Melatonin prevents progression/improves macular degeneration instead of causing it, as Ray surmises

[mangoes]

I just sent an email to Jeff Bowles, who did an extensive review of melatonin studies and mentions Peat in his bio, basically asking how he reconciled Peat's evidence of melatonin's harm with his own finding, substantiated by his own literature review, that melatonin in high enough doses will effectively cure Alzheimer's via a reduction of luteinizing hormone.

Oh wow that’s really interesting, I hadn’t heard of Jeff Bowles, I’ll have to look him up. I’d love to hear Ray’s responses to all this evidence, I remember him saying he wanted more debate type exchanges in his emails

 

[cjm]

Oh wow that’s really interesting, I hadn’t heard of Jeff Bowles, I’ll have to look him up. I’d love to hear Ray’s responses to all this evidence, I remember him saying he wanted more debate type exchanges in his emails

Credit due to @baccheion for mentioning him. I will post Jeff's reply as soon as I hopefully get one.

 

[cjm]

Ray says it can shrink your penis.

Yes, and it makes the brain sluggish and damages immunity.

"Many health food stores are now selling melatonin, to reduce sleep and " prevent cancer. " They have taken some information out of context, and don't realize how dangerous melatonin is. It makes the brain sluggish, causes the sex organs to shrink, and damages immunity by shrinking the thymus gland. It is the hormone of darkness and winter, and is produced in the pineal gland by any stress which increases adrenalin. Adequate sun light suppresses the formation of melatonin."

With regards to the latter claim about immunity, I posted a study earlier that showed exogenous melatonin protecting against the immune-suppressive effect of glucocorticoids.

Same researcher found melatonin to prevent thymus involution:

"The experiment illustrated in Table 2 confirms the effect of TRH in the prevention of thymus involution in AHA-lesioned mice (Groups A to E). In addition, it can be seen that the reconstituting activity of TRH is exerted even at the daily dose of 10 pg. Melatonin also possesses the capacity to largely induce a recovery of thymus weight and size (Group H)."

Sci-Hub | The Involvement of Pineal Gland and Melatonin in Immunity and Aging: II. Thyrotropin-Releasing Hormone and Melatonin Forestall Involution and Promote Reconstitution of the Thymus in Anterior Hypothalamic Area (Aha)-Lesioned Mice. Internatio

 

[burtlancast]

Wow.

Great find.

 

[golder]

Ray says it can shrink your penis.

Wow, where does he say this?

 

[cjm]

It seems like Ray made the claim about immunity based on this:

"In 1994 A.V. Sirotkin found that melatonin inhibits progesterone production but stimulates estrogen production, and it’s widely recognized that melatonin generally inhibits the thyroid hormones, creating an environment in which fertilization, implantation, and development of the embryo are not possible. This combination of high estrogen with low progesterone and low thyroid decreases the resistance of the organism, predisposing it to seizures and excitotoxic damage, and causing the thymus gland to atrophy." Aging Eyes

I couldn't get the full study for the 1994 citation but I did find a similar study done by Sirotkin in 1997:

"Both melatonin and serotonin were potent inhibitors of progesterone release."

Melatonin and serotonin regulate the release of insulin-like growth factor-I, oxytocin and progesterone by cultured human granulosa cells

~

The first appendix for the Bowles book Extreme Dose! Melatonin is a study with adrenal carcinoma cells showing melatonin to have an opposite effect (with strings attached):

"Results—The addition of ENL or END with melatonin to cAMP-stimulated cells (treated cells) resulted in significant decreases in estradiol, androstenedione, and cortisol concentrations at 24 and 48 hours, compared with concentrations in cells stimulated with cAMP alone (cAMP control cells). The addition of these compounds to cAMP-stimulated cells also resulted in higher progesterone and 17-hydroxyprogesterone concentrations than in cAMP control cells; aldosterone concentration was not affected by treatments. Compared with the content in cAMP control cells, aromatase content in treated cells was significantly lower."

Effect of combined lignan phytoestrogen and melatonin treatment on secretion of steroid hormones by adrenal carcinoma cells

I don't know, it doesn't feel like a solid refutation of Sirotkin.

