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Melatonin


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#1 simfish

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Posted 10 June 2006 - 09:09 AM


If your body is already producing plenty of melatonin, then could taking it potentially decrease the body's own production of melatonin? This question should also apply to other drugs that the body naturally produces.

#2 ajnast4r

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Posted 10 June 2006 - 02:26 PM

my understand is yes... its believed youre body will decrease endogenous melatonin if it is supplied from an exogenous source... but since most peoples melatonin levels start to decrease around 35-40, anyone of or over that age should be ok.

negative feedback regulation does NOT occur when introducing endogenous substances through exogenous means in all cases... its really specific to the substance.

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#3 starr

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Posted 10 June 2006 - 09:48 PM

I wonder what the consequences of taking 3-9 mgs of melatonin nearly every night for 8 years would be (which is what I did).

#4 Shepard

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Posted 10 June 2006 - 10:31 PM

There have been some indications of supplemental melatonin having other hormonal affects (other than endogenous melatonin), FYI.

At my age, I don't use it daily. I've debated whether or not it is worthwhile to use it a couple of times per week for extra antioxidant protection and other actions.

#5 ajnast4r

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Posted 11 June 2006 - 02:08 AM

I wonder what the consequences of taking 3-9 mgs of melatonin nearly every night for 8 years would be (which is what I did).


try sleeping without it

#6 zoolander

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Posted 11 June 2006 - 03:34 AM

negative feedback regulation does NOT occur when introducing endogenous substances through exogenous means in all cases


a strong and incorrect statement.

For example, if I increase my dietary iron intake and have enough iron the total iron binding proteins will decrease accordingly. Similarly, if I lack iron in my diet, iron bind protein content will increase. This is negative feedback regulation. When they measure your iron levels they do iron binding studies as well

Additionally, specific stimulating hormones levels work via negative feedback. For example, thyroid stimulating hormone (TSH) is sensitive to circulating thyroid hormones.

I will have a look into the situation re. melatonin and get back to you.

Starr, be more specific. Did you take 3mg or 9mg? What is your age and lifestyle like i.e shift worker (nightshift) or party animals who pulls all nighters

#7 syr_

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Posted 11 June 2006 - 09:26 AM

I have heard yes, and this is true with most (all?) hormones that your body produces.

#8 ajnast4r

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Posted 11 June 2006 - 02:18 PM

a strong and incorrect statement.

For example, if I increase my dietary iron intake and have enough iron the total iron binding proteins will decrease accordingly. Similarly, if I lack iron in my diet, iron bind protein content will increase. This is negative feedback regulation. When they measure  your iron levels they do iron binding studies as well

Additionally, specific stimulating hormones levels work via negative feedback. For example, thyroid stimulating hormone (TSH) is sensitive to circulating thyroid hormones.

I will have a look into the situation re. melatonin and get back to you.

Starr, be more specific. Did you take 3mg or 9mg? What is your age and lifestyle like i.e shift worker (nightshift) or party animals who pulls all nighters



im not incorrect. example: supplementing digestive enzymes does not decrease the bodys production of digestive enzymes.

not EVERYTHING produced by the body is downregulated when an outside supply is introduced.

#9 scottl

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Posted 11 June 2006 - 02:40 PM

negative feedback regulation does NOT occur when introducing endogenous substances through exogenous means in all cases... its really specific to the substance.


I do agree. Melatonin is one that supposedly does not. There are however other issue with meletonin.

Digestive enzymes, not so sure. There may be feedback, not sure it matters.

#10 starr

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Posted 11 June 2006 - 04:13 PM

I wonder what the consequences of taking 3-9 mgs of melatonin nearly every night for 8 years would be (which is what I did).


try sleeping without it


I have been for about 7 months now. I'm not the best sleeper though,. Lately it's been better.

#11 starr

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Posted 11 June 2006 - 04:25 PM

Starr, be more specific. Did you take 3mg or 9mg? What is your age and lifestyle like i.e shift worker (nightshift) or party animals who pulls all nighters


I said 3-9 mgs because I varied the dose. Sometimes 3, sometimes 6 sometimes 9. Occasionally even more. Towards the end I kept it mostly to 3. When I started it, it helped me stay on schedule for a 9-5 job and I also took it for the antioxidant properties. I'm 31 and self employed so my schedule is pretty flexible. I naturally tend toward staying up late (after 12) but I really don't party much at all anymore. My skin has been going to hell lately (thinning and loss of elasticity) but I don't know for certain if that has anything to do with the cessation of melatonin. I had to stop it for a month in order to properly take a test but I still haven't finished that test because my timing has never been right for it. I also wanted to see how I would do without it.

