Showing posts with label Ancel Keys. Show all posts
Showing posts with label Ancel Keys. Show all posts
Ancel Keys
The Truth:
- Ancel Keys did not drop any countries from the Seven Countries Study. His most famous graph—the first one up above—is from a different paper he presented at a World Health Organization (WHO) conference in 1955. The Seven Countries Study didn’t even launch until 1958, and entailed much more than just plopping numbers into a pretty curve. (That said, the Seven Countries Study had plenty of problems too; some are mentioned on this site.)
- Contrary to popular belief, the cherry-picked graph didn’t convince everyone that fat was evil. In fact, Keys was pretty much ridiculed for the weakness of his fat/heart disease theory by other scientists at the WHO meeting, and whenever his graph was cited in medical journals later on, it was usually paired with some criticism. Although Keys’ work definitely shaped our current beliefs about fat, this graph didn’t exactly take the world by storm. (More on this later.)
- When all 22 countries were analyzed, the association between fat and heart disease did not go away. It actually remained statistically significant (meaning it probably wasn’t due to chance). And to make matters worse, the paper frequently cited as a “rebuttal” to Keys shows pretty clearly that animal protein had an even stronger association with heart disease than total fat did. The China Study was right all along! Time to go vegan, you guys. (Just kidding. But this part is the most interesting of all, and we’ll examine it in excruciating depth in a moment.)
Although some of his saga has been misconstrued, Keys was still far from perfect—and his eventual role in demonizing saturated fats (while glorifying polyunsaturated fats) has led us down an unfortunate road. My goal is neither to nudge Mr. Keys into sainthood nor to perpetuate his villain status—only to lay out the history and data as objectively as possible.
Mediterranean diet and public health: personal reflections.
Mediterranean diet and public health: personal reflections.
Keys A1.
Abstract
Ancel Keys
Ancel Keys was an American physiologist, former chairman of the International Society of Cardiology, consultant to the World Health Organization and the UN Food and Agriculture Organization, and inventor of the K ration. During his professional career he founded the field of quantitative human biology, wrote the most complete account of the physiological, psychological, and cognitive effects of starvation (The Biology of Human Starvation, 1950), and helped establish the link between CVD and dietary cholesterol. Nicknamed Mr Cholesterol for his discoveries, he advocated for a healthy lifestyle that included a low-fat diet and regular exercise. He retired as head of the Laboratory of Physiological Hygiene at the University of Minnesota in 1972 but remained intellectually active through his 97th year. He died on 20 November 2004 at the age of 100.
Dr Keys’ interest in cardiovascular disease began after the Second World War with the realization that as food supplies in northern Europe became short the death rate from coronary artery disease (CAD) dropped. This observation, coupled with reports of an epidemic of myocardial infarctions (MI) among American executives, motivated Keys to launch one of the first prospective studies in CVD epidemiology, the Minnesota Business and Professional Men’s Study.[1] Along with Henry Taylor, Keys recruited 286 Minneapolis—St. Paul businessmen between the ages of 45 and 55 to submit to yearly physical examinations starting in 1947 in an attempt to discover the factors involved in “degeneration of the heart.” Starting in 1947 the researchers recorded weight, blood pressure, ECG results, and cholesterol levels (mean 6.2 to 9.4 mmol/L). The only significant predictor of later MI was a high total cholesterol level. Initially these observations were harshly criticized by commercial interests such as the meat and dairy industry.
After a series of smaller studies, Keys examined the dietary habits of middle-aged men of Japanese origin living in either their native Japan, Hawaii, or Los Angeles in 1956.[2] This study was based on the observation that rates of CAD are significantly higher in nisei—Japanese living in Hawaii and Los Angeles—than they are for native Japanese. In Los Angeles, rates of CAD in nisei were similar to rates in “local Caucasians.” For every native Japanese experiencing an MI, the Hawaiian nisei have four, and the Los Angeles nisei ten. Given the common genetic background of the subjects, Keys and his colleagues sought to examine how the “usual American mode of life” might play a role. An examination of the dietary patterns demonstrated that while native Japanese get only 13% of their calories from fats, the Hawaiian Japanese get 32% of their calories from fats, and the Los Angeles Japanese get 45% of their calories from fats. The subjects’ mean total cholesterol levels corresponded to the three dietary patterns: 3.11 mmol/L for native Japanese, 4.70 mmol/L for Hawaiian Japanese, and 5.50 mmol/L for Los Angeles Japanese.
Beginning in 1957 Keys and his colleagues began what would eventually be known as the Seven Countries Study by surveying 12 000 men aged 40 to 59 from 18 areas of seven countries (Italy, the Greek Islands, Yugoslavia, the Netherlands, Finland, Japan, and the United States).[3] Study communities were chosen for their contrasting dietary patterns and the relative uniformity of their rural laboring populations. Through central chemical analysis of the foods consumed by randomly selected families as well as diet-recall measures, Keys and his colleagues were able to determine that in societies where fat was a major component of every meal (i.e., the US and Finland), both the blood cholesterol levels and the heart-attack death rates were highest. Conversely, in cultures where diets were based on fresh fruit and vegetables, bread, pasta, and plenty of olive oil (i.e., the Mediterranean region) blood cholesterol was low and heart attacks were rare. The report published in 1970 had a decisive impact on CVD prevention, as it described one of the first studies to clearly show that dietary saturated fat leads to CVD, and that the relationship is mediated by serum cholesterol.
