by Joseph Brasco, MD
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Increased Saturated Fats
Of all our nutritional mantras, the one most widely and emphatically proclaimed is the relationship between saturated fats and coronary artery disease. One would think a "fact" so ingrained in our social psyche would be supported by mountains of evidence.
However, the reality is the data to support the "diet-heart hypothesis" is flimsy at best - non existent at worst. In an extensive review of existing studies, Ravnskov came to the conclusion that, "Few observations agree with the diet-heart idea, but a large number have falsified most effectively.
Man's diet possibly includes factors of importance to the vessels or the heart, but there is little evidence that saturated fatty acids as a group are harmful or that polyunsaturated fatty acids as a group are beneficial." In a similar review, Dr. Mary Enig was also unable to find a solid relationship between saturated fat consumption and coronary artery disease. She instead came to the conclusion that the inordinate increase in trans fatty acid consumption was more likely the causative factor.
When discussing the "dietary heart hypothesis", the work of Dean Ornish, M.D., is often cited as clinical evidence for the efficacy of dietary fat reduction. However, while Ornish is a major proponent of the "low fat diet", in his studies a number of coronary artery risk factors are addressed, in addition to the dietary changes.
In Ornish's work, study participants underwent vigorous lifestyle changes, which included smoking cessation, stress management, exercise and a low-fat (near vegan) diet (the only animal products allowed were egg whites and one cup of non-fat milk or yogurt per day).
After following these changes for one year, the experimental group did show an overall regression of atherosclerotic plaque, Ornish's study is extraordinarily important because he was able to demonstrate, in quantifiable terms to the medical community, that lifestyle changes could be as powerful as drugs in managing a serious disease. However, to extrapolate that this study proves the value of the low fat diet is fallacious.
Ornish manipulates four separate variables in his study, all of which have purported association with cardiovascular disease. To suggest that any one variable or combination of variables is more important than the other cannot be concluded from Ornish's data.
Even if diet alone is examined, there are multiple variables within the diet, that in and of themselves could have significance. Was it the omission of trans fatty acids (which have been linked to cardiovascular disease)? Was it the increase of antioxidants provided by the intake of fresh fruits and vegetables? Was it the fact that the experimental group experienced an average loss of 22 lbs?
Again, to conclude that it was the "low fat diet" which was primarily responsible for the experimental group's success (as the study is often interpreted), is quite disingenuous. A factor often overlooked in Ornish's work is the effect of low fat/high carbohydrate diets on lipid profiles. While it is true, the experimental group had an overall reduction in cholesterol, there was a concomitant reduction in HDL cholesterol with an increase in triglycerides.
Numerous recent studies have verified this dietary effect. Of these current studies, Berglund specifically looked at the response of the reduction in dietary total and saturated fats and HDL cholesterol subtypes. The study demonstrated a decrease in dietary total and saturated fat resulted in a significant decrease in HDL2 and HDL2b cholesterol concentrations. The authors concluded that the dietary changes suggested to be prudent for a large segment of the population will primarily affect the concentrations of the most prominent antiatherogenic HDL subpopulations.
Although definitive conclusions for the general population may be premature, in individuals demonstrating evidence of hyperinsulinemia and dyslipidemia (i.e. - Syndrome X) carbohydrate restriction is imperative for improved lipid profiles. In nutrition, as well as in life, balance is always the key. Nowhere is balance more crucial than in the discussion of dietary fats.
ANY diet, whether it be high fat - low fat (or anything in-between), if it promotes imbalances in fatty acid profiles, will in the long run have negative health consequences. In the mid '50s, the biochemist, anthropologist, and explorer Hugh Sinclair suggested an alternative explanation for the relationship between dietary fat and cardiovascular disease.
Sinclair noted that several people groups existed that consumed relatively high amounts of fat and yet were free of heart disease. Sinclair detailed the dietary habits of the Eskimos (previously discussed); the Masai people of Kenya who ate large quantities of ruminant milk and meat; and Jamaicans who ate large amounts of saturated fat in the form of coconut oil. All three groups, all consuming high fat diets, were relatively free from heart disease.
Sinclair suggested that the polyunsaturated profiles of these diets were protective, and concluded that the rise in cardiovascular disease was more related to their exclusion from the diet rather than the inclusion of saturated fats or cholesterol. Since Sinclair's day, our biochemical understanding of fat has increased exponentially. We now realize it is not just the polyunsaturated content of the diet, but the ratio of N-6 to N-3 polyunsaturates that may ultimately determine health.
