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11 Oct, 8 tweets, 2 min read
When megadoses of vitamin D supplements are taken orally, the body may actually shunt conversion away from the active form of vitamin D (1,25D), instead increasing production of its analogs in the epi-25D pathway
These analogs are significantly less calcemic, so this shunt may be used to minimize increases in serum calcium seen with excess vitamin D

Unfortunately this pathway has not been studied in humans, but we see this consistently in studies in rodents with supplemental vitamin D
Infants also demonstrate a higher ratio of epi-25D to 1,25D and 25D (aka D3), perhaps to preserve calcium in the skeletal system as much as possible during early development
It's also worth noting that some labs do not distinguish between epi-25D and 25D on bloodwork

The effects of both forms overlap so this may not make much of a difference, but it would be interesting if supplemental vitamin D increases epi-25D but doesn't affect D3 much
If you're wondering if your vitamin D blood test includes just standard 25D or has the potential for cross-reaction between analogs, just check the type of analysis used

The gold standard LC-MS analysis can distinguish between forms, while other types may not
An LC-MS/MS Method for Analysis of Vitamin D Metabolites and C3 Epimers in Mice Serum: Oral Supplementation Compared to UV Irradiation…
Epimers of Vitamin D: A Review…
The truth about vitamin D synthesis…

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More from @ck_eternity_

11 Oct
Bowel flush from high doses of magnesium is caused by excess of it reaching the large intestine/colon

Magnesium is hydroscopic, so it draws water more than other minerals, and past the small intestine there is almost no ability to absorb it so it pulls water into the bowel
The flush reaction is directly proportionate to the unabsorbed magnesium fraction

This also plays a role in why forms that are less soluble in water like magnesium hydroxide, citrate, or oxide, are the most laxative as they are the least well-absorbed
The solution to minimize flush is to opt for more soluble forms like magnesium chloride, and to space out intake as much as possible throughout the day

I like to fill a liter jar with water and add 1-2tsp mag chloride to gradually drink, start small (~0.5 tsp) and taper up
Read 4 tweets
11 Oct
The idea that free radicals = bad and antioxidants = good is a major oversimplification

When we talk about redox state it's not just about maintaining as little oxidation as possible, but rather keeping an appropriate balance in place between reduction and oxidation

Chemistry 101:

Put simply, oxidation refers to any chemical reaction involving the loss of an electron, when something is oxidized it just means that one of its electrons is transferred to another molecule
Reduction is the inverse of this, a molecule or atom gaining an electron from another molecule or atom

As you can see, it's impossible for reduction to occur without oxidation, and vice versa, hence the shorthand "redox" refers to this category of reactions
Read 16 tweets
9 Oct
The idea of a "debate" around CICO is pretty ridiculous, in the sense that the role that thermodynamics plays in metabolism is well-established and agreed on by everyone

What we're actually seeing is a shift in emphasis away from calories in and more towards calories out
What I mean by this is that more and more nutritionists seems to be recognizing the error in the initial premise of the amount of calories eaten being the only significant factor in weight gain/loss

This is obvious in cases like hypothyroidism, etc, where metabolism is impaired
This isn't a new idea or mutually exclusive with CICO, just a shift in emphasis from one side of the equation to the other

I think most everyone would agree that the amount of food you eat matters, but also that lack of exercise, hormone imbalance, etc, can impair weight loss
Read 8 tweets
8 Oct
I've been digging more into the connections between the "big three" sex hormones (testosterone, estrogen, and progesterone), and glutamatergic disorders like epilepsy
Interestingly, androgens like testosterone and DHT are actually anticonvulsant, which seems counterintuitive since they increase force production

This seems to result from their conversion into the neurosteroids androsterone and 3a-androstenediol which increase GABA sensitivity
Progesterone is also anticonvulsant as a result increased neurosteroid production, most notably allopregnanolone, but to lesser extent other dihydroprogesterone derivatives
Read 6 tweets
7 Oct
If I had a few million $ to allocate towards developing an herb into a medical therapy, conducting clinical trials on it, etc, I would choose bacopa

Specifically, the possible role of bacopa extracts in improving epilepsy long term
I've reviewed hundreds of rodent and human studies on various herbs and the potential benefits of bacopa in epilepsy have always stood out to me as being some of the most promising, yet the relevant human data seems to be totally lacking
When we consider the role that GABA/glutamate imbalances play in nearly every mental illness and neurodegenerative disorder, the potential applications of these herbs is extensive
Read 4 tweets
3 Oct
N-acetylserotonin, the chemical byproduct of serotonin and precursor to melatonin, acts as an agonist of the TrkB receptor (the same receptor that BDNF activates)

This is another interesting pathway by which MAO inhibition may enhance the actions of neurotrophic factors
Increasing serotonin is also known to raise BDNF levels itself via activation of various serotonin receptors, we see this in SSRI's and other serotonergic supplements/drugs

This pathway could replicate a portion of these effects even if serotonin is not increased significantly
Mostly I find this interesting in the context of beta-carboline containing herbs which act as mild reversible MAO inhibitors, like ginseng or polygala

Most herbs with these properties behave well in rodent metrics of increasing neurogenesis
Read 5 tweets

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