no evidence of clinical benefit in patients given a low fat diet and supplements of olive or corn oil[16]. Similarly, the MRC group added soyabean oil as a supplement to the diet and found no difference in the incidence of death or myocardial infarction compared to men taking their normal diet[17], but a similar study from Oslo did show a significant reduction in pooled coronary heart disease relapses after 5 years and fewer fatal myocardial reinfarctions by 11 years[18]. However, none of these produced a significant difference in total mortality.

Saturated fat reduction, vegetable oil supplements and lifestyle changes in keeping with the current recommendations of the American Heart Association were advised for both the intervention and control groups in a study of Indian patients randomized within 48 h of a suspected myocardial infarction, but in addition the intervention group received a diet high in dietary fiber, omega-3 fatty acids (from fish and nuts), antioxidant vitamins and minerals[19]. The intervention group achieved remarkable wide-ranging and sustained changes in their nutrient intake associated with a modest reduction in serum cholesterol and weight loss. Cardiovascular events were reduced in the intervention group after only 6 weeks and after 1 year there was a significant reduction in myocardial infarction, a 42% reduction in cardiac deaths and a 45% reduction in total mortality compared to the control group on the standard 'low fat' diet. The study does not seem to have been continued beyond on year.

The first successful dietary study to show reduction in overall mortality in patients with coronary heart disease was the DART study reported in 1989[20]. The three-way design of this 'open' trial compared a low saturated fat diet plus increased polyunsaturated fats, similar to the trials above, with a diet including at least two portions of fatty fish or fish oil supplements per week, and a high cereal fibre diet. No benefit in death or reinfarctions was seen in the low fat or the high fibre groups. In the group given fish advise there was a significant reduction in coronary heart disease deaths and overall mortality was reduced by about 29% after 2 years, although there was a non-significant increase in myocardial infarction rates. The reduction in saturated fats in the fish advice group was less than in the low fat diet group and there was no significant change in their serum cholesterol.

Finally, the more recent Lyon trial[21] used a Mediterranean-type of diet with a modest reduction in total and saturated fat, a decrease in polyunsaturated fat and an increase in omega-3 fatty acids from vegetables and fish. As in the DART study there was little change in cholesterol or body weight, but the trial was stopped early following a 70% reduction in myocardial infarction, coronary mortality and total mortality after 2 years.

The most effective diet for secondary prevention is therefore not reduction of saturated fats and cholesterol but appears to be an increase in polyunsaturates of both omega-6 and omega-3 fatty acids. Unfortunately, the design and conduct of these trials are insufficient to permit conclusions about which polyunsaturates and other elements of these diets are the most beneficial. The long term effects of these trials[20,21] and the compliance with the dietary regimes remain to be seen. But the mechanism of any benefit of the omega diets would appear not to be associated with reduction in the total or LDL cholesterol levels and may be more related to reduction of a thrombotic tendency.

The case for recommending similar changes in diet in primary prevention is less clear cut. Although the benefit of olive oil receives strong epidemiological support from several Mediterranean countries, particularly Crete, and short-term studies of diets rich in oleic acid (the principle monounsaturate in our diet) have demonstrated a reduced LDL susceptibility to oxidation, no formal randomized long-term trial of monounsaturates has yet been attempted. There is no consensus from population or cohort follow up surveys about the protective effects of increased fish consumption on coronary mortality. The recently published report from the physicians Health study[22] found no evidence of an inverse association between the intake of fish or fish oils and the risk of myocardial infarction and, while the highest coronary mortality was found among men who ate no fish, the risk did not decrease with increasing fish intake. At present, there does not appear to be any dietary advice which is effective in primary prevention.

Is drug treatment better?

An important aspect of the lipid-lowering dietary trials is that on average they were only able to achieve about a 10% reduction in total cholesterol. The results of recent drug trials have demonstrated that there is a linear relation between the extent of the cholesterol, or LDL, reduction and the decrease in coronary heart disease mortality and morbidity, and a significant effect seen only when these lipids are lowered by more than 25%[23].

