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  1. #1
    Novice MrMakaveli's Avatar
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    Bromo for fat-loss
    Anyone using it?

    If so, how bad are the cognitive effects? (I've heard bromo causes "brain fog") I'm debating on if I should wait until classes are over to start or not.

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    Bromocriptine for Weight Loss
    by Nandi


    Introduction

    Bromocriptine, a drug that mimics the action of the naturally occurring neurotransmitter dopamine, has a long history of use by body builders and life extension enthusiasts. The drug originally gained popularity due to its reputation for acting as a mild growth hormone secretagogue. This is paradoxical, since in people suffering from acromegaly, or growth hormone excess, bromocriptine has the opposite effect: it actually lowers GH levels. Bromocriptine has a number of other legitimate medical uses, including treatment of Parkinson's Disease and the lowering of prolactin levels in people suffering from prolactin secreting tumors. It has also been used successfully to treat hyperprolactinemia (elevated prolactin) that often occurs as a side effect of the administration of antipsychotic medications.


    Bromocriptine and Weight Loss


    Lately however, bromocriptine has gained prominence particularly on the World Wide Web as a weight loss agent. Perhaps no single person is more responsible for this resurgence of interest in the drug than Lyle McDonald, who popularized its anti-obesity properties in his recently published e-book (1). There are studies both in animals (2) and humans (3),(4) that support the ability of bromocriptine to reduce weight and body fat. The exact mechanism whereby dopaminergic agonists induce weight loss has not been elucidated.

    Studies in animals have shown mixed effects of dopaminergic agonists on lipid metabolism. When dopamine and SKF 38393, a D2 receptor agonist were administered to genetically obese mice, antilipogenic effects were observed in the liver, but a combination of both lipolytic and antilipolytic effects were demonstrated in adipose tissue. In adipose tissue lipoprotein lipase activity was decreased (an antilipogenic effect) where as beta-agonist stimulated lipolysis was decreased (5). Additionally, obese mice treated with dopaminergic agonists also exhibited reduced de novo lipogenesis (2). This is the process whereby dietary carbohydrates are converted to fat. Interestingly, while de novo lipogenesis is important in animals, its contribution to fat deposition in humans is relatively unimportant (6). When humans ingest excess carbohydrates, rather than being stored as fat, the carbohydrates are preferentially used as fuel, preserving fat stores that would have otherwise been oxidized. Here is a case where the results of animal studies do not necessarily carry the same implications for humans.

    Dopamine has also been implicated in appetite control. It has been postulated that dopamine modulates appetite by providing a reward stimulus, and that obese individuals have lower levels of dopamine receptors in certain portions of the brain (7). Hence to achieve the same "reward" from eating as normal individuals, obese individuals must eat more. This would provide some rationale for the treatment of obese individuals with dopaminergic agonists, but it is unclear whether normal body weight individuals possessing a normal density of dopamine receptors and/or normal dopaminergic activity in the brain would benefit from such treatment. The authors of the previously cited paper also acknowledged that it was unclear whether the relative paucity of dopamine receptors in the obese subjects was a cause or a result of their overeating. Since eating elevates dopamine levels, the brain could be compensating for elevated dopamine in chronic overeaters by downregulating the dopamine receptors. This latter possibility could call into question the use of dopaminergic agonists for appetite control. The result of increasing dopamine levels with agonists could lead to a further downregulation of the D2 receptors, leading to an increased desire to eat in order to further elevate dopamine levels. In a review of the above-cited study, Dr. Joseph Frascella of NIDA’s [National Institute of Drug Abuse] Division of Treatment Research commented on this positve feedback effect on D2 receptor downregulation:

    “This deficiency could be a double-edged sword that cuts both ways. First, the reduced reward experienced by people with this deficiency may make them more likely to engage in addictive behaviors. Then, the addictive behavior itself could make the deficit worse as the brain further lowers D2 levels in response to constant overstimulation of the reward pathway. “In the end, they could be much worse off biologically than when they started,”


    http://www.drugabuse.gov/NIDA_Notes...thological.html


    Another mechanism by which dopamine could suppress appetite is by antagonizing neuropeptide Y (NPY). As fat stores decrease during dieting, leptin levels fall. This signals an increase in NPY, which is a potent hunger inducing neuropeptide. Treatment of genetically obese mice with bromocriptine led to a decrease in the elevated levels of hypothalamic NPY in these animals (2). Again, the implications of these observations to normal humans are unclear.

