I like health and fitness I like bioenergetics I like biotech Follow me for the worst controlled N=1 experiments you've ever seen
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Yawning is typically triggered by a condition of poor oxygenation to the brain.
While exercising it's normal (blood goes to the muscles that are being worked). The temporary nature of this phenomena makes it protective and drives brain adaptations (via HIF-1a mostly and other pathways as well). It's one of many acute stressors that contributes to cumulative resilience often seen in trained atheletes.
This is also why yawning mid-day at rest is generally a bad thing and indicative that non-challenging conditions are depriving your brain of oxygen. The brain is then hypoxic as a baseline and this degree of **chronic** stress causes cumulative damage over time.
There must be an exact mechanism in which yawning occurs in scenarios like this, or other unusual scenarios where it feels like there is something happening
We are determined to find the source of this phenomenon
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Gaslight 👻 retweeted
Can we please remove all the neuroticism from the performance and longevity field
Why is everyone attracted to this field so damn neurotic
We need to focus on resiliency and defense, not fragility
Anti Fragile Longevity
Thrive DESPITE suboptimal inputs
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Gaslight 👻 retweeted
One shitty Iranian trial of 40 kids inflated Prozac’s benefit in two major meta-analyses. Remove the trial and the benefit halves. Think of this the next time your doctor condescends to you about “the Science.” This is the science.
Cochrane’s 2021 review found Prozac offered just 2.84 CDRS-R points over placebo (96-point range): “small and unimportant.” Kirsch’s adult analysis found 1.8 HAM-D points over placebo. That’s 40% below the NICE benchmark for a clinically meaningful benefit. These are the numbers behind all that hubris.
SSRIs are whole-body drugs whose full effects we still don’t understand. Even Prozac’s label admits its exact mechanism is unknown. And no, it’s not correcting a serotonin deficiency. That’s marketing.
Lilly’s own correspondence reveals instructions to code suicide attempts as “overdoses” and suicidal thoughts as “depression.” Courts have found antidepressants responsible for egregious homicides and murder-suicides, even at normal prescribed doses. Severe sexual side effects can persist for decades after stopping these drugs. For some people, getting off means years of careful hyperbolic tapering, down to fractions of a milligram.
And we’re giving these drugs to children like they’re Tylenol.
This has to stop.
This is certainly the most consequential paper published in child and adolescent psychiatry for the last few years. It shows that the meta-analyses that current child psychiatry guidelines rely on to recommend fluoxetine for depression were skewed by an unbelievable trial (n=40) in Iran which found an effect 15 times larger than the average.
When this trial is removed all meta-analyses find the same as a recent Cochrane analysis which found 'small and unimportant differences.'
The flawed meta-analyses by Zhou and @cipriani in the @TheLancet and Lancet Psychiatry need to be corrected.
And guideline committees need to update their guidance in the context of the harms of these drugs including withdrawal effects, sexual effects and agitation/akathisia and suicidality in a minority of youths exposed to them.
Link below
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Gaslight 👻 retweeted
Doing a year long conspiracy where I befriend both parties and get them both to take nasal oxytocin so I can secure my $20 chick fil a gift card
JUST IN: Ex-Tinder executive launches new dating app that allows complete strangers to “matchmake” singles they think should date — and earn financial rewards for successful picks.
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I am begging everyone to stop looking at rodent data for longevity, like omit it completely from your worldview on this topic specifically.
70-85% of control mice die from neoplastic early-life cancers. Their response to something like rapamycin, or hGH deficiency mutations DOES NOT translate to humans at all I promise.
The chief-most killers of humans in the developed world are atherosclerotic CVD (virtually 100% diet mediated) and late-life cancers (which is impart or primarily driven by immune exhaustion).
Telomere lengthening is an interesting route but I believe that it's more tertiary to cardiovascular and thymus regeneration.
The cardiovascular problem is largely due to the fact that aortic and arterial elastin does not grow in adulthood (it barely grows in childhood). If a tissue doesn't grow then it doesn't heal. Poor diet, lack of sleep, lack of activity, and an excess of stress causes a deterioration that (as of now) can't really be fixed.
