Travis Cox

@Aging_Scientist Your name is mentioned on the study titled "Supplements and Drugs Are Associated With Biological Age in a Cohort of Exceptionally Healthy Individuals" Within it states that CoQ10 and antihistamines improved biological age. Which form of CoQ10, and which antihistamines?

I will never understand the obsession with driving yourself, owning a car or living in the suburbs. My commute now is 35 mins (used to be a 15 min walk). Part of it I spend walking, which keeps me healthy. Part of the commute I spend studying anki flashcards, ordering lunch, talking to ChatGPT or answering texts and mails. The driver better focus on the road if they don't want to kill anyone. Driving is an expensive waste of time!

@hanz69er If I had poor reaction to ketotifen do you suspect I'd have a poor reaction to cyproheptadine? Ketotifen interrupted sleep.

The deeper I dig into histamine, the more I recognize it’s probably the driver for a lot of dysfunctional behavior in people—ADHD, OCD, procrastination, insomnia, rumination. Histamine is one of the core arousal/wakefulness neurotransmitters and gates dopamine, acetylcholine, glutamate, and the stress axis via H1/H3 receptors. Too little histamine means underaroused; too much means hypervigilant. In cases of low-level (or even full-blown) allergies and dysregulated mast cell degranulation, chronic nighttime exposure leads to poor sleep. Downregulated H1 receptor expression from chronic agonism then causes poor activation when needed, leading to ADHD and/or procrastination—a functional histamine deficit. Similarly, chronic excessive histamine drive leads to OCD and rumination because the mind cannot relax in its hypervigilant state, which also causes histamine-driven insomnia. Two tools that can help: 1. Cyproheptadine is an antihistamine with antiserotonin effects that blocks histamine at the receptor and blunts the cortisol effect driven by excess serotonin (from gut microbes). It also stimulates appetite, so keep that in mind. More of a sledgehammer than... 2. Ketotifen, a mast cell stabilizer, doesn’t cause the drowsiness that cyproheptadine does. It prevents pathological mast cell degranulation and is good for low-grade allergies. And of course, the Ray Peat Carrot Salad™️ and well-cooked white button mushrooms will bind bacterial endotoxin in the gut, which could be driving the histamine dysfunction leading to the above symptoms.

@timpjohansson You raised your eyebrows I. The first pic causing forehead wrinkles and reduced the hunter eye look, and got a tan/burn in the 2nd pic

2023 2026 avoiding sugar 350g sugar/day no alcohol glass of wine 3x/week ~20k steps ~7k steps gym 6x gym 3x coke zero milk, juice, water no sun sunmaxx

@MewingByMikeMew A device that does what thumbpulling can do would be more effective. You can only thumbpull manually for so long.

I think Thumb Pulling could be really effective, we need to make a detailed video on this.

@BerbarianWizard "fresh" lol. rFSH, spellcheck

@BerbarianWizard You generally don't need an AI anyway. TRT is fine. I'd remove AI and focus on fat loss to lower aromatization. HCG and fresh are fine to maintain HTPA. DHT can be a good addition. I'm not a big fan of HGH, easy to get sides with this. I'd consider GLP1 w/protein+exercise.

I’d remove testosterone, so no need for an AI like exemestane either. I’d also remove HCG and rFSH. I’d add low-dose progesterone, low-dose DHT, Epithalon, Pinealon, and Vilon. With that we might actually regenerate his thymus and reverse aging. I have doubts about HGH though.

@HansAmato What if you're too hot?

Worst sleep of my life lasted years. Over an hour to fall asleep. Up 3 times a night. Exhausted every morning regardless. Fixed in 1 hour by addressing something not a single doctor ever suggested testing. Every doctor I saw ran the same panel. Every doctor told me the same thing. Labs are fine. Sleep hygiene. Stress management. Maybe try melatonin. None of them tested free T3. None of them tested reverse T3. None of them asked what my body temperature was first thing in the morning or why my hands were cold at 2pm in summer. When I finally addressed my thyroid. small doses of T3 spread across the day. the change was immediate enough that I thought I'd imagined it. Fell asleep the same night within minutes. Slept through without waking. Woke up warm for the first time in years. Here's what I know now that I didn't know then: > The thyroid doesn't release hormone once a day in a single dose. > It releases small amounts continuously... maintaining stable levels around the clock. > When I replicated that pattern, small doses every 2 to 3 hours, the results were dramatic. > When I overdid it, same compound, higher dose, racing heart, wired, couldn't sleep at all. Same molecule. Completely opposite outcome based entirely on how I used it. The dosing protocol matters as much as the compound itself. Most people who try this and fail are failing at the protocol, not the hormone.

The first case of a SENS spinout getting this far! Massive congrats to Oki and his team.

@hov992 @gaezpeat 50mg are available

@TravisLongevity @gaezpeat The vials are most of the time 10mg. the daily dose is 5-10mg. the cycle is 10 days - 2 weeks long. This can be repeated twice per year.

JUST DID 1 mg EPITALON SubQ 3 hours before Sleep Epitalon is one of the best peptides you can do for your health - Reduce oxidative stress - Restore circadian rythm - Influence gene expression - Neuroprotective - Stimulate telomerase activity (delayed aging) AND MORE...

Section from Nature article showing LiC has stores in plaques more than LiO: “Li was highly concentrated in Aβ plaques after the administration of LiC, but to a much smaller extent after administration of LiO in both 3xTg and J20 mice" Nature article: nature.com/articles/s4158…

What if a drug existed based on the structure of lithium carbonate which delivered a drug payload directly to amyloid plaques to clear them out? Suddenly the strong affinity for the plaques is a great thing instead of a limiting factor. Brain aging damage reversal mechanism?