In the late 1960s the realization grew that prevention programs could not rely solely on protecting the most susceptible but must protect the entire population.[4] The Seven Countries Study helped confirm this and shift scientific and public attention to entire populations considered at risk.
Even though the three major preventable risk factors for CVD (elevated serum cholesterol levels, high blood pressure, and smoking) had been identified as early as 1956, the link between cholesterol and CAD required the results of large epidemiology studies before gaining widespread acceptance. As a result of corroborative evidence from prospective population studies such as the Framingham study, the scientific community refocused on systemic intervention studies to test whether reducing risk factors would reduce disease incidence.
These early trials examined the effects of diet or drug therapy in primary and secondary prevention populations. Dietary modification typically focused on a reduction of the total and saturated fat content, although some of the trials examined fat substitution using corn or soybean oil.[5,6] At the same time, the drug therapy trials focused primarily on clofibrate and niacin, colestipol, or gemfibrozil.[5,7-13] On the whole, the drug trials were more successful at lowering cholesterol than the dietary trials. Unsurprisingly, the reduction in cardiovascular mortality and total mortality was greater in the secondary prevention trials and appeared to be dependent on the baseline cholesterol levels; that is, the higher the baseline risk the greater the obtained benefit.[5] In fact, the LRC-CPPT[5,10,11] reported a “cholesterol benefit ratio”: for every 1% reduction in cholesterol a 2.5% reduction in CVD incidence was achieved.
The mid-1990s saw the emergence of mega-trials using lipid-lowering therapy with HMG-CoA reductase inhibitors (statins). There have been numerous trials examining different statins (lovastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin) in patients with a wide variety of clinical characteristics. These trials have focused on primary prevention, secondary prevention, acute coronary syndromes (ACS), and aggressive lipid lowering.
Secondary prevention and risk equivalents
The first of these trials was the landmark 4S study,[14] which demonstrated that in patients with established CAD and a cholesterol level between 5.5 and 8.0 mmol/L, treatment with simvastatin was associated with a significant reduction in coronary mortality, all-cause mortality, stroke, and need for revascularization without a compensatory increase in noncoronary mortality. As a result this trial established the safety of cholesterol-lowering therapy and absolved it of past concerns that they would result in increased noncoronary death.[9]
The first of these trials was the landmark 4S study,[14] which demonstrated that in patients with established CAD and a cholesterol level between 5.5 and 8.0 mmol/L, treatment with simvastatin was associated with a significant reduction in coronary mortality, all-cause mortality, stroke, and need for revascularization without a compensatory increase in noncoronary mortality. As a result this trial established the safety of cholesterol-lowering therapy and absolved it of past concerns that they would result in increased noncoronary death.[9]
The importance of treating the dyslipidemic patient with CVD or risk equivalents was reinforced in two subsequent trials with pravastatin. The LIPID trial[15] and the CARE trial[16] examined patients with established CAD and a serum cholesterol of 4.0 to 7.0 mmol/L (LIPID), and 3.2 to 6.2 mmol/L (CARE). Similar to 4S, these trials showed that pravastatin was effective at reducing CVD mortality, all-cause mortality, MI, need for revascularization, and stroke.
The largest placebo-controlled trial examining the efficacy of statin therapy was reported in 2002. The HPS study[17] examined over 20 000 high-risk patients with established CVD, diabetes, or treated hypertension and a cholesterol level greater than 3.5 mmol/L (mean total cholesterol 5.9 mmol/L, LDL-C 3.4 mmol/L) and randomized them to either simvastatin (40 mg daily) or placebo. After 5.5 years of treatment, simvastatin was associated with a significant reduction in all-cause mortality, CVD mortality, major cardiovascular events, need for revascularization, and stroke. These effects were similar among tertiles of LDL-C, suggesting that the threshold beyond which lowering LDL-C has no effect has not yet been reached.
Similarly, atorvastatin was demonstrated to be beneficial in high-risk patients with type 2 diabetes not known to have CAD in the CARDS trial,[18] where atorvastatin (10 mg daily) significantly reduced cardiovascular mortality, MI, stroke, and need for revascularization. In the AVERT trial,[19] treatment with atorvastatin was shown to be equivalent to angioplasty at reducing ischemic events in patients with one- or two-vessel CAD and an average LDL-C of greater than 3.0 mmol/L.
Primary prevention
While it is no surprise that treating the highest risk individuals (i.e., those with clinically established disease) will result in the greatest clinical benefit, these patients are estimated to make up less than 10% of the total population CVD burden. The first major trial focusing solely on primary prevention was the WOSCOPS trial,[20] which was published only 1 year after the 4S trial. Like 4S, it was a landmark trial that demonstrated a significant reduction in nonfatal MI, cardiovascular mortality, need for revascularization, and need for cardiac hospitalization in men with relatively high cholesterol levels, who received pravastatin (40 mg/day). In contrast to the earlier trials with clofibrate,[9] WOSCOPS did not demonstrate an increase in noncardiac death. As a result it established the benefit of treating dyslipidemic patients who were at high risk of developing clinically apparent CVD. This trial was followed by two others, AFCAPS/TexCAPS[21] in 1998 and ASCOT-LLA[22] in 2003, which demonstrated the efficacy of primary prevention in patients with near-normal cholesterol levels. (In the AFCAPS/TexCAPS trial, this meant total cholesterol of 5.7 mmol/L and LDL-C of 3.9 mmol/L, and in the ASCOT-LLA trial, this meant total cholesterol of 5.5 mmol/L and LDL-C of 3.4 mmol/L.)