    Both obesity and cocaine addiction have been linked to the dopaminergic reward pathway. As we have been discussing, food consumption elevates dopamine level, leading to a reward stimulus. In the case of cocaine, the traditional view has been that cocaine blocks the cellular dopamine transporter, blocking dopamine reuptake and increasing extracellular dopamine levels, again leading to reinforcing reward. However, this view has been called into question by the 1998 publication of a study showing that mice lacking the dopamine transporter develop cocaine addiction (8). According to the dopamine reward model of cocaine addiction, the lack of the dopamine transporter should have maintained chronically elevated dopamine levels, obviating any reward derived from cocaine use. Nevertheless the mice became addicted. The authors suggested that other neurotransmitter pathways, such as those mediated by serotonin may play a more important role in addiction. These ideas are supported by the fact that dopaminergic agonists, including bromocriptine, have not been useful in treating cocaine addiction (9).

    Is it possible that the food driven reward mechanism is also dopamine independent, or at least only partially dependent on dopamine? The successful use of fenfluramine as an anorectic agent suggests this could be the case. Fenfluramine stimulates the release of serotonin and is a potent reuptake inhibitor of serotonin into nerve endings. This increases levels of serotonin in the nerve synapse, increasing levels of serotonergic nerve transmission. In both animals and humans, fenfluramine induces lack of appetite leading to weight loss. Fenfluramine was withdrawn from the market in 1997 due to findings that its use was associated with valvular heart disease.



    Side Effects of Bromocriptine Treatment


    As with the majority of drugs bromocriptine has a number of well characterized side effects that seem more unpleasant than dangerous, and often abate during treatment. These include nausea, orthostatic hypotension, headaches, abdominal discomfort, nasal congestion, fatigue and constipation. Besides these there are two other potential side effects that are not as well characterized, that are controversial, and that are of particular interest to bodybuilders and other athletes. The first I would like to address is the possibility that bromocriptine may lower testosterone levels in normal men, as well as increase the ovarian aromatization of testosterone to estrogen in women. The second is the potential bromocriptine may have to suppress the immune system in normal humans.



    Bromocriptine and Steroidgenesis


    It has been appreciated for decades that elevated levels of prolactin in males (hyperprolactinemia) can suppress testosterone production. Hyperprolactinemia disrupts the hypothalamic-pituitary-gonadal axis in women as well, leading to amenorrhea and infertility. Since bromocriptine lowers prolactin levels, when bromocriptine is administered to these patients, normal sexual function is usually restored. What is less well known is that studies done both in vitro and in humans suggest that hypoprolactinemia (low prolactin levels) also leads to suppressed testosterone production. So prolactin appears to exert a biphasic effect: too much or too little can disrupt testicular function. Normal physiological levels of prolactin appear to be necessary for normal gonadal function. (10) (11). To quote from Marin-Lopez et al, (10), where sulpiride and bromocriptine were used respectively to induce hyper and hypoprolactinemia in normal males


    "the hyperprolactinemia induced a low basal level of testosterone with a higher response of this steroid to hCG...while the loss of the trophic effect of prolactin on gonadal steroidogenesis, as seen in hypoprolactinemia produces a decrease of basal testosterone levels without any alteration of the response of this steroid to hCG. We conclude that prolactin plays an important role in the steroidogenesis of Leydig cells in normal men.'' (11)
    Confusing the issue is the fact that several other studies both in vitro and in vivo have shown either no effect or an increase in testosterone production due to both prolactin and bromocriptine administration (12) (13).

    A number of experimental observations have led to several theories that could possibly explain how bromocriptine induced hypoprolactinemia suppresses testosterone production. Kovacevic and Sarac (14) proposed that bromocriptine competitively inhibits androgen production at the level of the testicular enzymes 17 alpha-hydroxylase and/or 17,20-lyase. These enzymes act at intermediate steps in the testicular production of testosterone. Aisaka et al. observed a decrease in luteinizing hormone (LH) levels that was mirrored by a decrease in testosterone after bromocriptine administration, suggesting that bromocriptine directly inhibits LH secretion from the pituitary (15). As we know, luteinizing hormone, or LH, secreted from the pituitary gland acts directly on testicular Leydig cells to stimulate testosterone secretion.

    On the other hand Suescun et al. observed a decrease in circulating testosterone after bromocriptine administration in men with no decrease in LH levels (16), consistent with a direct testicular action of bromocriptine, as proposed by Kovacevic.

