If you’ve ever needed a little help sleeping, you may have reached for a bottle of Melatonin. Little did you know, you may have a potent anabolic agent in your hands. Ok, so it’s not a steroid, and there are limitations and questions I have about this study, but I think you’ll find this one interesting.
First let’s talk a little about Melatonin and what does. If you happen to have a solid circadian rhythm, and you sleep in total darkness, then there is a little gland in your brain known as the Pineal gland, that will release a tryptamine type chemical otherwise known as N-acetyl-5-methoxytryptamine or Melatonin. Like I said previously, I have reason to suspect that many of us suffer from circadian disturbances and have excess light bleeding into our rooms at night when we sleep, and it doesn’t take a lot of light to affect, or rather disrupt Melatonin release. Even the late evening hours before you go to bed are supposed to be a time of very dim light. The Melatonin release is a slow and gradual one, and living in an artificially lit world is wreaking havoc on our Melatonin release.
Exposure to Room Light before Bedtime Suppresses Melatonin Onset and Shortens Melatonin Duration in Humans
Compared with dim light, exposure to room light before bedtime suppressed melatonin, resulting in a later melatonin onset in 99.0% of individuals and shortening melatonin duration by about 90 min. Also, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50% in most (85%) trials.
Melatonin does some really awesome things besides just signalling to the brain when darkness has arrived. In my opinion, we shouldn’t look at Melatonin as a hormone that tells us to sleep, we should look to sleep and darkness in order to increase Melatonin, and thus enhance our anti-aging efforts. Melatonin has been shown to reduce the damage seen in Parkinson’s.
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. It is characterized by a progressive loss of dopamine in the substantia nigra and striatum. However, over 70% of dopaminergic neuronal death occurs before the first symptoms appear, which makes either early diagnosis or effective treatments extremely difficult. Only symptomatic therapies have been used, including levodopa (l-dopa), to restore dopamine content; however, the use of l-dopa leads to some long-term pro-oxidant damage. In addition to a few specific mutations, oxidative stress and generation of free radicals from both mitochondrial impairment and dopamine metabolism are considered to play critical roles in PD etiology. Thus, the use of antioxidants as an important co-treatment with traditional therapies for PD has been suggested. Melatonin, or N-acetyl-5-methoxy-tryptamine, an indole mainly produced in the pineal gland, has been shown to have potent endogenous antioxidant actions. Because neurodegenerative disorders are mainly caused by oxidative damage, melatonin has been tested successfully in both in vivo and in vitro models of PD. The present review provides an up-to-date account of the findings and mechanisms involved in neuroprotection of melatonin in PD.
Melatonin even enhances weight loss.
The overall findings suggest that melatonin should be exploited as a therapeutic tool to prevent or reverse the harmful effects of obesity and its related metabolic disorders.
It seems like most of Melatonin’s benefits come from its downstream expression of other hormones and genes, and its extremely powerful anti-oxidant status.
Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction. Furthermore, clinical tests utilizing melatonin have proven highly successful; because of the positive outcomes of these studies, melatonin’s use in disease states and processes where free radical damage is involved should be increased.
Our data indicate that oral administration of melatonin to normal human males increases basal GH release and GH responsiveness to GHRH through the same pathways as pyridostigmine. Therefore it is likely that melatonin plays this facilitatory role at the hypothalamic level by inhibiting endogenous somatostatin release, although with a lower potency than pyridostigmine. The physiological role of melatonin in GH neuroregulation remains to be established.
And to finally get to our last, and most recent finding, Melatonin can help rapidly heal crushed muscle damage. NOW, before I post the excerpt I want to make my opinion clear on something. I am not a biologist, but everything I have learned thus far tells me that it is not entirely useful to compare blunt trauma type muscle damage with the kind of damage we do to our muscles during exercise. There are some similarities but I often wonder if this kind of trauma involves a different set of hormones, inflammation etc. It could be also argued that muscle damage is muscle damage. If anyone has something to share on this, please fire away!
These data support the hypothesis that melatonin supports muscle restoration after muscle injury, inhibits apoptosis via modulation of apoptosis-associated signaling pathways, increases the number of satellite cells, and reduces inflammation.
The two things I think are worth pointing out is that melatonin increased satellite cells and reduced inflammation, two very good things when it comes to recovery from exercise. But it should also be pointed out that these test subjects were rats AND they were given intraperitoneal administered doses of melatonin. That means it is injected directly into the body cavity (I know, it doesn’t sound pretty, at all…)
So what do we do to increase Melatonin levels? Well the easiest way would be to simply buy a bottle of it and pop it in your mouth. But what dosages are the best? Should you use Time-Release? Should you only take it at night? Will taking Melatonin disrupt your own body’s production of Melatonin?
I will be writing my next article to address these very questions shortly!