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Bromocriptine???
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hhajdo
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Cy-BORG
by Cy Willson
Q: What's your take on this bromocriptine stuff that's being touted as the latest and greatest fat burner?
A: Well, I guess I technically advocated (indirectly) the use of dopamine or a dopamine agonist back when I wrote the "Steroid Dieting" article. In it I mentioned that dopamine can exert many positive effects that will, in general, enhance lipolysis. (15-22) Do I believe we should all drop the use of ephedrine and caffeine in favor of bromocriptine? Not really.
When given to type-II diabetes, there was an increase in glycemic control but no change in body composition after sixteen weeks of treatment (measured via hydrostatic weighing and MRI for distribution of fat).
However, to be fair, these people were consuming a maintenance amount of calories. Also, there were two studies that were performed in obese subjects that found a significant reduction of body fat. In one study, 33 obese postmenopausal females were instructed not to alter existing exercise or eating programs during the treatment with bromocriptine over a six week period. What they found after six weeks via skin fold measurements was an 11.7% reduction of total body fat with a change in body weight of only 2.5%, suggesting a conservation of protein stores as well.
They also administered bromocriptine to patients who were being treated for non-insulin dependent diabetes with oral hypoglycemics or insulin. They found a 10.7% and 5.1% reduction of body fat, respectively. In yet another study, researchers took obese patients and instructed them to follow a moderately calorie-restricted diet over an eighteen-week period. This study was a double-blinded and placebo controlled. What they found was that bromocriptine significantly reduced body weight and body fat when compared to placebo. Glucose tolerance was also significantly improved. Again, skinfold measurements were taken to determine the loss of body fat.
Still, one overwhelming factor involved here is that all of the research was conducted using obese diabetics and in general, there was always an improvement in glycemic control with lower insulin levels and an overall enhancement in insulin-mediated glucose disposal. (23-25) Now, will this help those who aren't obese or diabetic? Well, I don't think it'll be that big of an advantage to those people, but it's still something that would make a nice adjunct.
If you were to monitor someone close enough, it's feasible that he or she could use ephedrine/caffeine along with small dosages of bromocriptine. Now I know some will say this isn't a good move since both could result in elevated blood pressure and heart rate, but the same is done with ephedrine/caffeine and T3. Come to think of it, ephedrine and caffeine are often referred to as a "dangerous combo" in literature. So the key is to simply start off using smaller dosages and slowly increase it so that you may reach a point where you receive the benefits yet don't experience any significant side effects.
Ephedrine and caffeine are surely more potent when you compare results of various studies. Ephedrine/caffeine has been shown to decrease body fat irrespective of calorie intake and has also produced greater results than bromocriptine in a shorter period of time.(26-28) Still, as you should cycle off of ephedrine and caffeine from time to time, using a dopamine agonist like bromocriptine during that time is a great idea as well.
If you really want to know the most potent combo, it's something that bodybuilders have been doing for some time now — combining T3 with some sort of beta-2 agonist like clenbuterol or a less selective one like ephedrine. It's been demonstrated that when humans are in a state of hyperthyroidism (which is the state you're in when using thyroid meds at higher dosages and you're euthyroid yourself), the lipolytic response to a norepinephrine is increased fivefold.
In another study it was shown to enhance beta adrenergic sensitivity by tenfold in adipocytes. In one last study, they'd shown a fifteen-fold increase in the responsiveness of adipocytes (from subcutaneous abdominal adipose tissue) to a selective beta 2 agonist while in a state of hyperthyroidism. This is thought to occur via increased beta 2 receptor number of density in adipose tissue.
Regardless of how you look at it, this is one hell of a potent stimulation of lipolysis. (29-32) Oh and just as some side notes, hypothyroidism obviously produces the opposite results and in response to starvation, beta 2 receptor number/density decreases.
Summary: Bromocriptine isn't a miracle drug, but not worthless either. I like ephedra/caffeine better, but bromocriptine may be something to use when cycling off ephedra/caffeine products. An ephedrine/caffeine stack is surely more potent.
15) Thiblin I, et al. "Increased dopaminergic and 5-hydroxytyrptaminergic activities in male rat brain following long-term treatment with anabolic/androgenic steroids." Br J Pharmacol 1999 Mar;126(6):1301-6
16) Samanin R, Garattini S. "Neurochemical mechanism of action of anorectic drugs." Pharmacol Toxicol 1993 Aug;73(2):63-8
17) Maxwell G, et al. "The effect of dopamine upon oxidative metabolism of brown fat adipocytes." Eur J Pharmacol 1985 Oct 22;116(3):293-7
18) Sandyk R. "Dopamine and insulin interact to modulate in vitro glucose transport in rat adipocytes." Int J Neurosci 1988 Nov;43(1-2):9-14
19) Lee TL, et al. "Activation of beta 3-adrenoreceptors by exogenous dopamine to lower glucose uptake into rat adipocytes." J Auton Nerv Syst 1998 Dec 11;74(2-3):86-90
20) Maxwell GM, et al. "Thermogenesis and the effect of injected catecholamines on the oxygen consumption of cafeteria-fed rats." Clin Exp Pharmacol Physiol 1988 May;15(5):391-400
21) Nakagawa M, et al. "The effects of dopamine infusion on the postoperative energy expenditure, metabolism, and catecholamine levels of patients after esophagectomy." Surg Today 1994;24(8):688-93
22) Pernet A, et al. "The metabolic effects of dopamine in man." Eur J Clin Pharmacol 1984;26(1):23-8
23) Pijl H, et al. "Bromocriptine: a novel approach to the treatment of type 2 diabetes." Diabetes Care. 2000 Aug;23(8):1154-61.
24) Meier AH, et al. "Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics."
Experientia. 1992 Mar 15;48(3):248-53.
25) Cincotta AH, Meier AH. "Bromocriptine (Ergoset) reduces body weight and improves tolerance in obese subjects." Diabetes Care 1996 Jun;19(6):667-70
26) Astrup A, et al. "The effect of ephedrine/caffeine mixture on energy expenditure and body composition in obese women." Metabolism 1992 Jul;41(7):686-688
27) Boozer CN, et al. "An herbal supplement containing Ma Huang-Guarana for weight loss: a randomized, double-blind trial." Int J Obes Relat Metab Disord 2001 Mar;25(3):316-324
28) Daly PA, et al. "Ephedrine, caffeine and aspirin: safety and efficacy for treatment of human obesity." Int J Obes Relat Metab Disord 1993 Feb;17: S73-S78
29) Richelsen B, Sorensen NS. "Alpha 2- and beta-adrenergic binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism." Metabolism 1987 Nov;36(11):1031-9
30) Hellstrom L, et al. "Catecholamine-induced adipocyte lipolysis in human hyperthyroidism." J Clin Endocrinol Metab 1997 Jan;82(1):159-66
31) Wahrenberg H, et al. "Adrenergic regulation of lipolysis in human adipocytes: findings in hyper- and hypothyroidism." J Clin Endocrinol Metab 1986 Sep;63(3):631-8
32) Wahrenberg H, et al. "Adrenergic regulation of lipolysis in fat cells from hyperthyroid and hypothyroid patients." J Clin Endocrinol Metab 1994 Apr;78(4):898-903
33) Sciarra F: Anti-estrogens and aromatase inhibitors: tamoxifen and testolactone. J Endocrinol Invest 1988;11:755-762.