The anecdotal evidence he presented for a progesterone increase was stronger in a sense (again from the book):

"My lab results for my blood test after I had been taking about 300 mg a night of melatonin for around two months showed that my LH levels dropped by 30% (from 6.9 to 4.9 [mIU/mL]) and my FSH levels by 13% (from 8.8 to 7.7[mIU/mL]). So the prediction seems to be true--melatonin really suppresses LH. I am a little disappointed that the FSH did not drop further. Maybe I will need to explore the idea of trying follistatin which selectively suppresses FSH. I did another test to see if the melatonin boosted my progesterone levels. My progesterone rose from 1.9 to 2.2 ng/ml by taking melatonin, a nice 15% increase. However, my starting pre-melatonin progesterone level of 1.9 was already way higher than the upper limit of the reference range of 1.4 for men. (I believe this is due to my habit of taking 100 mg of pregnenolone a day, which is a direct precursor to progesterone.) So my progesterone levels are sky-high while taking pregnenolone, and go even higher while taking melatonin! As predicted--thank you very much."

~

For fun, there are studies that show no effect:

"Melatonin had no effect on basal P or 17,6-estradiol production."

Effects of melatonin on progesterone production by human granulosa lutein cells in culture

Requires further review.

 

[cjm]

Credit due to @baccheion for mentioning him. I will post Jeff's reply as soon as I hopefully get one.

Jeff replied -- let's just say I didn't get a scientific critique. He hadn't read the article yet, but took a quick look, and replied he had no idea Ray was a certain way. I'm paraphrasing. He did point me towards his most recent blog article which talks about melatonin and aging.

 

[GreenTrails]

I just sent an email to Jeff Bowles, who did an extensive review of melatonin studies and mentions Peat in his bio, basically asking how he reconciled Peat's evidence of melatonin's harm with his own finding, substantiated by his own literature review, that melatonin in high enough doses will effectively cure Alzheimer's via a reduction of luteinizing hormone.

Thanks! I just recently read Jeff Bowles book, Extreme Dose! Melatonin The Miracle Anti-Aging Hormone Anti-Alzheimer's Hormone Anti-Baldness Hormone Menopause Reversal Hormone. I found it very interesting. I use melatonin and have used it for several years at 5 mg. nightly. I think it's great, helps me to sleep, and who doesn't need a good night's sleep every night? I don't know if I would use 75 mg., but I've tried 40 mg. for a few nights and didn't notice much difference from my usual 5 mg. dosage, so I've returned to the 5 mg.

I also recently read the book by Pierpaoli, The Melatonin Miracle, and it has a lot of information about Melatonin. He recommends a dosage of under 5 mg. per night. He says Melatonin is an "age-reversing, disease-fighting, sex-enhancing hormone". Nothing in either of these books about "penis-shrinking".

 

[GreenTrails]

It seems like Ray made the claim about immunity based on this:

"In 1994 A.V. Sirotkin found that melatonin inhibits progesterone production but stimulates estrogen production, and it’s widely recognized that melatonin generally inhibits the thyroid hormones, creating an environment in which fertilization, implantation, and development of the embryo are not possible. This combination of high estrogen with low progesterone and low thyroid decreases the resistance of the organism, predisposing it to seizures and excitotoxic damage, and causing the thymus gland to atrophy." Aging Eyes

I couldn't get the full study for the 1994 citation but I did find a similar study done by Sirotkin in 1997:

"Both melatonin and serotonin were potent inhibitors of progesterone release."

Melatonin and serotonin regulate the release of insulin-like growth factor-I, oxytocin and progesterone by cultured human granulosa cells

~

The first appendix for the Bowles book Extreme Dose! Melatonin is a study with adrenal carcinoma cells showing melatonin to have an opposite effect (with strings attached):

"Results—The addition of ENL or END with melatonin to cAMP-stimulated cells (treated cells) resulted in significant decreases in estradiol, androstenedione, and cortisol concentrations at 24 and 48 hours, compared with concentrations in cells stimulated with cAMP alone (cAMP control cells). The addition of these compounds to cAMP-stimulated cells also resulted in higher progesterone and 17-hydroxyprogesterone concentrations than in cAMP control cells; aldosterone concentration was not affected by treatments. Compared with the content in cAMP control cells, aromatase content in treated cells was significantly lower."

Effect of combined lignan phytoestrogen and melatonin treatment on secretion of steroid hormones by adrenal carcinoma cells

I don't know, it doesn't feel like a solid refutation of Sirotkin.