#12 manofsan

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Posted 11 June 2006 - 06:51 PM

Try the precursor, tryptophane, so that your body can manufacture the melatonin from it. Pure tryptophane is banned from direct sale, but you can buy it as an organic source, such as valerian root.

I find that taking folic acid around bedtime really helps me to sleep deeply for some reason. Perhaps it just helps the brain to recharge more efficiently. I find it's good to juggle the supplements periodically and not take the same thing all the time.

#13 ajnast4r

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Posted 11 June 2006 - 08:46 PM

Try the precursor, tryptophane, so that your body can manufacture the melatonin from it. Pure tryptophane is banned from direct sale, but you can buy it as an organic source, such as valerian root.



tryptophan is not banned anymore and is available publicly. FTH nutracueticals makes a great (but expensive) tryptophan. 1 gram at bed, with a 8oz glass of OJ and 5mg p-5-p, 1 hours before bed... should put you out like a light.

and valerian is not a source of tryptophan... the chemicals act (weakly) on gaba

#14 starr

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Posted 11 June 2006 - 10:20 PM

I have tryptophan (Dr.'s Best). It came back awhile ago. I did take it hoping to naturally increase my melatonin levels. I can't say I noticed much. I was taking a lot of aminos a couple months ago in pursuit of GH release. I can't say with total certainty but it seems that the *less* aminos I take before bed, the better I sleep. There very well could have been other factors waking/keeping me up (like trying to sleep on an empty stomach). I plan to try again in a month or so.

#15 zoolander

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Posted 11 June 2006 - 11:23 PM

I still can't believe that you made such a statement in the supplement fora. A fora that looks at how various supplements effect our cells at a genetic level and now you are defending it.

I will quote you again and explain why I said the remark was strong and incorrect.

negative feedback regulation does NOT occur when introducing endogenous substances through exogenous means in all cases... its really specific to the substance.


It's a strong comment because you placed emphasis on the not by typing it in caps i.e NOT. There is nothing wrong with making strong statements by doing this but you would usually need to following the statement with an accurate comment. You stated that negative feedback regulation does NOT occur.........in all cases. Would it be fair to say that if negative feedback regulation occurs in just one situation that the statement is NOT accurate?

I gave you 2 examples off the top of my head that pretty much invalidated your statement. I am sure that if I look into it further that I could find more examples.

Here I will expand on one of my examples. I mentioned a negative feedback regulatory process that occurs with dietary iron.

Iron absorbtion is regulated by three mechanisms:
1. Dietary regulator: a short-term increase in dietary iron is not absorbed as the mucosal cells have accumulated iron and "block" additional uptake.
2. Stores regulator: as body iron stores fall, the mucosa is signalled to moderately increase absorbtion.
3. Erythropoietic regulator: in response to anemia the erythroid cells will signal the mucosa to increase iron absorbtion more significantly.

All of these mechanisms are negative feedback. Of importance here though is the first of the three, Dietary regulation.

In humans approximately 70% of total body iron is found in hemoglobin. Because of storage and recycling very little (1-2mg) iron will need to be replaced from the diet on a daily basis. Any excess dietary iron is not absorbed or is stored in intestinal enterocytes. Regulation of iron absorption, recycling and release from intracellular stores is controlled by the actions of the hepatic iron regulatory protein hepcidin. Recent evidence has demonstrated that hepcidin functions by inhibiting the presentation of one or more of the iron transporters (e.g. DMT1 and Ireg1) in intestinal membranes. With a high iron diet the level of hepcidin mRNA increases and conversely its levels decrease when dietary iron is low. This is occurring simultaneous to reciprocal changes in the levels of the transporters.

Duodenal HFE expression and hepcidin levels determine body iron homeostasis: modulation by genetic diversity and dietary iron availability.

Ludwiczek S, Theurl I, Artner-Dworzak E, Chorney M, Weiss G.

Department of Internal Medicine, University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.

