There seems to be an inverse relationship between melatonin and insulin, with increases is insulin reducing melatonin release, and vice versa

This is actually thought to be mediated by melatonin receptors in the pancreas, and insulin receptors in the pineal gland
This may be a large part of how eating too close to sleep can cause disrupt/worsen sleep

It's also worth noting that insulin resistance seems to create a state of chronic low melatonin production, indicating that insulin resistance may also be tied to worsened sleep
Besides reducing insulin release, melatonin may actually improve insulin sensitivity (likely through activation of AMPK)

Melatonin supplements have been used for this purpose in a few clinical trials, and IMO this is one of the more viable reasons for short term supplementation
Interestingly, there's a body of research suggesting that the body actually requires some amount of glucose for adequate melatonin production to occur

I think this is most likely because glucose increases tryptophan uptake into the brain, the precursor to serotonin and melatonin
Insomnia experienced during long fasts or on the keto diet seems to be a result of this lowered tryptophan uptake, and lowered melatonin levels

Outside of longterm low/no carb intake however, this isn't really relevant, and isn't justification for a large meal before bed

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More from @ck_eternity_

26 Mar
Fermentation can increase folate content of food significantly

This is especially important with vegetable sources of folate, which typically contain mostly folinic acid which some individuals are unable to utilize as effectively as the active methylfolate
According to this study fermentation increased folate concentration, adding almost entirely the methylfolate form
sciencedirect.com/science/articl…
Fermenting grains also increases folate and other B-vitamin concentrations, in this study sourdough more than doubled folate levels
infona.pl/resource/bwmet…
Read 4 tweets
26 Mar
What many people don't realize about opiate withdrawal is that in many ways it resembles an immune response, complete with elevated cytokines, activation of inflammatory microglia in the nervous system, and changes in histamine levels
Symptoms like anhedonia, insomnia, anxiety, etc, stem from downregulation of dopamine and GABA receptors

While these are responsible for most of the psychological aspects of withdrawal, upstream of this the opiate receptors also regulate the immune system
For example, many opiate users report never getting sick

This actually occurs because opiates raise the threshold for illness/inflammation symptoms, though they don't suppress the immune system completely and may even potentiate other aspects of immune function
Read 4 tweets
21 Mar
I've been reviewing ashwagandha's impact on thyroid function, and honestly I think the risk of hyperthyroidism from taking it is overblown

The only studies I've found showing it increases thyroid function are in patients that already have hypothyroidism, not in healthy adults
It's well-known that cortisol has an antagonistic effect on every step in thyroid hormone synthesis, and ashwagandha is one of the most potent herbs at reducing cortisol, so from this perspective it makes sense that ashwagandha could have therapeutic value in hypothyroidism
However, I don't think this indicates a general ability to stimulate thyroid function in and of itself

Ashwagandha has some of the most impressive benefits I've ever seen that make it well worth consuming for many individuals
Read 8 tweets
18 Mar
The most potent phytoestrogen, coumestrol, found primarily in alfalfa and red clover, is one of the few phytoestrogens that actually has any ability to cause endocrine disruption (at least in rodent studies)

Surprisingly, it does this through its anti-estrogenic effects!
All phytoestrogens activate estrogen receptors far weaker than estrogen itself does, because of this they reduce estrogen receptor activation rather than increase it

In some cases this could be beneficial (ie in reducing breast cancer), but issues can still occur
The most potent phytoestrogens still bind to estrogen receptors as strogly as estrogen itself, without properly activating the receptors

This blocks the activity of estrogen, altering gene expression, and preventing feedback loops that regulate estrogen levels
Read 7 tweets
14 Mar
Personally I subscribe to the theory that the paleolithic diet was actually fairly low in animal fat

After the extinction of megafauna the remaining wild game would have been quite lean, similar to elk or venison today, since only large animals carry much body fat in the wild
At the time fat was prized due to its relative scarcity, and was likely divided among important individuals in the group like hunters or expectant mothers

We still see this in modern hunter-gatherer tribes today, groups like the Hazda eat mostly lean meat and moderate carbs
To an extent, animals with a high body fat % are a product of modern agriculture, which often encourages them to be sedentary and eat a caloric surplus

These practices serve to increase the weight of each individual animal so that they have more market value
Read 6 tweets
12 Mar
I've been working on ways to actively limit the effects on xenoestrogens beyond just limiting exposure

So far, the most promising compound I've found for this purpose is diindolylmethane, also known as DIM

Let me expand on this:
First, let's look at the primary mechanisms by which xenoestrogens cause endocrine disruption

They are thought to act primarily by binding to the aryl hydrocarbon (Ah) receptors, altering gene expression of hormone metabolism enzymes, and by binding to estrogen receptors
Activating of the Ah receptors is primarily what skew hormone balance by increase the conversion of testosterone into estrogen by aromatase

DIM is a weak but competitive ligand at both the Ah receptors and estrogens receptors, as well as a mild aromatase inhibitor
Read 9 tweets

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