Is reta worth using at 18

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Would it do anything at the age of 18
 
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no
 
HarveyJ07 said:
Would it do anything at the age of 18
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Only if youre trying to lose fat.

Reta is a triple agonist; so it targets GLP-1, GIP, and Glucagon. Other weight loss drugs are often GLP-1s as thats most common.

Lets look at the science:

GLP-1(also commonly taken on its own):
Naturally released from the gut when you eat, slows stomach digestion down, boosts insulin when glucose levels are high leading to better insulin sensitivity. It also works to reduce appetite signals in the brain.
It works by crossing blood brain burrier in both the Hypothalamus and the Brainstem. It activates POMC/CART neurons which are satiety signals, inhibits NPY/AgRP signals which are hunger-driving signals. It also has a slight effect on the nausea pathway (which is why some get nausea especially on higher doses). Something extremely fascinating is its effects on dopamine receptors, and how it dampens the to food cues (and possibly other addictive behaviors shown in studies).

GIP:
GIP is secreted in the small intestines when you eat, by K cells. It’s an insulinotropic, which means it works to boost insulin release only in a high glucose environment; meaning that insulin does not crash in a fasted state.
In the brain there is a receptor that makes part of the hypothalamus that uptakes GIP, while not greatly understood it is shown to boost the GLP-1s satiety signals (POMC/CART). Some more recent studies also show that the GIP may actually boost ones tolerance to the nausea caused by GLP-1 which in turn makes it more sustainable.

Glucagon:
Think of glucagon as insulins “counter” hormone. It is made by alpha cells in the pancreas. (Insulin stores, glucagon mobilizes). It is naturally released by 3 main activities: fasting, exercise, a blood sugar drop. In the hypothalamus it signals for the mobilization of energy (fat) which ALSO indirectly decreases hunger. This also ties back into energy expenditure pathways -> leading to a higher BMR (often side effected with higher RHR). In the liver, glucagon is released into the bloodstream and pushes fatty acid oxidation which produces more ketones. In fat tissue it simply encourages lipolysis(the breakdown of fat).
 
hej1377 said:
Whowver said that is an iqcell
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Well thank god ty for that i tried arguing but then i just got a bunch of insults thrown at me so i just gave up
 
stormlymikkel said:
Only if youre trying to lose fat.

Reta is a triple agonist; so it targets GLP-1, GIP, and Glucagon. Other weight loss drugs are often GLP-1s as thats most common.

Lets look at the science:

GLP-1(also commonly taken on its own):
Naturally released from the gut when you eat, slows stomach digestion down, boosts insulin when glucose levels are high leading to better insulin sensitivity. It also works to reduce appetite signals in the brain.
It works by crossing blood brain burrier in both the Hypothalamus and the Brainstem. It activates POMC/CART neurons which are satiety signals, inhibits NPY/AgRP signals which are hunger-driving signals. It also has a slight effect on the nausea pathway (which is why some get nausea especially on higher doses). Something extremely fascinating is its effects on dopamine receptors, and how it dampens the to food cues (and possibly other addictive behaviors shown in studies).

GIP:
GIP is secreted in the small intestines when you eat, by K cells. It’s an insulinotropic, which means it works to boost insulin release only in a high glucose environment; meaning that insulin does not crash in a fasted state.
In the brain there is a receptor that makes part of the hypothalamus that uptakes GIP, while not greatly understood it is shown to boost the GLP-1s satiety signals (POMC/CART). Some more recent studies also show that the GIP may actually boost ones tolerance to the nausea caused by GLP-1 which in turn makes it more sustainable.

Glucagon:
Think of glucagon as insulins “counter” hormone. It is made by alpha cells in the pancreas. (Insulin stores, glucagon mobilizes). It is naturally released by 3 main activities: fasting, exercise, a blood sugar drop. In the hypothalamus it signals for the mobilization of energy (fat) which ALSO indirectly decreases hunger. This also ties back into energy expenditure pathways -> leading to a higher BMR (often side effected with higher RHR). In the liver, glucagon is released into the bloodstream and pushes fatty acid oxidation which produces more ketones. In fat tissue it simply encourages lipolysis(the breakdown of fat).
Click to expand...
REP MEEEE:feelsgiga::feelsgiga::feelsgiga:
 
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stormlymikkel said:
Only if youre trying to lose fat.

Reta is a triple agonist; so it targets GLP-1, GIP, and Glucagon. Other weight loss drugs are often GLP-1s as thats most common.

Lets look at the science:

GLP-1(also commonly taken on its own):
Naturally released from the gut when you eat, slows stomach digestion down, boosts insulin when glucose levels are high leading to better insulin sensitivity. It also works to reduce appetite signals in the brain.
It works by crossing blood brain burrier in both the Hypothalamus and the Brainstem. It activates POMC/CART neurons which are satiety signals, inhibits NPY/AgRP signals which are hunger-driving signals. It also has a slight effect on the nausea pathway (which is why some get nausea especially on higher doses). Something extremely fascinating is its effects on dopamine receptors, and how it dampens the to food cues (and possibly other addictive behaviors shown in studies).

GIP:
GIP is secreted in the small intestines when you eat, by K cells. It’s an insulinotropic, which means it works to boost insulin release only in a high glucose environment; meaning that insulin does not crash in a fasted state.
In the brain there is a receptor that makes part of the hypothalamus that uptakes GIP, while not greatly understood it is shown to boost the GLP-1s satiety signals (POMC/CART). Some more recent studies also show that the GIP may actually boost ones tolerance to the nausea caused by GLP-1 which in turn makes it more sustainable.

Glucagon:
Think of glucagon as insulins “counter” hormone. It is made by alpha cells in the pancreas. (Insulin stores, glucagon mobilizes). It is naturally released by 3 main activities: fasting, exercise, a blood sugar drop. In the hypothalamus it signals for the mobilization of energy (fat) which ALSO indirectly decreases hunger. This also ties back into energy expenditure pathways -> leading to a higher BMR (often side effected with higher RHR). In the liver, glucagon is released into the bloodstream and pushes fatty acid oxidation which produces more ketones. In fat tissue it simply encourages lipolysis(the breakdown of fat).
Click to expand...
What would increase bonemass and height then that has low side effects
 
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