High Dose Melatonin Therapy

[Konstantin]

I am taking melatonin every day in dose from 1 to 6 mg ( usually 3mg ) for almost 4-5 years.
It helps me sleep better. The highest dose that I have tried was 9 mg. The only effect I noticed from this dose was good night sleep.

On a few occasions, I noticed that when I took the regular dose of melatonin of 3 mg that I can't fall asleep at all. I feel so fresh the whole night. It happens only a few times in all these years that I am taking melatonin.

When that happens I stop taking melatonin for a few days and then I restart taking melatonin again. This insomnia goes the next day when I stop melatonin.

I found one good and long article about melatonin

The Therapeutic Potential of Melatonin: A Review of the Science - PMC

www.ncbi.nlm.nih.gov

and here what is says about mega doses

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.[138] 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

Probably timing is also very important

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,[46,148] 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,”[27] melatonin administration that unduly prolongs the nocturnal melatonin rise, or that is given throughout the day, may exacerbate SAD[82] and bipolar and classic depression.[83] 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

Melatonin has also been suggested for use as a contraceptive for women,[145] which might raise the question of whether melatonin damages the female reproductive system. Notably, no side effects were reported in a report of a phase 2 clinical trial in which 1400 women were treated with 75 mg of melatonin nightly for 4 years.[145]

 

[s1mpleman]

Very interesting thanks for sharing. I've only gone up to 9mg which was taking in 3 pills back when I was first getting myself off pot to help me sleep. I found all it did then was make me really jittery but 1mg seemed to be perfect. I've found I can sleep without it totally fine now, but I get a much deeper sleep with it. It helped a lot at resetting my sleeping patterns too, it's a godsend when I have to travel to Brazil to see the wifes family.

I never considered a higher dose at all although I've heard quite a lot it isn't toxic at any level.

Thought I'd have a quick search through pubmed and found some interesting studies. One that even experimented with intravenous administration up till 100mg. Hope there helpful, I'm pretty astonished by the results.

Neuroprotective effects of high-dose vs low-dose melatonin after blunt sciatic nerve injury - PubMed

Our results suggest that melatonin, especially at a dose of 50 mg/kg, has a potent neuroprotective effect and can preserve peripheral neural fibers from lipid peroxidative damage after blunt trauma. With further investigations, we hope that these data may prove useful to clinicians who treat...

www.ncbi.nlm.nih.gov

Abstract
INTRODUCTION:
Melatonin, the secretory product of the pineal gland, has potent antioxidant properties. The aim of this study was to compare the effects of low-dose (10 mg/kg) vs high-dose (50 mg/kg) melatonin on early lipid peroxidation levels and ultrastructural changes in experimental blunt sciatic nerve injury (SNI). We believe this to be the first study to assess the dose-dependent neuroprotective effects of melatonin after a blunt peripheral nerve injury.
MATERIALS AND METHODS:
Rats were randomly allocated into 5 groups of 10 animals each. The SNI only rats underwent a nerve injury procedure. The SNI plus vehicle group received SNI and intraperitoneal injection of vehicle (diluted ethanol) as a placebo. The SNI plus low-dose or high-dose melatonin groups received intraperitoneal melatonin at doses of 10 mg/kg or 50 mg/kg, respectively. Controls had no operation, melatonin or vehicle injection. SNI was induced by clamping the sciatic nerve at the upper border of the quadratus femoris for 2 min.
RESULTS:
Sciatic nerve samples were harvested 6 h after nerve injury and processed for biochemical and ultrastructural analysis. Trauma increased the lipid peroxidation of the sciatic nerve by 3.6-fold (153.85 +/- 18.73 in SNI only vs 41.73 +/- 2.23 in control rats, P < 0.01). Low (P = 0.02) and high (P < 0.01) doses of melatonin attenuated the nerve lipid peroxidation by 25% and 57.25%, respectively (65.76 +/- 2.47 in high-dose vs 115.08 +/- 7.03 in low-dose melatonin groups).
DISCUSSION:
Although low-dose melatonin reduced trauma-induced myelin breakdown and axonal changes in the sciatic nerve, high-dose melatonin almost entirely neutralized any ultrastructural changes.
CONCLUSION:
Our results suggest that melatonin, especially at a dose of 50 mg/kg, has a potent neuroprotective effect and can preserve peripheral neural fibers from lipid peroxidative damage after blunt trauma. With further investigations, we hope that these data may prove useful to clinicians who treat patients with nerve injuries.