While it is no surprise that treating the highest risk individuals (i.e., those with clinically established disease) will result in the greatest clinical benefit, these patients are estimated to make up less than 10% of the total population CVD burden. The first major trial focusing solely on primary prevention was the WOSCOPS trial,[20] which was published only 1 year after the 4S trial. Like 4S, it was a landmark trial that demonstrated a significant reduction in nonfatal MI, cardiovascular mortality, need for revascularization, and need for cardiac hospitalization in men with relatively high cholesterol levels, who received pravastatin (40 mg/day). In contrast to the earlier trials with clofibrate,[9] WOSCOPS did not demonstrate an increase in noncardiac death. As a result it established the benefit of treating dyslipidemic patients who were at high risk of developing clinically apparent CVD. This trial was followed by two others, AFCAPS/TexCAPS[21] in 1998 and ASCOT-LLA[22] in 2003, which demonstrated the efficacy of primary prevention in patients with near-normal cholesterol levels. (In the AFCAPS/TexCAPS trial, this meant total cholesterol of 5.7 mmol/L and LDL-C of 3.9 mmol/L, and in the ASCOT-LLA trial, this meant total cholesterol of 5.5 mmol/L and LDL-C of 3.4 mmol/L.)
Despite this body of evidence, some controversy remains regarding the role of statins in primary prevention for members of populations at lower baseline risk, such as women, and for patients likely to have adverse drug reactions, such as the elderly. Even though analyses of the ASCOT trial have clearly established the beneficial role of statins in these populations (an observation that was supported by secondary prevention trials such as CARE, 4S, and TNT), pharmacotherapy remains recommended for high-risk individuals only.
Acute coronary syndromes
As discussed above, statins have been shown to be effective in patients with established, stable CAD. Given the theoretical pleotropic effects of statins on inflammation, plaque stabilization, and thrombogenicity, several studies have examined their potential utility in the immediate aftermath of an acute coronary syndrome (ACS). The first major trial to address this question was the MIRACL study,[23] which confirmed that lipid-lowering with atorvastatin (80 mg/day), when given 24 to 96 hours after admission for ACS, significantly reduced recurrent ischemic events in the first 16 weeks. PROVE-IT TIMI 22[24] elaborated on these results and demonstrated that intensive lipid-lowering reduced major cardiovascular endpoints in patients hospitalized for ACS (one-third with unstable angina, one-third with non-ST elevation MI, and one-third with ST elevation MI). Patients in the intensive arm were able to achieve an LDL-C level of 1.60 mmol/L in contrast to a level of 2.46 mmol/L achieved by those in the standard therapy arm, corresponding to a 2-year reduction in the composite of death, MI, or urgent revascularization as well as recurrent unstable angina.
As discussed above, statins have been shown to be effective in patients with established, stable CAD. Given the theoretical pleotropic effects of statins on inflammation, plaque stabilization, and thrombogenicity, several studies have examined their potential utility in the immediate aftermath of an acute coronary syndrome (ACS). The first major trial to address this question was the MIRACL study,[23] which confirmed that lipid-lowering with atorvastatin (80 mg/day), when given 24 to 96 hours after admission for ACS, significantly reduced recurrent ischemic events in the first 16 weeks. PROVE-IT TIMI 22[24] elaborated on these results and demonstrated that intensive lipid-lowering reduced major cardiovascular endpoints in patients hospitalized for ACS (one-third with unstable angina, one-third with non-ST elevation MI, and one-third with ST elevation MI). Patients in the intensive arm were able to achieve an LDL-C level of 1.60 mmol/L in contrast to a level of 2.46 mmol/L achieved by those in the standard therapy arm, corresponding to a 2-year reduction in the composite of death, MI, or urgent revascularization as well as recurrent unstable angina.
Aggressive lipid-lowering
The aggressive lipid-lowering strategy was further extended to patients with stable CAD in two separate trials published in 2005. The TNT trial[25] enrolled 10 000 patients with stable CAD and a baseline LDL-C of 3.4 to 6.5 mmol/L and then randomized them to low-dose (10 mg/day) or high-dose (80 mg/day) atorvastatin. The significantly lower serum LDL-C level achieved with high-dose atorvastatin (2.0 mmol/L vs 2.6 mmol/L) was associated with a reduction in major cardiovascular events, MI, stroke, and cardiovascular mortality without affecting total mortality. Similarly, the IDEAL trial[26] demonstrated a significant reduction in nonfatal MI and need for revascularization in the intensive lipid-lowering arm, where atorvastatin (80 mg/day) was used to achieve LDL-C 2.1 mmol/L versus the standard arm, where simvastatin (20 mg/day) was used to achieve LDL-C 2.7 mmol/L. Likewise, the recently completed JUPITER trial[27] showed that rosuvastatin (20 mg/day) resulted in a significant reduction in cardiovascular morbidity and mortality in patients without evidence of CVD, a low to normal LDL-C, and an elevated C-reactive protein level compared with placebo.
