Professor of behavioural genetics with my own twins. I mix behaviour and genetics @unitartu and @mcgillu to understand obesity. I also mix global music as a DJ.
i finally built the AI scribe i always wanted, fully open and on-device!! sound on 🔊
it listens to doctor and patient, writes every word while they're still talking, and the moment they hang up it drafts the note and maps the symptoms and risk factors to a possible stroke
How should PhD students leverage AI in their research? First, you should write papers where you leverage AI to analyze something at scale. There are many low-hanging fruit because gen AI is essentially still a new thing. Exploit it!🧵
Terrific @TheAtlantic piece on archaeologists' and anthropologists' slowly dawning realization that now-submerged areas on the coastal shelf--swathes of land drowned when the glaciers melted--may be where much of our species' early history took place. (Link in reply)
🗣️Postdoctoral Research position at the Montreal Neurological Institute: at least two years of secured funded for working on machine-learning analysis of biological-contextual data and body-brain interactions👉https://t.co/piGFjbUMUv
Being a parent of a teenager in the modern digital environment means begging your kid to play Minecraft or do *something* even slightly less brain-rotting than watching short video content from Spotify, which is what they're started doing because you've blocked all YouTube content from the XBox devices at the router level and turned off the WiFi and limited the carrier data throughput after 9PM for their smart phones, which they legitimately need because that is how their coaches communicate with them about cheer routines or band practice
And if you dare to complain about how annoying it is to have this second job as an IT admin just to keep your kids from guzzling down the worlds shittiest content, half the internet calls you a bad parent for not locking them down more and the other half calls you a bad parent for being a content Nazi
Before steamships, global trade followed the winds rather than the shortest route. This brilliant animation by @BartGonnissen uses 250,000+ historical ship positions (based on logs from 1750–1855) to reveal how winds shaped global shipping routes. Source: https://t.co/eU8waXbBvV
New blog post: I used Claude to audit the reproducibility of every journal paper I've been an author on in the last five years. Our commitment to openness meant that the code and data were available, but there were some significant issues. 🧵https://t.co/O5pkxUM4Jx
Le TGV Nouvelle Génération, co-conçu par Alstom et SNCF Voyageurs, a été inauguré aujourd’hui ! 🥳
Petit thread pour vous montrer en quoi c'est une fierté française. 🧵
This is what the Dzherelo underground school in Komyshuvakha looked like before and after the russian strike.
Opened in October 2025, it had modern classrooms and stood 7–8 metres underground. But it was never designed to withstand a FAB-3000 bomb.
russia struck while civilians were gathering to receive humanitarian aid.
They knew people were there.
31 killed. 48 still missing.
made a new https://t.co/aLKrkDy0Mg capsule for teaching factor analysis: Factor Lab. In the PLAY mode you have to guess the generating model based on observed correlations, and in the LEARN mode you can play around with seeing what correlational structures are implied by the model: https://t.co/0eUFXNse92
Aggregated knowledge from a small number of debates outperforms the wisdom of large crowds
This study asked a live crowd (N = 5,180) to respond to general-knowledge questions (eg "What is the height of the Eiffel Tower?")
Participants first answered individually, then deliberated and made consensus decisions in groups of five, and finally provided revised individual estimates.
Averaging consensus decisions was substantially more accurate than aggregating the initial independent opinions. In short, small groups beat the wisdom of crowds.
Combining as few as four consensus choices in small groups outperformed the wisdom of over 5,000 individuals.
The key was reasoning together--that aspect of collective deliberation allowed small groups to make more accurate estimates than massive crowds.
https://t.co/Yz23ELwgde
Most exercise and aging studies can't answer a basic question: is muscle deterioration from aging itself, or just from decades of moving less? A new Nature Aging study solved this by recruiting older adults who moved as much as people in their twenties.
The researchers from Amsterdam UMC and Maastricht University recruited four distinct groups: young adults in their twenties, older adults whose daily step counts and high-intensity activity matched the young group, older adults who had trained consistently for years (three structured hour-long sessions per week for over a year), and older adults with early physical impairment.
