Great article with old and new insights about melatonin which is more than a nighttime hormone related to sleep. It is a metabolic regulator essential to reduce inflamaging or aging. Melatonin production declines with age unless optimized with diet, exercise, lifestyle and supplementation.
To wit., more melatonin is produced in the gut (and locally used or consumed) than the pineal gland!
And melatonin stimulates repair of pancreatic tissue and by extension other tissue with regeneration potential. Especially note the improvement in bone marrow cell lineage. It is widely noted that immune function is either over expressed or under expressed in the aged leading to collateral tissue damage or increased vulnerability to inflammatory diseases or infections.
Two gut enzymes are responsible for producing more melatonin from dietary or consumed L-tryptophan. Perhaps everyone who is aging should consume tryptophan rich foods or take a supplement of L-tryptophan to reduce oxygen radicals that accelerate aging. Particularly relevant to persons with diseases associated with inflammation such as metabolic syndrome and its comorbidities that are often thought of as accelerated aging.
See bolded text below.
For sleep issues, previous studies in Japanese children showed sleep improvement with the following:
tryptophan rich breakfast,
one hour of bright sunlight before noon, and
Blue blocking sunglasses at night to reduce inhibition of melatonin production during the dark photoperiod.
Based on the evidence below regarding daytime gut production of locally used and locally consumed melatonin at low tissue levels of 5-10 and the pulsed brain levels during darkness of 150 the following conjecture:
Gut produced melatonin protects the soma or bodily production of oxygen radicals related to normal mitochondrial and digestive functions during the day and that nighttime pulses during rest allows the melatonin to optimize the tissue regenerative effect during restorative sleep.
Levels of 5-10 turn down the metabolic stove from burning hot to simmer, and levels of 150 during nighttime rest and sleep turns the stove almost off to maximize healing and recharging of enzymatic antioxidant systems within all cells.
Note that daytime melatonin turns off TNF alpha and other inflammatory cytokines and elevates Il-10 a marker of reduced inflammation!
The full article is available at the link below.
Protective Effect of Melatonin on Acute Pancreatitis
Abstract
Melatonin, a product of the pineal gland, is released from the gut mucosa in response to food ingestion. Specific receptors for melatonin have been detected in many gastrointestinal tissues including the pancreas. Melatonin as well as its precursor, L-tryptophan, attenuates the severity of acute pancreatitis and protects the pancreatic tissue from the damage caused by acute inflammation. The beneficial effect of melatonin on acute pancreatitis, which has been reported in many experimental studies and supported by clinical observations, is related to: (1) enhancement of antioxidant defense of the pancreatic tissue, through direct scavenging of toxic radical oxygen (ROS) and nitrogen (RNS) species, (2) preservation of the activity of antioxidant enzymes; such as superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPx), (3) the decline of pro-inflammatory cytokine tumor necrosis α (TNFα) production, accompanied by stimulation of an anti-inflammatory IL-10, (4) improvement of pancreatic blood flow and decrease of neutrophil infiltration, (5) reduction of apoptosis and necrosis in the inflamed pancreatic tissue, (6) increased production of chaperon protein (HSP60), and (7) promotion of regenerative process in the pancreas. Conclusion. Endogenous melatonin produced from L-tryptophan could be one of the native mechanisms protecting the pancreas from acute damage and accelerating regeneration of this gland. The beneficial effects of melatonin shown in experimental studies suggest that melatonin ought to be employed in the clinical trials as a supportive therapy in acute pancreatitis and could be used in people at high risk for acute pancreatitis to prevent the development of pancreatic inflammation.
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