Melatonin For Insomnia


Melatonin is a hormone that is produced by the pineal gland inside the brain. Its main function is to regulate the sleep-wake cycles of the human body. The secretion of melatonin is mainly dependent on the light levels. At night, the level of melatonin produced by the pineal gland rises. As our body gets older, the amount of melatonin secreted by the pineal gland tends to decrease. This is the reason why scientists believe young people can easily get a good night sleep. Older people will usually experience sleeping problems. When melatonin first came into popularity in the mid-1990’s, it was marketed for frequent travelers who wants to reset their body clocks to the new time zone as fast as possible. This makes melatonin a very popular food supplement for treating the symptoms of jet lag.

As melatonin became more and more popular, it was popularized as a “natural sleep aid” that is free from “hang-overs” and other side effects associated with sleeping pills. Over the course of time, researchers look for other possible use of melatonin. Melatonin is clinically proven and highly successful in making a person fall asleep easily. The sleep inducing effect of melatonin has no reported toxic side effects. Insomnia sufferers who are new to melatonin should start using the lowest dose of melatonin that is available. The usual starting dose is 0.5 to 1 mg taken 30 minutes before bedtime. If the initial dose is not effective, increase melatonin dosage by 0.5 mg on successive nights until you find the effective dosage. We want to use the lowest dose possible so that we can minimize the common melatonin side effects.

Some researchers recommend the use of sublingual melatonin, a form of melatonin supplement which is taken under the tongue. Sublingual melatonin is reported to be easily absorbed by the blood stream because it does not need to be digested. Regular melatonin supplements like the tablet and capsule form are absorbed through the stomach.

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Pharmacology and physiology of melatonin in the reduction of oxidative stress in vivo. Biol Signals Recept 2000 May-Aug; 9(3-4):160-71.

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