    Other studies have shown that lowering prolactin decreases the binding of LH to the Leydig cell LH receptor, with a concomittent reduction in androgen production (17). These researchers concluded that


    These results suggest that under normal conditions, endogenous prolactin plays a key role in maintaining the functional integrity of rat Leydig cells." (16)
    So perhaps by either lowering the affinity of the LH receptor to LH, or by directly decreasing LH receptor number, bromocriptine could lower testosterone production.

    As is obvious from the conflicting studies, and the variety of proposed mechanisms for bromocriptine induced testosterone suppression, there is much to be learned about the role of prolactin in maintaining normal testicular steroidogenesis.

    All of the studies thus far cited have been carried out in men. What about the effects of bromocriptine in normal women? As mentioned earlier in the article, hyperprolactinemia inhibits ovulation in both animals and humans. One interesting study showed that prolactin administered to rats decreased levels of ovarian aromatase. Conversely, when bromocriptine was administered, ovarian aromatase was increased (18). Is this of any relevance to human females? Perhaps, since the same phenomenon is observed during the follicular phase of the menstrual cycle: bromocriptine increases the estradiol/testosterone ratio as a result of increased aromatization of testosterone to estrogen (19).



    Bromocriptine and the Immune System


    A number of studies have shown that prolactin stimulates certain aspects of immunity, and that by lowering prolactin with bromocriptine many of the symptoms of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus can be ameliorated. A recent review by McMurray (20) provides an excellent overview of this topic. While this is certainly hopeful news for people suffering from these diseases, what are the implications for the immune lowering effects of bromocriptine in healthy people?

    One possibility is that by suppressing the prolactin mediated immune response, an individual could become more susceptible to tumor formation. (21). As Matera et al pointed out (22), prolactin specifically heightens the response of the cellular arm of the immune system. Recalling some basic immunology, the immune system has two components, the cellular arm and the humoral arm. The former is responsible for the direct attack on pathogens, while the latter involves the production of antibodies that mark pathogens for destruction, as well as creating a class of "memory" B cells that once primed by exposure to a pathogen, will respond vigorously the next time the body encounters the same invader. The cellular response is orchestrated by so called Th1 helper cells. The humoral response on the other hand is governed by another T cell subclass, the Th2 helper cells. These two T cell subclasses keep each other in check by controlling the production of cytokines that are mutually suppressive. So any immune stimulus that activates Th1 cells will suppress the Th2 response, and vice versa. So by suppressing prolactin (which heightens the cellular immune respons), cellular immunity is weakened.

    One point of possible concern is that many persons who are using or contemplating the use of bromocriptine also use anabolic-androgenic steroids (AAS). Like bromocriptine, Anabolic Androgenic Steroids (AAS) suppress the cellular arm of the immune system. They do so by stimulating Th2 cells, which as we discussed above, suppress the Th1 driven cellular response. So users of both Anabolic Androgenic Steroids (AAS) and bromocriptine could receive a double dose of immune suppression, leaving the body open to attack by pathogens, or conceivably more susceptible to the development of tumors. This latter possibility is potentially heightend by the fact that many Anabolic Androgenic Steroids (AAS) elevate IGF-1 levels, which have been implicated in tumorogenesis.

    It has also been demonstrated that prolactin opposes the immunosuppressive effects of glucocorticoids (21). Bromocriptine, by virtue of prolactin suppression, therefore may leave an overtrained or stressed individual more prone to the deleterious effects of elevated cortisol levels, including increased muscle catabolism, and an impaired immune response to exercise induced muscle damage, which is essential to growth.(Post exercise muscle damage is a powerful catalyst for growth. The muscles repair and rebuild so that they are bigger and stronger that before training. Suppressing this post exercise inflammation, whether with cortisol or NSAIDS, hinders growth.)



    Bromocriptine and Cognitive Impairment


    Dopaminergic agonists including bromocriptine exhibit mixed effects on cognitive ability when used to treat Parkinson’s patients, as well when administered to normal subjects. Swainson et al (23) showed that when administered to Parkinson’s patients, bromocriptine improved working spatial memory, while at the same time impairing so called “reversal learning” skills. This effect was subsequently reproduced in normal volunteers (24). In a reversal task, subjects have to learn that a previously rewarded stimulus now lacks reward, while the formerly neutral or negative stimulus now receives reward. This involves two stages: ceasing to respond to the former stimulus, while simultaneously learning to respond to a new stimulus.

    A real world example of working spatial memory is learning to adapt and respond to changing situations, as one would face during a chess game. An example of a reversal learning skill is the ability of a child who is repeatedly reprimanded for chatting to classmates to realize that it is expected of her to participate in classroom discussions.