34) Olin B (Ed): Facts and Comparisons. JB Lippincott Co, St Louis, MO, 1990.
35) Reynolds JEF (Ed): Martindale: The Extra Pharmacopoeia, (electronic version). Micromedex, Inc, Denver, CO, 1990.
36) Liu PY, Wishart SM, Handelsman DJ. "A double blind, placebo-controlled, randomized clinical trial of recombinant human chorionic gonadotropin on muscle strength and physical function and activity in older men with partial age-related androgen deficiency." J Clin Endocrinol Metab 2002 Jul;87(7):3125-35
by Cy Willson
Q: What's your take on this bromocriptine stuff that's being touted as the latest and greatest fat burner?
A: Well, I guess I technically advocated (indirectly) the use of dopamine or a dopamine agonist back when I wrote the "Steroid Dieting" article. In it I mentioned that dopamine can exert many positive effects that will, in general, enhance lipolysis. (15-22) Do I believe we should all drop the use of ephedrine and caffeine in favor of bromocriptine? Not really.
When given to type-II diabetes, there was an increase in glycemic control but no change in body composition after sixteen weeks of treatment (measured via hydrostatic weighing and MRI for distribution of fat).
However, to be fair, these people were consuming a maintenance amount of calories. Also, there were two studies that were performed in obese subjects that found a significant reduction of body fat. In one study, 33 obese postmenopausal females were instructed not to alter existing exercise or eating programs during the treatment with bromocriptine over a six week period. What they found after six weeks via skin fold measurements was an 11.7% reduction of total body fat with a change in body weight of only 2.5%, suggesting a conservation of protein stores as well.
They also administered bromocriptine to patients who were being treated for non-insulin dependent diabetes with oral hypoglycemics or insulin. They found a 10.7% and 5.1% reduction of body fat, respectively. In yet another study, researchers took obese patients and instructed them to follow a moderately calorie-restricted diet over an eighteen-week period. This study was a double-blinded and placebo controlled. What they found was that bromocriptine significantly reduced body weight and body fat when compared to placebo. Glucose tolerance was also significantly improved. Again, skinfold measurements were taken to determine the loss of body fat.
Still, one overwhelming factor involved here is that all of the research was conducted using obese diabetics and in general, there was always an improvement in glycemic control with lower insulin levels and an overall enhancement in insulin-mediated glucose disposal. (23-25) Now, will this help those who aren't obese or diabetic? Well, I don't think it'll be that big of an advantage to those people, but it's still something that would make a nice adjunct.
If you were to monitor someone close enough, it's feasible that he or she could use ephedrine/caffeine along with small dosages of bromocriptine. Now I know some will say this isn't a good move since both could result in elevated blood pressure and heart rate, but the same is done with ephedrine/caffeine and T3. Come to think of it, ephedrine and caffeine are often referred to as a "dangerous combo" in literature. So the key is to simply start off using smaller dosages and slowly increase it so that you may reach a point where you receive the benefits yet don't experience any significant side effects.
Ephedrine and caffeine are surely more potent when you compare results of various studies. Ephedrine/caffeine has been shown to decrease body fat irrespective of calorie intake and has also produced greater results than bromocriptine in a shorter period of time.(26-28) Still, as you should cycle off of ephedrine and caffeine from time to time, using a dopamine agonist like bromocriptine during that time is a great idea as well.
If you really want to know the most potent combo, it's something that bodybuilders have been doing for some time now — combining T3 with some sort of beta-2 agonist like clenbuterol or a less selective one like ephedrine. It's been demonstrated that when humans are in a state of hyperthyroidism (which is the state you're in when using thyroid meds at higher dosages and you're euthyroid yourself), the lipolytic response to a norepinephrine is increased fivefold.
In another study it was shown to enhance beta adrenergic sensitivity by tenfold in adipocytes. In one last study, they'd shown a fifteen-fold increase in the responsiveness of adipocytes (from subcutaneous abdominal adipose tissue) to a selective beta 2 agonist while in a state of hyperthyroidism. This is thought to occur via increased beta 2 receptor number of density in adipose tissue.
Regardless of how you look at it, this is one hell of a potent stimulation of lipolysis. (29-32) Oh and just as some side notes, hypothyroidism obviously produces the opposite results and in response to starvation, beta 2 receptor number/density decreases.
Summary: Bromocriptine isn't a miracle drug, but not worthless either. I like ephedra/caffeine better, but bromocriptine may be something to use when cycling off ephedra/caffeine products. An ephedrine/caffeine stack is surely more potent.
15) Thiblin I, et al. "Increased dopaminergic and 5-hydroxytyrptaminergic activities in male rat brain following long-term treatment with anabolic/androgenic steroids." Br J Pharmacol 1999 Mar;126(6):1301-6
16) Samanin R, Garattini S. "Neurochemical mechanism of action of anorectic drugs." Pharmacol Toxicol 1993 Aug;73(2):63-8
17) Maxwell G, et al. "The effect of dopamine upon oxidative metabolism of brown fat adipocytes." Eur J Pharmacol 1985 Oct 22;116(3):293-7
18) Sandyk R. "Dopamine and insulin interact to modulate in vitro glucose transport in rat adipocytes." Int J Neurosci 1988 Nov;43(1-2):9-14
19) Lee TL, et al. "Activation of beta 3-adrenoreceptors by exogenous dopamine to lower glucose uptake into rat adipocytes." J Auton Nerv Syst 1998 Dec 11;74(2-3):86-90
20) Maxwell GM, et al. "Thermogenesis and the effect of injected catecholamines on the oxygen consumption of cafeteria-fed rats." Clin Exp Pharmacol Physiol 1988 May;15(5):391-400
21) Nakagawa M, et al. "The effects of dopamine infusion on the postoperative energy expenditure, metabolism, and catecholamine levels of patients after esophagectomy." Surg Today 1994;24(8):688-93
22) Pernet A, et al. "The metabolic effects of dopamine in man." Eur J Clin Pharmacol 1984;26(1):23-8
23) Pijl H, et al. "Bromocriptine: a novel approach to the treatment of type 2 diabetes." Diabetes Care. 2000 Aug;23(8):1154-61.
24) Meier AH, et al. "Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics."
Experientia. 1992 Mar 15;48(3):248-53.
