Have you ever notice you get really sleepy after a big Thanksgiving meal?
This is what I like to call the "Thanksgiving dinner effect," it occurs as a result of a large meal containing high carbs and protein, particularly turkey
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Turkey is one of the foods highest in the amino acid tryptophan, which also happens to be the precursor to the neurotransmitters serotonin and melatonin
Tryptophan > 5HTP > serotonin > melatonin
For this cascade to occur in the brain, tryptophan must first cross the blood brain barrier, which regulates which substances enter the nervous system
Amino acids are able to pass through it, but particularly if insulin is present at the same time ncbi.nlm.nih.gov/pmc/articles/P…
Insulin is one of the most important hormones in the body, since its primary purpose is to drive glucose, amino acids, and nutrients into cells
This gives it the ability to lower blood sugar, but it also helps move amino acid neurotransmitter precursors into the brain
So when we eat a large meal containing both a high-tryptophan protein source and plenty of carbohydrates, not only do we take in more tryptophan than usual, but we also get more into the nervous system and produce more of these inhibitory neurotransmitters
On top of this synergy, insulin is also naturally inhibitory, increasing the activity of GABA signaling frontiersin.org/articles/10.33…
Carbohydrates activate insulin 100%, while protein activates it 60%, so large meals high in protein/carbs can even have this effect on their own
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While anemia is a risk factor for hair loss, interestingly enough so is iron overload
One of the first symptoms of hereditary hemochromatosis is hair loss, and this even seems to occur via similar mechanisms to androgenic alopecia
Androgen receptor activation in the scalp seems to trigger hair loss either partially or primarily via a signaling cascade involving TGF-beta
I've found a number of studies linking androgen receptor activation and TGF-beta in general, and they seem to potentiate each other
My impression is that this depends on the tissue the receptor is present in, having more influence in scalp and prostate, but not as much in other tissues
It may even explain why AR activation promotes body hair growth by not scalp hair growth, though this is mostly speculation
Alzheimer's disorder is often referred to as a metabolic disorder ("type III diabetes"), but I've come to view it as a circadian disorder
Disrupted circadian rhythm = rapid insulin resistance, combined with inability to clear amyloid plaques with glymphatic function impaired
This is in combination with other factors of course, neurodegeneration doesn't develop overnight
It does raise the question of how crucial of a role melatonin and sunlight play in the prevention of neurodegeneration, I'll link a few interesting articles below
Melatonin regulates Aβ production/clearance balance and Aβ neurotoxicity: A potential therapeutic molecule for Alzheimer's disease pubmed.ncbi.nlm.nih.gov/33254429/
Normally in undermethylation we see decreased levels of serotonin and dopamine activity at their receptors, since higher levels of DNA methylation can inhibit the reuptake of these neurotransmitters
This "mimics" the effects of SSRIs and DRIs to some extent
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However this can also be paired with more adrenaline and noradrenaline through a separate mechanism, where methyl groups are required to metabolize adrenaline
Because of this when methyl groups are depleted we see lower levels of metanephrine, an adrenaline metabolite
One of the main causes of niacin toxicity is the depletion of methyl groups, since niacin forms methyl-nicotinamide in the liver
This is paired with more adrenaline/noradrenaline, less betaine (a methyl donor in the liver), and high levels of homocysteine nature.com/articles/hr201…
Niacin deficieny causes tryptophan to be funneled away from serotonin production into endogenous niacin production
Some of the intermediates in the conversion are neurotoxic, especially quinolinic acid which imitates excess glutamate
This is often implicated in schizophrenia pathology
These intermediates are created due to lack of niacin stemming from dietary deficiency or higher demand to drive essential reactions like NAD+ creations
Reducing the formation of quinolinic and kynurenic acids is also one of the mechanisms through which niacin supplementation significantly improves some cases of schizophrenia
This seems to be especially useful in cases of overmethylation
If we look at the structure of cytochrome C oxidase, the rate limiting protein in energy production in mitochondria, it becomes obvious why light is so important
The heme and copper cores act as chromophores absorbing light and using it to excite electron transfer
If we compare the structure of chlorophyll (left) with hemoglobin (right) there is a distinct similarity
Both contain similar structures that harness light to drive redox reactions, this works via the photoelectric effect where the energy of light is transferred into electrons
Cytochrome C oxidase is the last protein in the electron transport chain, which operates by using a current of electrons to drive ATP production
It's absorption peaks in the 630-670nm range, red light, which is the part of the spectrum that penetrates the farthest into the body