Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte d-glucose transport
Now TRH stimulates prolactin and tsh and seasonal variation in receptor binding in both TSH and PRL has been associated with for example shifts between reproduction and feeding (complex but also happens through kisspeptin and neurpeptide y).
When you have digested that, carry on:
TRH:
"TRH has been used clinically for the treatment of spinocerebellar degeneration and disturbance of consciousness in humans.[1] Its pharmaceutical form is called protirelin (INN) (/proʊˈtaɪrɪlɪn/)."
Serum S-adenosylmethionine, but not methionine, increases in response to overfeeding in humans.
"Overfeeding did not alter serum concentrations of the SAM precursor, methionine or the products, S-adenosyl-homocysteine and homocysteine. The SAM/SAH (S-adenosylhomocysteine) ratio was unchanged in the total population, but increased in high-weight gainers (+52%, P=0.006, Pinteraction =0.005). Change in SAM correlated positively with change in weight (r=0.33, P=0.041) and fat mass (r=0.44, P=0.009), but not with change in protein intake or plasma methionine, glucose, insulin or low-density lipoprotein (LDL)-cholesterol.
Overfeeding raised serum SAM in proportion to the fat mass gained. The increase in SAM may help stabilize methionine levels, and denotes a responsiveness of SAM to nutrient state in humans. The role of SAM in human energy metabolism deserves further attention."
Neuroendocrine effects of S-adenosyl-L-methionine, a novel putative antidepressant.
"S-adenosyl-L-methionine (SAMe), a putative antidepressant, is a naturally occurring substance whose mechanism of action is still a matter of speculation. It has been recently postulated that SAMe may increase the dopaminergic tone in depressed patients. Since dopamine inhibits both thyrotropin (TSH) and prolactin secretion, we investigated the effects of treatment with SAMe on the TSH and prolactin response to thyrotropin-releasing-hormone (TRH) stimulation in 7 depressed outpatient women (mean age: 46.1 +/- 7.2 years) and 10 depressed outpatient men (mean age: 38.0 +/- 10.0 years) participating in a six-week open study of oral SAMe in the treatment of major depression. At the end of the study, there was a significant reduction after treatment with SAMe in the response of both prolactin and TSH to TRH stimulation in the group of depressed men compared to pre-treatment values. On the other hand, in the group of depressed women, the posttreatment prolactin response to TRH did not appear to change when compared to pre-treatment and the TSH response to TRH challenge tended even to augment slightly after treatment with SAMe. Our results, at least in depressed men, seem to support the hypothesis of a stimulating effect of SAMe on the dopaminergic system. "
The effect of S-adenosyl methionine on the TSH receptor function in human thyroid tissue: increase in binding of TSH and decrease in adenylate cyclase coupling.
" 125I-TSH binding to the pretreated membrane and adenylate cyclase activity of the membrane were examined. In contrast to the reported effect of AdoMet on the decrease in GH binding to lactogenic receptor, AdoMet 0.5 mumoles/ml significantly increased the binding of TSH to the receptor by increasing the affinity of the binding, whereas it decreased the coupling of adenylate cyclase significantly. The effect of AdoMet was partially counteracted by the pretreatment of the membrane with AdoHcy. This effect of AdoMet is very similar to that of diamide previously reported. The result implies that the effect is due to an alteration in the tertiary structure of receptor protein triggered by methylation. "
S-adenosyl-L-methionine restores prolactin receptors in the aged rabbit brain.
The number of prolactin (PRL) receptors in the hypothalamus and substantia nigra of aged rabbits is significantly lower than the number measured in young animals. The treatment of aged rabbits for 30 days with S-adenosyl-L-methionine (SAM) restored the number of PRL binding sites to levels found in the hypothalamus and substantia nigra from young animals. We did not observe a clear-cut difference between the dissociation constants of untreated young, and untreated or SAM-treated aged rabbits, whereas the binding capacity varied. Moreover, in vitro addition of SAM to hypothalamic membranes from aged rabbits resulted in a significant increase in the number of binding sites. This in vitro effect was antagonized by S-adenosyl-L-homocysteine, a specific in vitro inhibitor of methyltransferase activity. The reduction in the number of PRL receptors is assumed to be related to the decrease in membrane fluidity induced by aging, while its increase after SAM treatment might be ascribed to the ability of this methyl donor to increase the fluidity of cell membranes by stimulating phospholipid synthesis.
I STRONGLY SUSPECT that both ADHD and ASD can be helped by modulating methylation, especially when theres an autoimmune background such as elevated TSH and gut problems.
Get on SAM-E, even just 200mg might change your life within 3hours after taking your first pill.
