From the time I was a teenager, I always had the notion that the obese must be hiding a significant amount of muscle mass under their layers of fat. This idea came from the notion of progressive resistance training which held that the stimulus for increased muscle mass was being exposed to heavier and heavier loads. I was always told the origins of progressive resistance training were from Milo of Croton the ancient Greek wrestler. Legend was that this ancient strong-man had one at least six Olympic championships and that he trained over the four years leading up to the games by picking up and carrying a calf. As the animal matured, Milo was tasked with carrying a heavier and heavier load. Milo’s progressive weight-training program would culminate with him carrying the full grown bull into the Olympic stadium, carrying it the full length of the field where he would then kill, butcher, roast and eat his training medium.

I reasoned that the obese were very much like Milo. Carrying around with them a progressively increasing load that would necessitate the development of stronger muscles, I expected them to be hiding significantly enlarged muscles. I felt that if the obese would simply strip away their body fat and perform resistance training, they should be able to unveil a very pleasing physique. Consistent with this thinking, when I began training clients, I consistently overestimated the amount of resistance they should use in their workouts. I was always surprised to find that they would struggle and be unable to complete even a couple of reps. As I would adjust the resistance, the amount required would actually be much less than a typical non-obese subject of similar stature. In my flawed thinking, I always assumed this was due to a lack of toughness or discipline. I never considered that their muscles might be profoundly atrophied. After all, they had been “resistance training” their whole life. I would later reason that their “resistance training” was unrelenting, thus never allowing for recovery time and muscle growth. Never once did I consider that their nutritional status might have something to do with the problem.

My blind spot with regard to nutrition was typical of most HIT enthusiasts. Arthur Jones always pointed out that an intense training stimulus was the key to muscle growth. Once the stimulus was applied, any reasonable diet should allow results. It was even argued that progress should occur in the absence of good nutrition since a severe stimulus made muscle growth a survival mechanism. Mike Mentzer often described his feelings on the primacy of training over nutrition by telling a parable of a tanning enthusiast obsessing over the various types of tanning lotions without ever getting in the sun. I also held these beliefs well into my adulthood. Despite observing numerous clients with evidence to the contrary, I wrote in Ultimate Exercise, Bulletin #1 (published in 1998) that one could probably produce good gains on a diet of Skittles if the training stimulus was correct.

For more years than I care to admit, I persisted in these beliefs. I did so in spite of training numerous obese clients who were way weaker than I expected, and also in spite of looking at thousands of CT scans of obese patients. I was first challenged to think about the role of nutrition by Charlie Christian, MD (a Cardiothoracic surgeon and an owner of a SuperSlow training center (www.insideoutsidespa.com)). Dr. Christian gave a presentation at one of the SuperSlow conventions on the importance of Omega-3 fatty acids and Insulin control to metabolic health, and how this can synergistically improve results from high intensity training. Given my HIT background, I was fully prepared to poo-poo his arguments. However, the evidence presented in his lecture was overwhelming and irrefutable. The biggest influence on my thinking in this area came not from a fellow physician, but from an economist. I originally came across Arthur Devany (www.arthurdevany.com) by way of an article on Clarence Bass’ Ripped website (www.cbass.com). Dr. Devany developed the concept of Evolutionary Fitness. I will not attempt to give you a synopsis of his philosophy, but will instead refer you to his website. His insights on diet and insulin sensitivity are astounding and are the source for the discussion that follows.

Because of Dr. Devany, I was able to put together a picture that had been residing in my blind spot for most of my life. The key to the paradox of the obese-yet weak client was insulin sensitivity. The modern Western diet is very high in refined carbohydrates when compared to the diet in our evolutionary past. Also, the average modern human very rarely engages in intense exercise. In the face of very high carbohydrate intake, one’s glycogen stores will become completely full. A 75 kg person will store about 70 grams of glycogen in their liver and about 220grams in their skeletal muscle. Thus one can see that skeletal muscle is the major storage depot for glucose. Once the glycogen stores are completely full, glucose will begin to stack up in the blood stream. The evolutionary-based response is to increase insulin to drive more glycogen storage. However, pushing more glucose into a cell whose glycogen stores are full can be very damaging. The glucose cannot be stored, and instead attaches to other cell components by a mechanism called glycosylation. Imagine pouring honey onto the keyboard of your computer and you get an idea of the metabolic effect of glycosylation in the cell. This seemingly inappropriate response occurs because, from an evolutionary perspective, this is a novel metabolic event.

