If you actually review the unbiased literature on seed oils (not your little food guru blog articles, actual studies), this is exactly what those papers suggest is harmful, rather than seed oils inherently.
The Japanese eat a good amount of seed oils to compose their fat macro dietary intake, along with saturated fats in meats, O3 fats in seafood, and carbohydrates from rice, etc.
Pretty excellent longevity all things considered.
Most also eat much less fast food than the West.
Black seed oil has been consumed for a few thousand years, but never refried. Curious.
Now I’m not saying to go crazy with cooking/consuming industrialized vegetable/seed oils, just offering a newer perspective on the matter. Getting you to think beyond what others tell you to think.
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This paper hasn’t yet been replicated as far as I’m aware, but the results were extremely impressive and it was going around sometime last year in the fitness community.
Results demonstrated 66.5-95.4% improvement rates in atherosclerosis at a 10,800 FU/day.
Potential risks are, because it can lower blood pressure, potentially excessively decreasing blood pressure for those who are on BP medications.
Advised caution in those taking any sort of blood thinner medications such as Coumadin, also known as warfarin, and possibly also those who are on medications like Eliquis (another blood thinner prescribed for atrial fibrillation).
Effective management of atherosclerosis progress and hyperlipidemia with nattokinase: A clinical study with 1,062 participants pmc.ncbi.nlm.nih.gov/articles/PMC94…
I figure it can’t hurt to include as a preventative measure personally. I use PureBulk’s natto extract. 426mg is equivalent to about 10800 FU, give or take.
A major flaw I’ve found behind the “seed oil/PUFA = obesity” theory is that there is this mechanism confabulated regarding linoleic acid having a pro-endocannabinoidergic effect via CB1 receptor agonism (this part is true), but the faulty thinking here is that this can be extrapolated to THC activity in cannabis producing the “munchies” in regards to lack of satiety induction and the drive to continue eating.
There is also the theory that PUFA, specifically linoleic acid, is the sole cause of producing depression, which would go completely against the above theory. If we’re using THC’s pharmacology as the basis for these theories, how is it that linoleic acid is also the cause of depression if CB1 agonism generally produces a very strong anti-depressant effect, including via simply increasing endogenous endocannabinoid activity via resistance and/or cardio exercise?
Not only are there two totally different and separate mechanisms in which linoleic acid and THC influence CB1 receptors (LA metabolizing to arachidonic acid metabolites which are used to synthesize endogenous endocannabinoids, anandamide and 2-arachidonoylglycerol, and THC via direct partial non-selective activation), there is also a significant difference between each of their degrees of binding affinity, protein binding and duration of receptor stimulation, influence on specific brain regions in regards to downstream effects on factors like ghrelin, dopamine release increasing pleasure derived from food consumption, and overriding of satiety signals such as leptin.
One of the key factors I notice with those with flagrant digestive issues are a severe aversion to any sort of bitter foods or herbs/vegetables.
These two factors will often go hand in hand, typically dating back to a childish palate and/or downregulated taste receptors that require a reset after a lifetime of a Stupid American or ultra processed diet.
Aside from chloride, zinc, trimethylglycine/betaine, thiamine, and potassium, tasting bitter foods/herbs on the tongue regularly helps to keep stomach acid production high via the bitter taste receptor on the tongue. Activating the bitter taste receptors stimulates the vagus nerve, which goes on to stimulate salivation (digestive enzymes begin during proper mastication/chewing), and gastric secretions (stomach acid and digestive enzymes in the stomach).
This is absolutely CRUCIAL to optimal digestion of proteins, fibers, and fats.
This is one key reason why I highly recommend to stop being a pussy and to taste herbs like black seed oil directly on the tongue, capsules and softgels eliminating a good portion of the potential benefits you could be experiencing.
This is equally important in those who need to eat frequent, generally protein-rich meals throughout the day to stimulate and maintain muscle protein synthesis, i.e. bulking, such as bodybuilders and power lifters.
You really need to ensure you’re getting sufficient micronutrient and herbal bitter/vegetable intake. Especially important in the off season and even during prep for contests so you’re getting the most out of your food intake while avoiding potential bloating and related digestive issues that can negatively impact performance and aesthetics.
The problem I have with natural T boosters is they’re largely squeezing out additional adrenal androgen output, vs gonadal/testicular. Adrenal androgen production making up only about 3% of total testosterone and DHT production systemically. Shilajit being a prime example of this phenomena.
An exception to this obviously being micronutrients that directly influence antioxidant capacity or hypothalamic-pituitary-testicular axis in the gonads and natural aromatase inhibitors, which reduces total systemic estradiol and interrupts the negative feedback loop on gonadotrophin production (luteinizing hormone/LH and follicle stimulating hormone/FSH) via HPTA.
I’ve yet to see this having a sustained effect on the HPTA and resulting androgen production without using that acute energy and motivation to make serious dietary, lifestyle, and environmental changes.
Such as subcutaneous and visceral fat loss, which downregulates aromatase expression, thus having a more sustained effect on relieving that negative feedback loop on HPTA function.
Providing a surplus of micronutrients and sufficient macronutrients/calories that will enable the testicles to produce gonadotrophins without interference from lack of energy or excessive reactive oxygen species production (ROS/oxidative stress).
Or seriously altering indoor light environment and sunlight exposure practices to provide the proper stimulus to HPTA via the retinohypothalamic tract and removing the negative stimulus that interferes with this and produces excessive ROS, that is artificial blue light and nnEMF/RF.
Any so-called “testosterone boosters” will only have an acute effect on androgen hormones at best, and more generally will have a greater effect on catecholamine or adrenal steroid production.
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.