The anecdotal evidence he presented for a progesterone increase was stronger in a sense (again from the book):

"My lab results for my blood test after I had been taking about 300 mg a night of melatonin for around two months showed that my LH levels dropped by 30% (from 6.9 to 4.9 [mIU/mL]) and my FSH levels by 13% (from 8.8 to 7.7[mIU/mL]). So the prediction seems to be true--melatonin really suppresses LH. I am a little disappointed that the FSH did not drop further. Maybe I will need to explore the idea of trying follistatin which selectively suppresses FSH. I did another test to see if the melatonin boosted my progesterone levels. My progesterone rose from 1.9 to 2.2 ng/ml by taking melatonin, a nice 15% increase. However, my starting pre-melatonin progesterone level of 1.9 was already way higher than the upper limit of the reference range of 1.4 for men. (I believe this is due to my habit of taking 100 mg of pregnenolone a day, which is a direct precursor to progesterone.) So my progesterone levels are sky-high while taking pregnenolone, and go even higher while taking melatonin! As predicted--thank you very much."

~

For fun, there are studies that show no effect:

"Melatonin had no effect on basal P or 17,6-estradiol production."

Effects of melatonin on progesterone production by human granulosa lutein cells in culture

Requires further review.

Thank you for this information.

 

[cjm]

Thanks! I just recently read Jeff Bowles book, Extreme Dose! Melatonin The Miracle Anti-Aging Hormone Anti-Alzheimer's Hormone Anti-Baldness Hormone Menopause Reversal Hormone. I found it very interesting. I use melatonin and have used it for several years at 5 mg. nightly. I think it's great, helps me to sleep, and who doesn't need a good night's sleep every night? I don't know if I would use 75 mg., but I've tried 40 mg. for a few nights and didn't notice much difference from my usual 5 mg. dosage, so I've returned to the 5 mg.

I also recently read the book by Pierpaoli, The Melatonin Miracle, and it has a lot of information about Melatonin. He recommends a dosage of under 5 mg. per night. He says Melatonin is an "age-reversing, disease-fighting, sex-enhancing hormone". Nothing in either of these books about "penis-shrinking".

Melatonin does antagonize testosterone due to negative feedback from increased gonadotropin-inhibitory hormone (GnIH),

Melatonin Stimulates the Release of Gonadotropin-Inhibitory Hormone by the Avian Hypothalamus

Abstract. Gonadotropin-inhibitory hormone (GnIH), a neuropeptide that inhibits gonadotropin synthesis and release, was first identified in quail hypothalamus. G

academic.oup.com

Melatonin inhibits hypothalamic gonadotropin-releasing hormone release and reduces biliary hyperplasia and fibrosis in cholestatic rats - PubMed

Melatonin is a hormone produced by the pineal gland with increased circulating levels shown to inhibit biliary hyperplasia and fibrosis during cholestatic liver injury. Melatonin also has the capability to suppress the release of hypothalamic gonadotropin-releasing hormone (GnRH), a hormone that...

pubmed.ncbi.nlm.nih.gov

which lowers luteinizing hormone (LH), which is elevated in Alzheimer's (and worth lowering per Jeff's research) but which is promoting T release.

I think.

"Melatonin administration to intact animals significantly decreased both LH and testosterone levels (p<0.01). Co-administration of HCG [Human Chorionic Gonadotropin] +melatonin resulted in significant decreases in LH (p<0.001) and increases in testosterone levels (p<0.01)."

Melatonin inhibits testosterone secretion by acting at hypothalamo-pituitary-gonadal axis in the rat - PubMed

OBJECTIVES: We have investigated the changes in serum luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone levels together with testicular histology in both pinealectomized (PNX) and intact rats. MATERIAL and METHODS: Twenty-one animals were PNX and allowed to recover...

pubmed.ncbi.nlm.nih.gov

~

But as always, melatonin has no effect:

"The mean nocturnal LH, FSH, testosterone and inhibin β integrated nocturnal secretion values did not change during the treatment period. Likewise, their pulsatile characteristics during melatonin treatment were not different from baseline values. Taken together, these data suggest that long-term melatonin administration does not alter the secretory patterns of reproductive hormones in normal men."