The aggressive lipid-lowering strategy was further extended to patients with stable CAD in two separate trials published in 2005. The TNT trial[25] enrolled 10 000 patients with stable CAD and a baseline LDL-C of 3.4 to 6.5 mmol/L and then randomized them to low-dose (10 mg/day) or high-dose (80 mg/day) atorvastatin. The significantly lower serum LDL-C level achieved with high-dose atorvastatin (2.0 mmol/L vs 2.6 mmol/L) was associated with a reduction in major cardiovascular events, MI, stroke, and cardiovascular mortality without affecting total mortality. Similarly, the IDEAL trial[26] demonstrated a significant reduction in nonfatal MI and need for revascularization in the intensive lipid-lowering arm, where atorvastatin (80 mg/day) was used to achieve LDL-C 2.1 mmol/L versus the standard arm, where simvastatin (20 mg/day) was used to achieve LDL-C 2.7 mmol/L. Likewise, the recently completed JUPITER trial[27] showed that rosuvastatin (20 mg/day) resulted in a significant reduction in cardiovascular morbidity and mortality in patients without evidence of CVD, a low to normal LDL-C, and an elevated C-reactive protein level compared with placebo.
These clinical results for intensive lipid-lowering therapy were supported by three surrogate endpoint studies. The SCAT Trial[28] demonstrated significantly less angiographic progression of CAD in patients with near-normal cholesterol levels (mean total cholesterol 5.2 mmol/L, LDL-C 3.36 mmol/L) who underwent intensive lipid-lowering with simvastatin versus patients on placebo. More recently the REVERSAL[29] and ASTEROID[30] trials demonstrated that lowering LDL-C to a mean level of 2.0 mmol/L with atorvastatin (80 mg) and to 1.57 mmol/L with rosuvastain (40 mg) resulted in a slowing or even regression of coronary atherosclerosis as assessed by intravascular ultrasound.
Owing to the demonstrated benefits of intensive lipid-lowering therapy, most major lipid guidelines were revised between 2004 and 2007 (see Table). These guidelines rely on risk prediction scores that estimate an individual’s 10-year risk for heart disease as high, moderate, or low and recommend treatment accordingly.
The current Canadian Cardiovascular Society (CCS) guidelines[31] recommend that patients in the high-risk category be treated with a statin to achieve a reduction in LDL-C by more than 50% to a level of less than 2.0 mmol/L. The primary goal for patients in the moderate- and low-risk groups is a reduction in LDL-C of at least 40% from baseline, when levels are ≥3.5 mmol/L and ≥5.0 mmol/L, respectively.
The current Adult Treatment Panel III (ATP-III-R) guidelines[32] are similar to the CCS recommendations with comparable targets for each risk category. A key difference however is the inclusion of patients with a Framingham risk score of less than 10% in the moderate risk category if they have two CVD risk factors (smoking, hypertension, HDL-C < 1.1 mmol/L, a positive family history of premature CAD, and age ≥45 years in men and ≥55 years in women). The low-risk category for the ATP-IIIR includes patients with a less than 10% 10-year risk and 0–1 risk factors. The risk stratification tool used by the European Society of Cardiology (ESC) is the SCORE system, which considers patients with a 10-year risk of CVD death greater than 5% as high risk.[33] The ESC lipid guidelines recognize risk equivalents as a distinct category that warrant immediate treatment to high-risk targets. For patients with a SCORE rating greater than 5%, a 3-month trial of lifestyle measures is the recommended starting point. If after 3 months lipid levels remain above moderate- to low-risk targets and the SCORE rating remains greater than 5%, then intensive therapy to reach high-risk targets is recommended.
As discussed, statins have been shown to be safe and effective at lowering lipid levels (especially LDL-C) and protecting against CVD. Nevertheless there are situations where despite optimal doses, lipid levels remain suboptimal. For these patients there are two established options with more in development.
The first therapeutic approach is combination therapy with niacin. Several studies have reinforced the importance of simultaneously lowering LDL-C and increasing HDL-C. Early trials focusing on the combination of colestipol and niacin (CLAS, FATS) demonstrated a significant regression in coronary atherosclerotic lesions as well as a reduction in death, MI, angina, and need for revascularization.[34,35] The more recent HATS and ARBITER-2 studies found significant effects in surrogate (CIMT, angiographic stenosis) and clinical endpoints (death, MI, stroke, or revascularization) and confirmed the beneficial effect of adding niacin to statin therapy.[36,37]
The second therapeutic approach involves combining a cholesterol absorption inhibitor such as ezetimibe with a statin. Recently the ENHANCE trial[38] confirmed the efficacy of ezetimibe at lowering LDL-C; however, it did not show any additional improvement in the surrogate endpoint of carotid vascular disease over simvasatin therapy alone. Conversly, the recent SEAS study demonstrated no effect of ezetimibe on the progression of aortic stenosis, although there was a concomitant reduction in coronary events.[39]
In addition to the established armamentarium for lowering lipid levels, there are multiple agents in development that target novel components of the lipid pathway and atherosclerotic cascade. Perhaps the best known novel agents are in the class of the cholesterol ester transfer protein inhibitors, which are specifically designed to raise HDL-cholesterol. Their reputation was recently tainted when a phase 3 trial (ILLUMINATE) examining the safety and efficacy of torcetrapib was halted after an excess of deaths and cardiovascular events in the torcetrapib treatment group.[40] However, other novel agents in this class now being studied have not caused the same deleterious off-target effects seen with torcetrapib and appear to be safe. Other agents in development include antagonists of apolipoprotein B, the large protein that forms the backbone of all lipid molecules except HDL-C, as well as inhibitors of phospholipid A2, an enzyme that plays a critical role in the pathogenesis of atherosclerosis. Early studies show these agents are effective at reducing LDL-C levels and decreasing inflammation without significantly increasing adverse events.