Both dietary extremes discussed fail to introduce balance in this ratio. High carbohydrate diet due to their high grain and plant content will ultimately be low in N-3 fats (especially long chain N-3 fats - i.e. EPA/DHA), thus unbalancing the N-6/N-3 ratio. Low carbohydrate diets, in their popular form, rely heavily on commercially raised grain-fed meats and poultry (the fatty acid profile of the meat from wild game, free range beef and poultry have a significantly higher N-3 to N-6 ratio), eggs (free range hens also make better eggs) and cheeses.
A diet based on these foods will also greatly unbalance the N6/N3 ratio. Although the precise ratio remains controversial, the N6/N3 ratio should probably be in the range of 4-3/1 to optimize human health, western diets rich in vegetable oils, cereal grains and grain fed live stock, drive this ratio to an unprecedented 50-10:1. This imbalance may have implications in a host of diseases, including hyperinsulinemia, artherosclerosis and tumorgenesis.
When the diets of hunter-gatherer populations are studied, authors have concluded that their N6/N3 ratio varied between 4:1 to 1:1. This ratio appears to be biologically optimal. Based on these considerations, investigators, have advocated a return to dietary ratios of ancestral humans. A diet based on lean meats (wild game or free range livestock), fish, raw nuts and seed, vegetables, low glycemic fruit (paleocarbs) - "an evolutionary diet" - not only will be helpful in the management of obesity, but in a host of other common western diseases, including cardiovascular disease.
Dietary Protein and Cardiovascular Disease
Multiple recent studies have demonstrated the benefit of dietary fats (especially N-3 polyunsaturates and monounsaturates) in cardiovascular disease and in the reduction of cardiovascular risk factors. A more recent study trend has examined the possible beneficial role of dietary protein.
Wolfe has published numerous articles demonstrating the positive effects of the isocaloric substitution of protein for carbohydrate on lipid profiles. His studies have demonstrated a decreased LDL-C, an increased HDL-C, and reduction of triglycerides, thus reversing the dietary effects of increased carbohydrates. Wolfe states that substitution of carbohydrate for fat in the diet results in a reduction in HDL apoprotein transport rates along with increased catabolism of apolipoprotein A-1.
The decreases in plasma VLDL and LDL resulting from substitution of protein for carbohydrate in the diet may relate to either increased catabolism or decreased production. Thus, according to Wolfe's work, the simple dietary substitution of protein for carbohydrate could have profound health benefits.
Wolfe's data has recently been validated by Hu. In this study the dietary habits of over 80,000 women were examined. After controlling for variables, high protein intakes were associated with lowered risk of ischemic heart disease. Both animal and vegetable protein sources were protective. This inverse association was noted in women on both low fat or high fat diets. Wolfe's and Hu's work both indicate that dietary protein has cardioprotective properties independent of those of dietary fat.
Given the multiple health benefits ascribed to N-3 polyunsaturates and the evolving data regarding dietary protein - fish may be one of the best foods for human consumption. In a fascinating piece of epidemiological work, Marcovina compared 2 racially homogenous Bantu populations from Tanzania. The only appreciable difference between the groups was their dietary habits.
The Bantu living closer to the shore had a predominantly fish based diet, while the inland Bantu consumed an essentially vegan diet (a diet devoid of animal products ). When plasma lipoprotein (a) (an independent cardiovascular risk factor) levels were compared, those among the fish eating population were 40% lower. This suggests another cardioprotective aspect of fish consumption.
In a recent study by Mori, he demonstrated the inclusion of fish in a weight loss program yielded greater results than either fish consumption or weight loss alone in their obese subjects. The experimental group in their study demonstrated improved glucose, insulin and lipid metabolism, as well as greater reductions in blood pressure, heart rate and weight loss versus controls. This study suggests a novel approach to the dietary management of obesity and NIDDM.
Perhaps the most influential of the studies looking at the benefits of fish, was the Diet and Reinfarction Trial (also known as the DART trial). In this study, the authors demonstrated that the addition of a modest amount of fish (2-3g of EPA per week or the equivalent of 300g of fatty fish per week) reduced post myocardial infarction mortality by about 29% when compared to controls.
One of the more interesting aspects of the study was that the control group was instructed on the standard fat reduction diet and on average had lower cholesterol levels than did the experimental group. The authors theorized that the fish oils had a favorable effect on clotting mechanisms and blood platelets, as well as a potential anti-arrhythmic effect on the ischemic heart. The results of this study are profound, especially given the modest and otherwise innocuous interventions undertaken.
Given the evidence of the benefit of N-3 polyunsaturates, coupled with the potential benefits of dietary protein, fish clearly is a biologically superior food source. The isocaloric substitution of fish for dietary carbohydrates is not only evolutionary appropriate, by may have untoward health benefits from weight control to improved glucose homeostasis to cardiovascular disease prevention.
