Lucas Philip Sindlev @SindlevL

30 days of Wi-Fi (4G, 4h/day) damaged gonads (testes & ovaries) in adults. Offspring had ↑mortality, developmental defects (edema, curved spine, tail deformities) & anxiety-like behavior. Effects worsened with longer exposure. sciencedirect.com/science/articl…

Less protein, more lifespan! A comprehensive review of the merits of protein restriction for healthy aging A flip from the proteinmaxxing craze "cell.com/cell-press-blu…

Scientists may have uncovered one reason coffee is repeatedly associated with healthier aging and lower disease risk. Compounds in coffee appear to activate a receptor that helps protect cells from stress, inflammation, and damage. ow.ly/fHl650ZpokU

A new systematic review suggests that creatine monohydrate, a popular supplement for athletes, might help treat major depressive disorder. Evidence indicates that combining creatine with standard antidepressants or talk therapy tends to improve… dlvr.it/TTnLjR

A major new international study has found that muscle health likely plays a major role in whether people develop diabetes. ow.ly/JUHp50ZnGP0

There has never been a number for normal. Ask how much muscle ten weeks of lifting should add and the literature has not had a clean answer, because almost every synthesis has asked which training variable matters rather than how much growth to expect by when. A new preprint went after the second question with 3,237 observations drawn from 480 studies, modelling growth against training weeks and admitting only direct measurement of muscle by scan or biopsy. At the median study length of ten weeks, muscle size rose about 7 percent. From the same model the authors derived something the field has been missing: thresholds for what counts as a small, typical and large response. Roughly 2 percent is small, 7 percent typical, and 12 percent large. Growth also decelerated. Around ten weeks, muscle was accruing at about a quarter of a percent per week. Push the model out and the weekly increment stops being distinguishable from zero somewhere past a year of continuous training. Early weeks carry most of it. Then there is the finding that should change how you read every other hypertrophy paper. Measurement instrument moved the result almost as much as the training did. MRI cross-sectional area came in about 6 points lower than muscle biopsy fibre area, and about 4 points lower than ultrasound. Against a typical response near 7 percent, the window you look through is nearly as influential as three months of work. Inside the biopsies, type II fibre area also grew about 5 points more than type I. Two peer-reviewed syntheses sit comfortably alongside this. A Bayesian network meta-analysis of training prescription found that many combinations of load, sets and frequency produce hypertrophy without one clear optimum. A meta-regression of protein supplementation found its benefit on training-induced mass plateauing past moderate intakes. Both describe a system with diminishing returns rather than a linear dose you can keep escalating. Individual results were expected to land anywhere from slightly negative to above 20 percent, so the average is estimated far more precisely than any one person's outcome. Studies with more male participants showed larger effects. Age and training experience showed no consistent influence. And this is a preprint. It has not been peer reviewed, and the numbers may move. Roberts et al., preprint submitted June 2026. PROSPERO CRD42024498510 Currier et al., Br J Sports Med 2023. PMID 37414459

Melatonin decreases toxicity of methamphetamine. pubmed.ncbi.nlm.nih.gov/9723784/