Until 1994, the trials with lipid lowering therapy for primary and secondary prevention had been as disappointing and confusing as the trials with diet. They tended to show a reduction in coronary events, including deaths from myocardial infarction, but no reduction in overall mortality. Even though an excess of deaths from cancer and suicide was not shown to have any casual relationship with the treatment, there was no widespread acceptance of lipid lowering therapy.
This changed in 1994 with the publication of the seminal 4S study on secondary prevention of coronary heart disease in 4444 patients with cholesterol levels greater than 5.5 mmol . 1-1 who were randomized to treatment with simvastatin or placebo in addition to 'usual care' including dietary advice[24]. The 4S study showed highly significant (30%) reduction in cardiac events and deaths from myocardial infarction and, for the first time, in overall mortality. The benefits were apparent after 18 months and the difference between the treated and the control groups continued to increase over the five years of follow-up. The more recent CARE study showed a similar outcome with a 28% reduction in reinfarction using pravastatin in 4159 patients following myocardial infarction despite the fact their cholesterol levels before treatment were not high (mean 5.4 mmol . 1-1)[25]. As part of their usual care, patients in this study also received high levels of antiplatelet agents and beta-blockers and 55% had undergone revascularization with angioplasty or bypass surgery. There was no change in coronary heart disease deaths or in all-cause mortality. Over 5 years of follow-up in both these statin trials the treatment was extremely well tolerated with around 90% compliance and no serious effect, indeed there was almost no difference in the side-effect profiles between the statins and the placebo.

With primary prevention the results of treatment with the statins appears equally encouraging. The West of Scotland Coronary Prevention study treated over 6000 healthy men (aged 44-65 years) who had total cholesterol levels greater than 6.5 mmol . 1-1 with either pravastatin or placebo[26]. Again the trial was continued for 5 years, and normal advice was given to both the intervention and the control groups. The risks of death from coronary heart disease and non-fatal myocardial infarction were reduced significantly in the pravastatin group by 31%, and there was a non-significant but favourable trend for all-cause mortality (-22%) with no adverse effect on non-cardiovascular mortality.

The cost effectiveness of treatment with the statins has been assessed at current prices for both primary and secondary care. It varies greatly according to the risk, being obviously more efficient for those at the highest risk, but has been shown to be greater than drug treatment for mild-to-moderate hypertension which is widely endorsed and used in general practice. For those at lower risk, diet should be able to provide a cheaper regimen but at present none has proved sufficiently beneficial.


The commonly-held belief that the best diet for the prevention of coronary heart disease is a low saturated fat, low cholesterol is not supported by the available evidence from clinical trials. In the primary prevention, such diets do not reduce the risk of myocardial infarction or coronary or all cause mortality. Cost-benefit analyses of the extensive primary prevention programmes, which are at present vigorously supported by Governments, Health Departments and health educationalists, are urgently required.

Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested. The circumstantial evidence of benefit from oils, particularly olive oil, vegetables, fruit and fish is strong.

For those at high risk, drug therapy, with the statins provides effective primary and secondary prevention and should be considered, with or without a diet, in the same way as drug treatment for mild or moderate hypertension.
L.A. Corr, Guy's and St. Thomas' Hospitals, London, U.K.
M.F. Oliver, National Heart and Lung Institute, London, U.K.

