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BHPCausesTreatments-2
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This 2019 mini-review comes from urologists and prostate biologists in Vienna and Innsbruck. It summarizes what drives benign prostatic hyperplasia (BPH), the noncancerous growth of prostate tissue, and what it leads to clinically: an enlarged prostate and lower urinary tract symptoms. The authors focus mainly on the androgen pathway. Inside the prostate, testosterone is converted to the more potent dihydrotestosterone (DHT), which drives growth through the androgen receptor; finasteride and dutasteride block that conversion. They then survey newer contributors: the insulin-like growth factor (IGF) axis, estrogens, chronic inflammation, metabolic syndrome, obesity and genetics, and they briefly cover treatment. Several candidate interventions, including metformin, pomegranate extract and ginseng, have support only from rodent or cell studies.

By age 80, most men have benign prostatic hyperplasia, a slow, noncancerous overgrowth of the inner prostate. Many never notice it. Others get a weak stream, urgency and repeated trips to the bathroom at night. Even though BPH is so common, nobody can yet explain why one man ends up with a 40-gram prostate and another with a 200-gram one.

The authors start with the oldest and firmest piece of the puzzle: hormones. The testes make testosterone, and inside the prostate an enzyme called 5-alpha reductase converts it into dihydrotestosterone, or DHT, a far more potent androgen. Men castrated before puberty, and men born without a working form of the enzyme, do not develop enlarged prostates. This is why finasteride and dutasteride, which block the enzyme, shrink the gland by 20 to 30% and lower the chances of urinary retention and surgery. Androgens appear to be necessary but not sufficient, though. Testosterone falls with age while BPH rises, so something else must tip the balance.

The review points to three candidates. The first is a growth-factor network built around IGF. IGF is raised in BPH tissue and interacts with TGF-beta, a scar-promoting signal, in the prostate’s supporting tissue. The second is chronic inflammation, which is common in BPH specimens and has been linked to faster progression and a higher risk of urinary retention. The third is metabolism. In a Baltimore cohort, each extra point of body mass index went with about 0.4 milliliters of extra prostate volume, and severely obese men had roughly 3.5 times the odds of an enlarged gland compared with men of normal weight. The authors propose that insulin resistance, a hormonal shift toward estrogen, narrowed pelvic arteries and low-grade inflammation all feed prostate growth and urinary symptoms.

Genes matter too. Twin studies put the heritability of BPH and urinary symptoms at 50 to 70%, although only one genetic variant, in the vitamin D receptor gene, has held up consistently across populations.

The review also lists some intriguing leads. The diabetes drug metformin blunted testosterone-driven prostate growth in rats, and pomegranate extract, ginseng and vanillic acid had effects in animal models. None has been tested in a proper human trial.

One clinical point is easy to miss. Among older men with urinary symptoms, about 60% have an overactive bladder, while only 30 to 40% have a prostate that is actually obstructing urine flow. Prostate size alone is a poor guide to what is causing the symptoms.

The paper has clear limits. It is a narrative overview of 26 references, not a systematic analysis. The take-home is modest but useful. Androgens set the stage for prostate growth, and metabolic health and inflammation may decide how far it goes. No long-term trial has yet shown that improving those factors actually prevents BPH.

Actionable Insights

These points combine what the review says with well-established trial data. The review itself tested nothing.

  1. Keep weight and waist in check. Each BMI point was linked to about 0.4 mL more prostate volume, which is small on its own. Severe obesity, though, carried about 3.5 times the odds of an enlarged prostate (Cohen’s d about 0.7, a medium effect). Whether losing weight shrinks the prostate has not been tested.
  2. Stay active. Separate meta-analysis data, not covered in this review, link higher physical activity to up to 25% lower BPH risk.
  3. Find out what is causing your symptoms. Bladder overactivity is present in about 60% of older men with symptoms and obstruction in only 30 to 40%, so treatment should follow testing, not prostate size alone.
  4. Match the drug to the goal. Alpha-blockers ease symptoms quickly but do not shrink the gland. 5-alpha reductase inhibitors shrink it by 20 to 30%. In a four-year trial they cut acute urinary retention from about 7% to 3% and surgery from about 10% to 5%, so roughly 1 in 20 to 25 men treated avoids one of these events. Daily tadalafil gives a modest symptom benefit.
  5. Skip the unproven options. The evidence for metformin, pomegranate and ginseng in BPH is animal-only.