    In the experiment carried out by Swainson et al (24) mentioned above, normal volunteers were administered 1.25 mg of bromocriptine. One aspect of the study that is interesting is that only the subjects who showed relatively poor working spatial memory before bromocriptine administration showed an improvement after being given the drug, whereas no such correlation existed for reversal learning. Bromocriptine impaired reversal learning independently of a subject’s pre-administration reversal learning skills. The bromocriptine treated subjects performed better on the second round of reversal learning testing, which suggested to the researchers that bromocriptine impairs this aspect of cognition in novel situations more strongly than in familiar ones.

    Although there is no concrete explanation for the bromocriptine induced cognitive impairment, the authors theorize it is due to dopamine overload of the neural circuitry involved in reverse learning. Jentsch et al (25) showed that monkeys exhibited a similar impairment in reversal learning after cocaine administration. In this experiment food was placed under one of three novel objects and the monkeys learned to lift that object to obtain the food. When the food was subsequently placed under a different one of the three objects, placebo treated monkeys quickly learned to lift the new object to get the food, while the cocaine treated monkeys continued to lift the original object in search of food.

    The parallels between this experiment and the human reversal learning experiment are not surprising since cocaine elevates dopamine levels in certain portions of the brain, just as bromocriptine acts as a dopaminergic agonist in the brain. Dopaminegic overload is likely the cause of the impaired reverse learning in both experiments.




    Summary


    Just as users of Anabolic Androgenic Steroids (AAS) owe it to themselves to become familiar with the impact these drugs can have on a person's health, so should users, or potential users, of bromocriptine be aware of the possible health implications of its use. I've tried to point out some of the potential benefits of bromocriptine use (e.g. weight loss, treatment of autoimmune diseases) as well as some possible drawbacks (impaired gonadal function; immunosuppression). Like just about every other agent used to improve performance or lose weight, bromocriptine has its potential dark side as well.

    Feel free to debate and critique this piece. You may also of course contact the author. Critique and discuss here.


    References:

    (1) Bromocriptine; McDonald, Lyle

    (2) Int J Obes Relat Metab Disord 1999 Apr;23(4):425-31
    Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists.
    Scislowski PW, Tozzo E, Zhang Y, Phaneuf S, Prevelige R, Cincotta AH.

    (3) Diabetes Care 1996 Jun;19(6):667-70
    Bromocriptine (Ergoset) reduces body weight and improves glucose tolerance in obese subjects.
    Cincotta AH, Meier AH.
    .
    (4) Eur J Endocrinol 2002 Jul;147(1):77-84
    Dopaminergic tone and obesity: an insight from prolactinomas treated with bromocriptine.
    Doknic M, Pekic S, Zarkovic M, Medic-Stojanoska M, Dieguez C, Casanueva F, Popovic V.

    (5) Metabolism 1999 Aug;48(8):1033-40
    Bromocriptine/SKF38393 treatment ameliorates dyslipidemia in ob/ob mice.
    Zhang Y, Scislowski PW, Prevelige R, Phaneuf S, Cincotta AH.

    (6) Am J Clin Nutr 2001 Dec;74(6):707-8
    Am J Clin Nutr. 2001 Dec;74(6):737-46.
    No common energy currency: de novo lipogenesis as the road less traveled.
    Hellerstein MK.

    (7) Lancet 2001 Feb 3;357(9253):354-7
    Brain dopamine and obesity.
    Wang GJ, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, Fowler JS.

    (8) Nat Neurosci 1998 Jun;1(2):132-7
    Cocaine self-administration in dopamine-transporter knockout mice.
    Rocha BA, Fumagalli F, Gainetdinov RR, Jones SR, Ator R, Giros B, Miller GW, Caron MG.

    (9) Expert Opin Investig Drugs 2002 Apr;11(4):491-9
    The potential of dopamine agonists in drug addiction.
    Kosten TR, George TP, Kosten TA

    (10) Endocrinology 2001 Jan;142(1):308-18
    Biphasic action of prolactin in the regulation of murine Leydig tumor cell functions.
    Manna PR, El-Hefnawy T, Kero J, Huhtaniemi IT.

    (11) Invest Clin 1996 Sep;37(3):153-66
    Leydig cell function in hyper- or hypoprolactinemic states in healthy men
    Marin-Lopez G, Vilchez-Martinez J, Hernandez-Yanez L, Torres-Morales A, Bishop W.

    (12) Biol Reprod 1978 Feb;18(1):44-54
    Hormonal interactions in regulation of androgen secretion.
    Bartke A, Hafiez AA, Bex FJ, Dalterio S.

