You’ve learned a lot about fat loss in the last chapters. You've wrestled with catabolism and metabolic slowdown. You've taken a crash course in thyroid management. Many of you could jump into the diet right now and lose a good amount of weight, and might be able to reach your goal of a single-digit body fat percentage. However, many of you (especially women) would still encounter problems. In fact, you may already have discovered that there is a point when the stubborn fat stops melting away like the rest of the fat on the body. Some people have an alarming discrepancy between their upper and lower body fat, as if they had two different bodies glued together at the waist.
Bad things usually happen while chasing down the last of the sub-equator fat. Muscle wasting accelerates, especially in the lace. You may become so disheartened that you abandon the diet and start a rampage of binge eating, which puts the fat back on. In the worst-case scenario, the fat from bingeing lands preiasely where you don't want it: on your hips, thighs and but,
Your doctor will say that it's "genetic," or "a female thing,"
And you can't "spot reduce." For about 12 years, I've pursued this lower body fat problem in female bodybuilders. I've tried every technique, from traditional to harebrained — more exer-cise in the area, fancy French rub-on creams and injections, anti-estrogens and steroids. Most of them had absolutely no suc-cess at mobilizing fat out of these areas. Money mobilizes, yes. Fat, no.
Well, if I didn't keep pursuing this problem, then the chap-ter would end right here with, "Lower body fat? You're fucked." However, you will see that this chapter is gloriously exciting. Lower body fat can be dieted off (without liposuction). Lower body fat does not just have more fat cells. It responds differently to weight loss because its response to certain hormones differs markedly from most of the other fat on the body. These crazy fat cells are not only the last to reduce, but just as importantly, they can cause further metabolic slowdown and catabolic action in areas far away from your butt.
Although this chapter specifically discusses how to target lower body fat, you can think of it as a bridge. It's a continua-tion of the previous chapter's discussion of thyroid and a prequel to the upcoming chapter on thermogenic agents. This chapter contains elements common to all three areas.
I'll warn you before we get started that this chapter con-tains the most complex (and worthwhile) information about fat. As usual, I will try to simplify the scientific jargon, condense the information and skip over the unimportant stuff.
You've read the headline: "Mother Lifts Car to Free Trapped Child!" Perhaps friends have told you about the "rush" from jumping out of an airplane. Or perhaps you've been involved in a near-miss auto accident, after which you have uncontrollable shaking and nausea. All of these events have one thing in com-
: Adrenaline, the "fight or flight" hormone. Think of it as an octane booster to the body whenever you encounter a BIG stress.
In America, most physicians call this hormone epinephrine, and its close-acting sibling nor epinephrine. Europeans and most non-doctors call them adrenaline and noradrenalin. I'll use the adrenaline tag because it's easier to remember. (I'm one of the syllabically impaired.)
Adrenaline and noradrenalin are hormones, naturally pro-duced chemical messengers that impart instructions to various cells in the body. Adrenaline is produced by the two adrenal glands located over each kidney, which weigh about 5 to 7 grams each (for reference, an ounce is 28 grams). Noradrenalin, which is slightly different in chemical structure, is gener-ated at the nerve endings.
Why are there two sources for this hormone? Because noradrenalin can only be generated in the nerves of certain cells. Cells that don't get much blood circulation (like fat cells, for example) aren't candidates for adrenaline, which is circulated systemically.
Some people think that adrenaline is only released under extreme conditions, because that's when it's most noticeable. In reality both hormones are being produced and consumed continuously the adrenaline siblings affect many of the same systems as thyroid hormone — body temperature, blood pressure, inspiration and heart rate. In fact, the adrenalines and thyroid hormone have synergistic effects. Daily temperature fluctua-tions and fat distribution in part controlled by the adrenalines, which are properly called catecholamine.
Hormone receptors on cells are like assigned parking spaces, tailored in size and shape to each type of hormone.
Receptors for both adrenaline and noradrenalin are called adrenoreceptors. Adrenoreceptors are almost everywhere: in the blood, the organs, the muscles, and the fat cells.
Now it gets either interesting or too damn complicated, depending on what mood you're in. There are 4 types of these receptors (well, maybe 4-1/2), and each one communicates a different message to the cell. Sometimes a fat cell gets com-pletely different messages from its receptor sites. Lower body fat has very screwy adrenoreceptors, much like my crazy old granny in my basement. (Remember, she's in the freezer now.)
Although adrenaline was identified in 1895, it wasn't until 1948 that scientists figured out that they were dealing with Sibyl receptors. At first, they found two receptors and named them alpha and beta. Over the years, they discovered more receptors, which they named alpha- 1 (Al), alpha-2 (A2), beta-1 (Bl), beta-2 (B2) and the very shy beta-3 (B3). The A2s are bad, bad characters.
Fat cells have both Bl and A2 receptors. Fat cells don't get much blood circulation, so it is noradrenalin that attaches to these receptors.
Bl receptors send good messages. They activate lipase, the enzyme that breaks down fat. Lipase causes the fat cell to disas-semble itself, breaking down stored triglycerides into fatty acids and glycerol, which are used for energy throughout the body are the good guys, and it is noradrenalin that lights them up. Regular adrenaline would do the same thing if it could reach the receptor. However, fat doesn't have any major arteries or veins, only capillaries.