Context and Source

  • Open Access Paper: Pathophysiology of Benign Prostatic Hyperplasia and Benign Prostatic Enlargement: A Mini-Review
  • Institutions: Department of Urology, Kaiser Franz Josef Hospital, Vienna; Sigmund Freud Private University, Vienna; Department of Urology, Medical University of Innsbruck
  • Country: Austria
  • Journal: Gerontology (S. Karger AG), 2019
  • Impact evaluation: The impact score of this journal is 3.1, evaluated against a typical high-end range of 0 to 60+ for top general science and medicine journals, therefore this is a Medium impact journal.

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FishConsumptionCardioRisk-2
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A systematic review and dose-response meta-analysis pooled prospective cohort studies from Japan, one of the highest fish-consuming countries, to test whether the survival benefits linked to fish in Western populations hold when even the lowest eaters consume fish regularly. Of 16 eligible studies, nine entered the meta-analysis. Comparing the highest with the lowest intake groups, higher fish consumption was associated with a 6% lower risk of death from any cause and a 15% lower risk of cardiovascular death, with almost no disagreement between studies. A spline model suggested risk fell up to about 100 grams per day and then flattened, although formal dose-response tests were not statistically significant.

Japan is one of the few places on Earth where almost nobody avoids fish. That makes it an unusually good test bed for a question nutrition researchers have argued about for decades: do the survival benefits linked to fish in Western studies keep growing as intake climbs, or do they run out?

A team from Tohoku University, Kobe University, Japan’s National Institutes of Biomedical Innovation, Health and Nutrition, and the research institute of seafood company Nissui gathered every prospective cohort study of Japanese adults that tracked fish intake and later deaths. After reviewing 113 full-text articles, they found 16 relevant studies and pooled nine.

The headline result is consistent but modest. People in the highest fish-intake groups were about 6% less likely to die from any cause during follow-up than those in the lowest groups. For cardiovascular death, the gap was larger, about 15%. Unusually for nutrition research, the individual studies barely disagreed with each other, and removing any single study did not change the picture.

The twist is what “low intake” means in Japan. In American and European cohorts, the comparison group often eats almost no fish. In Japan, the bottom group in most studies still ate roughly 18 to 46 grams a day, a couple of servings a week or more. So this analysis asks a sharper question: if you already eat fish, does eating more still help? The answer appears to be a qualified yes.

The authors also tried to map the shape of the benefit. A flexible curve fitted to four studies suggested death risk kept falling until about 100 grams a day, around one and a half typical Japanese servings, and then leveled off. Earlier global analyses had placed that plateau nearer 60 grams. However, the formal tests for a dose-response trend were not significant, and the plateau was identified by eye. It is a hypothesis, not a finding.

There are reasons for caution beyond the usual “correlation is not causation.” Two studies carry about three-quarters of the statistical weight in each main analysis. For cardiovascular death, the dominant study comes from a cohort that began in the mid-1960s, received the lowest quality score in the set, and, like the second-largest contributor, measured stroke deaths rather than all cardiovascular deaths. The heart-attack evidence is thin. Fish intake was asked about once, at the start, by questionnaire, and people who eat more fish may differ in income, activity and overall diet in ways adjustment cannot fully capture. The authors themselves rate the certainty of the evidence as low.

The study was funded by Nissui, and two of the six authors work there. That does not invalidate the analysis, which was preregistered and follows standard methods, but readers should weigh it.

What emerges is reassuring rather than revolutionary. Fish appears to remain a sensible part of a long-lived diet even at intakes far above Western norms, with the clearest signal for stroke and cardiovascular death and diminishing returns somewhere near a daily serving. Whether the effect comes from omega-3 fats, protein, vitamin D, taurine, or simply eating less of something else remains open.