    (13) Clin Endocrinol (Oxf) 1982 Oct;17(4):345-52
    Relationship of changes in serum concentrations of prolactin and testosterone during dopaminergic modulation in males.
    Nakagawa K, Obara T, Matsubara M, Kubo M.

    (14) J Steroid Biochem Mol Biol 1993 Dec;46(6):841-5
    Bromocriptine-induced inhibition of hydroxylase/lyase activity of adult rat Leydig cells.
    Kovacevic R, Sarac M.

    (15) Nippon Naibunpi Gakkai Zasshi 1985 Jun 20;61(6):701-9
    The effects of bromocriptine on the pulsatile pattern and the circadian profile of gonadotropins and testosterone secretion in normal adult men
    Aisaka K, Ogawa T, Mori H, Kigawa T.

    (16) J Androl 1985 Jan-Feb;6(1):10-4
    Induced hypoprolactinemia and testicular steroidogenesis in man.
    Suescun MO, Scorticati C, Chiauzzi VA, Chemes HE, Rivarola MA, Calandra RS

    (17) Arch Androl 1979 Nov;3(3):219-30
    Prolactin and Leydig cell responsiveness to LH/hCG in the rat.
    Purvis K, Clausen OP, Olsen A, Haug E, Hansson V.

    (18) Biol Reprod 1983 Sep;29(2):342-6
    Inhibition of ovarian aromatase by prolactin in vivo.
    Tsai-Morris CH, Ghosh M, Hirshfield AN, Wise PM, Brodie AM.

    (19) Fertil Steril 1989 Jul;52(1):51-4
    Prolactin suppression by bromocriptine stimulates aromatization of testosterone to estradiol in women.
    Martikainen H, Ronnberg L, Puistola U, Tapanainen J, Orava M, Kauppila A.

    (20) Semin Arthritis Rheum 2001 Aug;31(1):21-32
    Bromocriptine in rheumatic and autoimmune diseases.
    McMurray RW.

    (21)J Neuroimmunol 2000 Sep 1;109(1):47-55
    Prolactin in autoimmunity and antitumor defence.
    Matera L, Mori M, Geuna M, Buttiglieri S, Palestro G.

    (22) Brain Behav Immun 1992 Dec;6(4):394-408
    Prolactin and prolactin secretagogues reverse immunosuppression in mice treated with cysteamine, glucocorticoids, or cyclosporin-A.
    Bernton E, Bryant H, Holaday J, Dave J.

    (23) Neuropsychologia 2000;38(5):596-612
    Probabilistic learning and reversal deficits in patients with Parkinson's disease or frontal or temporal lobe lesions: possible adverse effects of dopaminergic medication.
    Swainson R, Rogers RD, Sahakian BJ, Summers BA, Polkey CE, Robbins TW.

    (24) Psychopharmacology (Berl) 2001 Dec;159(1):10-20
    Improved short-term spatial memory but impaired reversal learning following the dopamine D(2) agonist bromocriptine in human volunteers.
    Mehta MA, Swainson R, Ogilvie AD, Sahakian J, Robbins TW.

    (25) Neuropsychopharmacology 2002 Feb;26(2):183-90
    Impairments of reversal learning and response perseveration after repeated, intermittent cocaine administrations to monkeys.
    Jentsch JD, Olausson P, De La Garza R 2nd, Taylor JR.

  3. #3
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    I'm currently using 2.5mg/day (taken before bed) while on fina. I stayed up for a couple hours after taking it and my stomach felt a bit uneasy for about 10 minutes... sinuses also got a bit congested. Other than that no sides. I'm not using it to drop fat though, so I can't comment on that effect... so far I don't see a difference, but that may be cause I'm eating 5-6k cals/day

  4. #4
    I am banned! Drveejay11's Avatar
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    Great post RoadHouse!

    Here's some more:

    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 ********* 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 *********ally 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, ********* 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 ********* 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 ********* derangements, such as slowed ********* 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 ********* 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 ********* 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 ********* 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 ********* 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, ********* 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, ********* 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.

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    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 ********* 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 ********* 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.

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    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, ********* 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 ********* 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: ********* 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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    Community Veteran JohnnyB's Avatar
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    Damn I burned 100 calories just reading those two posts

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    Hehehe........

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    This is like any other drug in the way that everyone will have a different reaction to it. Bromo tends to supress your appetite. With some people, 2.5mg is enough for an entire day. For others, 2.5mg would make them vomit. Personally, I could eat up 10mg of Bromo and not have it tickle my stomach. Just me and my opinion

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