Over the past 50 years the lipid hypothesis has grown from an obscure theory to a central concept in the practice of cardiovascular medicine and the prevention of heart disease. The concept began with the pioneering work of Dr Ancel Keys, who helped establish the epidemiological link between dietary fats, serum cholesterol, and atherosclerotic coronary and vascular disease. But the early observations would have meant nothing if large randomized trials had not confirmed the role of dyslipidemia in cardiovascular disease and the beneficial effects of contemporary lipid management.
The key to the management of dyslipidemia remains a balanced combination of education, early prevention, lifestyle modification (including a low-fat diet and regular exercise), and tailored pharmacotherapy. While controversies continue regarding what is the most appropriate target for lipid levels and whether monotherapy should be pursued over combination therapy, the fact remains that up to 50% of ischemic heart disease worldwide can be accounted for by dyslipidemia with treatment benefits “substantially greater than those associated with hypertension therapy.”[41] As such, the need for an aggressive and effective lipid-lowering treatment approach could not be more relevant.
Debate since 2000
In 2000, Uffe Ravnskov published his book The Cholesterol Myths and went on to found The International Network of Cholesterol Skeptics.[58]
The first major critical analysis of the Seven Countries Study was undertaken by Gary Taubes, in Good Calories, Bad Calories. Taubes was the original author of the major critiques of this study. All other subsequent authors have built upon Taubes critique.
The second major critique of The Seven Countries Study was published by Nina Teicholz, in The Big Fat Surprise. She was the first to analyze the problems with the data underlying Keys' Mediterranean data (which provided the foundation of the Mediterranean diet), and she was the first to establish that the survey in Crete was conducted during Lent, thereby causing Keys to dramatically undercount the amount of saturated fat eaten. Teicholz's book is the first systematic argument for how saturated fats had been unfairly demonized by Keys and why they are not, after all, bad for health. The role of both Taubes and Teicholz in shifting the debate on dietary fat has been covered in hundreds of newspaper and magazine articles.
In his 2009 video Sugar: The Bitter Truth, Robert Lustig says his purpose is to debunk the prior thirty years of nutrition research, specifically Keys.[59] Lustig gave details in his book Fat Chance: that Keys cherry-picked seven of 22 countries; consumption of trans-fat peaked in the 1960s and Keys failed to separate them out; results for Japan and Italy could be explained by either low saturated fat consumption or by low sugar consumption; and Keys wrote that sucrose and saturated fat were intercorrelated but failed to perform the sucrose half of his multivariate correlation analysis.[60] (All this work is based on Taubes' original analysis)
Controversy continues about the study itself, and about the strength and causality of the association between dietary fat and heart mortality, particularly as the study of cholesterol has become more sophisticated.[61][62] Reigniting the debate[63] was a meta-analysis in 2014 finding that "current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats".[64] However, this meta-study has also met with controversy and was corrected, with Willett continuing to defend reduced saturated fat in the diet.[65]
Taubes wrote two bestsellers, Good Calories, Bad Calories in 2007[66] followed by Why We Get Fat in 2010–2011.[67] Part I of Good Calories, Bad Calories relates how we came to believe dietary fat causes heart disease (Part II offers that carbohydrates cause the chronic diseases of civilization, and Part III explains obesity and calories).[68] Teicholz's international bestselling The Big Fat Surprise in part follows Taubes Part I. Her book is the first to make the comprehensive argument that saturated fat has been unfairly demonized and does not, after all, cause heart disease. Her book adds historical information about the vegetable oil industry and its influence on nutrition science. Her book also includes investigations into trans fats, tropical oils, and the Mediterranean diet, as well as the story of nutrition science post 1986 (where Taubes leaves off). Teicholz has since contributed for The BMJ, the New York Times, CNN.com, and the Wall Street Journal on the subject of saturated fat and dietary fat generally.
Taubes became a regular contributor to The New York Times opinion pages[69] and twice the paper gave Taubes a lead feature story in its Sunday magazine: "What if It's All Been a Big Fat Lie?" (2002)[70] and "Is Sugar Toxic?" (2011).[71]
In September 2014, Frank Hu led the 2015 Dietary Guidelines Advisory Committee's report on saturated fat and cardiovascular disease. Alice H. Lichtenstein said that the consensus is that a low-fat diet is "probably not a good idea" and that it might induce dyslipidemia. She said that the guidelines had changed (formerly recommending low fat, and now moderate fat) in 2000, and that the American Heart Association and the National Heart, Lung, and Blood Institute had revised guidelines as of 2000.[72] The group's Scientific Report of the 2015 Dietary Guidelines Advisory Committee says the average person in the U.S. consumes too much saturated fat. "Sources of saturated fat should be replaced with unsaturated fat, particularly polyunsaturated fatty acids."[63]
As of 2016, WebMD and the Mayo Clinic both recommended that its readers avoid or minimize saturated fats and replace them with polyunsaturated or monounsaturated fats.[73][74]
Saturated fat
A four-decades-old study — recently discovered in a dusty basement — has raised new questions about longstanding dietary advice and the perils of saturated fat in the American diet.
The research, known as the Minnesota Coronary Experiment, was a major controlled clinical trial conducted from 1968 to 1973, which studied the diets of more than 9,000 people at state mental hospitals and a nursing home.