Pharmacokinetics of high-dose intravenous melatonin in humans - PubMed

This crossover study investigated the pharmacokinetics and adverse effects of high-dose intravenous melatonin. Volunteers participated in 3 identical study sessions, receiving an intravenous bolus of 10 mg melatonin, 100 mg melatonin, and placebo. Blood samples were collected at baseline and 0...

www.ncbi.nlm.nih.gov

This crossover study investigated the pharmacokinetics and adverse effects of high-dose intravenous melatonin. Volunteers participated in 3 identical study sessions, receiving an intravenous bolus of 10 mg melatonin, 100 mg melatonin, and placebo. Blood samples were collected at baseline and 0, 60, 120, 180, 240, 300, 360, and 420 minutes after the bolus. Quantitative determination of plasma melatonin concentrations was performed using a radioimmunoassay technique. Pharmacokinetic parameters were estimated by a compartmental pharmacokinetic analysis. Adverse effects included assessments of sedation and registration of other symptoms. Sedation, evaluated as simple reaction times, was measured at baseline and 120, 180, 300, and 420 minutes after the bolus. Twelve male volunteers completed the study. Median (IQR) Cmax after the bolus injections of 10 mg and 100 mg of melatonin were 221,500.0 (185,637.5-326,175.0) pg/mL and 1,251,500.0 (864,375.0-1,770,500.0) pg/mL, respectively; mean (SD) t1/2 was 42.3 (5.6) minutes and 46.2 (6.2) minutes; mean (SD) Vd was 1.6 (0.9) L/kg and 2.0 (0.8) L/kg; mean (SD) CL was 0.0253 (0.0096) L/min · kg and 0.0300 (0.0120) L/min · kg; and median (IQR) AUC0- ∞ , 8,997,633.0 (6,071,696.2-11,602,811.9) pg · min/mL and 54,685,979.4 (36,028,638.6-105,779,612.0) pg · min/mL. High-dose intravenous melatonin did not induce sedation, evaluated as simple reaction times. No adverse effects were reported in the study.

The use of high-dose melatonin in liver resection is safe: first clinical experience - PubMed

Experimental data suggest that melatonin decreases inflammatory changes after major liver resection, thus positively influencing the postoperative course. To assess the safety of a preoperative single dose of melatonin in patients undergoing major liver resection, a randomized controlled...

www.ncbi.nlm.nih.gov

Abstract
Experimental data suggest that melatonin decreases inflammatory changes after major liver resection, thus positively influencing the postoperative course. To assess the safety of a preoperative single dose of melatonin in patients undergoing major liver resection, a randomized controlled double-blind pilot clinical trial with two parallel study arms was designed at the Department of General and Transplantation Surgery, Ruprecht-Karls-University, Heidelberg. A total of 307 patients, who were referred for liver surgery, were screened. One hundred and thirteen patients, for whom a major liver resection (≥3 segments) was scheduled, were eligible. Sixty-three eligible patients refused to participate, and therefore, 50 patients were randomized. A preoperative single dose of melatonin (50 mg/kg BW) dissolved in 250 mL of milk was administered through the gastric tube after the intubation for general anesthesia. Controls were given the same amount of microcrystalline cellulose. Primary endpoint was safety. Secondary endpoints were postoperative complications. Melatonin was effectively absorbed with serum concentrations of 1142.8 ± 7.2 ng/mL (mean ± S.E.M.) versus 0.3 ± 7.8 ng/mL in controls (P < 0.0001). Melatonin treatment resulted in lower postoperative transaminases over the study period (P = 0.6). There was no serious adverse event in patients after melatonin treatment. A total of three infectious complications occurred in either group. A total of eight noninfectious complications occurred in five control patients, whereas three noninfectious complications occurred in three patients receiving preoperative melatonin (P = 0.3). There was a trend toward shorter ICU stay and total hospital stay after melatonin treatment. Therefore, a single preoperative enteral dose of melatonin is effectively absorbed and is safe and well tolerated in patients undergoing major liver surgery.