Possible Alzheimer's treatment and novel brain aging reversal mechanism: You’ve likely heard of the Nature article “Lithium deficiency and the onset of Alzheimer’s disease” which implied that lithium orotate seemed to be a better form than lithium carbonate for Alzheimer's.

@hov992 @gaezpeat Khavinson*

@hov992 @gaezpeat You don't need 10 vials. They're either tiny mg amounts or you're reading wrong information. I believe the Khavison protocol was 5-10g a day for 10-20 days.

@Adityalch @RobDouglas @PGC1a_RB A good article and honestly lines up with my current philosophy in a lot of ways. I use Rapamycin and other catabolic longevity agents but it is in the context of a lifestyle and protocol that has sufficient anabolic signalling as well.

@TravisLongevity @RobDouglas @PGC1a_RB Richard's comments adds great points on how to get the AMPK mediated benefits I don't touch on in my article, in case you haven't read that too 🙌

My thoughts extending from @Adityalch's article: Rapamycin and metformin would make you weaker, reductively, and pharmacologically speaking, while testosterone makes one stronger Testosterone and androgens, in general, would constitutely activate anabolism through multiple forms of androgen receptor-mTOR The result is a tonic, constant elevation of mTOR signaling that goes well beyond what acute resistance training alone produces (just lift bro, no cardio) So by being on testosterone, you would benefit more off 'autophagy' based activity (maybe a more accurate description/explanation would be AMPK focused activity since activity driven AMPK activation leads to autophagy; yes I know both mTOR and autophagy occur in flux differently throughout different tissues depending and also vary depending on feeding/nutrition and activity type/driven status) Exogenous androgen users have strong mechanistic reasons to be more deliberate about incorporating AMPK-activating modalities, but the goal isn't simply to "balance out" mTOR, it's to preserve AMPK–mTOR oscillation and prevent a chronic anabolic lock-in state with potential downstream metabolic and cellular consequences The key insight is that these two pathways are not merely opponents but they form a required oscillatory circuit (AMPK-mTOR Oscillation Principle) AMPK, activated by increases in AMP/ATP ratio and calcium-dependent cues (such as during HIIT or LISS cardio), suppresses mTORC1 by phosphorylating TSC2 and raptor; when energy is restored, mTOR rebounds This bidirectional interplay ensures metabolic flexibility, where the cell cycles between anabolic growth and catabolic renewal Recent systems-level modeling (the Metabolic Overdrive Model, 2026) explicitly frames healthy adaptation as an AMPK–mTOR antiphase window; the absence of a 24–48 hour window where AMPK rises and mTOR dips is considered a signal of pathological "lock-in" (absence being no form of AMPK activation, where that be cardiovascular focused activity or periods of fasting [actual fasting, not just between meal quiet, quiescent, periods]) Professional bodybuilder, strength athletes, even recreational people, using AAS (even just 'TRT')push the system toward exactly this lock-in: persistent mTORC1 signaling, high-protein diets sustaining leucine-driven mTOR activation, insulinotropic supplements, and carbohydrate overfeeding can suppress AMPK and SIRT1 activity simultaneously This creates a cellular state mechanistically paralleling cancer cell metabolism; high energy throughput but low regulatory elasticity (constant high mTOR, low AMPK activation) The risks of sustained mTOR hyperactivation extend far beyond theoretical concern: - Insulin resistance through chronic MTORC1 activation - Autophagy suppression through constant mTORC1 activity - Cardiac pathology (enlarged heart) - Mitochondrial quality decline: AMPK drives mitophagy via PINK1/Parkin pathways and promotes lysosomal biogenesis; without periodic AMPK activation, dysfunctional mitochondria accumulate and are not recycled, impairing oxidative capacity over time Which is why, if on AAS (even TRT), cardio is a necessity ('living the lifestyle') Does Cardio "Balance" mTOR? The framing of "balance" is partially correct but mechanistically imprecise. AMPK activation via cardio does not simply "neutralize" mTOR — it provides periodic suppression intervals that allow cellular housekeeping Not only that but the AMPK/autophagy from more cardio activity is more 'powerful/beneficial' from that of any drug like rapamycin or metformin The reasoning isn't about "canceling gains" ('cardio kills gains bro'; fasting is bad for gains) but about preserving metabolic oscillation; the physiological rhythm between mTOR-driven anabolism and AMPK-driven cellular renewal

@Aging_Scientist Owning a car allows you to go where you want when you want without relying on public transport or needing to be near stranger on public transport. Having lived both ways I certainly prefer having a car.

@KumaniWest @doctormorphh What is your experience with DHTe? Have you looked into the esterified allopregnanolone?

@doctormorphh Test at 150-200mg or low dose DHTE is healthier then most peptides

The biggest issue with peptides is that they actually work and they are the gateway to steroids. People dont research a peptide before getting on and notice a lot of great effects. This extends into their steroid journey and then hop on gear without having researched it before, expecting a very similar risk:reward ratio. This will not be the case, there are a lot of things you should keep in check while on gear.

@m_goes_distance What could be unethical about biological age optimization?

just spent another week playing god - reviewed three germline editing startups and will write checks - injected peptides before a board meeting. nobody asked everyone noticed - had a conversation about designer embryo selection over lunch - funded a guy running longevity trials on himself out of a garage in SoMa - debated the ethics of biological age optimization with someone who has never checked their biological age - ended the week younger than I started it I will be forgiven bio/acc