During the 1950’s, scientific research on the biochemical mechanisms dictating fuel use confirmed that the elimination of carbohydrate from the diet in a rat for only a few days led to a loss in the ability of its liver to convert carbohydrate (glucose) into fat. The rate of fat-making from carbohydrate depends upon the quantity of carbohydrate available.

This is a very important point to remember as we proceed: the primary issue related to fat-making from carbohydrate — the ability to release fat from one’s fat stores and the ability to burn fat as fuel — depends upon one’s total daily exposure to glucose rather than upon the rate of its appearance in the blood

These early studies also looked at how interventions, such as various sorts of feeding, variations in diet composition, and even starvation, affected animal tissues. Striking changes were noted in the enzyme systems of animals that had been starved and then re-fed. Starvation for as few as forty eight-hours, followed by re-feeding, led to a one thousand-time increase in the enzymes that convert carbohydrate into fat!

Today, it’s well understood that these metabolic changes begin to occur within minutes of a change in the internal environment. In other words, exposure to glucose can cause an increase in the principal glucose-to-fat converting enzymes within minutes. Yet, on the other hand, as we’ve seen, changes at the cellular level and at the whole body level can often take several months to become fully developed. Adaptation time varies according to the tissue or cellular machinery under investigation.

Several popular diet books preach low-carbohydrate eating for five days, re-loading with a high-carbohydrate diet on the weekendfor the purpose of reloading the muscle’s glycogen, and then resuming the low-carbohydrate diet on the following Monday.

Based on what we’ve learned to this point, it’s clear how foolhardy such a regimen is; its basis resides in the supposed importance of glycogen for muscle building and endurance. One author goes so far as to say that fat-building won’t “turn-on” within the span of a forty eight-hour weekend. Sadly, this medical doctor hasn’t learned much about how enzymes work: It’s a scientific fact, well established in the literature that the five days of carbohydrate restriction (taught in this regimen) actually increase the ability of the enzymes to convert carbohydrates to fat.

When high rates of enzyme activity meet the large amounts of ingested carbohydrates that are generated in the weekend’s carb-loading phase, rapid fat-making from carbohydrate begins immediately, within minutes.

Considering the amount of information that’s available about organism adaptation, the true student in this field is surprised that so many obesity researchers, even those with training in biochemistry, fail to take all this information into account.

One of the leading and best-known medical Establishment doctors, Dr. J. P. Flatt from the department of biochemistry at the University of Massachusetts Medical Center seems totally unaware of these adaptations. Flatt has written extensively about his notion that carbohydrate balance is at the root of the obesity epidemic. He claims that evolution has led to a regulatory system that prioritizes adjustments of protein and glucose burning relative to the intake of protein and carbohydrates (glucose). This evolutionary priority, he says, takes preference over any attempt by the body to maintain fat balance.

He understands, however, that the fuel mix, burned by the body, is controlled by the fuels themselves and by the body’s hormonal response to these circulating fuels. Flatt is convinced that glycogen is important to blood glucose concentration and, therefore, attributes an undue importance to glucose (and glycogen) that isn’t supported by the best of current research. This, of course, is a central feature of the scientific belief based on glucose as the body’s primary fuel, biasing all of his science because the basic assumption upon which he draws his conclusions is flawed from the outset. Based on his observations, he has concluded that, over time, carbohydrate burning is essentially equal to its intake. His recommendations to people include restricting fat intake to avoid regaining weight after periods of dieting. His rationale is that body fat accumulates from the storage of dietary fats, not from the conversion of carbohydrate into body fat.

In his studies, technologically sophisticated, Dr. Flatt has committed the cardinal sin: failure to understand the relationship between carbohydrate and fat in the diet and, hence, failure to understand their consequent disposal. In his studies, he adds varying amounts of fat to the diet of someone habituated to carbohydrate consumption and then tests his ability to burn fat.

The ability to burn fat is a direct function of the amount of carbohydrate in the diet: the more carbohydrates that are consumed, the more the body loses its ability to burn fat.

Carbohydrates convert into body fat, and the newly formed fat is diverted into storage and away from burning because it blocks the metabolic pathways that lead to its own burning. As we’ve learned, any fat consumed along with the carbohydrate is diverted into storage as well because the pathway to fat burning is shut down.

In his studies, Flatt feeds fat along with carbohydrate and also experimentally over-feeds his subjects. His measurements of the subjects’ ability to oxidize (burn) fat are made on the day of the feeding experiment, or on the next day, but never after a longer interval to see how time affects fat burning through the mechanism of adaptation.

In all cases, the subjects are unable to burn the fat that’s consumed. To Dr. Flatt this means that there’s a lack of direct regulatory mechanisms which adjust fat burning to fat intake. These errors in fat balance, according to Dr. Flatt, become cumulative and gradually lead to an increase in the body’s fat mass. He recognizes that fat burning can increase but believes that this occurs only when one becomes fat. He also confuses his terms and argues that it’s a tenet of nutrition science that high-fat diets increase the incidence of obesity. If his research had been more wide-ranging, he would have understood that the high-fat diet, discussed in the studies he quotes, is always associated with a concomitant high level of carbohydrate intake.