During the study, which was paid for by the National Heart, Lung and Blood Institute and led by Dr. Ivan Frantz Jr. of the University of Minnesota Medical School, researchers were able to tightly regulate the diets of the institutionalized study subjects. Half of those subjects were fed meals rich in saturated fats from milk, cheese and beef. The remaining group ate a diet in which much of the saturated fat was removed and replaced with corn oil, an unsaturated fat that is common in many processed foods today. The study was intended to show that removing saturated fat from people’s diets and replacing it with polyunsaturated fat from vegetable oils would protect them against heart disease and lower their mortality.
So what was the result? Despite being one of the largest controlled clinical dietary trials of its kind ever conducted, the data were never fully analyzed.
Several years ago, Christopher E. Ramsden, a medical investigator at the National Institutes of Health, learned about the long-overlooked study. Intrigued, he contacted the University of Minnesota in hopes of reviewing the unpublished data. Dr. Frantz, who died in 2009, had been a prominent scientist at the university, where he studied the link between saturated fat and heart disease. One of his closest colleagues was Ancel Keys, an influential scientist whose research in the 1950s helped establish saturated fat as public health enemy No. 1, prompting the federal government to recommend low-fat diets to the entire nation.
“My father definitely believed in reducing saturated fats, and I grew up that way,” said Dr. Robert Frantz, the lead researcher’s son and a cardiologist at the Mayo Clinic. “We followed a relatively low-fat diet at home, and on Sundays or special occasions, we’d have bacon and eggs.”
The younger Dr. Frantz made three trips to the family home, finally discovering the dusty box marked “Minnesota Coronary Survey,” in his father’s basement. He turned it over to Dr. Ramsden for analysis.
The results were a surprise. Participants who ate a diet low in saturated fat and enriched with corn oil reduced their cholesterol by an average of 14 percent, compared with a change of just 1 percent in the control group. But the low-saturated fat diet did not reduce mortality. In fact, the study found that the greater the drop in cholesterol, the higher the risk of death during the trial.
The findings run counter to conventional dietary recommendations that advise a diet low in saturated fat to decrease heart risk. Current dietary guidelines call for Americans to replace saturated fat, which tends to raise cholesterol, with vegetable oils and other polyunsaturated fats, which lower cholesterol.
While it is unclear why the trial data had not previously been fully analyzed, one possibility is that Dr. Frantz and his colleagues faced resistance from medical journals at a time when questioning the link between saturated fat and disease was deeply unpopular.
“It could be that they tried to publish all of their results but had a hard time getting them published,” said Daisy Zamora, an author of the new study and a research scientist at the University of North Carolina at Chapel Hill.
Seven Countries Study HOAX
In the year 1958, Keys began the "Seven Countries Study" to examine the association between diet and cardiovascular disease in different countries. The results: countries that consumed the most fat had the most heart disease. Quick, announce to the world that dietary fat causes heart disease! What he failed to mention in his summation was that he LEFT OUT the countries where fat consumption was low but heart disease high, like Chile. He basically cherry picked certain countries to support his theory. Plus, he left out countries that consume tons of fat but have low heart disease statistics, like Holland and Norway. This study gained massive media attention, influencing dietary guidelines and still fooling the masses today who haven't learned otherwise, thanks to allopathic doctors and other Western (quack) MDs who never study a lick of nutrition.
Still, the new "saturated fat" guidelines received serious criticism at the time from respected scientists (who blamed sugar), but Time magazine didn't cover that. I guess those headlines wouldn't stand out so much, like mad scientists who propagate political agendas. The guidelines were picked up by the USDA, whose job it was to sell grains. How convenient! America was put on the low-fat, high-carb diet and had no idea where it was all headed. Without any scientific proof, America charged forward. Guess what began next? - The obesity epidemic and the diabetes epidemic. It's time to debunk this "cornerstone" of modern nutrition policy and the reason why health authorities help perpetuate the health avalanche.
You see, if you eat pesticide and insecticide food (most conventional and all GMO) and you become obese or get cancer, or both, then you are most likely a victim of misinformation, which has led to your demise. It is important to realize the massive significance here. Every decade or so, American media create and perpetuate new health lies, to keep the old ones alive and keep the "on the fence" health enthusiasts fighting the wrong battles. Since modern nutrition policy is based on completely fabricated lies and bad science, it's time to drop the "seven countries myth," eat the good fats and maintain the good kind of cholesterol.
Avocado: Recent research shows that the absorption of two key carotenoid antioxidants, lycopene and beta-carotene, increases significantly when fresh avocado or avocado oil is added to a salad, and doing so can increase absorption of carotenoids by between 200 and 400%. Though avocado is a "high-fat food" (about 85% of its calories come from fat), phytosterols are key supporters of the body system that keeps inflammation under control. This is well documented for helping arthritis sufferers. (http://www.whfoods.com)
Omega-3 Fatty Acids and Hemp Seed Oil: Omega-3 fatty acids can significantly reduce the risk of sudden cardiac death by as much as 45 percent, as demonstrated in a major study that involved more than 11,000 patients (GISSI Prevention study). These fatty acids also protect against stroke, improve blood pressure, reduce inflammation and can improve vascular function and lipid metabolism, just for starters. Check out the benefits of including more omega-3 in the diet:
• Smarter children - Children in mainstream primary schools taking DHA supplements were better behaved and showed increased reading ability.