Risk of Osteoporosis
Of all the potential negative side effects of dietary protein, the issue of osteoporosis is perhaps the most difficult to resolve. The literature is greatly divided on the topic, and clear recommendations are hard to find. In a recent study, Munger found that the intake of dietary protein, specifically from animal sources was associated with a reduced incidence of hip fractures in post menopausal women.
In the articles' discussion, a brief review of protein's controversial role in osteoporosis was undertaken. In the studies showing a potential benefit (as in the author's paper), it has been theorized that dietary protein may strengthen bone by its effect on the structure and function of bone-related proteins.
In studies demonstrating a negative effect, it has been argued that dietary protein (especially in the form of animal based protein) is a primary source of acid ash, which results in the acidification of urine. In order to buffer the urine and maintain acid-base homeostasis, calcium salts are mobilized from the skeleton, resulting in a net calciuria. Over time, this buffering of endogenous acids may contribute to a progressive decline in skeletal mass and, ultimately, lead to osteoporosis.
However, Wachman and Bernstein, the two authors who originally postulated this mechanism for osteoporosis, theorized that by increasing the dietary alkaline ash this process could be halted.
In a study by Sebastian., he was able to reduce calicuria and improve overall calcium/phosphorous balance by the administration of potassium bicarbonate as a buffering agent to postmenopausal women consuming an acid promoting diet. The authors suggest that potassium bicarbonate could be administered long-term as a novel means of preventing and treating postmenopausal osteoporosis.
In a 4-year longitudinal study by Tucker, he was able to demonstrate that a greater bone mineral density was associated with increased dietary potassium and magnesium levels, as well as increased consumption of fruits and vegetables. The authors concluded that this positive association was due to the beneficial effects of potassium and magnesium on calcium balance and bone metabolism, as well as the buffering properties of increased alkaline ash in the form of fruits and vegetables.
Given the divergent nature of the theories, it is highly probable that both have merit. With respect to protein's beneficial effects, protein is certainly necessary for proper bone matrix formation and metabolism. It is likely a chronic suboptimal intake will jeopardize this function. One could conjecture that the studies finding a negative association between protein and osteoporosis have somehow highlighted this aspect of the equation. Those studies finding a positive association between protein and osteoporosis are probably looking at the endogenous acid production issue.
In an article by Remer, he calculated the potential renal acid load (PRAL) of frequently consumed foods in order to help dietitians design diets of varying urinary pH. On their list, animal protein sources (as expected) were calculated to increase PRAL.
However, grain products, legumes and dairy products (especially hard cheeses) also increased PRAL. In fact , according to Remer's data brown rice had a greater PRAL than any of the meat products examined (with the exception of canned corned beef - if you want to call that meat).
Perhaps the most ironic of all, was Remer's finding that cheeses had the highest of the calculated PRALs. Parmesan, cheddar, and processed American cheese had PRALs almost 2 times any meat product. In light of Remer's data, the relationship of protein and osteoporosis cannot fully be determined without addressing the total dietary PRAL. The type of protein being consumed (lean meats vs. Processed meats vs. Cheese) and the other foods in the diet are likely to significantly affect the study's outcome.
The protein osteoporosis controversy was addressed in a review article by Spencer. According to the author, numerous studies have been published on the calcium-losing effect of protein. However, several aspects of the study conditions have to be considered in the interpretation of the results.
Some of these are the type of protein, such as purified proteins (which seem not to promote calciuria): the duration of the study (there may be a transient increase in calciuria followed by a normalization or reduction); whether the phosphorous (which has an independent calcium sparing effect) intake remained the same, was increased, or decreased; whether the diets were under strict control or with outpatient volunteers; whether the protein intake was changed from a low to a high protein intake or was changed from a normal to a high protein intake; and whether excessively high protein intakes were used.
All these factors affect urinary calcium excretion during high protein consumption. After reviewing the available data, based on the aforementioned criteria, the authors concluded, "to our knowledge, no convincing data have been published showing that a high protein diet, using complex proteins for prolonged periods of time under strictly controlled dietary conditions, causes calcium loss."
It is quite obvious that the role of dietary protein in calcium homeostasis is complex and multifactorial in nature. However, given the work of Remer, it may actually be the net PRAL of the diet that is most important in influencing the development of osteoporosis, rather than the diet's absolute protein content. Since most of the current low carbohydrate diets encourage the ample consumption of vegetables, this is likely to offset any potential acidifying effects of increased dietary protein.
In fact, given most individuals do not consume enough vegetables and fruits, these diets are likely to promote better acid-base balance then the average American diet. Unlike the more modified low carbohydrate diets, modern ketogenic diets may pose a risk for calciuria since they rely heavily on animal protein, cheeses, and cured meats, and are usually not salt restricted (the Cl ion- not the Nat ion - can also cause a renal acid load and subsequently calciuria).