25) Cincotta AH, Meier AH. "Bromocriptine (Ergoset) reduces body weight and improves tolerance in obese subjects." Diabetes Care 1996 Jun;19(6):667-70
26) Astrup A, et al. "The effect of ephedrine/caffeine mixture on energy expenditure and body composition in obese women." Metabolism 1992 Jul;41(7):686-688
27) Boozer CN, et al. "An herbal supplement containing Ma Huang-Guarana for weight loss: a randomized, double-blind trial." Int J Obes Relat Metab Disord 2001 Mar;25(3):316-324
28) Daly PA, et al. "Ephedrine, caffeine and aspirin: safety and efficacy for treatment of human obesity." Int J Obes Relat Metab Disord 1993 Feb;17: S73-S78
29) Richelsen B, Sorensen NS. "Alpha 2- and beta-adrenergic binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism." Metabolism 1987 Nov;36(11):1031-9
30) Hellstrom L, et al. "Catecholamine-induced adipocyte lipolysis in human hyperthyroidism." J Clin Endocrinol Metab 1997 Jan;82(1):159-66
31) Wahrenberg H, et al. "Adrenergic regulation of lipolysis in human adipocytes: findings in hyper- and hypothyroidism." J Clin Endocrinol Metab 1986 Sep;63(3):631-8
32) Wahrenberg H, et al. "Adrenergic regulation of lipolysis in fat cells from hyperthyroid and hypothyroid patients." J Clin Endocrinol Metab 1994 Apr;78(4):898-903
33) Sciarra F: Anti-estrogens and aromatase inhibitors: tamoxifen and testolactone. J Endocrinol Invest 1988;11:755-762.
34) Olin B (Ed): Facts and Comparisons. JB Lippincott Co, St Louis, MO, 1990.
35) Reynolds JEF (Ed): Martindale: The Extra Pharmacopoeia, (electronic version). Micromedex, Inc, Denver, CO, 1990.
36) Liu PY, Wishart SM, Handelsman DJ. "A double blind, placebo-controlled, randomized clinical trial of recombinant human chorionic gonadotropin on muscle strength and physical function and activity in older men with partial age-related androgen deficiency." J Clin Endocrinol Metab 2002 Jul;87(7):3125-35
hhajdo
New member
It's not needed during the fina cycle..
Some people use it to prevent gyno because they believe that fina causes an increase in prolactin levels...
I didn't see any studies which show that fina will affect prolactin levels, I think DaMan said that he'll do a blood test while on fina so maybe he has some more info...
I don't see any benefit in using bromo post cycle also..
Some people use it to prevent gyno because they believe that fina causes an increase in prolactin levels...
I didn't see any studies which show that fina will affect prolactin levels, I think DaMan said that he'll do a blood test while on fina so maybe he has some more info...
I don't see any benefit in using bromo post cycle also..
hhajdo
New member
It can be used as a fat loss aid:
Excerpt From Lyle McDonald's new book "Bromocriptine"
Chapter 1: Defining the Problem I always seem to start out these projects with a chapter on defining the problem. I'm not entirely sure if it's for the reader's benefit or my own. Either way it serves the same purpose. I try to solve body problems by first defining what those problems are, then figuring out what's causing the problems, and finally seeing if they can be fixed in any effective fashion. This booklet will follow that pattern.
So let's define the problem very succinctly: Your body hates you. Yeah, I said this in the foreword but it bears repeating. It's become one of my more common catch-phrases and I am quite serious about it. Actually, that sentence has it backwards. Your body loves you and wants to keep you alive; what it thinks is the right thing to do to keep you alive is generally contrary to your goals of less weight/fat and more muscle. Let me shorten the problem even more: dieting sucks. That's the real issue and topic of this book. Anyone who's tried to lose weight/fat (there is a difference) and failed, knows this to be true. Gaining weight is pretty easy for most folks, just eat and enjoy. Losing it is the real hassle. Sure, a genetically lucky few can do it without much effort but they aren't the ones reading this book.
There are good biological reasons for this discrepancy that you'll learn about in the next chapter.I'm fascinated with dieting and fat loss. I have been since the start of my career. It's the psychological profile that comes along with being a former fat kid. I've done/read most of the diets out there, tried all of the supplements, even a couple of the drugs. All this was in the quest to be lean and stay there. "Why?", you ask. I'll be honest: I want to fix myself. It's the same reason that nutcases become psychologists and fat girls become dietitians. They want to fix themselves, too. It's a common affliction. My friend Bryan Haycock, who has always wanted to be huge, has dedicated most of his time to studying muscular growth physiology for the same reason. He wants to be huge, so he researches muscle growth ; I want to be lean so I research fat loss. He and I make a very good team, especially when you throw in our endocrinology-obsessed buddy, Elzi Volk. The three of us have most of it covered.
Even at 10% bodyfat, I'm not happy. I know I'm lean, healthy, all of that. My doctor is thrilled and thinks I'm nuts to want to be leaner. So does my mom. They may not be wrong. But at 10% bodyfat, I'm simply not satisfied. The more athletic readers know what I'm talking about. Other readers may just think I'm nuts and obsessive. They may not be wrong either.
Losing weight/keeping it off As most people (well, the honest ones anyhow) will tell you, losing weight or fat isn't fundamentally that hard. I'll tell you that too. No magic diet is needed and even fat folks can lose weight: just diet and exercise. It's keeping it off for any decent period of time that is the hard part. Even a 5 to 10 pound weight loss in obese folks improves health indices, but keeping even that off for more than a little while is pretty rare.
Folks who want to get really lean without using drugs have to contend with muscle loss, crashing hormones and other problems. This is a problem I've been looking at for years and there are few real or good solutions. Most are just stopgaps or kludge fixes, nothing very permanent beyond 'Deal with it'. Drugs are the exception; drugs work wonderfully and solve many, many problems.That's the problem, what's the goal?So, we ask, what are we trying to accomplish exactly, in solving the problem described above. For the average person, losing weight and keeping it off without hunger and recidivism would be the goal. Fairly simple, really, but most people still fail miserably at it. For the obsessed like me, the ultimate goal would be losing all the fat you want without your body screwing you on the way down. In both cases, it'd be ideal if you could lose fat weight with no muscle loss, no metabolic slowdown, no crashing hormones, and no runaway appetite. If you could stay leaner without much effort that would be great too. If you're an athlete, being able to gain muscle without getting (too) fat would also be ideal.
It's not as simple as it sounds and most solutions to date have been only marginally successful, except for drugs of course. Drugs work great because they allow us to step outside of our normal physiology. Most of the dietary supplement strategies are aimed at correcting part of this problem; most try to mimic drugs and some actually succeed. Did I mention that drugs work great? Prohormones, anti-catabolics, fat-burners, appetite suppressants, protein powder, etc. are all attempts to fix some part of the overall metabolically screwed up picture. As most know, they only work to a small degree.