The immune issue is similar, @AbudBakri talks about this all the time so creds go to him for me knowing about it. The thymus rarely grows in adulthood and typically atrophies as you age. T-cells last for ~15 years after they're made so the process is very slow and you don't notice it until it's too late.
The latter of these two issues is actually a bit easier to solve (or at least it's more solved than the former currently). But if you can maintain the heart and large blood vessels as well as the immune system, you'll find significantly better health outcomes.
Regeneration is highly energy dependent and my entire point here is underpinned by metabolic throughput being maintained for as long as possible.
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A word of caution that’s a decade or maybe two decades late.
I would not currently inject gray-market “research peptides.” The sourcing and quality-control risks are simply too high.
The question isn’t whether peptides can work as signaling molecules (they can). It’s whether the vial contains the peptide it claims, at the stated dose, without microbial contamination, endotoxins, heavy metals, or peptide-related impurities.
The FDA does not verify the safety, effectiveness, or quality of compounded drugs before marketing. Does that mean every compounded product is unsafe? No. But the safeguards are different.
Until a specific research peptide has credible human evidence and a reliable source with transparent, independent testing, I would hold off.
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I don’t know dude it sounds to me, from how you’re describing the story events, that the girl thought you were passing and paid you a girl to “girl” compliment, which you would expect a troon to find validating.
You repaid this nicety by breaking down and throwing a fit, making her feel bad and apologizing for it.
Sounds like you’re the asshole here.
i rejoined the party and after a while the girl responsible found me and apologized profusely. i appreciated the apology and understood that she’d meant it as a compliment, but nonetheless i gently reminded her to be very cautious when speaking about a trans woman’s body.
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Started actually doing my rear delt work and it made my shoulder stop hurting on chest presses
#muchtoconsider
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Holy shit the comments under this post lmao
It's obvious that Jeremy fragrance is abusing GLP-1's, unknown stimulants (just guessing here because he is Germanic) + is experiencing "fragrance" toxicity side effects after decades of essentially snorting it every day.
Very sad to see, be careful.
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Gaslight 👻 retweeted
new study i read today ties increased ERR activity to antioxidant defense capability:
we know SLU-PP-915 + SLU-PP-332 "activate" the Estrogen Related Receptors (ERRs)
when we "activate" these receptors, this can cause a muscle fiber type shift away from glycolytic fibers toward more oxidative fibers.
just think fuel preference shifting more towards fatty acids instead of glucose, and the fiber becomes more endurance capable.
so how does this uniquely tie into antioxidant defense?
if there is a greater capacity to burn fatty acids for fuel, that frees up more glucose / glycolytic intermediates to be used for antioxidant defense.
basically we don't need the glucose as much to make energy with since fats are covering down, and we can send the glucose down alternative antioxidant defense pathways instead.
in this specific study:
Cardiolipin got fucked
↓
more ROS
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body turns up ERRs (ERRy shown here)
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fuel type shifts towards fats
↓
more glucose is spared to feed antioxidant defense and attenuate the ROS increase
study points out how this can be an adaptive response from the body to protect cellular integrity.
who knows how this translates with the SLU stuff. they weren't part of the study, just obviously where my mind goes since they're involved in the program.
nature.com/articles/s43587-0…
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This shit has to have @MartinShkreli shaking in his boots.
A new University of Arkansas Phase 1 trial was registered this month to study BPC-157 in humans after rotator cuff repair surgery.
- The study plans to enroll 30 patients and compare daily subcutaneous BPC-157 for 90 days against a control group.
- Researchers will be looking at recovery outcomes after surgery, with the trial currently scheduled to begin in January 2027.
For a compound that has exploded in popularity despite having very little quality human data, this is a significant development.
BPC-157 has spent years living almost entirely in animal studies, anecdotes and real-world use. Now we finally have a new prospective human trial to watch.
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