• Benefits pregnant women - Taking omega-3s during pregnancy reduces post-partum depression and results in healthier babies.
• Cancer prevention - Omega-3 fatty acids reduce inflammation and reduce the risk of cancer. (http://www.naturalnews.com)
Olive Leaf Extract: Olive leaf extract is one of nature's most incredible "cure all" medicines. Olive leaf extract has been said to kill virtually every virus and bacterial growth in existence. It is well known in the health enthusiast world as a natural remedy for high cholesterol, as it prevents the oxidation of LDL cholesterol, so it can't attach itself to arterial walls. This is significant considering that many sufferers of high cholesterol also suffer from high blood pressure and adult onset diabetes.
Remember the weight loss craze? Remember aspartame and the zero calories craze where everything was either labeled "light" or "zero"? Remember George W. Bush pushing his subsidized GMO corn on America? We feed the world! There is a plan to make you sick, folks, so don't underestimate the power of the "Seven Countries Study" or any scientist who makes the cover of some ever-so-popular and classic mainstream magazine!
Sources for this article include:
http://www.naturalnews.com
http://authoritynutrition.com
http://authoritynutrition.com
http://www.naturalnews.com
http://www.naturalnews.com
http://science.naturalnews.com
http://science.naturalnews.com
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Is "artery-clogging-saturated-fat" one word?
George McGovern led a U.S. senate committee in 1977 to publish the USA's first set of "Dietary Goals" so we could all "reverse the epidemic of heart disease" in the country. Certainly we need politicians telling us what to eat and what NOT to eat based on flawed science and money-making schemes (like margarine). All that heart disease in America couldn't be from all the processed foods since WWII. Certainly America did not hire Nazi scientists fresh out of prison to help develop food additives, preservatives, pharmaceuticals and vaccines 20 years prior to the "Seven Countries Study." From the designers of the Auschwitz gas chambers to the GMO food on your dinner plate, how could that be? Our government could never be so sinister, right? (http://www.naturalnews.com)Still, the new "saturated fat" guidelines received serious criticism at the time from respected scientists (who blamed sugar), but Time magazine didn't cover that. I guess those headlines wouldn't stand out so much, like mad scientists who propagate political agendas. The guidelines were picked up by the USDA, whose job it was to sell grains. How convenient! America was put on the low-fat, high-carb diet and had no idea where it was all headed. Without any scientific proof, America charged forward. Guess what began next? - The obesity epidemic and the diabetes epidemic. It's time to debunk this "cornerstone" of modern nutrition policy and the reason why health authorities help perpetuate the health avalanche.
You see, if you eat pesticide and insecticide food (most conventional and all GMO) and you become obese or get cancer, or both, then you are most likely a victim of misinformation, which has led to your demise. It is important to realize the massive significance here. Every decade or so, American media create and perpetuate new health lies, to keep the old ones alive and keep the "on the fence" health enthusiasts fighting the wrong battles. Since modern nutrition policy is based on completely fabricated lies and bad science, it's time to drop the "seven countries myth," eat the good fats and maintain the good kind of cholesterol.
Want some ibuprofen for that inflammation or organic fats to fight it?
Organic Coconuts and Coconut Oil: Coconut oil is one of the richest sources of saturated fat that you can find, with around 90% of calories as saturated fat. The initial studies on coconut oil that supposedly demonstrated that it was unhealthy used refined and hydrogenated coconut oil that contained trans fats! These studies have no relevance to unrefined, organic, virgin coconut oil. Populations that eat a large percentage of calories from coconuts are much healthier than Western nations and have little to no traces of cardiovascular disease, despite the high saturated fat consumption. It all depends on which kind of saturated fat - you see - there's the rub.Avocado: Recent research shows that the absorption of two key carotenoid antioxidants, lycopene and beta-carotene, increases significantly when fresh avocado or avocado oil is added to a salad, and doing so can increase absorption of carotenoids by between 200 and 400%. Though avocado is a "high-fat food" (about 85% of its calories come from fat), phytosterols are key supporters of the body system that keeps inflammation under control. This is well documented for helping arthritis sufferers. (http://www.whfoods.com)
Omega-3 Fatty Acids and Hemp Seed Oil: Omega-3 fatty acids can significantly reduce the risk of sudden cardiac death by as much as 45 percent, as demonstrated in a major study that involved more than 11,000 patients (GISSI Prevention study). These fatty acids also protect against stroke, improve blood pressure, reduce inflammation and can improve vascular function and lipid metabolism, just for starters. Check out the benefits of including more omega-3 in the diet:
• Smarter children - Children in mainstream primary schools taking DHA supplements were better behaved and showed increased reading ability.
• Benefits pregnant women - Taking omega-3s during pregnancy reduces post-partum depression and results in healthier babies.
• Cancer prevention - Omega-3 fatty acids reduce inflammation and reduce the risk of cancer. (http://www.naturalnews.com)
Olive Leaf Extract: Olive leaf extract is one of nature's most incredible "cure all" medicines. Olive leaf extract has been said to kill virtually every virus and bacterial growth in existence. It is well known in the health enthusiast world as a natural remedy for high cholesterol, as it prevents the oxidation of LDL cholesterol, so it can't attach itself to arterial walls. This is significant considering that many sufferers of high cholesterol also suffer from high blood pressure and adult onset diabetes.