Even the weight loss drugs introduced by the pharmaceutical industry have only been marginally successful. They are either appetite suppressants (such as Fen/Phen or Meridia) which stop working after a while (but see chapter 8 for a possible solution), thermogenics which have side effects, or compounds which impair fat absorption (such as Orlistat, and runaway diarrhea is the price you have to pay). A small weight loss occurs, maybe 5-10%, but that's about it. They are all ultimately sort of kludge fixes, which aren't addressing the real problem (hint: it's in the brain).
Drug-using bodybuilders/athletes don't have this problem, since they are replacing their body's normal hormones with drugs. Steroids, thyroid medication, injectable growth hormone, cortisol blockers, appetite suppressants, that's just a partial list of the chemical warfare that occurs in elite bodybuilding and athletics. Drugs allow those folks to do things that aren't 'normal' relative to human physiology. Drugs also make natural folks expect a lot more than is realistically possible; they wish they could pull off the magical body transformations without drugs, but they find out the hard way that it can't be done. Drugs can also come at a high cost: financial, legal, and possibly health-wise. This booklet is about fixing part of the problems. I don't claim to have the complete answer...yet. But as research builds up and we figure out what's causing the problem, we are getting closer to the answer. The drug bromocriptine, a very old drug with several uses totally unrelated to body composition, turns out to solve many of the problems that I talked about above. I'll present the data and mechanism soon. In addition, it's very safe at the doses needed, fairly inexpensive, legal, and not too hard to come by. So it meets my criteria for a good drug. Before you get the wrong idea, this booklet isn't only aimed at the psychos like me, who want to maintain single digit bodyfat year round without all of the associated problems. The data I'm going to present turn out to apply to dieters in general, because the mechanisms at the heart ofthe problem are the same.Losing 10 pounds and keeping it off long term is essentially the same as dieting to 'normal' bodyfat levels (11-18% in men, 21-28% in women) or getting even leaner. All three situations come with the same basic problems: hunger, metabolic slowdown, impaired fat burning, crashing hormones, all of which derail your efforts. The difference is merely one of degree: the person dieting to 'normal' isn't as badly off as someone dieting to 6% bodyfat. Since all of these problems ultimately stem from the same place (the brain, as it turns out) they end up having the same basic fix.
Defining the problem, part 1Ok, so the statement that dieting sucks doesn't really tell you much. Let's define the problem in a bit more detail. A quick look at the dieting literature shows an exceptionally poor rate of success. Depending on which data you believe, anywhere from 90% on up of dieters will gain back all of the lost weight within a few years. Some have even concluded that it's not worth attempting weight loss since nearly everyone fails.As I mentioned above, losing the weight/fat ultimately isn't the problem, keeping it off in the long-term is. Current research is focusing more on how to keep the weight off, since losing it isn't fundamentally that difficult. Eat less, exercise, weight usually comes off. Keeping it off long-term, there's the real problem, and it's where most people fail. There are many, many reasons for this of course, some physiological, some psychological. Changing long-term eating and behavior patterns is difficult, that's part of the psychology. And nobody really likes restriction even if it's self-imposed. Both cause anxiety which humans don't really like, so we revert to old habits. Physiologically, dieting and weight/fat loss cause a decrease in metabolic rate and energy/activity levels, along with a decrease in fat burning. Fat storage enzymes are increased as well, which means that the dieter's body is just waiting to start storing fat again. When (not if) the diet is broken, the pounds come back on, frequently with a little bit extra stored for good measure.The small percentage of dieters that do succeed long-term tend to show characteristic changes in things such as eating habits, exercise habits, regular self-monitoring to stay on the bandwagon and others. They make the changes and maintain them long term. They have to restrict calories to some degree for the rest of their lives to maintain the weight/fat loss. I suspect they're a little bit hungry and unhappy most of the time. Since nobody likes restriction or hunger, most people go back to old eating habits and gain all the weight back. An ideal solution would fix this problem.Defining the problem, part 2It's convenient for weight loss 'experts' to blame weight loss failures on willpower but that turns out to be a very simplistic (and not entirely correct) explanation. Quite literally, the brains of these individuals are the problem. Essentially, their brains 'want' that person to be fatter and are sending powerful appetite simulating signals to get those people to eat. That's on top of the other metabolic derangements, such as slowed metabolic rate and decreased fat burning, along with increased fat storage capacity, that occur.
Dieting athletes and bodybuilders have a slightly different set of problems although they turn out to be related in terms of the mechanism involved. Psychologically, the problems are less since most athletes equate suffering with progress in the first place, which is both good and bad. On the one hand, most athletes don't whine about being hungry or changing their habits, that's part of the price for playing. On the other, many confuse working harder with working smarter. What they lack in finesse, they make up for with pigheaded stubbornness. The real problems for this group are physiological. Without drugs (euphemistically referred to as 'props' or 'gear' in the subculture), natural athletes lose muscle mass at an alarming rate and have totally screwed-up hormone levels when they get very lean. Staying there, except for the genetically lean, is nearly impossible, as is making any real gains in muscle mass without gaining the bodyfat back. Getting lean beyond a certain point, in the range of 10-12% bodyfat for men and maybe 18-20% bodyfat for women, causes levels of testosterone, growth hormone, thyroid and the other 'good' hormones to crash. Levels of the 'bad' hormones such as cortisol skyrocket. Appetite soars through the roof. Muscle loss accelerates and getting rid of that last little bit of fat is a total pain as the body fights to keep you alive. For bodybuilders who only have to be lean for one day (contest day), it's no big deal. But stories of folks ballooning up after the contest are rampant. The physiology coupled with months of deprivation can lead to month long binges. As you might imagine, fat storage takes off. As it turns out, nearly all of the problems I described above are being controlled by the same basic systems and they turn out to be mostly in the brain. Appetite, hormones, the psychological drive for food, fat burning, etc. all under control of the same basic systems at a fundamental level. And it's your brain that is screwing you over. This is why the idea of "Just try harder" doesn't get very far. Your brain, which is feeding your urges about behavior, food, etc. is fighting against you. Did I mention that your body hates you? It does and, eventually, it's going to win.