HFE affects the interaction of transferrin bound iron with transferrin receptors (TfR) thereby modulating iron uptake. To study genetically determined differences in HFE expression we examined individual HFE levels in C57BL/Sv129 mice and assessed their relationship to the regulation of iron homeostasis in the duodenum and the liver, and their regulation by diet. We found an up to 14-fold variation in inter-individual expression of HFE mRNA in the duodenum. Mice with high duodenal HFE mRNA expression presented with significantly higher levels of TfR and DMT-1 mRNAs and an increased IRP-1 binding affinity as compared to mice with low HFE levels. Duodenal HFE expression was positively associated with serum iron and liver HFE levels. Dietary iron supplementation decreased HFE in the duodenum but not in the liver. This was paralleled by reduced amounts of DMT-1 and FP-1 in the duodenum while the expression of DMT-1, FP-1, and hepcidin in the liver were increased with dietary iron overload. Duodenal and liver HFE levels are regulated by divergent penetration of as yet unelucidated modifier genes and to a much lesser extent by dietary iron. These measures control duodenal iron transport and liver iron homeostasis by modulating HFE expression either directly or via stimulation of iron sensitive regulatory molecules, such as hepcidin, which then exert their effects on body iron homeostasis. Copyright 2004 Springer-Verlag

PMID: 15173932 [PubMed - indexed for MEDLINE]


Even the most basic of examples counters your statement. If ate pure glucose (exogenous mean) it would increase my blood glucose levels (endogenous substance). If I continue to eat glucose my blood glucose levels will continue to increase. High blood glucose (hyperglycaemia) is dangerous. If I apply your statement to this situation I should be able to eat as much glucose as I like regardless of my blood glucose level. I could eat myself into an extreme situation. However, this does not happen in healthy individuals. Why? because of negative feedback. A negative feedback mechanism that will decrease your appetite and/or make you feel ill to stop you from increasing your blood glucose to dangerous unhealthy levels.

Drinking to much alcohol results in intoxication. Intoxication = negative feedback.
Drinking to much water will distented your stomach/bladder and decrease your thirst. Distension = negative feedback

You did confuse a little when you followed up your statement with

negative feedback regulation does NOT occur when introducing endogenous substances through exogenous means in all cases... its really specific to the substance.


Your statement is an oxymoron.

ajnast4r said in response to my statements

im not incorrect.


You didn't use capitals this time. Perhaps you are not so sure this time

anjast4r said:

example: supplementing digestive enzymes does not decrease the bodys production of digestive enzymes.


I'm not arguing the reverse case that "negative feedback regulation ALWAYS occurs when introducing endogenous substances through exogenous means in all cases" you can present as many examples as you wish but it does not defend your statement as incorrect. However, all I have to do is give one example to show your statement as incorrect. I have given many examples.

anjast4r said:

not EVERYTHING produced by the body is downregulated when an outside supply is introduced.


You're using capitals again. This time it appears that you are trying to drive your point home. Again, what you just said does not defend your initial statement. It is merely a modifacation of what you said. Your initial statement doesn't say "not EVERYTHING" it says "does NOT occur....in all cases" which is like saying "NOTHING" and opposed to "not EVERYTHING".

You mentioned the word downregulated in the last statement. Are you talking about downregulation of receptors, as suggested in the original post by starr? or are you talking about the downregulation/realignment/control of a metabolic process i.e homeostasis?

Let me state this clearly....

my arguement is against the statement made as a strong black or white comment. Strong because emphasis was placed on the word "NOT" by using capitals and black or white because the comment "in all cases" was made.

I don't care if there are cases where negative feedback does not occur. I care about people who ask question being misinformed but such bold and incorrect statements.

Now lets move on to answering the question and exploring our options

#16 simfish

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Posted 12 June 2006 - 01:27 AM

Ok, does that also hold true with dopamine boosting drugs and the body's production of dopamine? I know thaat the body does something else with relation to dopamine though - it cuts down on its own dopamine receptors.

But DOES THE SAME apply to amino acids that the body naturally produces, like tyrosine? I've read something about people taking tyrosine supplements becoming tolerant to it... =/

#17 scottl

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Posted 12 June 2006 - 01:39 AM

Zoo,

I read that to mean does not occur in all cases=does not occur in 100% of cases so if 1 case is false what he said is correct according to how I read it and probably how he meant it. I now see how you could read it the other way but probably not how meant.

#18 scottl

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Posted 12 June 2006 - 01:40 AM

Actually you still can't tell from what I wrote above. Suffice to say those words can be taken two ways.

