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28 Sep, 4 tweets, 1 min read
Daily high-dose iodine supplementation (2 drops lugol's iodine) increases flouride and bromide excretion by 15x and 16x baseline levels respectively

This increased excretion is still present after 3 months of iodine use
naturallifeenergy.com/files/Iodine-r…
If you choose to use higher doses of iodine be sure to provide plenty of its cofactors selenium, riboflavin, and vitamin C as well

Magnesium and sodium may also be beneficial
I'd start with a lower dose and taper up intake, as I don't believe megadoses are necessary or advisable in many cases

Be aware that high doses of iodine can increase thyroid metabolism, and especially if not paired with proper selenium may contribute to thyroid disorders
That said, some researchers estimate that 90+% of the population may be deficient in iodine, so there are many benefits to supplementing it either in isolation (lugol's iodine) or food (sea vegetables, fish, and shellfish)

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More from @ck_eternity_

28 Sep
I believe it's no coincidence that inhibitory neurotransmitters release chloride ions into the neuron while excitatory neurotransmitters release calcium or sodium

Chloride belongs to the halide family of elements and is highly electronegative, it acts as a dielectric blocker
What this means is that it reduces the dielectric constant of cellular water and limits the DC electric current between neurons

While we mostly think of signaling between neurons in terms of neurotransmitter release, they also utilize electric conduction
It seems chloride was selected for specifically because of its electronegativity which allows it to block both electric and chemical signaling between neurons

Calcium and sodium seem to have the opposite effect, perhaps due to their electronegativity being 1/3rd that of chloride
Read 4 tweets
19 Sep
Berberine is notable among "anti-diabetic" herbs/supplements in the fact that it acts as a dipeptidyl peptidase-4 (DPP-4) inhibitor

DPP-4 is responsible for breaking down various peptides, including growth hormone, VEGF, and GLP-1, blocking it increases insulin activity
The "liptin" class of type 2 diabetes medication are based on this mechanism

Berberine shares other mechanisms with diabetes medications as well, such as activating AMPK (similar to metformin), but it is the only herbal compound I could find that inhibits DPP-4
DPP-4 inhibitors are known to increase satiation from food, lower blood glucose, and increase insulin release

AMPK activation may help to promote/maintain insulin sensitivity as well

According to one study, berberine may also reduce elevated total serum cholesterol as well
Read 5 tweets
14 Sep
Unfortunately, despite niacin raising HDL significantly, it doesn't actually improve heart disease

It originally looked very promising as a treatment for heart disease, but over the past few decades it hasn't panned out despite extensive research
ncbi.nlm.nih.gov/pmc/articles/P…
My theory is because in most individuals niacin raises HDL too much, putting it above the optimal range and actually increasing mortality

In theory, individuals with low HDL may still benefit by using niacin to put it back into this range
That said even in individuals with normal HDL niacin still does not increase heart disease, in the vast majority of cases it just has no effect, so there's no harm in taking it

Niacin is especially potent at increasing neuroplasticity, so there are many other mental benefits
Read 6 tweets
14 Sep
Heart disease stems from a combination of:

- inflammation
- elevated oxLDL cholesterol/lipids
- impaired methyl waste clearance (homocysteine)
- impaired reverse cholesterol transport (HDL)
- dysregulated iron/calcium metabolism
Interestingly, the reduction in heart disease seen with many statins in clinical trials may stem as much from their anti-inflammatory effects as their reduction in cholesterol synthesis, this study found positive effects even in those with normal LDL
nejm.org/doi/full/10.10…
More and more studies suggest that reducing inflammation is an important exis of heart disease prevention, similar to lipid markers
nejm.org/doi/full/10.10…
Read 4 tweets
7 Sep
Dissociation in depression and other mental illness is usually a result of excess glutamate activity, which triggers the release of inhibitory compounds like dynorphin/KYNA to protect the brain

They block dopamine, serotonin, and endorphins, limiting cognitive function
Dynorphin is actually in the endorphin class

It still relieves pain, but causes strong dysphoria, they've tried to create "non-addictive" pain meds that activate its receptor (the KOR) but most are rarely used as they often cause depressive symptoms
Dynorphin is also associated with trauma/PTSD especially

Since it blocks pain signaling while causing dysphoria, it disconnects the person from the traumatic experience

This again serves to prevent neurotoxic over-activation of neurons, another way the brain protects itself
Read 5 tweets
7 Sep
First off, let's look at the data extending back as far as possible

On the scale the dip looks almost meaningless, and likely had little impact on the daily caloric surplus that promotes obesity in the first place
I could take another zoomed in comparison like this and make the case that fat intake causes obesity, despite the fact that it doesn't inherently either

Graphs like these just arbitrarily connect effects of modernization with modern diseases, they're very weak evidence forms
Obesity is caused by taking in more energy than the body can metabolize

Metabolism can be affected by hormone status, circadian rhythm, muscle mass, etc, so these factors can reduce energy demand but caloric surplus is still the root cause
Read 6 tweets

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