Allopregnanolone And Initiation Of Puberty. Fine Tuning And Increasing Hormone Release

[Beefcake]

Stumbled across two interesting studies regarding allopregnanolone.

Allopregnanolone and puberty: modulatory effect on glutamate and GABA release and expression of 3α-hydroxysteroid oxidoreductase in the hypothalamus ... - PubMed - NCBI

These results suggest an important physiological function of allopregnanolone in the hypothalamus of the P rat where it might be involved in the 'fine tuning' of neurosecretory functions related to the biology of reproduction

Allopregnanolone induces LHRH and glutamate release through NMDA receptor modulation. - PubMed - NCBI

These results suggest an important physiologic function of allopregnanolone on the regulation of neuroendocrine function in female adult rats. Not only appears to be involved in enhancing LHRH release through modulation of NMDA receptors but also in the release of glutamate which is critical in the control of LHRH release.

This would mean that you could possibly cure low hormone output or weak hypothalamus function by boosting allopreg. Haiduts 5a-dhp and also pure pregnenolone seems to be a good place to start.
I’m interested more in how the body decides that now its time for puberty and how it decides to stop it? Do we know that it even stops? Or is it just a gradual decline in health after? Anyone got the answer as to how the body knows its in its teens?
All I know from googling this is that at a certain age your body starts making more LHRH. Well why would not allopreg be the initiator of this? Allopregnenolone could be responsible for the start of puberty? How does allopreg get increased?

 

[lampofred]

Stumbled across two interesting studies regarding allopregnanolone.

Allopregnanolone and puberty: modulatory effect on glutamate and GABA release and expression of 3α-hydroxysteroid oxidoreductase in the hypothalamus ... - PubMed - NCBI

These results suggest an important physiological function of allopregnanolone in the hypothalamus of the P rat where it might be involved in the 'fine tuning' of neurosecretory functions related to the biology of reproduction

Allopregnanolone induces LHRH and glutamate release through NMDA receptor modulation. - PubMed - NCBI

These results suggest an important physiologic function of allopregnanolone on the regulation of neuroendocrine function in female adult rats. Not only appears to be involved in enhancing LHRH release through modulation of NMDA receptors but also in the release of glutamate which is critical in the control of LHRH release.

This would mean that you could possibly cure low hormone output or weak hypothalamus function by boosting allopreg. Haiduts 5a-dhp and also pure pregnenolone seems to be a good place to start.
I’m interested more in how the body decides that now its time for puberty and how it decides to stop it? Do we know that it even stops? Or is it just a gradual decline in health after? Anyone got the answer as to how the body knows its in its teens?
Cheers

I think Dr. Peat wrote that a build up of PUFA/iron and the resultant metabolic stress is what triggers puberty.

 

[Beefcake]

I think Dr. Peat wrote that a build up of PUFA/iron and the resultant metabolic stress is what triggers puberty.

That seems dumb. So if you would avoid iron and PUFA you mean that you would have delayed puberty? But then once puberty starts it PUFA and iron lowers T levels? How would you develop with low T?

 

[lampofred]

That seems dumb. So if you would avoid iron and PUFA you mean that you would have delayed puberty? But then once puberty starts it PUFA and iron lowers T levels? How would you develop with low T?

This is how I understand it: PUFA initiates puberty because it's estrogenic. And estrogenic influences accelerate puberty/aging and decrease T. It's impossible to eat absolutely 0 PUFA. So the less PUFA you eat, the later you will hit puberty, but the more T you will have when you do hit it, and the slower your rate of aging will be.

 

[Beefcake]

This is how I understand it: PUFA initiates puberty because it's estrogenic. And estrogenic influences accelerate puberty/aging and decrease T. It's impossible to eat absolutely 0 PUFA. So the less PUFA you eat, the later you will hit puberty, but the more T you will have when you do hit it, and the slower your rate of aging will be.

Ok not convinced. Sure stress can be factors but I don’t think PUFA or Iron has anything to do with it. As the studies above show allopreg a strong neurosteroid seems to modulate the hypothalamus in puberty. Glutamate is a strong allopregnenolone booster probably to increase GABA A and lower glutamate as a feedback. I think the development of a aging brain from childhood into adulthood increases glutamate transmission thus increasing allopregnenolone untill it starts to initiate LHRH. So stress could be a initiator of that allopregnenolone respons. But I’d think it’s some NMDA receptor, glutamate sort of neruomodulatory switch that happens in that age thus leading to this cascade of hormones starting puberty.

Control of puberty by excitatory amino acid neurotransmitters and its clinical implications. - PubMed - NCBI

Excitatory amino acids, glutamate in particular, have a marked stimulatory effect on the reproductive axis, particularly at puberty.

 

[Beefcake]

This is how I understand it: PUFA initiates puberty because it's estrogenic. And estrogenic influences accelerate puberty/aging and decrease T. It's impossible to eat absolutely 0 PUFA. So the less PUFA you eat, the later you will hit puberty, but the more T you will have when you do hit it, and the slower your rate of aging will be.

