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First let's sum up what we want to do in terms of maximizing bodyfat loss during a diet. In the most general sense, we want to accelerate the rate of fat utilization by the body. Not only does this increase fat loss, it will exert a protein sparing effect. Let's look at how we might accomplish this dietarily.

By using MCT or DAG, we can provide dietary fatty acids to tissues like the liver and muscle at a more rapid rate. But that's only part of the picture and the low-carbohydrate phase is not very high in fat as you'll soon see. Quite in fact, you'll only be allowed a relatively small amount of fat during the diet phase but, if possible, that fat should come from either MCTs or DAGs. Coconut oil, which is half MCT can also be used.

We also want to accelerate the processes of mobilization from the fat cell, transport (via increased blood flow), and utilization in the muscle. Let's look at each.

First we want to lower insulin levels, which is easily accomplished by reducing dietary carbohydrate intake. This will have a natural effect of increasing catecholamine levels (especially in the first few days of carb restriction), but we can do more. Exercise is a natural choice, of course, and both weight training and aerobics (or interval training) will enhance catecholamine output (this effect is further enhanced on low-carbohydrates). Compounds such as ephedrine/caffeine or clenbuterol also enhance nervous system output, increasing fat mobilization (and possibly utilization in skeletal muscle). Both have anti-catabolic (protein sparing) effects.

So now we have enhanced nervous system output, both adrenaline and noradrenaline. Depending on the ratio of beta-1,2 to alpha-2 receptors in the fat cell, we might get a potent fat mobilization signal (high beta-1,2/low alpha-2) or a poor fat mobilization signal (if there are a lot of alpha-2 receptors and not very many beta-1,2 receptors). As mentioned, stubborn fat is known to have more alpha-2 receptors; this is especially true for women's hip and thigh fat and

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somewhat true for men's abdominal and low-back fat. As it turns out, beta- and alpha- receptors also affect blood flow to the fat cell; beta-receptors increase blood flow and alpha-receptors inhibit it. Though I'm not aware of any direct data, I suspect that the circulation to women's hips and thighs (and perhaps men's ab fat) has a preponderance of alpha-2 receptors which decrease blood flow.

As mentioned before, thyroid has a profound effect on adipose tissue blood flow but, short of using thyroid medication, there's not much we can do here. Fasting increases blood flow to fat cells and low-carbohydrate/ketogenic diets effectively mimic fasting. Aerobic exercise also increases blood flow to adipose tissue in addition to its other effects on calorie burning.

So, you ask, is there any way to inhibit alpha-2 receptors? Several years ago, Dan Duchaine introduced the world to yohimbe, a natural compound that inhibits alpha-2 receptors. Although not perfect orally, regular use (0.2 mg/kg of bodyweight) seems to help. Unfortunately, yohimbe (especially the bark) tends to cause side effects: sweating, a racing heart, and other problems. Yohimbine HCL (the drug form) eliminates many of these problems but poor blood flow to fat cells still limits its usefulness.

Given enough time, yohimbe will build up in the tissues and exert a greater effect (it's also likely that yohimbe improves blood flow to the fat cell). Recently, there have been a slew of topical yohimbe creams that purport to isolate the alpha-2 inhibition to the fat cell; you rub them on your stubborn fat areas and then go do cardio.

As it turns out, there is a dietary way to inhibit alpha-2 fat cells: raising blood fatty acids. When you lower carbohydrates to 20% of total calories or below, blood fatty acids increase (as a side-benefit, the catecholamine response to exercise is also increased when carbs are lowered this much).

After 3-4 days of exposure to fatty acids, alpha-2 receptors become inhibited naturally (without the side effects of oral yohimbe). Combined with aerobics, this is a potent way to get rid of stubborn fat. It also explains the previous observation that low-carbohydrate diets make mobilization/loss of women's stubborn fat easier: between the lowering of insulin and the fatty acid mediated inhibition of alpha-2 receptors, those fat areas were easier to get rid of. Of course, decreasing carbohydrates fits in nicely with our goal of lowering insulin in the first place.

So now we have large amounts of fatty acids floating around in the bloodstream. While this will, in general, increase fatty acid utilization by the body, we can do more. By depleting muscle glycogen with weight training (or even intensive endurance or interval training), we can upregulate CPT activity and enhance fat oxidation in the muscle. Depletion of liver glycogen (via carbohydrate restriction and exercise) will do this in the liver as well. As I mentioned previously, glycogen depletion also sets us up for compensation (and an anabolic rebound) later in the cycle.

Fundamentally, all I have described is a low-carbohydrate/ketogenic diet coupled with training which happens to address most, if not all, of the processes we are trying to optimize for fat loss. Which makes this as good a place as any to discuss ketosis.

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