#19 ajnast4r

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Posted 12 June 2006 - 02:10 AM

zoo, i love your posts... but thats a bit much. i have NO idea what youre trying to get at here... scott seems to have understood what i meant... maybe you are just misinterpreting it?


exactly what i mean was: negative feedback regulation does not occurr with 100% of substances.

that is not an incorrect statement... i really have no idea what ur getting at.

#20 zoolander

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Posted 12 June 2006 - 03:04 AM

exactly what i mean was: negative feedback regulation does not occurr with 100% of substances.


Ok. The above statement resolves the issue. I agree with the above statement ;)

It's quite a paradox in my situation because my grammer and spelling are not the best but I am very semantical. Especially when it comes to making bold statements.

Lets not forget that I am from another country and sometimes, even though english may be our primary language, differences will come into play.

In person I am very laid back when it comes to arguing a point. I slowly and calmly breakdown the arguement to get a better understanding. I have discovered that his approach tends to come accross as quite aggressive on-line in the cyber world.

Scottl, I guess you have seen me do this before [lol]

This situation arised as a result of a misunderstanding.

ajnast4r, I enjoy your posts as well.

Now come here and give me a hug before I pop off a rip the shit out of your arguement in shepards supplement regime post about fatty acid intake

Only Joking [tung] [lol]

#21 zoolander

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Posted 12 June 2006 - 05:02 AM

Let's us have a look at some of the original questions related to melatonin...

Simfish said:

If your body is already producing plenty of melatonin, then could taking it potentially decrease the body's own production of melatonin? This question should also apply to other drugs that the body naturally produces.


I can understand why you might think that melatonin supplementation might decrease the bodys own ability to secrete it but I am not aware of this happening with melatonin.

When taking a melatonin supplement before the onset of endogenous melatonin secretion i.e before bed at night, the dose of the supplement will be added to our our endogenous secretion. Hence, in most situation a low dose will be effective. You can start as low as 300mcg with some supplements. If you are taking melatonin after a nightshift you obviously will not have any endogenous secretion because of the light. Melatonin supplementation taken at any time during the day or night then 0.3-5mg of melatonin should be enough to induce sleep.

anjast4r said:

but since most peoples melatonin levels start to decrease around 35-40, anyone of or over that age should be ok.


Peiraoli has suggested in his book, The Melatonin miracle that endogenous melatonin decreases with age. Others have also found a decrease with age

Aging and the circadian rhythm of melatonin: a cross-sectional study of Chinese subjects 30-110 yr of age.

Zhao ZY, Xie Y, Fu YR, Bogdan A, Touitou Y.

Anti-Senility Research Center of Shandong, Shandong Academy of Medical Sciences, 250062 Jinan, PR China.

Although previous reports indicate that nocturnal plasma melatonin secretion declines with age, some recent findings do not support this point. In the present cross-sectional study, we documented serum melatonin concentrations at two time points, 02:00 and 08:00 h, in 144 persons aged 30-110 yr and found a significant age-related decline. It began around the age of 60 and reached a very significantly lower level in subjects in their 70s and over 80 yr of age (P < 0.01, when compared with age <60 yr). Nocturnal melatonin levels were higher among (post-menopausal only) women than men overall (P < 0.05). In the older age-groups, nocturnal melatonin levels did not differ between healthy controls and subjects with high blood pressure or ischemic heart disease. To further check these results, we also assessed the circadian pattern of serum melatonin in four subgroups of healthy men, aged 30-39, 40-49, 50-59, and 60-69 yr: blood samples were taken at 2 h intervals from 08:00 to 22:00 h and hourly from 22:00 to 08:00 h. Our results showed generally similar circadian melatonin patterns that peaked at night with very low levels during the daytime. No significant difference was found among the three younger groups, but nocturnal melatonin levels were significantly lower in the men in their 60s.

PMID: 12511033 [PubMed - indexed for MEDLINE]


However, some will disgree.....

Do plasma melatonin concentrations decline with age?

Zeitzer JM, Daniels JE, Duffy JF, Klerman EB, Shanahan TL, Dijk DJ, Czeisler CA.

Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

PURPOSE: Numerous reports that secretion of the putative sleep-promoting hormone melatonin declines with age have led to suggestions that melatonin replacement therapy be used to treat sleep problems in older patients. We sought to reassess whether the endogenous circadian rhythm of plasma melatonin concentration changes with age in healthy drug-free adults. METHODS: We analyzed the amplitude of plasma melatonin profiles during a constant routine in 34 healthy drug-free older subjects (20 women and 14 men, aged 65 to 81 years) and compared them with 98 healthy drug-free young men (aged 18 to 30 years). RESULTS: We could detect no significant difference between a healthy and drug-free group of older men and women as compared to one of young men in the endogenous circadian amplitude of the plasma melatonin rhythm, as described by mean 24-hour average melatonin concentration (70 pmol/liter vs 73 pmol/liter, P = 0.97), or the duration (9.3 hours vs 9.1 hours, P = 0.43), mean (162 pmol/liter vs 161 pmol/liter, P = 0.63), or integrated area (85,800 pmol x min/liter vs 86,700 pmol x min/liter, P = 0.66) of the nocturnal peak of plasma melatonin. CONCLUSION: These results do not support the hypothesis that reduction of plasma melatonin concentration is a general characteristic of healthy aging. Should melatonin replacement therapy or melatonin supplementation prove to be clinically useful, we recommend that an assessment of endogenous melatonin be carried out before such treatment is used in older patients.

PMID: 10569297 [PubMed - indexed for MEDLINE]


Starr said:

I wonder what the consequences of taking 3-9 mgs of melatonin nearly every night for 8 years would be (which is what I did).


I am not aware of any long-term administration studies on humans. There are studies with rats and flies. Here's one using rats

Effects of long-term administration of melatonin and a putative antagonist on the ageing rat.

Oaknin-Bendahan S, Anis Y, Nir I, Zisapel N.

Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Israel.

Adult rats were treated with either melatonin, the putative melatonin antagonist N-(2,4 dinitrophenyl)-5-methoxytryptamine (ML-23), their combination, or a vehicle for 16 months via the drinking water. The survival rates, serum testosterone and densities of 125I-melatonin binding sites in the medulla-pons and hypothalamus of the animals at the age of 27-29 months were significantly higher in the melatonin than vehicle-treated group. Surprisingly, ML-23 without or with melatonin, also prolonged the life-span of the aged animals. ML-23 treatment greatly increased 125I-melatonin binding in the medulla-pons whereas this increase was prevented by melatonin supplementation. Thus melatonin can attenuate age-related decrease in survival rates, testosterone and brain 125I-melatonin binding sites, while chronic blockade by the putative antagonist also elicits melatonin-mimetic responses, perhaps by effecting supersensitivity.

PMID: 7605949 [PubMed - indexed for MEDLINE]


so the consequences with long-term administration of melatonin in the above study was an attenuation (i.e to lessen) of age-related decreases in survival rates. I'm not sure what the rat dosage were in this study so I can't convert it into a human equivalent dose for you.

Starr, I'm thinking that you'll be ok and that no real harm has been done. But I can't back this statement up apart from trying to put some pieces together for you.

In regards to possible downregulation/desensitization of melatonin receptors.....all I could find was research that showed that even endogenous secretions within normal physiological levels, could desensitize receptors. Perhaps someone else can answer this question. I heard it asked a few times.

Melatonin desensitizes endogenous MT2 melatonin receptors in the rat suprachiasmatic nucleus: relevance for defining the periods of sensitivity of the mammalian circadian clock to melatonin.

Gerdin MJ, Masana MI, Rivera-Bermudez MA, Hudson RL, Earnest DJ, Gillette MU, Dubocovich ML.

Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Feinberg School of Medicine, Chicago, IL 60611-3008, USA.

The hormone melatonin phase shifts circadian rhythms generated by the mammalian biological clock, the suprachiasmatic nucleus (SCN) of the hypothalamus, through activation of G protein-coupled MT2 melatonin receptors. This study demonstrated that pretreatment with physiological concentrations of melatonin (30-300 pM or 7-70 pg/mL) decreased the number of hMT2 melatonin receptors heterologously expressed in mammalian cells in a time and concentration-dependent manner. Furthermore, hMT2-GFP melatonin receptors heterologously expressed in immortalized SCN2.2 cells or in non-neuronal mammalian cells were internalized upon pretreatment with both physiological (300 pM or 70 pg/mL) and supraphysiological (10 nM or 2.3 ng/mL) concentrations of melatonin. The decrease in MT2 melatonin receptor number induced by melatonin (300 pM for 1 h) was reversible and reached almost full recovery after 8 h; however, after treatment with 10 nM melatonin full recovery was not attained even after 24 h. This recovery process was partially protein synthesis dependent. Furthermore, exposure to physiological concentrations of melatonin (300 pM) for a time mimicking the nocturnal surge (8 h) desensitized functional responses mediated through melatonin activation of endogenous MT2 receptors, i.e., stimulation of protein kinase C (PKC) in immortalized SCN2.2 cells and phase shifts of circadian rhythms of neuronal firing in the rat SCN brain slice. We conclude that in vivo the nightly secretion of melatonin desensitizes endogenous MT2 melatonin receptors in the mammalian SCN thereby providing a temporally integrated profile of sensitivity of the mammalian biological clock to a melatonin signal.

