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_
