Leptin and Male Reproduction: Relationship to our current PCTs

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    Leptin and Male Reproduction: Relationship to our current PCTs


    ScienceDirect - Molecular and Cellular Endocrinology : Leptin in male reproduction: the testis paradigm

    Leptin in high circulating concentrations or low concentrations in the brain can inhibit testosterone production
    ......


    http://jcem.endojournals.org/content/84/10/3673.full

    Tamox and Torem Raise leptin (granted post menapausal)
    http://www.sciencedirect.com/science...78512200001213


    Aromasin lowers leptin. I always knew why i added it in my pct, but an AI may not be warrented for the entire PCT
    http://aacrmeetingabstracts.org/cgi/...ct/2006/1/98-b


    couldnt find good evidence on Clomiphene.

    Can you give insight. on PCT, I have my way of doing it personally and always works well.

    i know of many many supplements to reduce circulating leptin levels but is this a concern.

    Also can this be a plause for a low carb high calorie diet for PCT to minimize leptin production by insulin stimulation

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    any estrogen agonist such as SERM's will increase leptin, also GH peptides WILL increase leptin, and the main reason that testosterone drops is the rise in cortisol with the drop in GnRH. The reason people gain weight is because they litterally exchange testosterone for estrogen with the exception of SERM's where there is a drop in estrogen at the HPTA. As you can see I am not a fan of peptides during pct, especially Ghrelin mimickers.
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    Quote Originally Posted by andrew732 View Post
    any estrogen agonist such as SERM's will increase leptin, also GH peptides WILL increase leptin, and the main reason that testosterone drops is the rise in cortisol with the drop in GnRH. The reason people gain weight is because they litterally exchange testosterone for estrogen with the exception of SERM's where there is a drop in estrogen at the HPTA. As you can see I am not a fan of peptides during pct, especially Ghrelin mimickers.
    GH peptides or even ghrelin agonists work by keeping leptin levels low hence the hunger.

    theres a difference though with levels in the ARC nucleus vs other places in the hypothalamus as well as circulating levels..
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    Ghrelin always boosts leptin, its a proven fact....
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    Quote Originally Posted by andrew732 View Post
    Ghrelin always boosts leptin, its a proven fact....
    so why in a state of low leptin does it rise?

    ill re research but i know the low leptin raises ghrelin as a part of NPY and agouti.

    The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review.

    Klok MD, Jakobsdottir S, Drent ML.
    Source

    Department of Endocrinology, VU University Medical Center, Amsterdam, the Netherlands.

    Abstract

    Leptin and ghrelin are two hormones that have been recognized to have a major influence on energy balance. Leptin is a mediator of long-term regulation of energy balance, suppressing food intake and thereby inducing weight loss. Ghrelin on the other hand is a fast-acting hormone, seemingly playing a role in meal initiation. As a growing number of people suffer from obesity, understanding the mechanisms by which various hormones and neurotransmitters have influence on energy balance has been a subject of intensive research. In obese subjects the circulating level of the anorexigenic hormone leptin is increased, whereas surprisingly, the level of the orexigenic hormone ghrelin is decreased. It is now established that obese patients are leptin-resistant. However, the manner in which both the leptin and ghrelin systems contribute to the development or maintenance of obesity is as yet not clear. The purpose of this review is to provide background information on the leptin and ghrelin hormones, their role in food intake and body weight in humans, and their mechanism of action. Possible abnormalities in the leptin and ghrelin systems that may contribute to the development of obesity will be mentioned. In addition, the potentials of leptin and ghrelin as drug targets will be discussed. Finally, the influence of the diet on leptin and ghrelin secretion and functioning will be described.
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    Quote Originally Posted by andrew732 View Post
    Ghrelin always boosts leptin, its a proven fact....
    http://diabetes.diabetesjournals.org...50/2/227.short

    here GH peptides
    http://jcem.endojournals.org/content/83/9/3062.short

    stimulates leptin in arc nucleaus thus increases in Ftty acd oxidation
    http://jcem.endojournals.org/content/83/9/3062.short

    difference in circulating vs levels in arc nucleaus of hypothalamus
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    I am going to address this thread generally instead of responding to individual posts per se. I hope I am adequately giving retort to everything that has been discussed.

    So...everyone is on the same page...

