In my experience, speaking with thousands of people about insulin resistance and disease, some health practitioners find my evidence-based conclusions hard to accept.
Specifically, some wrestle with the idea that dietary fat is an essential part of a healthy diet and that, rather than fat, carbohydrates are the nutrient that warrants scrutiny. My study and ultimate appreciation for dietary fat started with the realization that dietary fat is the only nutrient that does not increase insulin and by helping maintain lower levels of insulin, dietary fat is the one nutrient that helps most with insulin sensitivity.
In this instance, two topics in particular often need to be resolved: 1) obesity and 2) heart disease. And rightly so; global levels of obesity continue to increase and heart disease is the leading killer. However, even more prominent than obesity or heart disease is insulin resistance—the single most common health disorder in the world (affecting half of all adults in the USA, Mexico, China, and India); and insulin resistance increases obesity and heart disease! And this matters.
Calorie vs. Hormone
As we learn more about the powerful and essential role of the hormone insulin to promote fat gain, we invariably are forced to reconcile the fattening effects of insulin with the laws of thermodynamics. If hormones (i.e., insulin) make us fat, and it is impossible for an organism to gain fat without increased insulin, how do we account for a caloric imbalance?
We all accept, whether we acknowledge, that the energy we consume in food has two metabolic/thermodynamic fates: it is stored or used. This prevalent paradigm is what causes us to look at fat gain or loss as contingent on being in caloric gain or loss, respectively. However, changing the way we eat changes the math.
A LCHF diet has more “wiggle room” regarding caloric balance than the traditional LFHC diet. This is why people adhering to a calorie-unrestricted LCHF diet can lose more fat than people following the classic calorie-restricted LFHC diet , despite significantly more calories .
First, a LCHF diet increases metabolic rate. The best example of this is a study that rotated obese and overweight subjects through four diets that differed in composition of fat and carbohydrate. Importantly, all of the diets were isocaloric—the number of calories the subjects were consuming was identical throughout. Metabolic rate (measured by resting energy expenditure) was the lowest during the lowest-fat diet and increased steadily through the four diets as fat content increased and carbohydrate content decreased. In the end, the metabolic rate of subjects when on the LCHF was roughly 100 calories per day higher than when these same subjects adhered to a LFHC diet .
Second, a LCHF diet introduces a third option for energy. Rather than having to be stored or used, a LCHF diet allows energy to be simply lost from the body. By keeping insulin low, the liver makes ketones from fat and while ketones can be and are used by the body for energy, they are also removed from the body through urine and breathing. This is unique to ketones—these little pieces of fat allow the laws of thermodynamics to remain in place while providing a novel “bypass”.
Dietary Fat vs. Plasma Fat
The fat in our blood appears to matter very much for heart disease risk. However, against popular sentiment, the fat we eat is not the fat circulating in our blood.
Cholesterol levels in the blood are one of the most sought after blood markers for one’s risk of cardiovascular complications. They may also be one of the most misunderstood. For decades, we have vilified cholesterol due to its apparent role in causing cardiovascular problems like atherosclerosis. However, since the very beginning of the onslaught, scientists have argued that cholesterol is a terrible predictor of heart disease and mortality. Within the discussion of cholesterol, the cholesterol carrier known as the low-density lipoprotein (LDL) has been labeled the great villain of heart disease for decades, despite conflicting evidence .
With LDL in the crosshairs, dietary fat became the match that lights the fuse—eating more fat can raise total cholesterol levels in part through increased LDL cholesterol levels. However, a few decades ago we learned that LDL cholesterol is not a series of identical molecules—they can vary in size and the size of the LDL particle matters. People with smaller, more dense LDL particles, referred to as “pattern B”, are roughly three times more likely to experience a heart attack when compared with people whose LDL particles are larger and more buoyant, known as “pattern A” . Theoretically, the size of the particle is important due to its likelihood of invading the walls of blood vessel and initiating the cascade of events that leads to atherosclerosis. Naturally, the smaller and denser particle is able to invade the blood vessel wall more easily than the larger and buoyant particle.
Paradoxically, eating more fat prompts LDL cholesterol to be more “pattern A”—it produces a larger and buoyant LDL particle in the blood. One study revealed this finding by placing 20 men on either a traditional high-carbohydrate diet or a low-carbohydrate ketogenic diet for six weeks . Not only did insulin come down significantly, but on average the subjects on the carbohydrate-restricted diet experienced an increase in LDL size. Importantly, even those who were considered “pattern B” subjects became demonstrably more “pattern A” due to the increased LDL particle size. A second study conducted an almost identical dietary intervention, but followed over 100 subjects for six months . Total cholesterol dropped more in the low-fat group than the low-carbohydrate group, but, once again, in addition to greater weight loss and reductions in insulin, subjects in the low-carbohydrate ketogenic diet group had substantially greater improvements in LDL particle size. In particular, the number of large LDL particles almost doubled, while the low-fat group had no change.
Unfortunately, the process of determining LDL particle size is not as simple as most blood tests; the specific laboratory test is not widely available, is expensive, and has not reached widespread clinical awareness or practice. Thankfully, there is a surrogate marker that can be used as an estimate of LDL size. By comparing the levels of two blood lipids that are always measured, namely triglycerides and HDL cholesterol, we receive a ratio that can accurately indicate LDL size. Specifically, by dividing triglycerides (in mg/dl) by HDL cholesterol (in mg/dl), a number around 2.0 and above suggests a person very likely has a preponderance of small, denser LDL particles (i.e., pattern B). In contrast, having a ratio less than ~2.0 equates to tending to have larger, buoyant LDL particles (i.e., pattern A) [429, 430].
By accepting the utility of the TG:HDL ratio, we are able to look at more evidence to explore the effect of diet in more detail. One noteworthy study separated subjects into one of three groups: 1) a calorie-restricted low-fat group; 2) a calorie-restricted moderate-fat Mediterranean diet group (with more fat coming from fish and nuts); and 3) a calorie-unrestricted low-carbohydrate group. Again, the group eating fewer carbohydrates had the greatest changes; the low-carbohydrate group, despite eating as much as they wanted (and losing the most weight), had the greatest reduction in TG:HDL ratio, with the moderate-fat group in second place and the low-fat group coming in last with the least degree of TG:HDL reduction.
About Benjamin Bikman, Ph.D. – Ben earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. Currently, his professional focus as a scientist and professor (Brigham Young University) is to better understand chronic modern-day diseases, with special emphasis on the origins and consequences of obesity and diabetes. He frequently publishes his research in peer-reviewed journals and presents at international science meetings.
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