The effect of high dose melatonin on cardiac ischemia- reperfusion Injury - PubMed

Our study suggests that high dose melatonin, appears to offer protection against cardiac ischemia-reperfusion injuries in rats by scavenging the free radicals and could have a potential clinical use in the management of myocardial ischemia.

www.ncbi.nlm.nih.gov

Abstract
PURPOSE:
Melatonin, the most potent scavenger of toxic free radicals, has been found to be effective in protecting against pathological states due to the release of reactive oxygen species. This study was performed to establish the effect of high dose melatonin on protection against ischemia- reperfusion (I/R) injury in rat hearts.
MATERIALS AND METHODS:
Forty male Sprague-Dawley rats were used in this study. They were separated into four groups of ten rats each. A left coronary artery occlusion was induced in the rats by ligating the artery for 20 minutes and then releasing the ligation (reperfusion) afterwards. The control group was Group A. Group B was subjected to myocardial ischemia-reperfusion without any treatment, while Group C underwent myocardial ischemia-reperfusion with a melatonin treatment before the ischemia. Group D was subjected to myocardial ischemia-reperfusion with a melatonin treatment before the reperfusion. After 20 minutes of reperfusion, blood samples were obtained from each group for biochemical studies, and the animals were sacrificed for histological and, immunohistochemical examinations of the myocardial tissue.
RESULTS:
We found that the cardiac troponin T(cTn-T) levels were significantly increased in Group B when all groups were compared. In the Group C rats treated with melatonin, the cTn-T values were significantly lower than those in Groups B and D. In addition, malondialdehyde (MDA) and antioxidant enzymes including, superoxide dismutase (SOD) and myeloperoxidase (MPO) were lower than those in Group B in the melatonin treated groups. The differences were statistically significant (p < 0.05). Histopathologic and immunohistopathologic studies also supported the effectiveness of melatonin.
CONCLUSION:
Our study suggests that high dose melatonin, appears to offer protection against cardiac ischemia-reperfusion injuries in rats by scavenging the free radicals and could have a potential clinical use in the management of myocardial ischemia.

 

[s1mpleman]

Just found two more to add.

The first they found a reduction in oxidative damage from ALS and the second one deals with melatonin and radiation therapy.

Reduced oxidative damage in ALS by high-dose enteral melatonin treatment - PubMed

Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by...

www.ncbi.nlm.nih.gov

Abstract
Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by classical antioxidants. In preparation of a possible future clinical trial, we explored the potential of melatonin as neuroprotective compound and antioxidant in: (1) cultured motoneuronal cells (NSC-34), (2) a genetic mouse model of ALS (SOD1(G93A)-transgenic mice), and (3) a group of 31 patients with sporadic ALS. We found that melatonin attenuates glutamate-induced cell death of cultured motoneurons. In SOD1(G93A)-transgenic mice, high-dose oral melatonin delayed disease progression and extended survival. In a clinical safety study, chronic high-dose (300 mg/day) rectal melatonin was well tolerated during an observation period of up to 2 yr. Importantly, circulating serum protein carbonyls, which provide a surrogate marker for oxidative stress, were elevated in ALS patients, but were normalized to control values by melatonin treatment. This combination of preclinical effectiveness and proven safety in humans suggests that high-dose melatonin is suitable for clinical trials aimed at neuroprotection through antioxidation in ALS.

Randomized phase II trial of high-dose melatonin and radiation therapy for RPA class 2 patients with brain metastases (RTOG 0119) - PubMed

High-dose melatonin did not show any beneficial effect in this group of patients.

www.ncbi.nlm.nih.gov

Abstract
PURPOSE:
To determine if high-dose melatonin for Radiation Therapy Oncology Group (RTOG) recursive partitioning analysis (RPA) Class 2 patients with brain metastases improved survival over historical controls, and to determine if the time of day melatonin was given affected its toxicity or efficacy. RTOG 0119 was a phase II randomized trial for this group of patients.
METHODS AND MATERIALS:
RTOG RPA Class 2 patients with brain metastases were randomized to 20 mg of melatonin, given either in the morning (8-9 AM) or in the evening (8-9 PM). All patients received radiation therapy (30 Gy in 10 fractions) in the afternoon. Melatonin was continued until neurologic deterioration or death. The primary endpoint was overall survival time. Neurologic deterioration, as reflected by the Mini-Mental Status Examination, was also measured.
RESULTS:
Neither of the randomized groups had survival distributions that differed significantly from the historic controls of patients treated with whole-brain radiotherapy. The median survivals of the morning and evening melatonin treatments were 3.4 and 2.8 months, while the RTOG historical control survival was 4.1 months.
CONCLUSIONS:
High-dose melatonin did not show any beneficial effect in this group of patients.

