> there is quite literally no good evidence that boosters for Covid do anything for otherwise healthy people who have already been infected
Before I dive back into the literature, as you claim to be stating this in good faith... is the "good" load-bearing here? Relentlessly attacking methodology is an easy way to make this kind of general claim.
Also, are you talking narrowly about a group of people that has had COVID but never had a prior COVID vaccination? (In which case is it still a "booster"?) Or is a proper steelman of your position that anyone that has had COVID, regardless of prior vaccinations exposure, does not benefit from additional vaccination in any meaningful sense?
The hypothesis (I'm paraphrasing) is the fructose severely downgrades the mitochondria (this is well established).
The part that is really interesting to me is that patients with alzheimer's have huge amounts of fructose in their brains (that's covered the in the podcast).
So, lots of fructose, mitochondria impacted, thus neurons degraded. Makes sense to me.
As far as alternative hypothesis, there aren't any good ones that I'm aware of.
Alzheimer's disease is a specific subtype of dementia; this article seems to be more focused on vascular dementia (or at least vascular risk factors) -- why I was curious about the relationship between e.g. smoking and fructose.
The association of fructose has been studied directly in the context of AD, and the hazard ratio is modest (and not necessarily dose-dependent) [0]:
> After adjustment for sex, age, MMSE at baseline, education level, SBP, treatment of hypertension, LDL, uric acid, prevalent diabetes mellitus, current smoking, alcohol consumption, dietary fiber intake, total energy intake, sugar in beverage, seafood, red meat, fried foods, animal fat, personal income, marital status, physical activity index, and BMI in the Cox regression model, participants with consumption of fructose more than 7 servings/week showed a higher risk of all-cause dementia and AD dementia (HR: 1.49, 95% CI: 1.14–1.84, P for trend < 0.001 for all-cause dementia; HR: 1.60, 95% CI: 1.22–2.01, P-trend < 0.001 for AD dementia) than subjects with no consumption for fructose. And the results remained comparable for participants with medium consumption of fructose (HR: 1.46, 95% CI: 1.30–1.79, for all-cause dementia; HR: 1.52, 95% CI: 1.14–1.91, for AD dementia) (see Table 2).
I haven't seen anything about the fructose content of brains of AD patients; do you have a (preferably non-video) reference / source?
> 7g of acetaminophen can kill you, and 12g is likely to [3]
I agree that people should be cautious, but I think you are significantly misunderstanding [3].
"Toxicity" != death -- toxicity is merely "some evidence of a toxic effect" -- possibly as simple as a transiently abnormal blood test with no symptoms or sequelae, ever.
Single (accidental) doses of up to 200 mg / kg are routinely recommended to be managed at home [0], i.e. "you don't really need to go to the emergency department for this." For me, a fairly average 79kg male, this would be about 16g.
Please consult with your local poison control if you have concerns or questions!
In many people a momentary drop to the 80s or even below is not an emergency or anything close to it. Not saying that it is good.
Someone that is awake, sitting up, and struggling to breathe should be considered an emergency regardless of oxygen levels (and in this situation 80% would be very concerning).
EDIT: your comment is otherwise entirely correct, particularly at sea level.
One a friend and I hooked ourselves up to continuous pulse oximetry and had a contest to get the lowest recorded oxygen level. We tried everything we could think of, from just holding our breath to end-expiratory breath holding to hyperventilating to clear O2 (I used to do some recreational free-diving) beforehand to exercising (jumping jacks)...
Neither of us could get it below 98%, and this was at a mile of elevation (UNMH in Albuquerque).
It is pretty easy if you use the Wim Hof method. Breathe deep and fast for a few minutes, to the point where you get dizzy or feel weird sensations. Then exhale and stop breathing while being fully relaxed. I've done this while hooked to a pulse oximeter and it takes quite a while before O2 actually starts dropping (especially because the effect can be delayed in your limbs), but once it starts you'll pretty quickly run into the regime where a normal oxi will start an alarm because O2 is too low. You can even go below 85% without losing consciousness, because your limbs will desaturate faster than your brain. It's also not uncomfortable, because rising CO2 is what causes breathing reflex, but you dropped its levels far below the threshold by hyperventilating first.