BPC-157 accelerates tendon repair. onlinelibrary.wiley.com/doi/epdf/10.10…

Fermented foods lowered inflammation over 17 weeks. Adding more fiber did neither. That's the finding from a Stanford randomized trial, and it should reframe how we think about feeding the gut. Researchers assigned healthy adults to one of two microbiome-targeted diets, high-fiber or high-fermented-food, and ran deep immune and microbiome profiling across 17 weeks. The expectation going in was intuitive: fiber feeds your bacteria, so more of it should mean a healthier microbiome and lower inflammation. That's not what happened. The high-fiber group's inflammatory markers stayed flat. Its primary immune outcome, a composite cytokine response score, was unchanged from start to finish. And microbial diversity, one of the more reliable markers of gut resilience, held steady rather than rising. The fermented-food group moved both. Inflammation declined steadily across the trial. Diversity climbed. Fiber feeds bacteria the substrate they can digest. The study captured a signature of exactly this - i.e., the microbiome's glycan-degrading enzyme capacity rose while overall diversity stayed flat, consistent with the existing community upregulating rather than broadening Fermented foods appear to do something structurally different. Live microbes plus the metabolic byproducts of fermentation seem to expand diversity directly, rather than by feeding what's already there. Greater diversity tracks with lower inflammatory load, and the fermented arm moved that lever while the fiber arm did not. One detail worth sitting with: fiber wasn't inert for everyone. High-fiber consumers split into three distinct immune trajectories, and which one you landed in tracked your baseline microbiome diversity. Fiber's effect was contingent on the gut that received it. People starting with more diverse microbiomes likely respond differently than this average suggests. Limitations: Eighteen people per arm, healthy adults, 17 weeks. Inflammatory markers are intermediate biology, not clinical endpoints. Fiber's metabolic and cardiovascular benefits are established on separate, far larger evidence, and this trial doesn't touch them. But for the specific job of moving the microbiome and inflammation, piling on more fiber wasn't the lever. The fermented foods, however, moved the needle. Wastyk, Sonnenburg et al., Cell 2021.

@moizali Just bought these - super sweet. Are they a modified or bred variety?

Almost every rule about when to take a supplement was invented rather than measured. The default is that it does not matter. Creatine saturates muscle over days, so the only variable is whether the dose was taken. Magnesium and vitamin C have no absorption reason to be scheduled. For this group, adherence is the entire protocol, and advice about morning versus evening is preference presented as pharmacology. Two compounds need a condition rather than a clock. Fat soluble vitamins are absorbed with dietary fat, and moving vitamin D to the largest meal of the day raised blood levels in patients who had been failing to respond. That study was small and had no control arm, so treat it as a sensible default rather than a measured effect size. The stronger case is omega-3. Ethyl ester fish oils, which is most of what is sold, require pancreatic lipase to cleave the ethyl group before the fatty acids can be absorbed, and that enzyme is released in response to fat entering the small intestine. Free fatty acid and triglyceride forms are less dependent on it. The instruction is not a time of day. It is that the capsule needs to arrive alongside food containing fat, which a black coffee does not provide. Three compounds have genuine schedules, and each has a mechanism behind it. Iron raises the hormone that blocks its own absorption. A dose of oral iron increases hepcidin, which suppresses uptake for roughly the next day. In iron depleted women, taking iron on alternate days rather than consecutive days raised cumulative fractional absorption from 16.3 to 21.8 percent and increased total iron absorbed from 131 to 175 milligrams. The same investigators found that splitting a daily dose into twice daily gave no advantage over a single morning dose. More frequent is not more absorbed. Caffeine outlasts the evening. Its half life sits near five hours in most adults and considerably longer in some, which means a dose taken six hours before bed still has a substantial fraction circulating at lights out. When 400 milligrams was given at zero, three, and six hours before habitual bedtime, all three timings disrupted sleep relative to placebo, measured both by report and by a validated home monitor. The six hour condition is the one worth knowing, because it is well outside what most people treat as a cutoff. Note the dose is high, roughly four cups of coffee. Melatonin is a timing signal rather than a sedative. Its effect on the circadian system follows a phase response curve, so administration in the evening shifts the clock earlier while administration in the morning shifts it later. Taken at the wrong point relative to your own rhythm, it moves you in the direction you did not want. This is why melatonin timing is not a matter of optimisation. Timing is the mechanism. What deserves less attention is mineral separation. The instruction to space iron away from calcium comes from single meal absorption studies, where the effect is large and real. When the same question was asked over six months in iron replete adults taking calcium with meals, haemoglobin, haematocrit, ferritin and zinc protoporphyrin were all unchanged. Absorption from one meal does not predict status across months, because uptake adjusts to demand. The separation advice retains force where it originated, in people with high iron requirements or existing deficiency, and little elsewhere. The usable test is whether a rule traces to something physical. Fat, a hormone, a half life, a circadian curve. If it does not, it is probably an absorption study that never became an outcome study. Stoffel et al., Lancet Haematol 2017 · PMID 29032957 Drake et al., J Clin Sleep Med 2013 · PMID 24235903 Minihane and Fairweather-Tait, Am J Clin Nutr 1998 · PMID 9665102 Blair and Dhillon, Am J Cardiovasc Drugs 2014 · PMID 25234378 Lewy and Sack, J Biol Rhythms 1997 · PMID 9406034

