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CLIFFS
1. Reta is not a drug. It's a signal.
2. How reta works
Goes straight to your hypothalamus (your brain's central command center).
It specifically targets something called Pro-opiomelanocortin (POMC). When these neurons get activated, they release Alpha-melanocyte-stimulating hormone (a-MSH), a neuropeptide that binds to Melanocortin 4 (MC4R), a G-protein-coupled receptor in your brain that plays a crucial role in regulating energy balance and appetite.
This is the biochemical equivalent of slamming down the off switch on your appetite.
It suppresses Neuropeptide Y (NPY), which is the most powerful hunger-signaling molecule that your body produces.
full. Reprogramming your brain's definition of hunger.
It binds to GLP-1 and GIP, you know these receptors on the beta cells, which trigger G-protein coupled receptor cascades that skyrocket intracellular cyclic AMP (cAMP), this amps up glucose-dependent insulin secretion.
These processes only occur when glucose is high; no more wild spikes.
While simultaneously telling the alpha cells to stand down, shutting down all unnecessary glucagon output.
The best part is, this happens in your liver. Reta binds to glucagon receptors on hepatocytes (cells) in your liver. Cyclic AMP (cAMP) activates Protein kinase A (PKA) which phosphorylates (a biochemical process where a phosphate group is added to a molecule, such as a protein or sugar) and activates hormone sensitive lipase HSL (a key intracellular enzyme that breaks down stored lipids, such as triglycerides and cholesterol esters, into free fatty acids and cholesterol, primarily in adipose tissue).
HSL is the enzyme that unlocks your fat cells, hydrolyzing stored triglycerides into free fatty acids, which you're going to burn, and then it floods your bloodstream with all this fuel ready for oxidation to be used. Turning your body into a fat-burning machine.
3. microdosing myths
This triple agonism creates a self-reinforcing, very powerful feedback loop drastically reducing caloric intake, highly sensitizing insulin response, and maxing out basal energy expenditure.
Reta's terminal half-life is approximately 144 hours about 6 days.
The Importance of Steady State Concentration
Requires a steady state concentration. (therapeutic equilibrium where the concentration in the bloodstream stays within a consistent range over time, rather than continuously building up or falling off)
The time to reach steady state is determined by half half-life. It takes four to five half-lives to reach 94 to 97%.
** 6 day half life = 24-30 days **
The weekly dosing interval is not arbitrary because the 7-day injection perfectly reinforces the plasma concentration just as it begins to decline from the previous dose. So it maintains that very crucial, very stable therapeutic plateau.
If you microdose, you can never go through the 4 to 5 half-lives to reach the 94 to 97% of steady state concentration, which means you'll never get to the 24 to 30 day mark, which, for reta is required.
The fallacy of: "tiny doses every day because you get fewer side effects and you get the same benefits."
For example, 0.1 milligrams daily versus 2.5 milligrams weekly means that the amount administered is likely less than the daily clearance rate, which we already learned is required.
You perpetually operate in what's called the distribution phase. You're trying to fill a bathtub with a thimble while the drain is wide open.
You never get to the therapeutic steady state that's required for efficacy. Rewiring of the hypothalamic set point requires a very strong, sustained signal.
A weekly dose provides days-long signals that carve new fullness pathways into your brain's neural architecture. A microdose is a weak, fleeting signal.
1. Reta is not a drug. It's a signal.
2. How reta works
Goes straight to your hypothalamus (your brain's central command center).
It specifically targets something called Pro-opiomelanocortin (POMC). When these neurons get activated, they release Alpha-melanocyte-stimulating hormone (a-MSH), a neuropeptide that binds to Melanocortin 4 (MC4R), a G-protein-coupled receptor in your brain that plays a crucial role in regulating energy balance and appetite.
This is the biochemical equivalent of slamming down the off switch on your appetite.
It suppresses Neuropeptide Y (NPY), which is the most powerful hunger-signaling molecule that your body produces.
full. Reprogramming your brain's definition of hunger.
It binds to GLP-1 and GIP, you know these receptors on the beta cells, which trigger G-protein coupled receptor cascades that skyrocket intracellular cyclic AMP (cAMP), this amps up glucose-dependent insulin secretion.
These processes only occur when glucose is high; no more wild spikes.
While simultaneously telling the alpha cells to stand down, shutting down all unnecessary glucagon output.
The best part is, this happens in your liver. Reta binds to glucagon receptors on hepatocytes (cells) in your liver. Cyclic AMP (cAMP) activates Protein kinase A (PKA) which phosphorylates (a biochemical process where a phosphate group is added to a molecule, such as a protein or sugar) and activates hormone sensitive lipase HSL (a key intracellular enzyme that breaks down stored lipids, such as triglycerides and cholesterol esters, into free fatty acids and cholesterol, primarily in adipose tissue).
HSL is the enzyme that unlocks your fat cells, hydrolyzing stored triglycerides into free fatty acids, which you're going to burn, and then it floods your bloodstream with all this fuel ready for oxidation to be used. Turning your body into a fat-burning machine.
3. microdosing myths
This triple agonism creates a self-reinforcing, very powerful feedback loop drastically reducing caloric intake, highly sensitizing insulin response, and maxing out basal energy expenditure.
Reta's terminal half-life is approximately 144 hours about 6 days.
The Importance of Steady State Concentration
Requires a steady state concentration. (therapeutic equilibrium where the concentration in the bloodstream stays within a consistent range over time, rather than continuously building up or falling off)
The time to reach steady state is determined by half half-life. It takes four to five half-lives to reach 94 to 97%.
** 6 day half life = 24-30 days **
The weekly dosing interval is not arbitrary because the 7-day injection perfectly reinforces the plasma concentration just as it begins to decline from the previous dose. So it maintains that very crucial, very stable therapeutic plateau.
If you microdose, you can never go through the 4 to 5 half-lives to reach the 94 to 97% of steady state concentration, which means you'll never get to the 24 to 30 day mark, which, for reta is required.
The fallacy of: "tiny doses every day because you get fewer side effects and you get the same benefits."
For example, 0.1 milligrams daily versus 2.5 milligrams weekly means that the amount administered is likely less than the daily clearance rate, which we already learned is required.
You perpetually operate in what's called the distribution phase. You're trying to fill a bathtub with a thimble while the drain is wide open.
You never get to the therapeutic steady state that's required for efficacy. Rewiring of the hypothalamic set point requires a very strong, sustained signal.
A weekly dose provides days-long signals that carve new fullness pathways into your brain's neural architecture. A microdose is a weak, fleeting signal.