 

[Mrs. Peel]

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

Um, does this mean that if you have light sensitivity (or damage to retinal photoreceptors) that taking melatonin makes it worse?

 

[Oxajil]

Um, does this mean that if you have light sensitivity (or damage to retinal photoreceptors) that taking melatonin makes it worse?

That's a reference to this study (poor rats!): Link

Abstract:

Melatonin increases photoreceptor susceptibility to light-induced damage.

Melatonin is an indolamine hormone synthesized in the retina and pineal gland. It is thought to act as a paracrine neurohormone in the mammalian retina. Pinealectomy has been shown to protect photoreceptors from light-induced damage, and melatonin treatment has been reported to increase the degree of photoreceptor damage in albino rats. To determine how melatonin influences photoreceptor survival, the effect of melatonin administration on light-induced retinal damage was studied. Melatonin was administered to albino rats by intraperitoneal injections at various times before or after light exposure. The rats were exposed to high-intensity illumination (1600 lux) for 24 hr to induce photodamage, then returned to cyclic lighting for 12 days. After this, they were killed, and their eyes were removed and examined histologically. Measurements of the outer nuclear layer (ONL) thickness were taken at 12 different loci around the circumference of the retinal sections. The animals that received daily melatonin injections (100 micrograms) in the late afternoon (3 hr before lights off) for 1-3 days before photodamage showed an approximate 30% greater reduction compared with sham control animals in ONL thickness in the superior quadrant, the area most susceptible to light damage. Melatonin injections given after the photodamage did not affect ONL thickness. Although retinal susceptibility to light damage varied with time of day, the degree to which melatonin increased the degree of damage appeared unaffected by the time of day. These results suggest that melatonin may be involved in some aspects of photoreceptor sensitivity to light damage.

So, if I understand correctly, in simple terms, melatonin injections before the rats were exposed to a lot of light, led to additional eye damage. But melatonin injections after the exposure of light led to no additional eye damage. Which may translate to: Don't take melatonin in the morning or maybe even early afternoon (but midafternoon is okay as mentioned earlier). Or: If you're planning to look straight at the sun or staying in a very bright place, you might want to take melatonin later! It can be tricky translating such studies.

FWIW: I have corneal scar tissue, and I used to be very sensitive to light, leading me to wear sunglasses most of the time, but that went away at some point and now I only have to do it on some summer days when it's very light out there. I'm saying this because I regularly took/take melatonin for periods of time one to several hours before sleep, and it never affected my sensitivity in a negative way. I doubt that a high concentration of melatonin would. Though perhaps (just a guess though!) taking it late afternoon and/or evening (if single dose; evening) would be the safe route if you have high sensitivity to light.

Hope this helps!

 

[s1mpleman]

So, if I understand correctly, in simple terms, melatonin injections before the rats were exposed to a lot of light, led to additional eye damage. But melatonin injections after the exposure of light led to no additional eye damage. Which may translate to: Don't take melatonin in the morning or maybe even early afternoon (but midafternoon is okay as mentioned earlier). Or: If you're planning to look straight at the sun or staying in a very bright place, you might want to take melatonin later! It can be tricky translating such studies.

FWIW: I have corneal scar tissue, and I used to be very sensitive to light, leading me to wear sunglasses most of the time, but that went away at some point and now I only have to do it on some summer days when it's very light out there. I'm saying this because I regularly took/take melatonin for periods of time one to several hours before sleep, and it never affected my sensitivity in a negative way. I doubt that a high concentration of melatonin would. Though perhaps (just a guess though!) taking it late afternoon and/or evening (if single dose; evening) would be the safe route if you have high sensitivity to light.