The brain and setpointIn the last five years or so, obesity research has exploded into a whole new realm. Rather than focusing on idiotic topics such as "Why fiber is good for weight loss" the current focus is on the biological mechanisms that drive eating behavior, maintain bodyweight at certain levels, and control the partitioning of calories (where they go after you eat them). It's been suggested for decades (since at least the 50's) that the body tries to maintain some type of 'setpoint' level of bodyweight or bodyfat and will try to maintain that level. While that's a little bit simplistic, it turns out to be more true than not. Simply put (the details are coming later), the brain has sort of a preconceived notion of how fat it wants you to be, a setpoint as it were. A great deal of this 'setpoint' is imprinted at a very early age (1). Like when you're in the womb and the first few months of life early. Quite literally, what your mom did while she was pregnant is affecting you now. If she was obese (or, as it turns out, undernourished), you're more likely to be overweight and have trouble losing and keeping weight and fat off. You probably have more fat cells than you'd otherwise have, as well as a brain that 'wants' you to be fat. Other aspects of your physiology, such as hormonal axes, may also be imprinted while you're in the womb (2). This probably contributes to the problems folks have losing fat as well. So if you have problems with losing fat or with your hormone levels, just blame your mom. She should appreciate that. In addition to your early childhood, what you did during puberty as well as what you do as an adult can affect setpoint. It looks like overeating for long periods of time or staying fat long enough can cause setpoint to go up (above where it was when you were born). Contrary to popular belief, you can also add fat cells if you stay fat/overeat for extended periods, and this may affect setpoint as well as your propensity to put fat back on after you diet. Pregnancy appears to raise setpoint a bit in women too. It's bringing setpoint back down that's the problem. The whole setpoint concent is pretty easy to demonstrate in animals, although harder to measure in humans. You can breed rats who will avidly defend a given setpoint. By defend I mean this: when you overfeed them, their metabolic rate increases, they become more active, and they will automatically decrease food intake. This brings them back to their setpoint level where everything normalizes again. In contrast, when you underfeed them their metabolic rate decreases, they decrease their activity, and increase food intake (3), which brings them back to their setpoint again. They make a useful model because scientists can biopsy their little rat brains and see what's happening chemically and figure out what's driving the process. When they are below their setpoint, their little rat brains undergo characteristic changes that cause things to occur: slowed metabolic rate, hunger, etc. Once bodyfat increases, their brains think everything is normal, and brain chemicals normalize. You can also breed rats with a high setpoint to begin with. If you maintain them at a bodyweight that's lower than their setpoint, even if they aren't actively dieting, their brains and the rest of their rat physiology will show the same changes as if they were starving. As soon as you fatten them up to their setpoint, their brains go 'Aahhh' and everything becomes normal, at which point they start to defend that setpoint. A fed rat brain is a happy rat brain, or something like that. Humans show some of the same tendencies as the rats mentioned, and the same basic neurochemistry too. The big difference is that we appear to defend against underfeeding a whole lot better than against overfeeding. That is, overfeed someone and you generally don't see major increases in metabolic rate or decreases in hunger. There are exceptions, people who burn off extra calories through fidgeting and other activities; they tend to stay very lean and have trouble gaining weight (4). They also have appetites that shut off readily when they overeat. They are not most people and we hate them. The only pleasure we might derive in this regards is knowing that they will be the first to die if a famine ever comes. In most people, when you overfeed, metabolic rate goes up a little and hunger decreases a little, if at all. Excess calories are stored as fat with excellent efficiency in most people except those lucky suckers who burn the majority off (4). To get far ahead of myself, these lucky folks will likely turn out to be very leptin sensitive, a topic that will make sense in a few chapters. Everyone else will be found to be suffering from some degree of leptin resistance. It's when you underfeed people that the problems start: hunger soars, metabolic rate and hormones crash, fat burning slows down, muscle loss goes up, everything I mentioned up above happens. Your body hates you and defends better against underfeeding than it does against overfeeding. This actually makes good evolutionary sense.
What does evolution have to do with it? Now you're wondering about that last sentence, how did being fat and defending against underfeeding/starvation make good evolutionary sense? Even if you weren't wondering, I'm going to tell you. I have to justify the cost of this booklet somehow. During most of our evolution, being fat up to a point was actually beneficial, because it helped us to survive when food was unavailable. In ancient times, that was usually about half of the year. People would typically fatten up during the summer when food was available, to ensure that they could survive the winter when food wasn't around. The increased bodyfat would give them the stored energy to get through the winter on top of helping to keep them warm. It's only in recent times where being fat is a health risk, mainly because people get fat, and stay fat for extended periods. The normal starvation period that we evolved on, which leaned us out for half of every year, doesn't occur anymore. Modern life is one long fattening cycle (readers who are powerlifters can think of it as one long bulking cycle). In contrast, being skinny meant that you tended to die when food wasn't available because you starved to death that much sooner. The folks who could best deal with starvation, by slowing metabolic rate and all the rest, survived, and we carry their genes (5). This is called the Thrifty Gene hypothesis, in case you care.
To your body, dieting is fundamentally identical to starvation, it differs only in extremity. In both cases, you're eating less than your body needs and, in both cases, your body adapts pretty much the same. That is, your body doesn't 'know' that you're only dieting for 8 weeks to look good in a bathing suit. If only 'knows' that you're eating less, and adapts accordingly. You'll find out how it 'knows' in the next chapter. While I'm on the topic, a little more bad news for female readers. We've known for years that women have a harder time losing and keeping off weight, no matter what they do. In addition to having a lower metabolic rate overall, women's bodies generally adapt faster and harder to caloric restriction or exercise than men's bodies do (6). To put it in the above terms, their bodies appear to defend against weight loss even moreso than men's do. Oh yeah, they also don't burn off excess calories as well with overfeeding (4). As my friend Elzi Volk says "When it comes to fat loss, women are screwed."
Again, this makes evolutionary sense. Since women were ultimately responsible for the survival of the human race (since they give birth to and take care of the children), the ones who could stay alive the longest during the winter famine were the ones who passed on their genes (7). This is the reason that women have a much harder time losing fat (and keeping it off) than men. The exact mechanisms by which women's bodies are able to do this are still under study. Figuring out what is the problem with women and fat loss and fixing it is one of my next projects. For now, just accept that it sucks to be female if you want to lose fat. You can do it, but it's harder.
Summing up So, the basic problem is this: Your body appears to have a set idea of how fat it 'wants' you to be. That's your 'setpoint' and how high or low it is depends on what your mom did when she was pregnant, what you did during puberty, and what you've done as an adult. This causes your brain to set things up to try and keep you at that weight, more or less. To a degree, it can adapt metabolism, etc. up and down in response to over- and under-feeding respectively. But, in general, for clear evolutionary reasons, your body works far harder against you when you underfeed than when you overfeed. Essentially, your body wants to keep you at a certain level of bodyfat which is usually higher than you want, because it thinks that the next famine could be around the corner. If food becomes unavailable tomorrow, you'll live longer if you're fatter. In a few thousand years, once our bodies have figured out that famines aren't coming, maybe our genetics will adapt. Until then, metabolic slowdown and all the rest is the price to pay for dieting. In addition, in response to that famine, your body has an extremely well developed way of keeping you alive, slowing metabolic rate, making you less active so that you burn less calories, making you hungry as hell so you'll go look for what food might be available, decreasing fat burning, and many others. All are aimed at helping you to survive until food becomes available. And, as far as your body is concerned, dieting is really no different than starvation. The only real difference is one of extreme, eating something versus eating nothing. In both cases, your body 'knows' that you're eating less than you should, and it adapts accordingly. So how do we fix it? The first step to solving that problem is to figure out how the body is performing this trick, the mechanism: knowing you're starving and adapting. Then we see if we can do anything about it.