A2s are the bad guys. They block lipase in the fat cell. Worse, A2s also encourage the formation of triglycerides in the cell. A2s also (this was included at no extra charge) decrease the
Generation of noradrenalin at the nerve sites. Less noradrenalin-line means that the good B1s don't light up as brightly Oh well lower body fat doesn't have many B1s anyway. The picture looks pretty grim: fat cell disassembly is blocked, more fat is stored, and — I almost forgot — body temperature is slightly reduced, did I leave anything out? Ummm, yes. Low-calorie diets cause an increase in the number of the A2 receptors.
Let's envision how your lower body fat works. Lower body fat cells have very few Bl receptors, so they do riot release much stored fat. They have a vast number of those pesky A2 receptors. When you go on a low-calorie diet, the following things will happen:
1. Fat is lost first and fastest at the cells with lots of Bl recep-tors.
2. Very little fat is lost in the fat cells that have lots of A2 receptors.
3. Eventually, your noradrenalin levels drop, reducing your body temperature.
4. The number of A2 receptors increases. The last of the fat becomes so hard to mobilize that the body will have to use more amino acids (from muscle) for fuel.
5. When you finally give up on the diet, even so-called nor-mal eating will cause new fat accumulation right in the fat cells that have just increased their number of A2 receptors.
At first glance, it looks like you're screwed. It's not your Thyroid. It's not an estrogen problem. Neither steroids nor anti-estrogens will help. Ephedrine doesn't fit too well into the Bl receptor. Besides, there aren't very many Bis in lower body fat. It would be perfect if only we could get rid of the A2s or maybeMove them around a little...
Wait a minute. With all of the anti-this and anti-that products available, isn't there something that would block A2s from accepting noradrenalin? Perhaps there's something that would leave the rest of the adrenoreceptors alone. If there is, gimme, gimme, gimme! I gotta have it! NOW!
This wonderful product, this A2 antagonist, already exists. It's been around a long time, and it's not even high tech. It's a nat-ural herb that even has PDA approval! It's yohimbe, the herb from the African tree bark, the male erection pill. Why hasn't it been used in the past for fat reduction? There isn't much scien-tific research on A2 receptors or their relationship with fat cells. Even though this herbal product has monumental implications for dieters, its entry in the Physicians' Desk Reference doesn't mention fat reduction at all.
I would like to say that all you have to do is take a magic pill like yohimbe (actually, 4 to 5 pills) and voila, your lower body fat would take care of itself. I hate to rain on the parade, but yohimbe is not perfect in oral form.
Let me remind you that fat cells don't have very good blood circulation — what little there is comes from capillaries. Unfortunately, to adequately saturate the lower body fat recep-tors with yohimbe, you would be overdosing the rest of the receptors in the body Yohimbe is a wonderful idea, but just tak-ing a pill won't produce optimal results.
Yohimbe effect needs to be localized. Doctors pooh-pooh spot reduction as a bogus marketing scam, like fat massage or cellulite wraps. On the contrary, new research shows that lower body fat reduction can be achieved with creams or direct injec-tion into the fat.
You may have heard of aminophyline cream, an over-the-Counter asthma medication that appears to measurably reduce body fat. We don't quite know if this is caused by true lipid reduction or just a reduction of the water in and around the fat cell. Technically, aminophyline is supposed to be potentiating Bl receptors. However, stubborn fat doesn't have many Bl receptors. Direct local injection of yohimbe would work better.
Now that you understand adrenoreceptors, I can explain their interaction with thyroid hormone. Thyroid hormone stim-ulates muscle cells to burn more energy Through the B2 recep-tor, both adrenaline and noradrenalin also send a heat message to the muscle cell. On a low-calorie diet, heat production from thyroid hormone decreases, which causes an increase of A2 activity and an attenuation of the B2 receptors. Sure, you could maintain body temperature by increasing thyroid medication, but you'd have to take so much that you would suppress natural TSH and thyroid hormone production. An additional hazard is that more thyroid hormone would speed up processes that shouldn't be accelerated, like heart rate, respiration and blood pressure.
Trying to keep body temperature optimal on a low-calorie diet by taking too much thyroid hormone will cause hyperthyroidism, even though your temperature is in the optimal range. Thyroid dosage should be optimized before you diet. The free T3 levels you found while at maintenance calories should not be increased while dieting. The interplay of low calories, thermogenic products and thyroid hormones can make maintaining opti-mal body temperature can be a real juggling act.
Although we've discussed lower body fat exclusively; which is usually a "woman thing," A2 receptors are present in outer areas. Future research may find that fat distribution is intimately tied into A2 receptor distribution. Many
Builders, who have no lower body fat problems, have had a hard time stripping away body fat in the lower back area. Would yohimbe work in these areas? Or are androgen steroid receptors making the fat stubborn? We don't know, but the grand exper-iment is continuing.
Source: http://www.saanabolicreview.co.za/ugly.html
Common misspellings of (Ugly) Lower Body Fat: (gly) (guly) (igly) (ufly) (ugky) (ugl) (ugli) (uglt) (uglu) (ugly (ugy) (uhly) (ulgy) (uly) (ygly) bady bdoy bdy bidy bod bodi bodt bodu bofy bosy boy boyd bpdy dat fa far fay fot fqt fst ft gat kower lawer liwer loeer loer loqer lowe lowee lowet lowir lowr lowrr lowwr lpwer lwer lwoer nody obdy vody
