Dave Scolte

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Dave Scolte

Dave Scolte

@DaveScolte

100% MADE IN USA ethical jewelry coming soon. 🇺🇸 Health & Aging. Beauty & Art. Microbiology student. Nothing online is medical advice.

Utah, USA Katılım Ocak 2026
327 Takip Edilen30 Takipçiler
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Maziyar PANAHI
Maziyar PANAHI@MaziyarPanahi·
🚨 Over 1 billion rows of psychiatric genetics data. Now on Hugging Face. ADHD. Depression. Schizophrenia. Bipolar. PTSD. OCD. Autism. Anxiety. Tourette. Eating disorders. 12 disorder groups. 52 publications. Every GWAS summary statistic from the Psychiatric Genomics Consortium. Before: wget, gunzip, 20 minutes debugging separators, repeat 50 times. Now: one line of Python.
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Dave Scolte
Dave Scolte@DaveScolte·
The constant switching back and forth between fad diets is likely causing dysregulation. There’s a reason the Mediterranean and Japanese diets work, and it’s not because they’re fat-free keto carboloading raw sugar. pmc.ncbi.nlm.nih.gov/articles/PMC10…
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Parmita Mishra
Parmita Mishra@parmita·
Longevity influencers be like: WE WILL LIVE TO 489 YEARS BY THE NEXT DECADE. WE WILL NEVER EVEN HEAR OF CANCER AGAIN. BECAUSE THE AGING PATHWAY TAKES CARE OF CANCER!!!!! AND HAVE YOU LOOKED AT HOW JELLYFISH ARE IMMORTAL. END OF TRANSMISSION
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Crémieux
Crémieux@cremieuxrecueil·
Reminder: Waymo is so safe that if every car was driven like a Waymo, about 9% of America's life expectancy gap would disappear. 9 percent! Americans die in car accidents *that often*.
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Crémieux@cremieuxrecueil

About 10% of America's life expectancy shortfall is due to motor vehicle accidents—fixed by Waymo and Tesla. About 18% is overdoses—that's fading now. And the lion's share of the rest is obesity-related. America will soon be buying its way out of its poor life expectancy issue.

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Parmita Mishra
Parmita Mishra@parmita·
Great question. If cancer happens when a single cell picks up mutations and starts dividing uncontrollably: then bigger animals (with way more cells) + longer lifespans (more time for mutations to accumulate) should get way more cancer. But they don't. (1/)
The Last Species@lemurian_master

@parmita asking as a retard, why can't we put more copies of TP53gene in humans ?

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Abud Bakri MD
Abud Bakri MD@AbudBakri·
The question is why do so many people get their tonsils out? And what are the long term effects of this re: - autoimmunity - cancer “The thymus is known to be the site of extensive T-cell development and maturation, but there is also evidence that a stepwise program of T-cell development occurs within the human tonsils”
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Dave Scolte
Dave Scolte@DaveScolte·
@cremieuxrecueil They literally just compounded high antioxidant/nutrient ingredients into it, like matcha and dark chocolate. It’s going to be okay everyone, have some ice cream.
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Crémieux
Crémieux@cremieuxrecueil·
There's a common claim that nutrition researchers 'can't explain' why ice cream seems to be healthy. But the initial research on this subject was p-hacked, not robust, and under closer examination, it doesn't hold up at all.
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Dave Scolte
Dave Scolte@DaveScolte·
My favorite science concept is “it depends” I really don’t like seeing certainty in the medical field on anything from vaccines to peptides, because it all just depends.
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Charles Swanton
Charles Swanton@CharlesSwanton·
People often ask how breakthroughs occur in cancer biology-often the story is more complex - the survival plot for myeloma outcomes is extraordinary - improvements come about in incremental steps - in my lifetime treatment of Myeloma has almost transformed into a curable disease
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cardoso
cardoso@Cardoso·
Hora do remédio, mas como não sou bobo, cortei as pontinhas pra não machucar a garganta.
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David Sinclair
David Sinclair@davidasinclair·
Here's my take on your paper: Cellular senescence or "zombie cell" events happen when a cell experiences too much genetic or epigenetic noise, caused by cellular damage (e.g. DNA breaks) or telomere erosion Your study of a Lewis Lung Carcinoma (LLC) mouse model indicates training the immune system to recognize senescent cells shrinks tumors. Why test this at all? Senescent cells are thought to be a protective mechanism that helps prevent cancer. With epigenetic and telomere erosion over time, senescent cells accumulate & secrete inflammatory factors. By the time we are 50, out fat, for example, is riddled with these cells. If you stained them blue with beta-galactosidase, a 20 year old's fat would be light blue and I, at 56, would have navy blue fat Increasingly, it looks like they also influence how the immune system behaves, in part by expressing cell surface proteins like PD-L1 that can dampen CD8 T cell activity That is why senolytics that kill zombie cells have generated so much interest. Removing them seems to restore tissue function and potentially improve immune surveillance against cancer At the same time, the biology in the paper is likely layered. CD8 T cells seem to be involved, which is good. But senescent cells may both suppress immunity and serve as targets themselves. So it’s possible the effects reflect a combination of clearing those cells and reactivating immune responses against tumors Either way, it points to an important direction, one that connects aging biology directly to cancer therapy.
Dr. Thomas Ichim@exosome

Greatest antiaging scientist is @davidasinclair I wonder what he thinks of our #senovax antiaging vaccine pmc.ncbi.nlm.nih.gov/articles/PMC12…

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Dave Scolte@DaveScolte·
@DagobertIX @exosome @davidasinclair Yes several studies now show that clearing senescent cells may be detrimental in the long run. Essentially exhausting regeneration pathways instead of directly addressing them. Though intermittent use like with plasmapheresis or staggered mTOR inhibitors is interesting.
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𒀭𒄑𒂆𒈦™
𒀭𒄑𒂆𒈦™@DagobertIX·
@exosome @davidasinclair For anti-aging, I believe in senomorphics more than senolytics, and think removing senescent cells is risky because you need to make sure the stem cells are capable of replacing them, and the senescent cells could also be stem cells
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Dave Scolte
Dave Scolte@DaveScolte·
@iamnickelsteel1 @davidasinclair We have a plethora of research showing transient states, like obesity, do transfer epigenetic markers to offspring; so this would make sense regardless. Healthy sperm = healthy children
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Nickel Steel
Nickel Steel@iamnickelsteel1·
In mice, sure, dietary inputs like resveratrol can tweak epigenetics and even sperm biology. But jumping from that to stable, meaningful inheritance is a big leap. biology might be more stateful than we thought, where your condition today can subtly echo into the next generation, not as destiny, but as bias.
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David Sinclair
David Sinclair@davidasinclair·
CRAZY IF TRUE PAPER: A new study in mice reports that resveratrol intake by old male mice (or directly treating their sperm) changes the metabolism of embryos & pups, "potentially through alterations in sperm telomere length and epigenetic modifications" 🤯
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