References:
1. Levin BE. The obesity epidemic: Metabolic imprinting on genetically susceptible neural circuits. Obes Res (2000) 8: 342-347.
2. Phillips DWI. Fetal growth and programming of the hypothalamic-pituitary-adrenal axis. Clinical and Experimental Pharmacology and Physiology (2001) 28: 967-970.
3. Levin BE and AA Dunn-Meynell. Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity Am J Physiol (2002) 282: R46-R54.
4. Vanltallie TB. Resistance to weight gain during overfeeding: a NEAT explanation. Nutr Rev. (2001) 59:48-51.
5. Arye Lev-Ran. Human obesity: an evolutionary approach to understanding our bulging waistline. Diabetes Metab Res Rev (2001) 17: 347-362.
6. Westerterp KR. Nutritional Implications of Gender Differences in Metabolism: Energy Metabolism, Human Studies in Gender Differences in Metabolism: Practical and Nutritional Implications ed. Mark Tarnopolsky.CRC Press. 1999.
7. Hoyenga KB and KT Hoyenga. Gender and energy balance: sex differences in adaptations for feast and famine. Physiol Behav (1982) 28: 545-563.
Excerpt From Lyle McDonald's new book "Bromocriptine"
Chapter 1: Defining the Problem I always seem to start out these projects with a chapter on defining the problem. I'm not entirely sure if it's for the reader's benefit or my own. Either way it serves the same purpose. I try to solve body problems by first defining what those problems are, then figuring out what's causing the problems, and finally seeing if they can be fixed in any effective fashion. This booklet will follow that pattern.
So let's define the problem very succinctly: Your body hates you. Yeah, I said this in the foreword but it bears repeating. It's become one of my more common catch-phrases and I am quite serious about it. Actually, that sentence has it backwards. Your body loves you and wants to keep you alive; what it thinks is the right thing to do to keep you alive is generally contrary to your goals of less weight/fat and more muscle. Let me shorten the problem even more: dieting sucks. That's the real issue and topic of this book. Anyone who's tried to lose weight/fat (there is a difference) and failed, knows this to be true. Gaining weight is pretty easy for most folks, just eat and enjoy. Losing it is the real hassle. Sure, a genetically lucky few can do it without much effort but they aren't the ones reading this book.
There are good biological reasons for this discrepancy that you'll learn about in the next chapter.I'm fascinated with dieting and fat loss. I have been since the start of my career. It's the psychological profile that comes along with being a former fat kid. I've done/read most of the diets out there, tried all of the supplements, even a couple of the drugs. All this was in the quest to be lean and stay there. "Why?", you ask. I'll be honest: I want to fix myself. It's the same reason that nutcases become psychologists and fat girls become dietitians. They want to fix themselves, too. It's a common affliction. My friend Bryan Haycock, who has always wanted to be huge, has dedicated most of his time to studying muscular growth physiology for the same reason. He wants to be huge, so he researches muscle growth ; I want to be lean so I research fat loss. He and I make a very good team, especially when you throw in our endocrinology-obsessed buddy, Elzi Volk. The three of us have most of it covered.
Even at 10% bodyfat, I'm not happy. I know I'm lean, healthy, all of that. My doctor is thrilled and thinks I'm nuts to want to be leaner. So does my mom. They may not be wrong. But at 10% bodyfat, I'm simply not satisfied. The more athletic readers know what I'm talking about. Other readers may just think I'm nuts and obsessive. They may not be wrong either.
Losing weight/keeping it off As most people (well, the honest ones anyhow) will tell you, losing weight or fat isn't fundamentally that hard. I'll tell you that too. No magic diet is needed and even fat folks can lose weight: just diet and exercise. It's keeping it off for any decent period of time that is the hard part. Even a 5 to 10 pound weight loss in obese folks improves health indices, but keeping even that off for more than a little while is pretty rare.
Folks who want to get really lean without using drugs have to contend with muscle loss, crashing hormones and other problems. This is a problem I've been looking at for years and there are few real or good solutions. Most are just stopgaps or kludge fixes, nothing very permanent beyond 'Deal with it'. Drugs are the exception; drugs work wonderfully and solve many, many problems.That's the problem, what's the goal?So, we ask, what are we trying to accomplish exactly, in solving the problem described above. For the average person, losing weight and keeping it off without hunger and recidivism would be the goal. Fairly simple, really, but most people still fail miserably at it. For the obsessed like me, the ultimate goal would be losing all the fat you want without your body screwing you on the way down. In both cases, it'd be ideal if you could lose fat weight with no muscle loss, no metabolic slowdown, no crashing hormones, and no runaway appetite. If you could stay leaner without much effort that would be great too. If you're an athlete, being able to gain muscle without getting (too) fat would also be ideal.
It's not as simple as it sounds and most solutions to date have been only marginally successful, except for drugs of course. Drugs work great because they allow us to step outside of our normal physiology. Most of the dietary supplement strategies are aimed at correcting part of this problem; most try to mimic drugs and some actually succeed. Did I mention that drugs work great? Prohormones, anti-catabolics, fat-burners, appetite suppressants, protein powder, etc. are all attempts to fix some part of the overall metabolically screwed up picture. As most know, they only work to a small degree.
Even the weight loss drugs introduced by the pharmaceutical industry have only been marginally successful. They are either appetite suppressants (such as Fen/Phen or Meridia) which stop working after a while (but see chapter 8 for a possible solution), thermogenics which have side effects, or compounds which impair fat absorption (such as Orlistat, and runaway diarrhea is the price you have to pay). A small weight loss occurs, maybe 5-10%, but that's about it. They are all ultimately sort of kludge fixes, which aren't addressing the real problem (hint: it's in the brain).
Drug-using bodybuilders/athletes don't have this problem, since they are replacing their body's normal hormones with drugs. Steroids, thyroid medication, injectable growth hormone, cortisol blockers, appetite suppressants, that's just a partial list of the chemical warfare that occurs in elite bodybuilding and athletics. Drugs allow those folks to do things that aren't 'normal' relative to human physiology. Drugs also make natural folks expect a lot more than is realistically possible; they wish they could pull off the magical body transformations without drugs, but they find out the hard way that it can't be done. Drugs can also come at a high cost: financial, legal, and possibly health-wise. This booklet is about fixing part of the problems. I don't claim to have the complete answer...yet. But as research builds up and we figure out what's causing the problem, we are getting closer to the answer. The drug bromocriptine, a very old drug with several uses totally unrelated to body composition, turns out to solve many of the problems that I talked about above. I'll present the data and mechanism soon. In addition, it's very safe at the doses needed, fairly inexpensive, legal, and not too hard to come by. So it meets my criteria for a good drug. Before you get the wrong idea, this booklet isn't only aimed at the psychos like me, who want to maintain single digit bodyfat year round without all of the associated problems. The data I'm going to present turn out to apply to dieters in general, because the mechanisms at the heart ofthe problem are the same.Losing 10 pounds and keeping it off long term is essentially the same as dieting to 'normal' bodyfat levels (11-18% in men, 21-28% in women) or getting even leaner. All three situations come with the same basic problems: hunger, metabolic slowdown, impaired fat burning, crashing hormones, all of which derail your efforts. The difference is merely one of degree: the person dieting to 'normal' isn't as badly off as someone dieting to 6% bodyfat. Since all of these problems ultimately stem from the same place (the brain, as it turns out) they end up having the same basic fix.
