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Yeah but so they can't be used for a bodybuilder as you want to increase the weight and if when you do it suppress your appetite you are fucked : /Remember it only feels like an appetite suppressant until you hit the weight homeostasis for that dose.
It's not a diet pill that reduces appetite regardless of weight.
If the room temperature (weight) and the thermostat (glp) are matched, nothing is happening. That's what a maintainance dose is. You feel normal. There's no appetite suppression. Drop more weight and appetite fires up to bring weight back up. Gain weight, and appetite suppression returns.
GLPs turn the thermostat down.
This is the mechanism of action people can't seem to grasp. It's not even specific to the drug, it's the body's natural weight regulation system.
But in the absence of this knowledge, that the body seeks to maintain energy homeostasis, and weight issues, underweight and overweight are usually attributable to a malfunction in this system, it's a paradigm shift in thinking that's going to be difficult to grasp.
Yeah but so they can't be used for a bodybuilder as you want to increase the weight and if when you do it suppress your appetite you are fucked : /
Btw I'm not sure you are right here @Ghoul because for example, on sema I was gaining weight at 1mg and my appetite suppression was non existent when instead at first it was very strong but on both instant I kept my same weight. So the appetite suppression just became less and less with time without my weight changing, surely not decreasing.
If it was like you are saying I should have got a stronger appetite suppression when I tried to bulk on it instead nothing happened except I had excellent BG control.
Lol, thanks immensely for your continued input here and in other threads."I am a walking glp-1 encyclopedia"
Lol, thanks immensely for your continued input here and in other threads.
Things i now worry about since last time we spoke:
- Is there a risk for pancreatic cancers with GLPs?
- In follow up of these drugs creating antibodies if using incorrect dilution rates and or dosage protocols, or start/stopping protocols, is there increased risk for autoimmune responses suppressing our natural or unnatural hormone functioning? GH as an example, but other hormones maybe as well?
- If so, how can one be comfortable using these, when it might destroy other processes in our bodies?
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Units are nanomolars, lower is better. The relative percentages are hard to express, but <1 is "high" 1-100 is "moderate" and >100 is "low".
Source for sema:
Discovery of the Once-Weekly Glucagon-Like Peptide-1 (GLP-1) Analogue Semaglutide - PubMed
Liraglutide is an acylated glucagon-like peptide-1 (GLP-1) analogue that binds to serum albumin in vivo and is approved for once-daily treatment of diabetes as well as obesity. The aim of the present studies was to design a once weekly GLP-1 analogue by increasing albumin affinity and secure...pubmed.ncbi.nlm.nih.gov
Imma skip the others for now unless anyone cares. Much of this data is non-specific and proprietary.
From [1]: "In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids intotriglycerides, (3) increase insulin receptor number, and (4) increase sensitivity of insulin-stimulated glucose transport."
"With that in mind, the following hypothesis may be proposed: individuals with a condition of increased GIP responsiveness may be more prone to obesity and hyperinsulinemia. Increased GIP responsiveness may manifest itself in the form of either increased affinity for GIP by GIP receptors, increased GIP receptor number, or increased synthesis and secretion of GIP following normal meal stimulation. The increased GIP responsiveness would likely increase insulin release resulting in greater and prolonged hyperinsulinemia. To compound this abnormality, GIP can also increase the affinity of the insulin receptor for insulin as well as increase the insulin-like effects in fat cells, all of which may serve to increase efftciency in the accumulation of triglycerides in fat cells. Thus, anecdotal accounts of individuals accumulating fat tissue mass at greater rates under normal meal conditions maybe a consequence of increased GIP responsiveness. Such individuals have greater efficiency in fat storage as a result of increased GIP and insulin responses when compared with normal persons." [1].
Also respected and well know member Type-IIx said
GIP functions in fat cells to increase fat accrual. [1].
So why are people here saying GIP stimulates lipolysis? Who is correct?
Thanks, now we know the nanomolars how can we find out how much glp1 there is in 2.5mg tirz and what is the dose equivalent on semaglutide?
Paradoxically, it does both. I'm going to use somewhat imprecise analogies to try and make this understandable.
Like GLP, GIP is released in response to food intake. It preps fat for energy storage, by increasing blood flow and other mechanisms. The same process that allows fat to more easily store excess energy also eases the path for lipolysis (releasing stored energy) in a calorie deficit.
Considering GIP is naturally secreted when taking IN food, storage from the presence of excess calories would be far more likely than release through lipolysis.
Basically it "opens the door" of fat cells through which energy can enter OR exit.
Here's the magic. GIP also induces satiation through a direct effect in the brain. "Ahhh, we've eaten enough" it whispers to the hypothalamus.
But with Tirz, this is all happening in the absence of food intake, you feel satiated, the "door" of fat cells are opened and you get some of your energy requirement satisfied from lipolysis (fat loss).
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Thank you for explaining.
Do you think bodybuilders should be concerned with using tirz for bulking?
Surely you wouldn't want to use this in an energy surplus then
I know Type-IIx suggests we use Semaglutide
In a small group of diabetics in this study, in a normal Tirz dose induced calorie deficit, abdominal visceral fat was significantly reduced, liver fat was significantly reduced. Abdominal subcutaneous fat increased, but to a much smaller degree than abdominal visceral fat decreased. This is a healthy recomposition of fat.
Was these diabetics training and eating enough protein? gaining fat isn't uncommon for those crash dieting/ consuming low calories as you are losing lean body mass so end up in a skinny fat position
Thanks