[1] Diet and cardiovascular disease (COMA Report) 1984, Report on health and social subjects-28, DHSS, HMSO.
[2] National Cholesterol Education Program Expert Panel on detection, evaluation and treatment of high blood cholesterol in adults. First report - Arch Int Med 1988: 148:36-39, Second report - Circulation 1994: 89: 1329-445.
[3] Pyorala K, De Backer G, Poole-Wilson P, Wood D. Prevention of coronary heart disease in clinical practice. Recommendations of the Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension. Eur Heart J 1994: 15: 1300-331
[4] Keys A. Seven Countries, A multivariate analysis of diet and coronary heart disease. Cambridge and London: Harvard University Press, 1980.
[5] Ascherio A, Rimm EB, Giovannucci EL, et al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States, BMJ 1996: 313: 84-90.
[6] Turpenien O, Karvonen MJ, Pekkarinen M, et al. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study, Int J Epidemiol 1979: 8: 99-118.
[7] Hjermann I, Velve Byre K, Holme I, Leren P. Effect of diet and smoking in the incidence of coronary heart disease. Lancet 1981: ii: 1303-10
[8] Strandberg TE, Salomaa VV, Naukkarinen VA, et al. Longterm mortality after 5 year multifactorial primary prevention of cardiovascular diseases in middle-aged men. JAMA 1991: 266: 1229-9.
[9] Franz D, Dawson EA, Ashman PL, et al. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey, atherosclerosis 1989: 9: 129-35.
[10] World Health Organization European Collaborative Group, European collaborative trial of multifactorial prevention of coronary heart disease. Lancet 1986: 1: 869-72.
[11] Neaton JD, Blackburn H, Jacobs D, et al. Serum cholesterol level and mortality: findings for men screened in the Multiple Risk Factor Intervention Trial. Arch Int Med 1992: 152: 1490-500.
[12] The Multiple Risk Factor Intervention Trial Research Group. Mortality after 16years for participants randomized to the Multiple Risk Factor Intervention Trial. Circulation 1996: 94: 946-51.
[13] Research Committee to the Medical Research Council. Low fat diet in myocardial infarction. A controlled trial Lancet 1965: ii: 501-4.
[14] Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Low fat, low cholesterol diet in secondary prevention of coronary disease. Adv Exp Med Biol 1978: 109: 317-30.
[15] Dayton S. Pierce ML, Hashimoto S, et al. A controlled clinical trial of a diet high in unsaturated fat preventing complications in atherosclerosis. Circulation 1969: 39/40: suppl. 11-63.
[16] Rose GA, Thomson WB, Williams TR. Corn oil in the treatment of ischaemic heart disease. BMJ 1965: 544: 1531-3.
[17] Research Committee to the Medical Research Council: Controlled trial of soya-bean oil in myocardial infarction. Lancet 1968: ii: 693-700.
[18] Leren P. The Oslo-Heart Study: eleven year report. Circulation 1970: XLII: 935-42.
[19] Singh RB, Rastogi SS, Verma R, et al. Randomized controlled trial of cardioprotective diet in patients with recent myocardial infarction: results of one year follow up. BMJ 1992: 304: 1015-18.
[20] Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989: ii: 757-61.
[21] de Logeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet 1994:343: 1454-59.
[22] Ascherio A, Rimm EB, Stampfer MJ, Giovannucci EL, Willett WC. Dietary intake of marine n-3 fatty acids, fish intake and the risk of coronary disease among men. N Engl J Med 1995: 332: 977-82.
[23] Holme I. Relation of coronary heart disease incidence and total mortality to plasma cholesterol reduction in randomized trials: use of meta-analysis. Br Heart J 1993: 69: S42-50.
[24] Scandinavian Simvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994: 344: 1383-9.
[25] Sacks FM, Pfeffer MA, Moye LA, et al., for the Cholesterol and Recurrent Events trial investigators. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels, N Engl J Med 1996: 35: 1001-9.
[26] Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia, N Engl J Med 1995: 333: 301-7.

Monday, March 26, 2007

Graveline on "Behavior Change"

Another one of the good guys whom I have read and learned a lot from. I really suggest you get and read his book. I have.
"Statin Drugs - Side Effects and The Misguided War on Cholesterol".
Low Cholesterol and Behavioral Change

Among the side effects reported from statin drug use have been a broad complex of emotional and behavioral symptoms. Case reports by anxious patients, concerned family members of caregivers have included aggressiveness, hostility, irritability, paranoia, road rage type outbursts, homicidal ideation, severe depression resistant to most therapies and as a natural follow-on to depression, a number of suicides have been reported where family members assert vehemently that, “It was the statin that did it.”

Dolichol inhibition is suspected as a major contributor to such behavioral change because of its established role in neuropeptide formation, where it orchestrates the processes of peptide strand formation in the endoplasmic reticulum and Golgi apparatus.