    Ghrelin, is the "hunger hormone" which prompts you to want to eat. About every 30 minutes, the stomach secretes this substance when ITS EMPTY. It wasn't even identified until 1999 and that after secretion makes it's way to the brain, where it goes into three separate parts: (1) the hypothalamus, which includes the hunger AND satiety centers (perhaps you can already see overlap); (2) the hindbrain, which controls the body's instinctive processes; and (3) the midbrain...the part that produces feelings of pleasure and contentment (if you read the AAS/PCT thread, you can see how this part of the brain overlaps during many different activities). Now, once in the hypothalamus, ghrelin triggers the release of neuropeptide Y, which activates those familiar feelings of hunger.

    When your stomach is filled, however, the ghrelin surges abate while another brain-gut process begins. An empty stomach is typically the size of your fist. As it fills with food, it stretches; when that occurs, three hormones are released from the gut and travel to the brain to relay the message that you are full and should stop eating. The first of these in cholecystokinin (CCK), which is released from the upper intestines. When it reaches the brain, it increases the feeling of satisfaction and encourages you to to stop eating. This hormonal signal does not last long, however, which is essentially why the other two are needed (it's also the reason - for any supplement history buffs out there that the CCK product by Pinnacle years ago ended up being a big flop).

    Think of these hormones, glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY), as the second line of fire. Released after CCK, they strongly inform the brain that you are full, while also telling the stomach to slow down its release of food into the intestines until any food in the stomach has been adequately digested. This usually accounts for the extremely full feeling when you simply cannot eat another bite - and why you still feel that way two-three hours later (think buffet eating).

    What happens, however, when you refuse to listen to those first and second rounds of warnings sent to you by these gut hormones to tell you that you are full? Thankfully, the body comes prepared with the release of yet another hormone: LEPTIN (the reason for this entire thread). Discovered a few years before ghrelin (1994), this appetite-suppressant is actually produced by your own adipose (fat) cells. Generally speaking, the higher your body fat, the more leptin you produce. Like the previous hormones mentioned, leptin travels to the hypothalamus - only it actually turns off hunger and stimulates the burning of calories.

    The problem - you knew there had to be a catch - is that leptin does NOT always function the way it is supposed to. Although most overweight and obese individuals have elevated leptin levels, many times their bodies do not respond normally to it, or their leptin stops working. In other words, they have developed leptin resistance because their bodies have produced so much that it has becomes numb to this effect. The good news for those overweight and obese is that when you lose enough weight, your cells begin to respond normally to leptin, it will suppress hunger again.

    SO - leptin and ghrelin are "essentially" antagonists (I use essentially because it's not 100%).

    Now, on to the post-menopausal studies...the biggest confounding variable to be concerned with when trying to extrapolate anything from those trials is that the aged (including your post-menopausal subjects) are harboring a boat-load of extra aromatase in heightened levels of adipose (yes, its a sad fact that we do usually gain weight when we are older and with it comes the estrone guys) and you might be surprised to learn but it is not usually the svelte lady who participates for said study. The best thing you can do to make this a non-issue; non-cyclical concern is stay thin. So now that you've shut off your other big source for estrogen, you can worry about the modest estrogen agonism offered by any SERM (and remember, that is tissue specific).

    With the use of SERMs, AIs, etc... you are likely to decrease FAT CELLS (leptin's source) which means...of course you'd see leptin go down. But keep in mind, that is only because your cells are becoming inherently more responsive to it. If you look at the first study on hypothalamic control of testosterone production, you must understand that it suggests this is a HIGH circulating concentrations and LOW hypothalamic ones that inhibit testosterone. In other words, HIGH fat (high circulating levels) and LOW response (at the hypothalamus, a la ... leptin resistance) is completely what we'd expect. This does NOT denounce the use of SERMs and AIs as having a pertinent role in PCT; it just means you should use caution when approaching PCT as a fat guy (i.e. - you should have gotten body fat levels down a bit before you embarked on the cycle).


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    Quote Originally Posted by dinoiii View Post
    I am going to address this thread generally instead of responding to individual posts per se. I hope I am adequately giving retort to everything that has been discussed.

    So...everyone is on the same page...

    Ghrelin, is the "hunger hormone" which prompts you to want to eat. About every 30 minutes, the stomach secretes this substance when ITS EMPTY. It wasn't even identified until 1999 and that after secretion makes it's way to the brain, where it goes into three separate parts: (1) the hypothalamus, which includes the hunger AND satiety centers (perhaps you can already see overlap); (2) the hindbrain, which controls the body's instinctive processes; and (3) the midbrain...the part that produces feelings of pleasure and contentment (if you read the AAS/PCT thread, you can see how this part of the brain overlaps during many different activities). Now, once in the hypothalamus, ghrelin triggers the release of neuropeptide Y, which activates those familiar feelings of hunger.