PMID: 15522910 [PubMed - indexed for MEDLINE]


I'm currently taking melatonin. I believe the benefits out weigh the possible risks. The possible risks are mainly there because we do not know what long-term supplementation will bring in humans. So cycle your supplementation. I take it 5 days a week and have 2 days off. Then every 3 months I have 2 weeks off. I do this with all my supplements.

But common on let's have a look at the benefits

Biochim Biophys Acta. 2006 Apr 17;

Melatonin as antioxidant, geroprotector and anticarcinogen.

Anisimov VN, Popovich IG, Zabezhinski MA, Anisimov SV, Vesnushkin GM, Vinogradova IA.

Department of Carcinogenesis and Oncogerontology, N.N. Petrov Research Institute of Oncology, Pesochny-2, St. Petersburg 197758, Russia.

The effect of the pineal indole hormone melatonin on the life span of mice, rats and fruit flies has been studied using various approaches. It has been observed that in female CBA, SHR, SAM and transgenic HER-2/neu mice long-term administration of melatonin was followed by an increase in the mean life span. In rats, melatonin treatment increased survival of male and female rats. In D. melanogaster, supplementation of melatonin to nutrient medium during developmental stages produced contradictory results, but and increase in the longevity of fruit flies has been observed when melatonin was added to food throughout the life span. In mice and rats, melatonin is a potent antioxidant both in vitro and in vivo. Melatonin alone turned out neither toxic nor mutagenic in the Ames test and revealed clastogenic activity at high concentration in the COMET assay. Melatonin has inhibited mutagenesis and clastogenic effect of a number of indirect chemical mutagens. Melatonin inhibits the development of spontaneous and 7-12-dimethlbenz(a)anthracene (DMBA)- or N-nitrosomethylurea-induced mammary carcinogenesis in rodents; colon carcinogenesis induced by 1,2-dimethylhydrazine in rats, N-diethylnitrosamine-induced hepatocarcinogenesis in rats, DMBA-induced carcinogenesis of the uterine cervix and vagina in mice; benzo(a)pyrene-induced soft tissue carcinogenesis and lung carcinogenesis induced by urethan in mice. To identify molecular events regulated by melatonin, gene expression profiles were studied in the heart and brain of melatonin-treated CBA mice using cDNA gene expression arrays (15,247 and 16,897 cDNA clone sets, respectively). It was shown that genes controlling the cell cycle, cell/organism defense, protein expression and transport are the primary effectors for melatonin. Melatonin also increased the expression of some mitochondrial genes (16S, cytochrome c oxidases 1 and 3 (COX1 and COX3), and NADH dehydrogenases 1 and 4 (ND1 and ND4)), which agrees with its ability to inhibit free radical processes. Of great interest is the effect of melatonin upon the expression of a large number of genes related to calcium exchange, such as Cul5, Dcamkl1 and Kcnn4; a significant effect of melatonin on the expression of some oncogenesis-related genes was also detected. Thus, we believe that melatonin may be used for the prevention of premature aging and carcinogenesis.

PMID: 16678784 [PubMed - as supplied by publisher]


1. Anti-oxidant
2. Anti-aging
3. Anticarcinogen

Sounds like other supplements should take a leaf out of melatonins' book

Edited by chrono, 09 October 2010 - 02:31 PM.
fixed quote tag


#22

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Posted 16 June 2006 - 08:37 PM

I need to take melatonin. I found that before I started using melatonin I could sleep late on the weekends - no problem. Now, I can't really sleep late on the weekends if the sun is shining. I can sleep in a little longer on a cloudy day.

This is the effect I believe it should cause for someone (who needs it), sensitivity to change in light influencing the sleep/wake cycles.