Hope this helps!

Good points, and I was under a similar understanding.

I also suffer from Anterior Uveitis (a lot less now thanks to diet changes) and have taken melatonin on a night with no adverse effects on my eyes sensitivity FWIW.

 

[Gaby]

I just finished reading "Extreme Dose Melatonin - The Miracle Anti-Aging Hormone, Anti-Alzheimer's Hormone, Anti Baldness Hormone, Menopause Reversal Hormone" by Jeff T. Bowles:

Melatonin – Jeff T Bowles

Is the fastest reading ever! Jeff T. Bowles is also the author of "Miraculous Results - Extremely High Doses of Vitamin D3" which we discussed elsewhere in this forum. Or at least I remember reading it and several members experimenting with his recommendations.

Bowles theorizes that one of the most important functions of the luteinizing hormone (LH) is to drive the destruction of tissue as we age (as opposed to when we are young). So LH attacks the brain in Alzheimer's disease. He quotes research pointing to the fact that an LH suppressing drug stop Alzheirmer's disease on its track, in women only. He explains, at least theoretically, why it didn't work in men and it has to do with the rest of the hormones. More specifically, he argues that men will only be protected by increasing their progesterone levels. This is where melatonin comes in.

He quotes research of melatonin's protective effects in Alzheimer's disease (AD), and he highlights how melatonin suppresses LH. He quotes his own blood tests which show how his LH levels dropped by 30% by taking 300mg of melatonin at night for two months. Not only that, his progesterone levels rose by 15%.

He argues that progesterone is one of the best neuroprotective substances on earth and himself takes 100mg of pregnenolone a day, which is a precursor for DHEA, progesterone, etc. He explains the levels of LH, progesterone and other hormones as we age and tells the story of how women delayed menopause by taking melatonin in high doses. Some women who already had menopause, started menstruating again.

His advice for people with initial stages of AD: for women, 75mg melatonin at night, and might even boost to 500mg. The same advice goes for men, except it would be 125mg of melatonin. He also suggests 200 to 400mmg of pregnenolone. However, he highlights the following:

It would be best to boost your melatonin doses gradually -- get used to 3mg, over a week or so, then go to 6mg, for a week, then 12mg, etc, doubling the dose every time you get used to the old dose. Why?

Because some of his friends started with 100 mg and didn't notice anything. On the 3rd day, it hit them: they got a bad case of dizziness or vertigo. He speculates that it is like fasting, some people get dizzy after several days of fasting.

After 12mg are reached, he suggests 24, then 48, then 75mg. For men, 96, then 120. He quotes results of members of his yahoo group where loved ones seemed to have recovered short-term memory despite the initial stage of AD. Anecdotally, he says that one member who only took coconut oil for one month, had pregnenolone levels increased by 250%!

Melatonin increases most of the "good" hormones and decreases most of the "bad" hormones, and it decreases all reproductive hormones regardless if they are good or bad.

Bowles also confesses to bad effects of melatonin among his members: higher chance of shingles, further thinning of hair if your father had thin hair, further thickening of hair if your father had thick hair. There was a case of recurrence of Lyme's disease.

He also quotes most of the papers on the protective effects of nicotine and smoking in AD, but he argues that it is due to the fact that smoking causes LH suppression. Same with smoking benefits in endometrial cancer, Parkinson's disease, Tourette's syndrome, etc.: smoking reduces LH.

LH levels go from 60% to 1100% increase in males by age 80. In females, +2600%. He speculates that progesterone protects women at some point, but that these levels might explain why AD is more common in elderly women than in elderly men.

So the above is the short version. He is fond of speculating very creatively. Furthermore, he has published papers. For instance:

The Evolution of Aging: A New Approach to an Old Problem of Biology - PubMed

Most gerontologists believe aging did not evolve, is accidental, and is unrelated to development. The opposite viewpoint is most likely correct. Genetic drift occurs in finite populations and leads to homozygosity in multiple-alleled traits. Episodic selection events will alter random drift...

pubmed.ncbi.nlm.nih.gov

This theory suggests that the protective effect of smoking and ibuprofen for Alzheimer's disease is caused through LH suppression.