    When your stomach is filled, however, the ghrelin surges abate while another brain-gut process begins. An empty stomach is typically the size of your fist. As it fills with food, it stretches; when that occurs, three hormones are released from the gut and travel to the brain to relay the message that you are full and should stop eating. The first of these in cholecystokinin (CCK), which is released from the upper intestines. When it reaches the brain, it increases the feeling of satisfaction and encourages you to to stop eating. This hormonal signal does not last long, however, which is essentially why the other two are needed (it's also the reason - for any supplement history buffs out there that the CCK product by Pinnacle years ago ended up being a big flop).

    Think of these hormones, glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY), as the second line of fire. Released after CCK, they strongly inform the brain that you are full, while also telling the stomach to slow down its release of food into the intestines until any food in the stomach has been adequately digested. This usually accounts for the extremely full feeling when you simply cannot eat another bite - and why you still feel that way two-three hours later (think buffet eating).

    What happens, however, when you refuse to listen to those first and second rounds of warnings sent to you by these gut hormones to tell you that you are full? Thankfully, the body comes prepared with the release of yet another hormone: LEPTIN (the reason for this entire thread). Discovered a few years before ghrelin (1994), this appetite-suppressant is actually produced by your own adipose (fat) cells. Generally speaking, the higher your body fat, the more leptin you produce. Like the previous hormones mentioned, leptin travels to the hypothalamus - only it actually turns off hunger and stimulates the burning of calories.

    The problem - you knew there had to be a catch - is that leptin does NOT always function the way it is supposed to. Although most overweight and obese individuals have elevated leptin levels, many times their bodies do not respond normally to it, or their leptin stops working. In other words, they have developed leptin resistance because their bodies have produced so much that it has becomes numb to this effect. The good news for those overweight and obese is that when you lose enough weight, your cells begin to respond normally to leptin, it will suppress hunger again.

    SO - leptin and ghrelin are "essentially" antagonists (I use essentially because it's not 100%).

    Now, on to the post-menopausal studies...the biggest confounding variable to be concerned with when trying to extrapolate anything from those trials is that the aged (including your post-menopausal subjects) are harboring a boat-load of extra aromatase in heightened levels of adipose (yes, its a sad fact that we do usually gain weight when we are older and with it comes the estrone guys) and you might be surprised to learn but it is not usually the svelte lady who participates for said study. The best thing you can do to make this a non-issue; non-cyclical concern is stay thin. So now that you've shut off your other big source for estrogen, you can worry about the modest estrogen agonism offered by any SERM (and remember, that is tissue specific).

    With the use of SERMs, AIs, etc... you are likely to decrease FAT CELLS (leptin's source) which means...of course you'd see leptin go down. But keep in mind, that is only because your cells are becoming inherently more responsive to it. If you look at the first study on hypothalamic control of testosterone production, you must understand that it suggests this is a HIGH circulating concentrations and LOW hypothalamic ones that inhibit testosterone. In other words, HIGH fat (high circulating levels) and LOW response (at the hypothalamus, a la ... leptin resistance) is completely what we'd expect. This does NOT denounce the use of SERMs and AIs as having a pertinent role in PCT; it just means you should use caution when approaching PCT as a fat guy (i.e. - you should have gotten body fat levels down a bit before you embarked on the cycle).


    D_
    thanks for responce.

    now what if its a bulking cycle and one wants to use nolva on cycle to ward gyno. and in PCT to recover and you inevitably got more fatt accumalted then you wanted to.

    how would you tackle the possible small leptin resistance from increased adipose accumulation from getting worse.

    its obvious that sdome people go way overboard with their bulk.

    Any advice to those on this subject matter?

    and i completely understand leptin resistance and understand the difference in circulating levels vs hypothalmic levels.

    Thanks for clearing this up. because i felt it was important.
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    On spot info but as I thought it seems as though GHRP-6 is slightly negative on testosterone output or slightly positive? Correct me if I am misunderstanding this Dr.D.
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    Sorry to be a pain but I cannot help but to notice this statement on the study with aromasin and leptin. " One possible explanationfor this distinct effect of exemestane on plasma leptin maybe the weak androgen effects of exemestane and its major metabolite17-hydro-exemestane"
    Even though Formestane and exemestane are closely related, I thought formestane was clearly more "androgenic" as it becomes an active steroid more readily than exemestane. Could it had been that they were using low doses of Formestane?
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    Great discussion!

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    bump dr H.

    in PCT, fairly lean, going to dose PM to increase leptin during sleep so i can hopefully burn more fat.

    what do you think. Is this why some people get leaner in PCT (when normal weight, or not leptin resistant)
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