I have heard people say they have tried melatonin and it gave them vivid dreams. I think those vivid or weird dreams may be an indication that this person does NOT need to supplement melatonin. But, that is just my guess.

If I had to cycle it I don't know what else I would use because I do think my body needs to supplement melatonin. I can forget to take it sometimes and will notice the difference. Cycling is not an option for me now; but who knows if that might change at some point.

#23 zoolander

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Posted 17 June 2006 - 09:06 AM

I have heard people say they have tried melatonin and it gave them vivid dreams. I think those vivid or weird dreams may be an indication that this person does NOT need to supplement melatonin. But, that is just my guess.


We all dream. It has been found that most animals and mammals dream. All except the ant eater. Maybe it's their diet?

So the fact that your friends are having vivid or weird dreams whilst taking melatonin and that you think that they do NOT need to supplement melatonin doesn't really make sense. I would think that taking something that increases your dream recall or increases the vividness of your dreams would be a bonus and not a negative.

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Posted 19 June 2006 - 01:51 PM

We all dream. It has been found that most animals and mammals dream. All except the ant eater. Maybe it's their diet?

So the fact that your friends are having vivid or weird dreams whilst taking melatonin and that you think that they do NOT need to supplement melatonin doesn't really make sense. I would think that taking something that increases your dream recall or increases the vividness of your dreams would be a bonus and not a negative.


This is not just something I have heard about. You can find many references to melatonin and vivid dreams in google.

http://www.google.co...in dreams vivid

Dream recall is a problem for some. (Little or no dream recall is actually a sign of a vitamin b6 deficiency.) But having wildly vivid dreams can be a problem for some people. Think of them as nightmares, perhaps. Most people do say that taking melatonin and having these wild dreams is not an improvement. Some people don't like the vivid dreams they have on melatonin. Moderation with everything.

For some people dreams can be weird enough without them getting more intense sometimes. This is different than restoring dream recall. Restoring dream recall would be an improvement, but having dreams that leave someone shaken up in the morning is not a good sign. And I think that may mean that melatonin is not needed by that person.

"I would think that taking something that increases your dream recall or increases the vividness of your dreams would be a bonus and not a negative." Sorry but we are not talking about restoring dream recall. Dream recall is fine but if the dream content gets too intense for some people then it can be a problem. Melatonin can change your dreams and cause you do wake up wondering what the hell all those images are about, more so than normally. How is that an improvement?

#25 zoolander

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Posted 20 June 2006 - 02:15 PM

The dreams are a manifestation of the subsconscious mind. From what you have said sounds as though the melatonin is helping these people sleep and dream normally. It sounds as though these people cannot and do not won't to deal with their dreams. If this is the case they probably need to see someone to help them. The dreams are as much as part of them as their left arms.

I do not think meltonin is to blame for the dreams.

If meltonin makes them dream then tell them to stay away from phenibut. Phenibut makes my dreams feel more realistic than my awake state. It's amazing

#26 xanadu

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Posted 20 June 2006 - 09:10 PM

Piracetam seems to make me dream.

#27 Centurion

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Posted 21 June 2006 - 12:30 AM

I rarely recall my dreams

#28

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Posted 26 June 2006 - 04:51 PM

I rarely recall my dreams


You may have a vitamin b6 deficiency. This can be serious because your body is not able to convert tryptophan into serotonin. Tryptophan does have some toxicity.

Little or no dream recall is a good sign of a vitamin b6 deficiency. Unless you have some GI problem you may have the same condition I have, pyroluria. You can read on the symptoms of pyroluria and see if you match any of them.

http://www.drkaslow..../pyroluria.html

#29 Shepard

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Posted 26 June 2006 - 06:10 PM

You can read on the symptoms of pyroluria and see if you match any of them.


Not the best idea.

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#30 emerson

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Posted 26 June 2006 - 06:46 PM

Dream recall also tends to be somewhat lowered in people not getting enough sleep. I'd say that accounts for a good percentage of the population at the moment.

I always feel so new-agey when going into the subject of dreams. But sometimes it's hard to resist. Keeping a journal of dreams upon waking is the best way I can think of to improve recall. Certainly seems like a good first measure before resorting to potentially unneeded medication. For someone with little to no dream recall it usually starts out as just vague feelings scribbled on paper, but for most people the training usually can extend that at a fairly rapid pace.




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