The only metabolic defense against this situation is to decrease the sensitivity of the insulin receptors on the surface of the muscle cell. Glucose that is stacked up in the bloodstream in the face elevated insulin levels can only have one metabolic destination…synthesis into triacylglycerol. These elevated insulin levels cause a 30-fold increased rate of transport of glucose into the fat cells where it is converted to triacylglycerol (fat). Also, in the presence of high insulin the liver also coverts glucose to fat but attaches it to a protein-coated package for transport to the fat cells (VLDL or very low density lipoprotein). In the chronically overfed state, the body protects itself by decreasing the sensitivity of insulin receptors on the muscle cells and preserving (actually increasing) insulin sensitivity on the fat cells. By this mechanism blood sugar can be held in check without making the interior of the cells a syrupy mess, and energy is stored for future starvation (which never comes). The problem is, insulin not only controls glucose homeostasis, it is a major hormone for nutrient storage and all of the anabolic processes of the body. In the state we describe above, a vicious form of nutrient partitioning begins to occur. Nutrients used for growth and differentiation are shunted away from the muscle and the liver and are diverted to body fat. The muscles become smaller and weaker and the liver becomes infiltrated with fat as it desperately tries to produce VLDL. The liver’s ability to synthesize proteins used for nutrient transport and immunologic function is greatly compromised. When these proteins decline, important nutrients cannot be moved about and the blood loses its osmotic force. The lack of circulating protein causes the blood to be hypo-osmotic. Fluid then moves passively to the tissue spaces to try to equalize osmotic pressure, resulting in a puffy edematous appearance.

Through knowledge of the above mechanisms, I began to notice things about my obese ER patients that I had failed to notice in my 19 years of practice. I began to pay attention to CT scans of patients. The images of CT scans represent transverse slices through the body, much like the slices of a spiral-cut ham. On abdominal CT scans I could really notice the consequences of the metabolic processes described above. The most readily obvious finding is the bizarre appearance of a normal size person entrapped in a fatty prison. In many cases, the cumulative width of the pannus of fat on either side, exceeded the width of the normal person trapped inside. The fat was not just on the surface, though. There was fat in the intra-abdominal cavity, layered on the mesentery between the intestines, and it was marbled throughout the liver, and it was packed around the kidneys. This layering of intra-abdominal fat made CT interpretation easier, as it spread out the organs of interest, and inflammation in the surrounding fat was easy to visualize. Even more astounding than the abundance of fat, was the lack of muscle. The atrophy was truly profound. The rectus abdominus, the internal and external obliques, and transversus abdominus muscles, which are normally 1-2 cm thick were only millimeters in thickness. The lumbar extensor muscles, were so atrophied that open spaces were evident between the cord-like bundles and the muscle did not extend above the spinous processes, or beyond the transverse processes of the vertebra. What, in the well-developed state was as thick as the barrel of a baseball bat, was now smaller than a paper towel tube. For 18 years of practice, I had never really noticed what was in front of my face the whole time.

With this new knowledge in hand I began to find explanations for symptoms that I had never been able to explain before. I even had to coin new diagnostic phrases. The first diagnostic dilemma solved was why so many obese people had ventral hernias. A ventral hernia is a defect in the abdominal wall that allows the viscera to protrude through. Occasionally, the protruding intestines can become entrapped and their blood supply can be strangulated, requiring emergency surgery. These hernias were occurring because the very thin abdominal muscles were being stretched beyond their capacity by the accumulation of intra-abdominal fat. Another diagnostic dilemma that was solved was concerning numerous obese patients with severe bilateral flank pain. These patients had undergone numerous studies including plain-film x-rays, urinalysis, CT scanning, renal ultrasounds and colonoscopy that were all read as normal. These patients would show up at the ER “at the end of their rope”, begging for pain relief. When I looked over their studies with my new perspective in hand, I noticed something profoundly wrong on their CT scans. Normally, when a physician looks at an abdominal CT, he or she is focused on the intra-abdominal structures. What I discovered was the answer was revealed when you focused on the abdominal wall muscles. The flank pain was coming from incredibly thin and weak oblique and transversus abdominus muscles being stretched over the iliac crests of the hip area. These patients were literally bursting at the seams. When I applied an abdominal binder (basically a heavy-duty girdle), their pain went away. I actually had to make up a diagnosis for this one- lateral abdominal diastasis. Obese patients will also commonly present with unexplained pain and paresthesias on the front of their thighs. Numerous studies including MRI of the spine searching for disc herniation fails to find an answer. What I have found is that the weakened rectus abdominus muscle protrudes on its inferior aspect over the inguinal ligament. This produces an impingement of the lateral cutaneous nerve of the thigh and the cutaneous branches of the genitofemoral nerve which causes pain on the front of the thigh. This can also be seen in the later stages of pregnancy for similar reasons.

The important concept behind all of this is not that the obese have these problems just because of excess body fat. These problems occur because of muscle atrophy that occurs as a result of nutrient partitioning that occurs with the metabolic derangements associated with a modern diet. These problems can be reversed by restoring a normal metabolic environment and a return to proper insulin sensitivity. Following a diet that is in line with our ancient ancestors will decrease the massive sugar load of the modern diet. High intensity exercise will empty the largest glucose reservoir in the body, making improved insulin sensitivity possible. The situation is somewhat like a tub overflowing, you want to turn of the faucet and unplug the drain. In short, eat a natural evolutionary-based diet, and workout hard, so that a brief and infrequent workout is necessary. If you do these two things, almost everything else will fall into place. A combination of a hunter-gatherer diet as detailed at www.arthurdevany.com, and high intensity strength training as advocated in Body by Science www.bodybyscience.net will set into motion a reversal of this tragic disorder. Get started today, because it’s a slippery slope to the scooter store.

Doug McGuff, MD