Eat more seafood, eliminate industrialized vegetable/seed oils and fast food.
Unbound copper and iron accumulation in tissue. Increase magnesium, retinol, BOUND copper, zinc, vitamin D (midday UVB sunlight exposure), vitamin C, thiamine, riboflavin, niacin, B6, folate, and cobalamin intake.
Inositol hexaphosphate/IP6 and melatonin (fix circadian biology, see the sunrise every single day) can help to reduce the hydroxyl radical production (iron oxidation).
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If you ignored my yearly warnings to START NOW on midday UV sunlight exposure and last winter ended up turning out rough for you, you need to read this so you don’t have to repeat it again.
You should only ever resort to supplements acutely to restore levels if deficient and below 30ng/mL on blood work, otherwise even if you just buy the Phillips bulbs and a basic set up instead of Sperti or a Chroma (safety and protection of the bulb is a highly concerning matter), you should be using UV light and I’ll tell you exactly why.
Cholecalciferol (vitamin D3 and what you think of when you hear “vitamin D”) is only ONE vitamin D complex metabolite of literally dozens.
There are dozens of different metabolites, both active and used as storage, of vitamin D that are highly important factors for vitamin D receptor (VDR) binding, organ receptor affinity and specificity, storage capacity, interchangeability throughout different contexts (i.e. low external UV, external temp dropping, healthy people demonstrating their own UV spectrum emission internally to influence the metabolites produced from dietary intake via cold exposure, etc.), and antiviral effects.
UVB exposure to the 7-dehydrocholesterol content of the skin forms pre-vitamin D3, which is unstable and undergoes thermal isomerization to vitamin D3.
Supplements won’t generate lumisterol and tachysterol from further UVB exposure to the pre-vitamin D3 formed in the skin.
In the presence of ROS, photosensitizing agents, and longer UV exposure, we also get 5,6-trans-vitamin D3, suprasterols, isotachysterols, and cholesta-5,7,9(11)-triene.
I’ve seen the theory that this association with cannabis usage and lower BMI is caused by a downregulation of CB1 receptors via chronic intake, but the same downregulation would occur with linoleic acid that gets stored in subcutaneous fat as they’re released and metabolized: a chronic supraphysiological activation of CB1R by endocannabinoids.
That’s not to mention the numerous other herbs and spices with agonistic activity at CB1R that are associated with lower BMI and reduced risk of obesity as well.
Lots of holes in this theory, back to the drawing board.
Estrogen in itself is pro-GABA and neuroprotective. Estrogen dominance or, more accurately, the imbalance between hormones, metabolites, and neurosteroids is anti-GABA or excitatory. A handful of the estrone metabolites is more specifically anti-GABA.
Serotonin is both inhibitory and excitatory depending on receptor and subreceptor unit site binding, typically tending towards more inhibitory, or pro-GABA. Hence why increasing it is effective in cases of obsessive-compulsive disorder and anxiety.
Nitric oxide in itself is pro-GABA, peroxynitrites without being effectively neutralized or recycled are anti-GABA.