Physical activity may help protect the aging brain for nearly a decade. Older adults with a higher VO₂ peak had larger cortical brain volumes and better memory years after a 5-year exercise intervention, regardless of whether they had been assigned to high-intensity, moderate-intensity training, or standard physical activity guidelines. The group following the guidelines also experienced the least hippocampal volume loss, even four years after the intervention ended. High-intensity training was not superior for preserving hippocampal volume in this study, which I found genuinely surprising. This does not mean HIIT harms the brain. Entering older age with strong cardiorespiratory fitness, and continuing to stay active, may matter more for long-term brain health than following any one specific training intensity/exercise prescription.

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@BrandonLuuMD Have you tried isotonic sodium/saline nasal sprays every morning? For me, they lower inflammation and get me through the day. Doesn't burn or sting like fluticasone propionate nasal sprays.

A growing body of evidence suggests that time zone changes also affect the trillions of bacteria living in our intestines....a phenomenon known as "gut jet lag". ow.ly/KnHx50ZsV9P

A first-in-human phase 1 study of an allogeneic, clinical-grade #iPSC-derived neural stem/progenitor cell product in patients with subacute complete #SpinalCordInjury demonstrates clinical #feasibility and long-term #safety. #SCI #StemCellTherapy #RegenerativeMedicine nature.com/articles/s4159…

At the cellular level, your body has about forty different ages (according to one of the largest aging studied ever run and published this week) A new study in Nature Medicine took blood from 60,542 people, measured over 7,000 proteins, and traced them back to the specific cell types that made them: brain cells, muscle cells, lung, gut, bone marrow. Then they built a separate "aging clock" for each one. The finding: your cell types don't age in sync. Your muscle can be a decade older than your liver. Your brain's support cells can be racing ahead while your immune cells stay young. One to three percent of people have ten or more cell types aging fast all at once. Fast-aging brain support cells (astrocytes) flagged future Alzheimer's about as strongly as the highest-risk Alzheimer's gene. Fast-aging muscle cells flagged ALS more than three years before diagnosis. Aging airway cells stacked on top of smoking to push lung cancer risk higher still. But the one to sit with is muscle. Across all forty-plus cell types, accelerated muscle aging was the single strongest predictor of dying from any cause. Not brain, not heart. Muscle. muscle is the most modifiable tissue you have. This study can't prove training rewinds the clock, but everything we already know points the same way. Muscle loss tracks death in every population it's been measured in, and the protein signatures behind this clock are the same ones tied to how your muscle is built and how well it makes energy. The strongest death-predictor in the body is also the one you have the most power over. Normal cellular aging: 9 in 10 alive at fifteen years. More than twenty cell types aging fast: about 1 in 3. this isn't a test you can buy. It's a research finding from banked blood, in a group skewing older and mostly white. Younger, more diverse validation comes next.

A new study reveals that night owls experience significantly higher body fat percentages, visceral adiposity, elevated blood glucose, and poorer lipid profiles compared to morning types. ow.ly/K4nv50ZnHul

Gene engineering #probiotics to express cxcl13 increases efficacy of #cancer #immunotherapy. science.org/doi/10.1126/sc…

In #multiplesclerosis B cell depletion causes IgA producing B regulatory cells to enter circulation. How interesting?? science.org/doi/10.1126/sc…

New episode of Lifespan: Inside the World’s First Age Reversal Trial. New updates on how the trial is going & how to maximize vision! youtu.be/VZDgTe5NDkQ?si…