However, since most people are in ketosis for only a short period of time (after which they are theoretically supposed to transition into a modified low carbohydrate diet), it is unlikely that these diets will significantly contribute to an individual's overall risk for osteoporosis.
Kidney and Liver Damage
While it is generally accepted that people with pre existing kidney and liver disease will benefit from some level of protein restriction there is no data to support proposition that increased dietary protein will actually cause kidney or liver damage.
In a study by Blum, he examined the kidney function of a group of healthy individuals consuming an ad lib. high-protein diet, as compared to a group of healthy vegetarians (Isn't that an oxymoron?). At the study's end, the authors concluded that protein does not affect kidney function in normal kidneys, and it does not influence the deterioration of kidney function with age.
The relationship of protein and the liver is somewhat more complex. Although there is no evidence that increased dietary protein will cause permanent liver damage, there is an actual dietary "protein ceiling". According to Rudman there is a lever at which dietary protein intake can exceed the liver's ability to metabolize it to the urea, thus leading to a build up of intermediary metabolites. These metabolites can subsequently lead to a toxic state in the affected individual.
The level of protein at which this will occur varies, but it is thought to be possible when protein makes up 30-40% of the calories in an eucaloric diet (the percent calories from protein can be higher in a hypocaloric diet).
"Rabbit Starvation" (a term coined by V. Stefansson to describe the phenomenon of excessive dietary protein) often occurred among explorers who would live for long periods of time on extremely low fat small game animals (i.e. rabbits). The condition was marked by nausea, vomiting, weight loss and fatigue. "Rabbit Starvation" was reversible when the percentage of daily calories from protein began to drop. Although the "Rabbit Starvation" phenomenon could effect an individual consuming a ketogenic diet, it is highly improbable.
In general, if one is consuming commercially available meats (even chicken), the percentage of calories from fat would be too high to induce this condition. In the modified low carbohydrate diets, due to the varied food sources, the risk of protein toxicity, for all practical purposes, is non-existent.
Conclusion
A critical reading of the current literature certainly supports the dietary trends of decreased carbohydrate intake (especially of neocarbs), increased protein intake, and increased fat intake (especially of monounsaturates and N-3 polyunsaturates). The data that supports these contentions comes from a wide spectrum of disciplines, including the basic sciences, medical science, epidemiology, and anthropology.
The one dietary program that addresses these principles in full, is the so called "evolutionary diet." The modern inception of this prehistoric lifestyle would favor the consumption of lean meats (preferably wild game or non-grain fed, free-range domesticated animals), fish, seafood, vegetables, fruits, raw nuts, and seed. Notably absent from this dietary genre are dairy products, cereal grains, beans, legumes and concentrated sweets (except for perhaps the occasional foray into raw honey!).
Adherence to these dietary guidelines will not only address obesity, but may also prove helpful in the management of everything from NIDDM to diseases of autoimmunity to cardiovascular illnesses. The guidelines are broad, but can be made quite specific depending on the goals, lean body mass, activity level, and overall health of the patient.
In the last few years, there has been a literal explosion of data in the nutritional sciences. Sometimes when addressing this data, we are put in the uncomfortable situation of realizing that today's facts are rapidly becoming tomorrow's fiction. However, by keeping an open mind and always questioning what we think we know, we will be able to provide our patients with the best and most innovative care possible.
Dr. Mercola's Comment:
My congratulations to Dr. Brasco for compiling such an outstanding review of the concerns that some have when confronted with the "low carb" diet. Dr. Brasco is a close personal friend and is also the physician who covers for me when I go out of town.
He is an internist and gastroenterologist and I believe one of the best in the country. It is a strange paradox of medicine that most GI specialist know virtually nothing about nutrition. That is certainly not true of Dr. Brasco who is clearly one of the leading nutritional GI specialists in the country.
I typically warn my patients that the diet recommended is NOT low carbohydrate but full of vegetables which are the good carbohydrates. Dr. Brasco provides an incredible review of the literature and some very sound scientific support for what appears to be the diet most of us were designed to eat.
I frequently explain to patients that part of the reason for the confusion on the carbohydrate issue is the fact that not all carbohydrates are created equal. The glycemic index mentioned above is one science tool that is used to explain this, but most patients have a hard time with this concept.
I give them an analogy to think of grains and most below ground vegetables as a simple train. Each car in the train represents a simple sugar molecule which is easily broken down once it reaches the digestive system.
I then ask them to visualize that same train but this time stacked 20 to 50 high with other trains and each train care interconnected to the cars above them. This is an accurate representation of the much more highly complexed and branched sugar molecules that are present in most above ground vegetables.
They have multiple bonds connecting each of the sugar molecules and take the body a long time to break them down. The extra time allows the body to slowly use the sugar and thus not have to secrete large amount of insulin to store the excess.
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