Long-term melatonin administration does not alter pituitary-gonadal hormone secretion in normal men

Abstract. The role of melatonin in the regulation of reproduction in humans is still controversial. In the present study the effects of melatonin were examined,

academic.oup.com

 

[Mufasa]

I think most anti-oxidants can give some positive effects, but too much of it always leads to reductive stress in the end.
I'm sure that I have overdosed on many anti-oxidants including melatonin in the past, in the spirit that free radical damage leads to aging.
I experienced good effects of all of them in the short term, but in the long term, I was only getting weaker and weaker.

I guess the effects or reductive stress can be hard to find out in a study, because this is just what happens with aging, and it happens gradually, year by year more and more tissue getting in a reduced environment. Until at some point, it is so bad, that you will experience, any of the diseases related to reductive stress: cardiomyopathy, pulmonary hypertension, neurological disorders, Parkinson’s disease, Alzheimer’s disease, insulin resistance, metabolic syndrome, rheumatoid arthritis, kidney diseases, and cancer.

The paradox is that, if your cells are experiencing reductive stress, it leads to more oxidative stress, than what would have happened if you have none of it, and you were metabolizing oxygen at a high rate (and producing a lot of free radicals in that process). It seems like the body is much better able to avoid damage of free radicals if they are generated during oxidative metabolism.

I would stay away from supplementing anti-oxidants. If the body makes them itself, fine, it probably knows what it wants, but if you are deliberately forcing the redox balance of your body to "reduction", I think you are doing the exact opposite of what Ray Peat is all about.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents (Pérez-Torres, et al., 2017)
Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD+/NADH, NADP+/NADPH, and GSH/GSSG, to a more reducing state. Overexpression of antioxidant enzymatic systems leads to excess reducing equivalents that can deplete reactive oxidative species, driving the cells to RS. A feedback regulation is established in which chronic RS induces OS, which in turn, stimulates again RS. Excess reducing equivalents may regulate cellular signaling pathways, modify transcriptional activity, induce alterations in the formation of disulfide bonds in proteins, reduce mitochondrial function, decrease cellular metabolism, and thus, contribute to the development of some diseases in which NF-κB, a redox-sensitive transcription factor, participates. Here, we described the diseases in which an inflammatory condition is associated to RS, and where delayed folding, disordered transport, failed oxidation, and aggregation are found. Some of these diseases are aggregation protein cardiomyopathy, hypertrophic cardiomyopathy, muscular dystrophy, pulmonary hypertension, rheumatoid arthritis, Alzheimer’s disease, and metabolic syndrome, among others. Moreover, chronic consumption of antioxidant supplements, such as vitamins and/or flavonoids, may have pro-oxidant effects that may alter the redox cellular equilibrium and contribute to RS, even diminishing life expectancy.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents

Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD[+] /NADH, NADP[+] /NADPH, and GSH/GSSG, to a more reducing state. ...

www.ncbi.nlm.nih.gov

 

[Korven]

I think most anti-oxidants can give some positive effects, but too much of it always leads to reductive stress in the end.
I'm sure that I have overdosed on many anti-oxidants including melatonin in the past, in the spirit that free radical damage leads to aging.
I experienced good effects of all of them in the short term, but in the long term, I was only getting weaker and weaker.

I guess the effects or reductive stress can be hard to find out in a study, because this is just what happens with aging, and it happens gradually, year by year more and more tissue getting in a reduced environment. Until at some point, it is so bad, that you will experience, any of the diseases related to reductive stress: cardiomyopathy, pulmonary hypertension, neurological disorders, Parkinson’s disease, Alzheimer’s disease, insulin resistance, metabolic syndrome, rheumatoid arthritis, kidney diseases, and cancer.

The paradox is that, if your cells are experiencing reductive stress, it leads to more oxidative stress, than what would have happened if you have none of it, and you were metabolizing oxygen at a high rate (and producing a lot of free radicals in that process). It seems like the body is much better able to avoid damage of free radicals if they are generated during oxidative metabolism.