Defining the problem, part 1Ok, so the statement that dieting sucks doesn't really tell you much. Let's define the problem in a bit more detail. A quick look at the dieting literature shows an exceptionally poor rate of success. Depending on which data you believe, anywhere from 90% on up of dieters will gain back all of the lost weight within a few years. Some have even concluded that it's not worth attempting weight loss since nearly everyone fails.As I mentioned above, losing the weight/fat ultimately isn't the problem, keeping it off in the long-term is. Current research is focusing more on how to keep the weight off, since losing it isn't fundamentally that difficult. Eat less, exercise, weight usually comes off. Keeping it off long-term, there's the real problem, and it's where most people fail. There are many, many reasons for this of course, some physiological, some psychological. Changing long-term eating and behavior patterns is difficult, that's part of the psychology. And nobody really likes restriction even if it's self-imposed. Both cause anxiety which humans don't really like, so we revert to old habits. Physiologically, dieting and weight/fat loss cause a decrease in metabolic rate and energy/activity levels, along with a decrease in fat burning. Fat storage enzymes are increased as well, which means that the dieter's body is just waiting to start storing fat again. When (not if) the diet is broken, the pounds come back on, frequently with a little bit extra stored for good measure.The small percentage of dieters that do succeed long-term tend to show characteristic changes in things such as eating habits, exercise habits, regular self-monitoring to stay on the bandwagon and others. They make the changes and maintain them long term. They have to restrict calories to some degree for the rest of their lives to maintain the weight/fat loss. I suspect they're a little bit hungry and unhappy most of the time. Since nobody likes restriction or hunger, most people go back to old eating habits and gain all the weight back. An ideal solution would fix this problem.Defining the problem, part 2It's convenient for weight loss 'experts' to blame weight loss failures on willpower but that turns out to be a very simplistic (and not entirely correct) explanation. Quite literally, the brains of these individuals are the problem. Essentially, their brains 'want' that person to be fatter and are sending powerful appetite simulating signals to get those people to eat. That's on top of the other metabolic derangements, such as slowed metabolic rate and decreased fat burning, along with increased fat storage capacity, that occur.
Dieting athletes and bodybuilders have a slightly different set of problems although they turn out to be related in terms of the mechanism involved. Psychologically, the problems are less since most athletes equate suffering with progress in the first place, which is both good and bad. On the one hand, most athletes don't whine about being hungry or changing their habits, that's part of the price for playing. On the other, many confuse working harder with working smarter. What they lack in finesse, they make up for with pigheaded stubbornness. The real problems for this group are physiological. Without drugs (euphemistically referred to as 'props' or 'gear' in the subculture), natural athletes lose muscle mass at an alarming rate and have totally screwed-up hormone levels when they get very lean. Staying there, except for the genetically lean, is nearly impossible, as is making any real gains in muscle mass without gaining the bodyfat back. Getting lean beyond a certain point, in the range of 10-12% bodyfat for men and maybe 18-20% bodyfat for women, causes levels of testosterone, growth hormone, thyroid and the other 'good' hormones to crash. Levels of the 'bad' hormones such as cortisol skyrocket. Appetite soars through the roof. Muscle loss accelerates and getting rid of that last little bit of fat is a total pain as the body fights to keep you alive. For bodybuilders who only have to be lean for one day (contest day), it's no big deal. But stories of folks ballooning up after the contest are rampant. The physiology coupled with months of deprivation can lead to month long binges. As you might imagine, fat storage takes off. As it turns out, nearly all of the problems I described above are being controlled by the same basic systems and they turn out to be mostly in the brain. Appetite, hormones, the psychological drive for food, fat burning, etc. all under control of the same basic systems at a fundamental level. And it's your brain that is screwing you over. This is why the idea of "Just try harder" doesn't get very far. Your brain, which is feeding your urges about behavior, food, etc. is fighting against you. Did I mention that your body hates you? It does and, eventually, it's going to win.
The brain and setpointIn the last five years or so, obesity research has exploded into a whole new realm. Rather than focusing on idiotic topics such as "Why fiber is good for weight loss" the current focus is on the biological mechanisms that drive eating behavior, maintain bodyweight at certain levels, and control the partitioning of calories (where they go after you eat them). It's been suggested for decades (since at least the 50's) that the body tries to maintain some type of 'setpoint' level of bodyweight or bodyfat and will try to maintain that level. While that's a little bit simplistic, it turns out to be more true than not. Simply put (the details are coming later), the brain has sort of a preconceived notion of how fat it wants you to be, a setpoint as it were. A great deal of this 'setpoint' is imprinted at a very early age (1). Like when you're in the womb and the first few months of life early. Quite literally, what your mom did while she was pregnant is affecting you now. If she was obese (or, as it turns out, undernourished), you're more likely to be overweight and have trouble losing and keeping weight and fat off. You probably have more fat cells than you'd otherwise have, as well as a brain that 'wants' you to be fat. Other aspects of your physiology, such as hormonal axes, may also be imprinted while you're in the womb (2). This probably contributes to the problems folks have losing fat as well. So if you have problems with losing fat or with your hormone levels, just blame your mom. She should appreciate that. In addition to your early childhood, what you did during puberty as well as what you do as an adult can affect setpoint. It looks like overeating for long periods of time or staying fat long enough can cause setpoint to go up (above where it was when you were born). Contrary to popular belief, you can also add fat cells if you stay fat/overeat for extended periods, and this may affect setpoint as well as your propensity to put fat back on after you diet. Pregnancy appears to raise setpoint a bit in women too. It's bringing setpoint back down that's the problem. The whole setpoint concent is pretty easy to demonstrate in animals, although harder to measure in humans. You can breed rats who will avidly defend a given setpoint. By defend I mean this: when you overfeed them, their metabolic rate increases, they become more active, and they will automatically decrease food intake. This brings them back to their setpoint level where everything normalizes again. In contrast, when you underfeed them their metabolic rate decreases, they decrease their activity, and increase food intake (3), which brings them back to their setpoint again. They make a useful model because scientists can biopsy their little rat brains and see what's happening chemically and figure out what's driving the process. When they are below their setpoint, their little rat brains undergo characteristic changes that cause things to occur: slowed metabolic rate, hunger, etc. Once bodyfat increases, their brains think everything is normal, and brain chemicals normalize. You can also breed rats with a high setpoint to begin with. If you maintain them at a bodyweight that's lower than their setpoint, even if they aren't actively dieting, their brains and the rest of their rat physiology will show the same changes as if they were starving. As soon as you fatten them up to their setpoint, their brains go 'Aahhh' and everything becomes normal, at which point they start to defend that setpoint. A fed rat brain is a happy rat brain, or something like that. Humans show some of the same tendencies as the rats mentioned, and the same basic neurochemistry too. The big difference is that we appear to defend against underfeeding a whole lot better than against overfeeding. That is, overfeed someone and you generally don't see major increases in metabolic rate or decreases in hunger. There are exceptions, people who burn off extra calories through fidgeting and other activities; they tend to stay very lean and have trouble gaining weight (4). They also have appetites that shut off readily when they overeat. They are not most people and we hate them. The only pleasure we might derive in this regards is knowing that they will be the first to die if a famine ever comes. In most people, when you overfeed, metabolic rate goes up a little and hunger decreases a little, if at all. Excess calories are stored as fat with excellent efficiency in most people except those lucky suckers who burn the majority off (4). To get far ahead of myself, these lucky folks will likely turn out to be very leptin sensitive, a topic that will make sense in a few chapters. Everyone else will be found to be suffering from some degree of leptin resistance. It's when you underfeed people that the problems start: hunger soars, metabolic rate and hormones crash, fat burning slows down, muscle loss goes up, everything I mentioned up above happens. Your body hates you and defends better against underfeeding than it does against overfeeding. This actually makes good evolutionary sense.