 

[Anamarija]

It would be best to boost your melatonin doses gradually -- get used to 3mg, over a week or so, then go to 6mg, for a week, then 12mg, etc, doubling the dose every time you get used to the old dose. Why?

Thank you Gaby, great info.

This is from book Ronald Ross Watsona - Melatonin in the Promotion of Health:

In the past 50 years since the discovery of MEL, we have witnessed an emergence of a plethora of information from studies on a wide group of animals, including vertebrates and invertebrates, and plants subjected to MEL, the most unique and wonder molecule among all the known substances in areas covering endocrinology, pharmacology, physiology, psychology, chronobiology, and environmental biology. The most remarkable feature of this pineal hormone is its synthesis in the synchronization with the environmental light/dark (LD) conditions. In all the animals investigated so far, irrespective of their habit, MEL synthesis in a 24-hour cycle reaches peak during the dark phase. As a hormone, MEL afforded the first opportunity for its use as a chronobiological marker, particularly for those who are engaged in circadian studies. It plays a central role in primary circadian pacemaker (suprachiasmatic nucleus, SCN) to synchronize the body functions to LD cycle of the environment. Accordingly, this hormone is considered as a “chronobiotic molecule,” or the “hormone of darkness.” Molecular biology study dealing with its biosynthetic enzymes and their genes, molecular regulators, degradation byproducts, and the mechanisms of signaling in a cell has opened up a new chapter in circadian research. Carefully controlled studies in different animals, including the human, have implicated MEL in the control of a wide variety of body functions ranging from aging to aggression,
hibernation to hypertension, jet lag to seasonal affective disorders, sleep to stress, and reproduction to tissue regeneration. More recent studies revealed that MEL, because of its lipophilic nature, can cross the plasma membrane of any cell and thereby has free access to all the tissues, organs, and systems in the living body and by acting as a potent scavenger of free radicals may play an important role in combating oxidative stress in a metabolically active cell [7]. Moreover, MEL is known to be involved in complex processes of cellular protection and apoptosis. A rapidly expanding body of literature suggests that MEL as a biomarker of circadian dysfunctions may play pivotal roles in various neurodegenerative or neurological diseases. As a result, MEL has become a potent candidate for investigation in several disciplines of experimental biology and pathophysiology signifying its importance in clinical and therapeutic research. The aim of this review is to track the progress in research from discovery of MEL to its potential use in therapy by focusing the most fascinating, and arguably important, data gathered in recent past. We emphasize mostly on recent review articles, including ours, as they included many original findings that contributed to the current state of knowledge.

 

[Laura]

This is really starting to sound like a potential rejuvenating/life extending therapy.

I guess we should note that the mice that had eye issues were albinos and albinos in general have eye issues to begin with so I don't think Mrs. Peel has anything to worry about.

Also, the protocol for building up to the high doses sounds better. Obviously, starting too big too fast is what I did wrong and I sure did have vertigo and feel half drunk for a few days!!! I'm going to go at it again in the right way!

 

[liam1310]

I'm using melatonin for years now, never anymore than 3mg, most of the time I use liquid or Swanson Melatonin capsules, other ingredients are rice flour and gelatin. 3mg 120 capsules, it also comes in 10mg 60 capsules.

I took 6mg last night, first time taking more than 3mg, didn't notice much of a difference, just a good night's sleep, l will experiment with increasing the dose.

Thanks for the info guys.

 

[s1mpleman]

Also, the protocol for building up to the high doses sounds better. Obviously, starting too big too fast is what I did wrong and I sure did have vertigo and feel half drunk for a few days!!! I'm going to go at it again in the right way!

Wow, if that's how you felt from your staggered attempts I can only imagine what the 100mg intravenous study participants experienced after that dose.

 

[Laura]

I just finished "The Melatonin Miracle" by Walter Pierpaoli, MD. etc and William Regelson, MD. It's pretty much about the basics of melatonin, where it is produced, what it does, interactions with body systems, that sort of thing. The book talks about how they came to the idea that it can reverse aging and also that it is an anti-cancer element in the body. The solution presented is supplementation.