They took muscle biopsies before and after a one-hour cycling session, then measured over 24,000 gene transcripts, 135 metabolites, and 1,383 lipid species.
By matching activity levels between young and older groups, any molecular differences couldn't be blamed on the older adults simply moving less. This isolated aging from inactivity for the first time at this molecular depth.
Key findings:
• The defining molecular signature of muscle aging is an energy crisis. Comparing young adults to activity-matched older adults, 1,106 genes were downregulated with age. These genes build the mitochondrial machinery that produces cellular energy: ATP synthase, cytochrome c oxidase, and NADH dehydrogenase subunits. Mitochondria are the power plants of cells, converting nutrients into ATP, the energy currency cells use to function. When these genes decline, cells lose their ability to generate energy efficiently.
• NAD+ levels declined and triglycerides accumulated inside aging muscle. NAD+ is a molecule required for energy production and cellular repair. Lower NAD+ means less capacity to convert fuel into usable energy. Triglycerides are stored fats, their accumulation inside muscle indicates unburned fuel piling up as the tissue loses its ability to process it.
• More than half the molecular signature of muscle aging was absent in trained older adults. Specifically, 57.1% of age-related gene downregulation and 55.9% of upregulation were missing in the trained group. Their muscle resembled young adults far more than their chronological age would predict.
• The changes training preserved were specifically the energy metabolism ones. Genes like NDUFS1 and COX5A, which were depleted in normally active and impaired older adults, sat at youthful levels in the trained group across all five mitochondrial respiratory complexes. The single most prominent feature of muscle aging turned out to be the single most preventable.
• Being generally active was not enough. Structured training was the difference. The normally active older adults walked as much as young adults, and their energy metabolism genes declined anyway. What preserved the youthful molecular profile was structured, sustained training. Filling a step counter and being genuinely trained are not equivalent at the molecular level.
• Roughly half of muscle aging persisted regardless of training. Changes in genes controlling synaptic transmission (how nerves communicate with muscle) and WNT signaling (a pathway regulating tissue maintenance and stem cell function) appeared in all older adults, trained or not. This unavoidable half is where drugs will have to work.
• The fittest muscle mounted the largest inflammatory response to exercise. All groups activated stress and immune genes after exercise, including IL6, IL1B, and TNF. But the magnitude scaled with fitness. Trained older adults most closely resembled young adults in their response, followed by normally active, with impaired older adults showing the most blunted response. The stress response to exercise appears to be the mechanism of adaptation, not damage to be minimized.
This raises a concern about anti-inflammatory longevity strategies. If the inflammatory stress response is how exercise produces its benefits, chronically suppressing inflammation may blunt the adaptation that exercise depends on. It doesn't mean inflammation is beneficial in general, but the timing and context matter.
A separate discovery: the proteasome appears to regulate NAD+. The proteasome is the cellular machinery that breaks down damaged proteins. When researchers inhibited it, NAD+ levels rose in both muscle and liver cells to a degree comparable to NAD+ precursor supplements. This opens a new route to understanding NAD+ decline that operates through protein turnover rather than just supplying more raw material.
The study draws a clear line between what lifestyle can address and what will require therapeutics. The energy metabolism decline, mitochondrial deterioration, and NAD+ depletion that define muscle aging are largely preventable through structured training. The synaptic and signaling changes that persist in all older adults represent the unavoidable half where drugs will need to work.
The decisions made about structured training in midlife determine which molecular trajectory muscle follows in later decades. Half of muscle aging is optional. The other half isn't. Knowing which changes belong to each category is knowing where behavior ends and biology takes over.
@gmiller@JonathanAnomaly@leonardocaff A narrowing of human personality variation based on today's preferences, normalizing embryo selection and stigmatizing unassisted procreation and thus subjecting women to the risks of stimulation and retrieval unnecessarily, narrowing human genetic diversity based on a proxy...