I would stay away from supplementing anti-oxidants. If the body makes them itself, fine, it probably knows what it wants, but if you are deliberately forcing the redox balance of your body to "reduction", I think you are doing the exact opposite of what Ray Peat is all about.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents (Pérez-Torres, et al., 2017)
Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD+/NADH, NADP+/NADPH, and GSH/GSSG, to a more reducing state. Overexpression of antioxidant enzymatic systems leads to excess reducing equivalents that can deplete reactive oxidative species, driving the cells to RS. A feedback regulation is established in which chronic RS induces OS, which in turn, stimulates again RS. Excess reducing equivalents may regulate cellular signaling pathways, modify transcriptional activity, induce alterations in the formation of disulfide bonds in proteins, reduce mitochondrial function, decrease cellular metabolism, and thus, contribute to the development of some diseases in which NF-κB, a redox-sensitive transcription factor, participates. Here, we described the diseases in which an inflammatory condition is associated to RS, and where delayed folding, disordered transport, failed oxidation, and aggregation are found. Some of these diseases are aggregation protein cardiomyopathy, hypertrophic cardiomyopathy, muscular dystrophy, pulmonary hypertension, rheumatoid arthritis, Alzheimer’s disease, and metabolic syndrome, among others. Moreover, chronic consumption of antioxidant supplements, such as vitamins and/or flavonoids, may have pro-oxidant effects that may alter the redox cellular equilibrium and contribute to RS, even diminishing life expectancy.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents

Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD[+] /NADH, NADP[+] /NADPH, and GSH/GSSG, to a more reducing state. ...

www.ncbi.nlm.nih.gov

Nice post!

I like to think of optimal oxidative metabolism driven by thyroid as being a flame that's burning nice and hot, cleanly - versus reductive (hypothyroid) metabolism where the flame is weak and produces a sooty smoke.

I think this is what ends up happening to long-term vegans and calorie restriction people. In an effort to prolong aging by not eating too much/"bad stuff" they actually produce more ROS and paradoxically age way faster. They would probably be better off eating a bunch of burgers and fries instead.

 

[cjm]

I think most anti-oxidants can give some positive effects, but too much of it always leads to reductive stress in the end.
I'm sure that I have overdosed on many anti-oxidants including melatonin in the past, in the spirit that free radical damage leads to aging.
I experienced good effects of all of them in the short term, but in the long term, I was only getting weaker and weaker.

I guess the effects or reductive stress can be hard to find out in a study, because this is just what happens with aging, and it happens gradually, year by year more and more tissue getting in a reduced environment. Until at some point, it is so bad, that you will experience, any of the diseases related to reductive stress: cardiomyopathy, pulmonary hypertension, neurological disorders, Parkinson’s disease, Alzheimer’s disease, insulin resistance, metabolic syndrome, rheumatoid arthritis, kidney diseases, and cancer.

The paradox is that, if your cells are experiencing reductive stress, it leads to more oxidative stress, than what would have happened if you have none of it, and you were metabolizing oxygen at a high rate (and producing a lot of free radicals in that process). It seems like the body is much better able to avoid damage of free radicals if they are generated during oxidative metabolism.

I would stay away from supplementing anti-oxidants. If the body makes them itself, fine, it probably knows what it wants, but if you are deliberately forcing the redox balance of your body to "reduction", I think you are doing the exact opposite of what Ray Peat is all about.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents (Pérez-Torres, et al., 2017)
Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD+/NADH, NADP+/NADPH, and GSH/GSSG, to a more reducing state. Overexpression of antioxidant enzymatic systems leads to excess reducing equivalents that can deplete reactive oxidative species, driving the cells to RS. A feedback regulation is established in which chronic RS induces OS, which in turn, stimulates again RS. Excess reducing equivalents may regulate cellular signaling pathways, modify transcriptional activity, induce alterations in the formation of disulfide bonds in proteins, reduce mitochondrial function, decrease cellular metabolism, and thus, contribute to the development of some diseases in which NF-κB, a redox-sensitive transcription factor, participates. Here, we described the diseases in which an inflammatory condition is associated to RS, and where delayed folding, disordered transport, failed oxidation, and aggregation are found. Some of these diseases are aggregation protein cardiomyopathy, hypertrophic cardiomyopathy, muscular dystrophy, pulmonary hypertension, rheumatoid arthritis, Alzheimer’s disease, and metabolic syndrome, among others. Moreover, chronic consumption of antioxidant supplements, such as vitamins and/or flavonoids, may have pro-oxidant effects that may alter the redox cellular equilibrium and contribute to RS, even diminishing life expectancy.

Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents

Reductive stress (RS) is the counterpart oxidative stress (OS), and can occur in response to conditions that shift the redox balance of important biological redox couples, such as the NAD[+] /NADH, NADP[+] /NADPH, and GSH/GSSG, to a more reducing state. ...

www.ncbi.nlm.nih.gov

I resonate with your stance but I want to be specific about melatonin in this thread. There's no question melatonin can be beneficial, e.g., lowering LH to alleviate Alzheimer's symptoms, and no LD-50 has been set for it:

"The acute toxicity of melatonin as seen in both animal and human studies is extremely low. Melatonin may cause minor adverse effects, such as headache, insomnia, rash, upset stomach, and nightmares. In animals, an LD50 (lethal dose for 50% of the subjects) could not be established. Even 800 mg/kg bodyweight (high dose) was not lethal. Studies of human subjects given varying doses of melatonin (1–6.6 g/day) for 30–45 days, and followed with an elaborate battery of biochemical tests to detect potential toxicity, have concluded that, aside from drowsiness, all findings were normal at the end of the test period"

The Therapeutic Potential of Melatonin: A Review of the Science

But it seems like harm from melatonin might be due to timing of administration:

"Although melatonin is a potential adjunctive agent in the treatment of cancer and immune deficiency, poorly timed administration can produce opposite effects. Melatonin injections given in the morning stimulate tumor growth, whereas the same doses in midafternoon have no effect but in the evening have a retarding effect. And although some people with depression may suffer from a “low melatonin syndrome,” melatonin administration that unduly prolongs the nocturnal melatonin rise, or that is given throughout the day, may exacerbate SAD and bipolar and classic depression. Finally, animal studies have shown that moderately large doses of melatonin (equivalent in one study to about 30 mg in adult humans) increased light-induced damage to retinal photoreceptors." (same link)

 

[GreenTrails]

Melatonin does antagonize testosterone due to negative feedback from increased gonadotropin-inhibitory hormone (GnIH),

Melatonin Stimulates the Release of Gonadotropin-Inhibitory Hormone by the Avian Hypothalamus

Abstract. Gonadotropin-inhibitory hormone (GnIH), a neuropeptide that inhibits gonadotropin synthesis and release, was first identified in quail hypothalamus. G

academic.oup.com

Melatonin inhibits hypothalamic gonadotropin-releasing hormone release and reduces biliary hyperplasia and fibrosis in cholestatic rats - PubMed

Melatonin is a hormone produced by the pineal gland with increased circulating levels shown to inhibit biliary hyperplasia and fibrosis during cholestatic liver injury. Melatonin also has the capability to suppress the release of hypothalamic gonadotropin-releasing hormone (GnRH), a hormone that...

pubmed.ncbi.nlm.nih.gov

which lowers luteinizing hormone (LH), which is elevated in Alzheimer's (and worth lowering per Jeff's research) but which is promoting T release.

I think.

"Melatonin administration to intact animals significantly decreased both LH and testosterone levels (p<0.01). Co-administration of HCG [Human Chorionic Gonadotropin] +melatonin resulted in significant decreases in LH (p<0.001) and increases in testosterone levels (p<0.01)."

Melatonin inhibits testosterone secretion by acting at hypothalamo-pituitary-gonadal axis in the rat - PubMed

OBJECTIVES: We have investigated the changes in serum luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone levels together with testicular histology in both pinealectomized (PNX) and intact rats. MATERIAL and METHODS: Twenty-one animals were PNX and allowed to recover...

pubmed.ncbi.nlm.nih.gov

~

But as always, melatonin has no effect:

"The mean nocturnal LH, FSH, testosterone and inhibin β integrated nocturnal secretion values did not change during the treatment period. Likewise, their pulsatile characteristics during melatonin treatment were not different from baseline values. Taken together, these data suggest that long-term melatonin administration does not alter the secretory patterns of reproductive hormones in normal men."

Long-term melatonin administration does not alter pituitary-gonadal hormone secretion in normal men

Abstract. The role of melatonin in the regulation of reproduction in humans is still controversial. In the present study the effects of melatonin were examined,

academic.oup.com

Thanks for this information. It appears to me that melatonin may not be good for males, but for females a decrease in LH would be a good thing, I would think. At menopause the LH goes up, and at the same time the thymus shrinks because the melatonin is greatly reduced from what it is in a younger woman. Supplementing melatonin as well as supplementing thymus seems to me to be a good strategy for women. The book by Jeff Bowles says as much; " NIH News: New paper suggests elevated LH behind Alzheimer's Disease".