Dr. Flatt’s influence upon his scientific colleagues and the medical and scientific communities of which he is a member has been profound; they have tended to accept his theories without protest. Examples of such unquestioning acceptance follow in the words of excellent scientists who’ve made extraordinary contributions to traditional science. This is, of course, yet-another example of the constraints imposed by a faulty belief system upon what should be unhampered scientific vision. Even those at the highest level of the Academy don’t escape criticism on this score. These misrepresentations then filter out into the news media through journalists and, then, out into society via journalism and its layman “experts.” Dr. Neil Ruderman, one of the most respected researchers working in obesity, diabetes, and pure research, recently referenced Dr. Flatt’s work:

Also relevant to this issue is the notion that obesity is a disorder of fat partitioning. This conception is based on the observation that humans and experimental animals generally are able to adjust rates of carbohydrate and amino acid (protein) oxidation (burning) to the amounts of these nutrients in their diet, but they are less able to adjust fat oxidation to fat intake. It has been suggested that for this reason some humans and experimental animals are more prone to obesity than others when placed on a diet with high-fat content. Although the notion of fat partitioning has led to many recommendations concerning the fat content of our diet, a mechanistic explanation for the adipogenic (fat-making) effect of a high-fat, high-calorie diet, has not come forth, nor is it clear why certain individuals and animals are more likely to become obese than others when ingesting it.

Dr. Ruderman is, undoubtedly, unaware of the interrelationship between carbohydrate and fat use throughout the whole range of a widely varying intake of different proportions of carbohydrates and fat. His viewpoint is that of a respected scientist, but one who is still a captive of the regrettable glucose belief system. As we’ve learned, the studies that related high-fat diets to obesity always used diets that were made up of a mixture of carbohydrates and fat. It seems that this brilliant researcher is unaware that in these studies the carbohydrates have never been reduced to a point or level that would truly indicate what happens to human physiology when it’s subjected to a true low-carbohydrate diet.

Dr. J. D. McGarry, recently deceased, formerly of the University of Texas Southwestern Medical Center, also reflects a viewpoint similar to Dr. Ruderman’s. Dr. McGarry was technically one of the best metabolism researchers in the world and his contributions to our understanding of metabolism are unparalleled. In 1980, he and his group were able to finally unravel the complexities of fuel metabolism, putting a close to a frantic research effort that had been on-going during the previous fifty years. Nonetheless, his vision was profoundly constrained by the glucose-loving belief system within the constraints of which he labored. In a discussion that I had with him while writing Ultimate Diet Secrets, the furthest he could go in agreeing with my thesis was that the low-carbohydrate diet might be interesting to look at. In his recent paper describing the cause of Type 2 diabetes Dr. McGarry wrote:

The concept that a lower than normal capacity to burn fat might be a predictor of insulin resistance receives support from both human and animal studies. For example, Astrup et al. showed that obese women who achieved a normal bodyweight by caloric restriction did not increase lipid oxidation appropriately in response to a fat meal when compared with women who had never been obese…

Kelly et al. showed directly that in obese humans the muscle bed has a diminished capacity to oxidize (burn) fatty acids. The above considerations lend weight to the notion that a substantial ability of muscle to oxidize fatty acids is an important contributor to the genesis of insulin resistance.

He concludes this landmark paper by suggesting that the development of new drugs might increase the capacity of the enzymes that dictate a muscle’s fat-burning capacity. Unfortunately, he’s unaware that we have the power to do exactly that right now, without expensive and dangerous drugs: All that we need to do is reduce our carbohydrate intake below a certain threshold. This, of course, along with exercise, is the answer and solution to Type 2 diabetes. I argue, therefore, that glucose is directly responsible for the rapidly growing number of diabetics and that one of the actions causing this disease is the process of glycation, as we’ve seen.

The most fascinating feature of Dr. McGarry’s 2002 paper is that it is an important first shot in a long-awaited revolution: the overthrow of the glucose-loving belief system and the triumph of the as yet unaccepted changeover to a belief that fat is good, as long as carbohydrate is restricted. Sadly, with his death, he’ll no longer be able to participate in that revolution. In his paper, he makes a list of all that we know, and don’t know, about diabetes. In his work, Dr. McGarry suggests that the impasse in solving the dilemma of the cause of diabetes may relate to the fact that our traditional campaign has been largely glucose-focused and that a more fat-focusedapproach may be better rewarded

In Dr. McGarry’s view, the diabetic state is caused by a breakdown in the body’s ability to handle fat and is, therefore, not primarily a disturbance in sugar metabolism. This is an earth shattering proclamation because the focus of diabetes research and treatment has always been directed to strategies having to do with glucose.

It’ll be decades, if ever, before clinicians who treat and study diabetes accept the idea that diabetes is fundamentally a disease in which there’s a breakdown in the body’s ability to deal with fat and that the disturbance in its ability to handle glucose is secondary to the fat-handling problem.

It’s my contention that the fat-handling problem is directly related to the body’s inability to deal with large amounts of glucose as well as fat and glucose together. The response to glucose consumption is a disruption in the ability to deal with fat. This is why I argue that one of the primary solutions to Type 2 diabetes lies in consuming fewer carbohydrates.

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