Imagine, every thought, sensation or emotion we have ever had, dependant upon the make-up of this protein linkage, comparable to popcorn on a string, where everything depends upon what protein and what position it has. There is no doubt about this important role of dolichols. Nor is there any doubt about dolichol inhibition with statin drug use. Just as cholesterol synthesis is inhibited by reductase inhibitors of the mevalonate pathway, so must dolichols (and CoQ10) for their formation depends upon the integrity of this same pathway. The finding of emotional and behavioral consequences of statin drug use should come as no surprise for dysfunction of dolichol managed pathways seems all but inevitable.

Additionally, that low cholesterol plays an important role in cognition and behavior independent of glial cell inhibition, is now well known to exist via the seleno-protein pathway. When disrupted this pathway leads to cognitive dysfunction as well as myopathy.

Now we find a study on the American Journal of Epidemiology by Zhang, Muldoon and others (yes, the same Muldoon having reported 100% cognitive dysfunction among statin users) reporting on the association of low serum cholesterol with negative mood, decrements of cognitive function and various types of aggressive behavior in adolescent children.

This association is not minor and was based upon detailed and well-controlled studies of a large population group and, surprisingly, existed only for the non-African-American segment of the group studied. When all the possible confounding factors were accounted for, the tendency for violence and aggressiveness persisted among Caucasian children and adolescents.

The authors report an across the board correlation of low cholesterol with many other studies including those with conduct disorders, violent behavior, criminals and psychiatric patients and even controlled dietary studies of non-human primates, reflecting on a species correlation. The result is a strong positive correlation between low cholesterol and aggressiveness.

So, if a surprisingly large segment of our society is already aggression prone because of low serum cholesterol, can you imagine the effect of wide scale use of statins to lower the cholesterols even more?

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

Prager on "Evil"

Yup! Here's another good man whom I believe has much to say to us today. Not only an author but also good on the radio.
New Form of Evil Is Why America Has Not Won Iraq War
By Dennis Prager
Tuesday, March 27, 2007I never thought we could see a new form of evil. After the gas chambers of the Holocaust, the tens of millions murdered in the Gulag, the forced starvation in the Ukraine, the hideous medical experiments on people by the Germans and the Japanese in World War II, the torture chambers in all police states, I had actually believed that no new forms of evil existed.
I was wrong.
Of course, for sheer cruelty, one cannot outdo the Nazis; no depiction of hell ever matched the reality of Auschwitz and Bergen-Belsen. But while Islamists and Baathists in Iraq have not devised new forms of torture -- there probably are no new ways left -- they have devised a new form of evil: murdering, maiming and torturing as many innocents among their own people as possible.
I do not know of an analogous form of evil. When the Allies conquered Nazi Germany, disaffected Nazis did not go around murdering and cutting off the heads of fellow Germans in order to make the Allies leave. Nor did disaffected Japanese blow up Japanese students so as to make the American occupation of Japan untenable.
Here is the latest example of this new form of evil as reported by the Associated Press: "Maj. Gen. Michael Barbero, deputy director for regional operations on the Joint Staff, said . . . the vehicle used in the attack [on Iraqi civilians] was waved through a U.S. military checkpoint because two children were visible in the back seat. He said this was the first reported use of children in a car bombing in Baghdad. 'Children in the back seat lowered suspicion, (so) we let it move through, they parked the vehicle, the adults run out and detonate it with the children in the back,' Barbero told reporters in Washington."
These same "insurgents" routinely blow up children who line up to receive candy from U.S. troops. Likewise, college students are targeted for death, as are men lining up to apply for civilian jobs, men and women attending mosques, physicians in hospitals, and so on. The more innocent the Iraqi, the more likely he or she is to be targeted for murder.
I submit that there was no way to anticipate this. And no one did. This includes all those who predicted a civil war in Iraq between Shiites and Sunnis. I include myself among those who predicted savagery in Iraq. On a number of occasions prior to our invasion of Iraq, I recounted to my radio listeners this chilling story:
As a young man, in 1974, I was riding on a bus traveling from Beirut to Damascus. The man I sat next to was an English-speaking Iraqi whom I asked at one point in our conversation, "Can you describe your nation in a sentence?" "No problem," he immediately answered. "We Iraqis are the most barbaric people in the world."
I obviously never forgot that man's words, and therefore anticipated great cruelties in Iraq. But neither I nor anyone who predicted a civil war had so much as a premonition of this unprecedented mass murder of the men, women and children among one's own people as a military tactic to defeat an external enemy.
It is, therefore, unfair to blame the Bush administration for not anticipating such a determined "insurgency." Without the mass murder of fellow Iraqis, there would hardly be any "insurgency." The combination of suicide terrorists and a theology of death has created an unprecedented form of "resistance" to an occupier: "We will murder as many men, women and children as we can until you leave." Nor is this a matter of Sunnis murdering Shiites and vice versa: college students, women shopping at a Baghdad market and hospital workers all belong to both groups. Truck bombs cannot distinguish among tribes or religious affiliations.
If America had to fight an insurgency directed solely against us and coalition forces -- even including suicide bombers -- we would surely have succeeded. No one, right, left or center, could imagine a group of people so evil, so devoid of the most elementary and universal concepts of morality, that they would target their own people, especially the most vulnerable, for murder.
That is why we have not yet prevailed in Iraq. Even without all the mistakes made by the Bush administration -- and what political or military leadership has not made many errors in prosecuting a war? -- it could not have foreseen this new form of evil we are witnessing in Iraq.
That is why we have not won.
There are respectable arguments to be made against America's initially going into Iraq. But intellectually honest opponents of the war have to acknowledge that no one could anticipate an "insurgency" that included people leaving children in a car and then blowing them up.