50 Years of Skewed "Facts"
Welcome to the land where wheat, corn, bread and hydrogenated cooking oils are the staple diet, and where people still can't differentiate the good fats from the bad ones. Just as we have good water (spring water) and bad water (fluoridated tap water), we have good fat and bad fat. But Ancel Key's research targeted all fats as bad for the heart.Remember the weight loss craze? Remember aspartame and the zero calories craze where everything was either labeled "light" or "zero"? Remember George W. Bush pushing his subsidized GMO corn on America? We feed the world! There is a plan to make you sick, folks, so don't underestimate the power of the "Seven Countries Study" or any scientist who makes the cover of some ever-so-popular and classic mainstream magazine!
Sources for this article include:
http://www.naturalnews.com
http://authoritynutrition.com
http://authoritynutrition.com
http://www.naturalnews.com
http://www.naturalnews.com
http://science.naturalnews.com
http://science.naturalnews.com
Read more
Ancel Keys
Keys started his academic career as a biologist, obtaining his MSc and PhD in Berkeley in 1928 and 1930 respectively. After that, he specialized in physiology by pursuing a PhD at Cambridge, which he received in 1936. By the late 1950s, Keys had made significant contributions to the fields of osmoregulation, high altitude physiology, the nutritional basis of human performance and the biology of human starvation and rehabilitation.
By starting the SCS, Keys could pursue the question of how dietary fat influenced blood cholesterol. He formulated the first ideas and assembled a team of like-minded scientists around him. During the first era of the SCS, it was Keys more than anybody else who was the driving force behind it. Although the still-unfolding story of dietary fat proved more complex than Keys envisioned. He was pioneering in the right direction – pointing out the cardioprotective effect of the Mediterranean diet and the ‘Keys equation’ on the effect of different dietary fatty acids on serum cholesterol levels, both of which still widely studied today.
Keys was professor and director of the Laboratory of Physiological Hygiene at the University of Minnesota, School of Public Health between 1940 and 1972. He received various honors from the countries he worked in, and he and his wife Margaret wrote two bestselling cookbooks: Eat Well and Stay Well (1959), and How to Eat Well and Stay Well the Mediterranean Way (1975). He remained dedicated to the SCS until the end of his long life.
Ancel Keys
A year or so before the video was posted, Lustig gave a similar talk to a conference of biochemists in Adelaide, Australia. Afterwards, a scientist in the audience approached him. Surely, the man said, you’ve read Yudkin. Lustig shook his head. John Yudkin, said the scientist, was a British professor of nutrition who had sounded the alarm on sugar back in 1972, in a book called Pure, White, and Deadly.
“If only a small fraction of what we know about the effects of sugar were to be revealed in relation to any other material used as a food additive,” wrote Yudkin, “that material would promptly be banned.” The book did well, but Yudkin paid a high price for it. Prominent nutritionists combined with the food industry to destroy his reputation, and his career never recovered. He died, in 1995, a disappointed, largely forgotten man.
Perhaps the Australian scientist intended a friendly warning. Lustig was certainly putting his academic reputation at risk when he embarked on a high-profile campaign against sugar. But, unlike Yudkin, Lustig is backed by a prevailing wind. We read almost every week of new research into the deleterious effects of sugar on our bodies. In the US, the latest edition of the government’s official dietary guidelines includes a cap on sugar consumption. In the UK, the chancellor George Osborne has announced a new tax on sugary drinks. Sugar has become dietary enemy number one.
Ancel Keys
This is one of those “gotta bust me some myths no matter where they come from” blog posts. And by that, I mean I’m about to challenge a story that’s been so well-circulated among paleo, low carb, and real-food communities that most of us have filed it away in a little brain-folder called “Things We Never Have to Question Because They’re So Ridiculously True.”
I’m talking about the late, great Ancel Keys, and his equally late (but maybe not as great) role in the history of heart disease research. The oft-repeated tale goes something like this:
Once upon a time, a scientist named Ancel Keys did an awful thing. He published a study about different countries that made it look like heart disease was associated with fat intake. But the truth was that he started out with 22 countries and just tossed out the ones that didn’t fit his hypothesis! When other researchers analyzed his data using all the original countries, the link between fat and heart disease totally vanished. Keys was a fraud, and he’s the reason my mom made me eat skim milk and Corn Chex for breakfast instead of delicious bacon and eggs. LET HIS SOUL BURN. BURN! BUUUUUURN!
Depending on who tells the story, some of the details (and wishes for eternal hellfire) may differ. But in many cases, Keys’ infamous cherry-picking is attributed to his Seven Countries Study, a landmark project that helped sculpt our common beliefs about fat. Even the Seven Countries Study page on Wikipedia—the first hit when you Google “Seven Countries Study”—says that Keys shamelessly erased the data he didn’t like:
The study began with a great many more countries … but Keys deleted the countries whose results did not match his pre-conceived conclusions, leaving him with only Japan, Italy, Great Britain, Australia, Canada and the US. Full disclosure would have made a great deal of difference.
Ditto for the page on Ancel Keys himself:
Keys collected data on deaths from coronary heart disease and fat consumption from 22 countries. Despite the fact that 22 countries provided statistics, Keys cherry-picked the data from the 7 countries which supported his theory that animal fat was the main cause of coronary heart disease in order to publicize his opinions. The results of what later became known as the “Seven Countries Study” appeared to show that serum cholesterol was strongly related to coronary heart disease mortality both at the population and at the individual level.
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