This is interesting

Control of puberty by excitatory amino acid neurotransmitters and its clinical implications. - PubMed - NCBI

The pulse frequency of hypothalamic GnRH secretion increases at the onset of puberty. In rodents and primates, this process involves facilitatory and inhibitory effects mediated through hypothalamic N-methyl-D-aspartic acid (NMDA) and gamma-aminobutyric acid (GABA) receptors, respectively. Precocious puberty was observed in an 11-month-old girl with nonketotic hyperglycinemia. This was thought to result from the effect of high concentrations of glycine (112 micromol/L in cerebrospinal fluid; normal, 3-12) acting on NMDA receptors as a coagonist of glutamate. Regression of pubertal development during anticonvulsive treatment with GABA agonists (loreclezole and vigabatrin) suggested that the stimulatory effects of glycine could be overcome by GABA receptor-mediated inhibition. These two hypotheses were tested in the in vitro model of the explanted hypothalamus from infantile (15-day-old) male rats. Glycine concentrations of 1-10 micromol/L increased the pulse frequency of GnRH secretion. This acceleration was prevented by 7-chlorokynurenic acid, a glycine antagonist at the NMDA receptor complex, and by the GABA agonist loreclezole. In addition, loreclezole and vigabatrin suppressed the developmental increase in the frequency of pulsatile GnRH secretion. The observation of precocious puberty in an infant with hyperglycinemia followed by pubertal regression during GABA agonist therapy and the in vitro findings in hypothalamic explants suggest that stimulatory inputs mediated through NMDA receptors and inhibitory inputs through GABA receptors are involved in the initiation of puberty.

So this means that glycine supplements possibly in children could cause an early puberty since glycine activates the NMDA receptor aswell. Glycine also stimulates allopreg. Just like we know taurine and glycine upregulates 5-ar and hormone release at the hypothalamus.

 

[lampofred]

Ok not convinced. Sure stress can be factors but I don’t think PUFA or Iron has anything to do with it. As the studies above show allopreg a strong neurosteroid seems to modulate the hypothalamus in puberty. Glutamate is a strong allopregnenolone booster probably to increase GABA A and lower glutamate as a feedback. I think the development of a aging brain from childhood into adulthood increases glutamate transmission thus increasing allopregnenolone untill it starts to initiate LHRH. So stress could be a initiator of that allopregnenolone respons. But I’d think it’s some NMDA receptor, glutamate sort of neruomodulatory switch that happens in that age thus leading to this cascade of hormones starting puberty.

Control of puberty by excitatory amino acid neurotransmitters and its clinical implications. - PubMed - NCBI

Excitatory amino acids, glutamate in particular, have a marked stimulatory effect on the reproductive axis, particularly at puberty.

Peat says PUFA/estrogen is what shifts the balance from GABA to glutamate.

 

[Beefcake]

Peat says PUFA/estrogen is what shifts the balance from GABA to glutamate.

Can you show me a link to this.

 

[lampofred]

Can you show me a link to this.

Suitable Fats, Unsuitable Fats: Issues in Nutrition -- "The ability of nerve cells to become quiescent after excitation is essential to learning and perception. This ability is lost with aging, as the functional balance in the brain shifts away from GABA-ergic to glutamatergic nerves. The polyunsaturated fatty acids promote the excitatory nervous state."

That's where he directly talks about PUFA, in several other articles he talks about how estrogen increases glutamate and decreases GABA. Since PUFA is one of the most estrogenic things in existence, that indirectly implies that PUFA increases glutamate and decreases GABA.

 

[Alex Jaramillo]

Stumbled across two interesting studies regarding allopregnanolone.

Allopregnanolone and puberty: modulatory effect on glutamate and GABA release and expression of 3α-hydroxysteroid oxidoreductase in the hypothalamus ... - PubMed - NCBI

These results suggest an important physiological function of allopregnanolone in the hypothalamus of the P rat where it might be involved in the 'fine tuning' of neurosecretory functions related to the biology of reproduction

Allopregnanolone induces LHRH and glutamate release through NMDA receptor modulation. - PubMed - NCBI

These results suggest an important physiologic function of allopregnanolone on the regulation of neuroendocrine function in female adult rats. Not only appears to be involved in enhancing LHRH release through modulation of NMDA receptors but also in the release of glutamate which is critical in the control of LHRH release.

This would mean that you could possibly cure low hormone output or weak hypothalamus function by boosting allopreg. Haiduts 5a-dhp and also pure pregnenolone seems to be a good place to start.
I’m interested more in how the body decides that now its time for puberty and how it decides to stop it? Do we know that it even stops? Or is it just a gradual decline in health after? Anyone got the answer as to how the body knows its in its teens?
All I know from googling this is that at a certain age your body starts making more LHRH. Well why would not allopreg be the initiator of this? Allopregnenolone could be responsible for the start of puberty? How does allopreg get increased?

I think caffeine has been vital for me the last few years in fighting depression. Which is no surprise since it raises allopregnenolone not only on paper but in my own experience.