“It is better to know nothing than to keep in mind fixed ideas based on theories whose confirmation we constantly seek, neglecting meanwhile everything that fails to agree with them.” -Claude Bernard. An Introduction to the Study of Experimental Medicine. 1957 (1).
Most people are acutely aware that obesity is increasing unabated (2). The Centers for Disease Control and Prevention (CDC) note:
“During the past 20 years there has been a dramatic increase in obesity in the United States. In 2009, only Colorado and the District of Columbia had a prevalence of obesity less than 20%. Thirty-three states had a prevalence equal to or greater than 25%; nine of these states (Alabama, Arkansas, Kentucky, Louisiana, Mississippi, Missouri, Oklahoma, Tennessee, and West Virginia) had a prevalence of obesity equal to or greater than 30%.”
Also, not a single state met the CDC’s goals set ten years ago to reduce obesity to 15 percent of the population in the U.S.
For most the previous decade (from March 2003 to June 2007 for the subjects) researchers embarked on a journey to help determine why we might get fat, and how we can lose the excess pounds (5). The report was recently published in the Annals of Internal Medicine, which was the longest randomized trial of a low carbohydrate diet compared to a low-fat, low calorie diet.
On the surface of it, the study was asking some simple questions: if we want to lose weight will we be more likely to do it if we cut back on the fat in the diet or on the carbohydrates? And if we care about doing this in the most healthful possible way, which one of these two approaches will leave us with the least likelihood of contacting heart disease – the lowest cholesterol, LDL (i.e., the “bad cholesterol”) and blood pressure, the highest HDL (the “good cholesterol”)?
After seven years and $4 million in government funding, the study published gave us some definitive answers. It also shed light on what may be one obvious reason why the country is enduring an obesity epidemic, and why we haven’t been able to achieve even a modicum of success in the last half-century in stemming the tide of obesity and, for most of us, losing any weight ourselves.
The answer: Scientific ineptitude.
The report was so flawed that I felt compelled to alert the press, and my story was picked up by the LA Times (3). While I’m grateful that the Times ran the story, I have more to tell.
In this multiple part series, I’m going to closely scrutinize the study in question and hopefully shed some light on what is wrong with the current design of diet studies and the field of nutrition in general.
In doing so, I hope to explore and investigate health and disease, overweight and obesity, as well as the field of nutrition (and much of the bad science that accompanies it), and what we can do to cure the obesity epidemic, and eliminate the diseases of civilization - Alzheimer's disease, atherosclerosis, asthma, cancer, chronic liver disease or cirrhosis, Chronic Obstructive Pulmonary Disease, Type 2 diabetes, heart disease, metabolic syndrome, Crohn's disease, nephritis or chronic renal failure, osteoporosis, acne, stroke, depression and obesity (4).
The article by Foster et al. (5) starts by noting the clinical superiority of a low-carbohydrate diet for inducing weight loss when compared to a low-fat, low-calorie diet in the short-term (6 months) (6-10).
The authors also discuss that longer-term (1 to 2 years) results have been mixed. Two studies demonstrated greater weight loss with the low-carbohydrate diet when compared with “low-fat diets” (10, 11) while four other studies showed no statistical difference (6, 12-14).
The results of these diet studies will be discussed in a future blog post in greater detail, but let’s learn a little more about these diets and why they have been prescribed for weight loss and health.
The idea behind The Atkins Diet and the efficacy of low-carbohydrate diets is essentially that the dietary carbohydrates are fattening, not the calories. The general theory can be summarized by some of the conclusions that Gary Taubes (15) made in his book, Good Calories, Bad Calories:
“Insulin is the primary regulator of fat storage. When insulin levels are elevated, we stockpile calories as fat. When insulin levels fall, we release fat from our fat tissue and burn it for fuel. . . .By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity. . . .The fewer carbohydrates we eat, the leaner we will be.”This is the ‘Carbohydrate Hypothesis’ for weight regulation. In this approach, individuals can eat meat, fish, fowl, and eggs without restraint. Therefore, the protocol of a “low-carbohydrate” diet generally is ad libitum. Indeed, all of the aforementioned studies (5-14) follow this design.
The theory behind a low-fat diet for weight loss is less clear. If the hypothesis is that dietary fats are fattening, not the calories, then we should expect the protocol of the diet also to be ad libitum. However, this is not the case. Most “low-fat” diets seem to imply that caloric restriction is included. In fact, in all of the studies referenced above that include low-carbohydrate ad libitum diets, the “low-fat” diets were restricted in calories.
Nutritionists and researchers will point out that fat is more calorically dense (9 kcal/g) than carbohydrates and protein (4 kcal/g), and therefore, if people limit their fat intake, they will also limit their caloric intake. This would imply that the low-fat group would not need to be restricted in calories since they’re restricting fat intake. However, invariably the diet studies include caloric restriction as part of a low-fat diet, which implies that individuals wouldn’t otherwise limit their caloric intake on this regimen.
Many public health authorities hold the assumption that too much dietary fat causes heart disease, and too many calories causes weight gain (i.e., the calories-in/calories-out hypothesis). This is supposedly why the diet studies include caloric restriction as part of the low-fat diet, which in many cases invalidates their research hypothesis.