There are no real details about any cases that tell you how much of anything was given, for how long, etc, so don't get it expecting that. I only took a few notes as follows:

Pineal gland senses and reacts to other types of EM fields besides light; this can interfere with the production of melatonin which may be one factor behind the increase in cancer since the beginning of the widespread use of electricity, artificial lighting, appliances, etc. It may not be just light... EMFs may trigger the growth of cancer cells by blocking the anti-cancer action of melatonin.

Melatonin helps normalize cholesterol levels and blood pressure.

Zinc supplements are needed by older people; melatonin is closely involved in zinc transport, so the fall of levels of one is associated with the other.

For insomnia or restless, broken sleep:

Tak 1 mg melatonin. If you are not asleep in 30 minutes take another 1 mg. If in 30 min, not asleep, repeat with another 1 mg, up to 5 mg. (I guess if 5 doesn't work, you could start higher the next night with 2 mg, then another 2 mg in 30 min, and so on.)

Anyway, after you finally do get a night's sleep (having found the amount that does the job), continue taking that amount every night for 2 weeks for a reset, and then, if you are in the "anti-aging" set, go to your normal supplementation amount.

Anti-aging:

Age	Dose 30 minutes before sleep time
40-44	.5 to 1 mg
45-54	1 to 2 mg
55-64	2 to 2.5 mg
65-74	2.5 to 5 mg
75 plus	3.5 to 5 mg

If groggy next day, reduce your dose by 1/2 mg. Try that, if still groggy, reduce again. Obviously, if the suggested amounts don't do the job, you can try upping it by 1/2 mg at a time.

Now, this book says that everyone in the above age brackets should be taking melatonin in these amounts or something close because it is by that much that the pineal's ability to produce it declines at those ages. Book says if you do this, you can reverse aging and prevent cancer and a host of other problems.

Synthetic melatonin is preferred.

 

[zhenqing]

This is all very fascinating!

I've been using melatonin for years as well, but only for my insomnia. I've started taking 1mg dose back in 2011 or so, after I saw melatonin mentioned here on the Forum, but 1mg didn't do much for me, so I increased to 5mg, and that worked wonders for quite a while, until I had to increase to 10mg a few years back (because my life got more and more stressful).

It takes around half an hour to an hour for me to get sleepy, and then I sleep like a baby, and I never feel groggy in the morning (assuming I went to bed at a reasonable hour and slept a reasonable amount, which for me is not less than 7 hours and no more than 8 hours).

If I skip even one day of taking melatonin, my insomnia returns. So it's been a godsend for me, because the usual prescribed drugs for sleeplessness are awful.

 

[Laura]

This is all very fascinating!

I've been using melatonin for years as well, but only for my insomnia. I've started taking 1mg dose back in 2011 or so, after I saw melatonin mentioned here on the Forum, but 1mg didn't do much for me, so I increased to 5mg, and that worked wonders for quite a while, until I had to increase to 10mg a few years back (because my life got more and more stressful).

It takes around half an hour to an hour for me to get sleepy, and then I sleep like a baby, and I never feel groggy in the morning (assuming I went to bed at a reasonable hour and slept a reasonable amount, which for me is not less than 7 hours and no more than 8 hours).

If I skip even one day of taking melatonin, my insomnia returns. So it's been a godsend for me, because the usual prescribed drugs for sleeplessness are awful.

Do you live in a high EMF environment? People who do, probably have worse sleep and will need more.

I'm just wondering if people who do will have to take higher doses than the book recommends. Of course, it is going to be very individual and people will have to find their proper dosage.

Anyway, everything I've been reading is very positive for this therapy. And let's face it, sleep is very important in these times, and repairing DNA damage too. We are simply bombarded with evil frequencies and it's only going to get worse with that 5G business. We need all the help we can get.

 

[zhenqing]

Do you live in a high EMF environment? People who do, probably have worse sleep and will need more.

I'm not sure, Laura. I live in a city, not the biggest (population a little more than 100k), but it's a city nonetheless. I'm afraid I don't have much knowledge in the matter of EMF yet (i.e what constitutes as high EMF environment) . I've always thought that my sleeplessness was caused by my chronic stress/anxiety, but of course the real cause may be more complicated than that.

I'll be changing my environment for a few weeks in a couple of days (sort of vacation time) - it's going to be interesting to observe if/how my body and mind is going to react.