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14 Jan, 7 tweets, 2 min read
This is one quite a few people seem to believe, so let me clarify a few things:

1. Seed oils do not turn into plastic no matter how much heat they're exposed to, a process called polymerization occurs, but in this case it's unrelated to plastics
From a chemistry standpoint some of the most well-known polymers are plastic compounds, but by definition a polymer is just a long chain of repeating molecular structures

DNA is a polymer, as are many proteins oh, seed oils forming polymers doesn't mean they are suddenly plastic
2. On a similar note, hydrogenation is not as bad as it sounds either, it's simply the process of adding hydrogen to convert a fat from being polyunsaturated to being saturated

Hydrogenation is often demonized as well, and there's a grain of truth here, though it isn't harmful
What's actually harmful is partial hydrogenation, which results in the creation of cardiotoxic trans fats

This was a major issue in food production that was only realized fairly recently, and was responsible for the high trans fat content of processed foods containing these oils
The good news is though that as of January 1st, 2021, partially hydrogenated oils as food ingredients were banned in the US, so unless some companies are still breaking the law they are absent from the market

I'm not sure about their legal status in other countries
Interestingly many of the handful of human studies actually showing an increase in heart disease from seed oil consumption are confounded by using partially hydrogenated oils and not controlling for the effect of trans fats

The Boston coronary study is a great example of this
All in all margarine is still trash, and you'd be better off consuming cold-pressed oils or whole foods in general, but that said it's nowhere near as bad as stuff like this makes it out to be, at least with the current legal restrictions

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More from @ck_eternity_

6 Jan
I've often seen the argument that high saturated fat in isolation will not increase athlerosclerosis, since while it increases LDL it does not increase very small LDL particles which are known to be the most likely to cause plaque

Unfortunately, this does not seem to be the case
This study looked at the effects of a high saturated fat diet on LDL particle size and found that while it had no effect on very large or very small particles, it did still increase small and medium particles
journals.plos.org/plosone/articl…
Like many aspects of nutrition the issue of particle size is a spectrum

While the increase from very high saturated fat inake is made up of larger particles, the high number of particles overall will offset this significantly
Read 4 tweets
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

(thread)
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
Read 12 tweets
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

(thread)
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…
Read 6 tweets
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
Read 8 tweets
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/
Read 5 tweets
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

(thread)
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…
Read 13 tweets

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