It would be interesting to observe the results of a low-fat, ad libitum diet compared to a low-carbohydrate, ad libitum diet – or a low-fat, ad libitum diet compared to a low-carbohydrate, calorie-restricted diet; would the researchers note the distinction? You would think they would, however in most cases the investigators didn’t see fit to note that one diet is restricted in calories (low-fat), while the other is not (low-carbohydrate) when discussing the results of their studies.
Low-fat diets have generally been advocated not only for weight loss, but for heart-health as well, based on the diet-heart hypothesis. This is the theory that saturated fat, and in earlier versions (public health authorities are fond of tweaking their hypotheses to maintain them, rather than discard, as would be the case if they were adhering to the scientific method), dietary cholesterol, raise serum cholesterol and raise the risk of cardiovascular disease and heart attack.
Dietary cholesterol has been exonerated by most proponents of the diet-heart hypothesis for its role in significantly altering dietary cholesterol levels and heart disease (16), even by Ancel Keys (17), who many people would credit with creating this resonating implication. It’s also known that our bodies are adapted to adjust serum cholesterol metabolism to dietary cholesterol intake (18). If we eat more dietary cholesterol, our body will adjust by synthesizing less in the body. If we eat less dietary cholesterol, we synthesize more. There are a number of books (19-21, 29, 31) that discuss and dismantle the idea that dietary cholesterol (as well as dietary saturated fat) causes heart disease.
In 1957, Keys proposed a formula for predicting serum cholesterol (22) based on the amount of polyunsaturated and saturated fat in the diet. Keys concluded that dietary saturated fat raised serum cholesterol, while polyunsaturated fat lowered it based on selected short-term data from the same decade, and stated that saturated fat is the primary dietary influence on serum cholesterol.
In 1973, in a critical examination of the diet-heart hypothesis, Reiser (23) noted:
“the message that everyone is in serious danger of coronary heart disease if he does not restrict the amount of saturated fat in his diet is being propagandized by every known medium of communication: lectures, newspapers, radio, television, films, and booklets, with the obvious hope that every listener and reader will apply it to himself. If the question were academic it would not be too serious. Unfortunately, the following on faith of the advice to reduce saturated and animal fat ingestion runs the risk of the consequences of any food fad: extremism and unbalanced diets.”
While the low-carbohydrate diet is deemed faddish by public health authorities, it’s more likely to be the opposite: a high-carbohydrate, low-fat diet is more of a fad than an Atkins diet.
Resier notes that “perhaps the most telling argument” against the idea that saturated fat raises serum cholesterol “comes out of the effort to pinpoint the responsible fatty acids.” Reiser makes the point that short-chain fatty acids, stearic acid, and palmitic acid, all saturated fats, are not effective in raising serum cholesterol. “How is it possible, therefore, to attribute the phenomenon of hypercholesteremia to saturated fatty acids?”
Also of note, the studies on dietary fat and serum cholesterol usually compare saturated fats to vegetable oils, which Reiser refers to as “an error in experimental design leading to erroneous interpretation of results.”
Stephan Guyenet states (24):
“The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect may have more to do with LA lowering blood cholesterol than saturated fat raising it.”
Guyenet points to a 2003 study by Muller et al. (25) with similar conclusions by the authors:
“The most important finding of this study was that lowering total saturated fat in the form of coconut oil, from 22.7 to 10.5 E% without change in the P/S ratio did not lower total or LDL cholesterol, but significantly reduced HDL cholesterol.”
In sum, Guyenet notes, “if saturated fat influences total cholesterol or LDL concentration at all, the effect is modest and is dwarfed by other factors.”
To wit, recent studies have been suggesting that there is no association between saturated fat and cardiovascular disease. Siri-Tarino et al. (26) wrote in The American Journal of Clinical Nutrition in 2010:
“A focus of dietary recommendations for cardiovascular disease (CVD) prevention and treatment has been a reduction in saturated fat intake, primarily as a means of lowering LDL-cholesterol concentrations . . . . In summary, although substitution of dietary polyunsaturated fat for saturated fat has been shown to lower CVD risk, there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate. Furthermore, particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.”
The same authors conducted a meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease (27). They concluded:
“there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of [coronary heart disease] or [cardiovascular disease].”
In August, 2010, researchers completed a study looking at saturated fat intake and mortality from cardiovascular disease in Japan. The authors concluded, “[Saturated Fat] intake was inversely associated with mortality from total stroke, in this Japanese cohort.” Note that in Japan, stroke causes more death than heart disease (28). The authors found that the people who ate the most saturated fat had less (although, not statistically significant) heart attack risk as those who ate the least.
Another point that should be noted is the idea that elevated total serum cholesterol causes heart disease is dubious, at best. This will be discussed later.
Most researchers seem to agree that the weight loss when achieved on a low-fat diet is due to the decreased intake in calories, however, the reduced caloric intake evidently needs to be prescribed by investigators in order for dieters to lower it. Conversely, many of the same researchers will interpret the same findings on a low-carbohydrate diet, that these dieters, too, will decrease caloric intake, however involuntarily since they are not restricted in calories. This may not necessarily be the case, and this will be discussed later, but it’s negligent for the researchers to omit discussion as to why the low-carbohydrate dieters consume fewer calories than baseline.
It’s worth noting that the title of the Foster et al. (5) study excludes the fact that the low-fat group was also restricted in calories, while the low-carbohydrate diet was unrestricted in calories: “Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet.” This is a critical point and will be discussed in future posts.
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