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CK

@ck_eternity_

15 Dec 21

Most people see a meteor as the ultimate symbol of mass extinction, in reality though we should be looking at oxygen the same way

The first major extinction event on earth was known as the great oxidation event and occurred as a result of increased O2 in the atmosphere

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At this point the earth was still covered in single-celled organisms

Opportunistic cyanobacteria developed photosynthesis as a way to leverage the abundant CO2 in the atmosphere for energy production, however the fundamental metabolism of other cells wasn't configured for this

Molecular oxygen is highly reactive with certain forms of minerals, particularly the water-soluble ferrous form of iron

This reactivity leads to the creation of a cascade of free radicals in response to the formation of iron oxide, I've discussed this often in health/disease

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CK

@ck_eternity_

25 Nov 21

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…

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CK

@ck_eternity_

23 Nov 21

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

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CK

@ck_eternity_

22 Nov 21

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/

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CK

@ck_eternity_

16 Nov 21

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…

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CK

@ck_eternity_

16 Nov 21

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

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