Dennis Prager is a radio show host, contributing columnist for Townhall.com, and author of 4 books including Happiness Is a Serious Problem: A Human Nature Repair Manual.

Sunday, March 25, 2007

Why the Low-Fat Diet is Stupid and Potentially Dangerous

Be it known there is controversy in this subject. Here is a scholarly, well written and well documented article that bears scrutiny. Verify what he says and if, as he states, the evidence is significant, act on it. Note that the last 1/3 of this article is composed of references so please do your Due-Diligence. Though it's a bit long I believe it is worth the read. Else I would not have posted it in its entirety.

Here is a quote from near the end of the article. "NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part."
Why the Low-Fat Diet is Stupid and Potentially Dangerous

Anthony Colpo, February 23, 2006.
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.

Such stupidity makes my head spin…

First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.

My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that wouild have made lipid-phobes like Ornish and Pritikin proud.

For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.

My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!

Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.

Basically, I felt like crap!

It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.

When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"

While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!

Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!

Why the Low-Fat Diet is a Big Fat Fraud

One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
   1) Directly slashing your intake of important vitamins and fatty acids;
   2) Reducing the absorption of crucial fat-soluble vitamins;
   3) Decreasing the absorption of important minerals.

You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!

The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).

The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.

Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!

Absorb This!

Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).

When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).

The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)

Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.

Making a Bad Situation Worse

The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).

The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.

Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.

It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).

A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).

Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!

Low-Fat, Low Omega-3

Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.

Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)

So what has this all got to do with low-fat eating? Everything!

Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).

Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).

When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).

Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!

Speaking of scrambled brains…

Nature's Anti-Depressant: Fat!

Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!

In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.

The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.

The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!

Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.

Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)

Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.

The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape

For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).

Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.

The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)

Fatless Shrugged

It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser. Low-Fat Diets Lower Testosterone

Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.

Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.

So too can low-fat diets.

Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).

Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).

It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.

Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune FunctionDiet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.

Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).

In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).

It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).

For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.

The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).

There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!

Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.

After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!

Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).

After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).

If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.

It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.

So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?

I truly doubt it…

If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.

The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg'dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.

In Search of the Elusive 'Negative Fat Intake'!

The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!

The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!

But the Japanese Eat a Low-Fat Diet…Don't They?

Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)

If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).

OK, So What About the Mediterranean Diet?

A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!


Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).


I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!

The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.

References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.

To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, and defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.

NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first). However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com


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