What does evolution have to do with it? Now you're wondering about that last sentence, how did being fat and defending against underfeeding/starvation make good evolutionary sense? Even if you weren't wondering, I'm going to tell you. I have to justify the cost of this booklet somehow. During most of our evolution, being fat up to a point was actually beneficial, because it helped us to survive when food was unavailable. In ancient times, that was usually about half of the year. People would typically fatten up during the summer when food was available, to ensure that they could survive the winter when food wasn't around. The increased bodyfat would give them the stored energy to get through the winter on top of helping to keep them warm. It's only in recent times where being fat is a health risk, mainly because people get fat, and stay fat for extended periods. The normal starvation period that we evolved on, which leaned us out for half of every year, doesn't occur anymore. Modern life is one long fattening cycle (readers who are powerlifters can think of it as one long bulking cycle). In contrast, being skinny meant that you tended to die when food wasn't available because you starved to death that much sooner. The folks who could best deal with starvation, by slowing metabolic rate and all the rest, survived, and we carry their genes (5). This is called the Thrifty Gene hypothesis, in case you care.
To your body, dieting is fundamentally identical to starvation, it differs only in extremity. In both cases, you're eating less than your body needs and, in both cases, your body adapts pretty much the same. That is, your body doesn't 'know' that you're only dieting for 8 weeks to look good in a bathing suit. If only 'knows' that you're eating less, and adapts accordingly. You'll find out how it 'knows' in the next chapter. While I'm on the topic, a little more bad news for female readers. We've known for years that women have a harder time losing and keeping off weight, no matter what they do. In addition to having a lower metabolic rate overall, women's bodies generally adapt faster and harder to caloric restriction or exercise than men's bodies do (6). To put it in the above terms, their bodies appear to defend against weight loss even moreso than men's do. Oh yeah, they also don't burn off excess calories as well with overfeeding (4). As my friend Elzi Volk says "When it comes to fat loss, women are screwed."
Again, this makes evolutionary sense. Since women were ultimately responsible for the survival of the human race (since they give birth to and take care of the children), the ones who could stay alive the longest during the winter famine were the ones who passed on their genes (7). This is the reason that women have a much harder time losing fat (and keeping it off) than men. The exact mechanisms by which women's bodies are able to do this are still under study. Figuring out what is the problem with women and fat loss and fixing it is one of my next projects. For now, just accept that it sucks to be female if you want to lose fat. You can do it, but it's harder.
Summing up So, the basic problem is this: Your body appears to have a set idea of how fat it 'wants' you to be. That's your 'setpoint' and how high or low it is depends on what your mom did when she was pregnant, what you did during puberty, and what you've done as an adult. This causes your brain to set things up to try and keep you at that weight, more or less. To a degree, it can adapt metabolism, etc. up and down in response to over- and under-feeding respectively. But, in general, for clear evolutionary reasons, your body works far harder against you when you underfeed than when you overfeed. Essentially, your body wants to keep you at a certain level of bodyfat which is usually higher than you want, because it thinks that the next famine could be around the corner. If food becomes unavailable tomorrow, you'll live longer if you're fatter. In a few thousand years, once our bodies have figured out that famines aren't coming, maybe our genetics will adapt. Until then, metabolic slowdown and all the rest is the price to pay for dieting. In addition, in response to that famine, your body has an extremely well developed way of keeping you alive, slowing metabolic rate, making you less active so that you burn less calories, making you hungry as hell so you'll go look for what food might be available, decreasing fat burning, and many others. All are aimed at helping you to survive until food becomes available. And, as far as your body is concerned, dieting is really no different than starvation. The only real difference is one of extreme, eating something versus eating nothing. In both cases, your body 'knows' that you're eating less than you should, and it adapts accordingly. So how do we fix it? The first step to solving that problem is to figure out how the body is performing this trick, the mechanism: knowing you're starving and adapting. Then we see if we can do anything about it.
References:
1. Levin BE. The obesity epidemic: Metabolic imprinting on genetically susceptible neural circuits. Obes Res (2000) 8: 342-347.
2. Phillips DWI. Fetal growth and programming of the hypothalamic-pituitary-adrenal axis. Clinical and Experimental Pharmacology and Physiology (2001) 28: 967-970.
3. Levin BE and AA Dunn-Meynell. Defense of body weight depends on dietary composition and palatability in rats with diet-induced obesity Am J Physiol (2002) 282: R46-R54.
4. Vanltallie TB. Resistance to weight gain during overfeeding: a NEAT explanation. Nutr Rev. (2001) 59:48-51.
5. Arye Lev-Ran. Human obesity: an evolutionary approach to understanding our bulging waistline. Diabetes Metab Res Rev (2001) 17: 347-362.
6. Westerterp KR. Nutritional Implications of Gender Differences in Metabolism: Energy Metabolism, Human Studies in Gender Differences in Metabolism: Practical and Nutritional Implications ed. Mark Tarnopolsky.CRC Press. 1999.
7. Hoyenga KB and KT Hoyenga. Gender and energy balance: sex differences in adaptations for feast and famine. Physiol Behav (1982) 28: 545-563.
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