Interesting. As I noted above (though typo O2 -> CO2), I used the same technique you describe, which I learned in free diving, and was not able to get below 98%, at altitude.
I'm quite sure no freediving instructor would ever teach you this particular method, because it is a surefire way to die underwater on your first attempt. Free diving breathing techniques usually revolve around lowering your heart rate, not lowering CO2. Wim Hof trainers will also tell you to never to use this method when near water.
As for the specifics that may have prevented you from doing what you wanted: If you breathe too shallow or too slow, you won't clear enough CO2. In freediving this is normal (even wanted), but for Wim Hof practice it means you didn't do it right. You really have to breathe so deep and fast that you enter an uncomfortable zone. It's not unlike physical exercise, except it's mostly mental.
> I'm quite sure no freediving instructor would ever teach you this particular method, because it is a surefire way to die underwater on your first attempt
Definitely no instructor involved, just a dumb 20 year-old living in Puerto Rico. It admittedly was dangerous, but I am living evidence that it was far from a "surefire" way to die. It was one of a hundred ways in which I put my life at risk during my 20s. ¯\_(ツ)_/¯
> As for the specifics that may have prevented you from doing what you wanted: If you breathe too shallow or too slow, you won't clear enough CO2.
I'm confident I was doing it sufficiently well to accomplish a longer period of breath holding than I otherwise would have been able to sustain, as evidenced by having done so (in addition to the usual symptoms of lightheadedness, confusion, loss of vision, near-syncope -- yes I agree quite uncomfortable). I know people on HN love to idolize Wim Hof, but in this context minute ventilation is not that difficult of a concept; I'm usually able to estimate the response in a paralyzed patient's PCO2 fairly well when making changes to their tidal volume and rate.
I didn't search for too long, but here's at least one relevant document, in which otherwise untrained subjects were able to achieve a substantial reduction in CO2 (17.4 vs 29.0) with a mere 15 seconds of hyperventilation, leading to an extra 23 seconds of breath holding prior to involuntary breathing moments. The peripheral O2 sat nadir in the hyperventilation group appears to have been identical to the non-hyperventilation group after the first trial (Fig 8b, looks like ~94%) and was only statistically significantly lower on trials 2-5: <https://pmc.ncbi.nlm.nih.gov/articles/PMC10363065/>
90 seconds of breath hold is still way too little to see oxygen drops in a finger pulse oxi. Also explains why you didn't die free-diving. Even with no training you can go much longer than that before risking a blackout (at least under normal circumstances). In fact training free-diving is all about CO2 tolerance and relaxation, so you won't even be able to store more O2. When I was reaching the 80s, I was doing 3+ minute breath holds. The first ~2 minutes my oxi stayed at full O2 sat with basically no change. In principle you should be able to induce a blackout yourself using this method without feeling an urgent need to breathe - if you do the prep stage hard enough. Just make sure you only do this when lying down in a safe position.
Can’t claim to know for sure, but I’d assume some kind of measurement limitations: the resolution and upper/lower limits of pulse ox are probably calibrated to some medical need, not to detect changes beyond what’s medically necessary
This was using equipment in the emergency department of our state's only L1 trauma center and comprehensive stroke center; I presume it was decent as far as medical monitoring equipment goes.
Before I dive back into the literature, as you claim to be stating this in good faith... is the "good" load-bearing here? Relentlessly attacking methodology is an easy way to make this kind of general claim.
Also, are you talking narrowly about a group of people that has had COVID but never had a prior COVID vaccination? (In which case is it still a "booster"?) Or is a proper steelman of your position that anyone that has had COVID, regardless of prior vaccinations exposure, does not benefit from additional vaccination in any meaningful sense?
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