 

[golder]

Thanks for this information. It appears to me that melatonin may not be good for males, but for females a decrease in LH would be a good thing, I would think. At menopause the LH goes up, and at the same time the thymus shrinks because the melatonin is greatly reduced from what it is in a younger woman. Supplementing melatonin as well as supplementing thymus seems to me to be a good strategy for women. The book by Jeff Bowles says as much; " NIH News: New paper suggests elevated LH behind Alzheimer's Disease".

Do you also think supplementing thymus is unadvisable for men?

 

[cjm]

It appears to me that melatonin may not be good for males

Only thing I would add is it's not good for male sex drive, but it could be good for a male with Alzheimer's. Bowles applied his research to evolutionary theory and discovered male sex traits exist primarily to defend against predation. They are not selected for longevity.

 

[GreenTrails]

Do you also think supplementing thymus is unadvisable for men?

Probably would depend on the man's age. Healthy ounger men no doubt have a thymus that's functioning well.

 

[Peeno]

Melatonin is anti estrogenic and promotes progesterone action via upregulating progesterone receptors. Melatonin is fantastic.

 

[GreenTrails]

Do you also think supplementing thymus is unadvisable for men?

In the book, The Melatonin Miracle, by Walter Pierpaoli, M.D., he says that the pineal gland is the "aging clock". He says that we age because our pineal function declines over time, and as it does it produces less melatonin, and this, in short, produces the cascade of events that we know as aging. Melatonin specifically stimulates the thyroid gland and the thymus gland, both of which are involved in the production of T cells, crucial for maintaining a strong immune system (p. 150).

As I understand it, the thymus is of a considerable size at birth and up until adolescence, then begins to get smaller, until at age 75 a person's thymus has disappeared and has turned into fatty tissue. Older people typically have a diminished immune system; their T cells are not nearly as aggressive as they were when they were younger which makes them more vulnerable to infections.

In the book, the author talks about experiments where the pineals were removed from young mice and transplanted into old mice. A single pineal gland in its membrane was positioned on the tip of a needle and gently inserted into the thymus of the older mice. The mice that had received the pineal transplants appeared to grow young, their fur improved, their activity level increased and they looked and acted like much younger mice. Both their immune response and thyroid function were equal to those of much younger animals. The thymus glands of the transplanted mice, which are usually shrunken and atrophied in mice of their age, had been restored to their youthful size and condition. This suggested that the way melatonin restores immune function is by rejuvenating the thymus gland. (p. 62-63)

 

[golder]

In the book, The Melatonin Miracle, by Walter Pierpaoli, M.D., he says that the pineal gland is the "aging clock". He says that we age because our pineal function declines over time, and as it does it produces less melatonin, and this, in short, produces the cascade of events that we know as aging. Melatonin specifically stimulates the thyroid gland and the thymus gland, both of which are involved in the production of T cells, crucial for maintaining a strong immune system (p. 150).

As I understand it, the thymus is of a considerable size at birth and up until adolescence, then begins to get smaller, until at age 75 a person's thymus has disappeared and has turned into fatty tissue. Older people typically have a diminished immune system; their T cells are not nearly as aggressive as they were when they were younger which makes them more vulnerable to infections.

In the book, the author talks about experiments where the pineals were removed from young mice and transplanted into old mice. A single pineal gland in its membrane was positioned on the tip of a needle and gently inserted into the thymus of the older mice. The mice that had received the pineal transplants appeared to grow young, their fur improved, their activity level increased and they looked and acted like much younger mice. Both their immune response and thyroid function were equal to those of much younger animals. The thymus glands of the transplanted mice, which are usually shrunken and atrophied in mice of their age, had been restored to their youthful size and condition. This suggested that the way melatonin restores immune function is by rejuvenating the thymus gland. (p. 62-63)

Thanks for this, great read.
Im so surprised Peat doesn’t even acknowledge the thymus regeneration potential of melatonin. I’ve never heard him say a good word about melatonin but I’ve heard him make several positive remarks on the thymus. Very strange.