Actionable Insights

These are associations, not proven effects, so treat them as reasonable bets rather than guarantees.

  1. If you eat little or no fish, moving toward regular intake is the change best supported by this and earlier data. The Japanese results suggest benefit continues up to roughly 100 grams a day (about 700 grams, or six 4-ounce servings, a week), with little extra beyond that.
  2. Expect a small individual effect. Moving from the lowest to the highest intake group was linked to about 6% lower relative risk of death from any cause. Applied to the death rate in these cohorts (about 12.6% over 4 to 19 years), that is roughly 0.5 to 0.7 fewer deaths per 100 people, so about 140 to 210 people would need to make the change to avoid one death. In standardized terms that is a Cohen’s d of about 0.03, far below the 0.2 conventionally called “small.”
  3. The cardiovascular signal is stronger: 15% lower relative risk, about 0.5 fewer cardiovascular deaths per 100 people, around 200 people per death avoided (d about 0.09). Most of this evidence concerns stroke.
  4. Whole fish is not the same as capsules. Fish-oil supplement trials are mixed, so these data do not justify pills as a substitute.
  5. At intakes near 100 grams a day, favor low-mercury species such as sardines, salmon, Atlantic or Pacific mackerel and small whole fish. Contaminants were not assessed.

Context and Source

  • Open Access Paper: Fish intake and mortality in Japan, a high fish-consuming country: a systematic review and dose-response meta-analysis of cohort studies, Published: 23 October 2026.
  • Institutions: Food and Health Science Research Institute, Nissui Corporation (Tokyo); Tohoku University Graduate School of Medicine and Graduate School of Biomedical Engineering (Miyagi); Yokohama University of Pharmacy (Kanagawa); National Institutes of Biomedical Innovation, Health and Nutrition (Osaka, corresponding author Haruki Momma); Kobe University (Hyogo)
  • Country: Japan
  • Journal: European Journal of Clinical Nutrition (Springer Nature)
  • Funding and conflicts: Funded by Nissui Corporation, a major Japanese seafood company; the two lead-listed contributors from Nissui (Yokoi, Kato) are employees.
  • Impact evaluation: The impact score of this journal is 3.2, evaluated against a typical high-end range of 0 to 60+ for top general science and medicine journals, therefore this is a Medium impact journal.

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CreatineMuscle10G-2
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A 12-week randomized, double-blind trial from Texas A&M University tested 10 grams per day of creatine monohydrate in 64 sedentary adults aged 45 to 65. Participants first chose whether to join a supervised resistance and aerobic training program with a modest calorie deficit or to keep their normal routine, and were then randomly assigned to creatine or a maltodextrin placebo. Creatine increased DXA-measured lean mass by roughly 1.1 to 1.3 kg relative to placebo in both settings, improved leg and bench press strength, and produced a larger drop in body fat percentage when combined with exercise and dieting. The authors also report gains on some memory tests, lower HbA1c and better lipid profiles.

Most people who diet in middle age lose more than fat. A meaningful share of the weight that comes off is muscle, the tissue that keeps us strong, mobile and metabolically healthy as we age. A new trial from Richard Kreider’s Exercise and Sport Nutrition Lab at Texas A&M asks whether one of the cheapest and best-studied supplements available, creatine monohydrate, can shift that trade in our favor.

The team recruited 73 healthy but sedentary adults aged 45 to 65, most of them overweight. Each volunteer chose whether to join a supervised program of resistance and aerobic training three times a week, paired with a diet cut by 300 to 500 calories a day, or to carry on as usual. Within each group, participants were randomly assigned to 5 grams of creatine twice daily or an identical-looking carbohydrate powder for 12 weeks. Sixty-four finished.

The muscle results are the strongest part of the paper. In the exercise and diet group, creatine users ended with about 1.1 kg more lean mass than placebo users, whose lean mass barely moved. Creatine users who did no training gained a similar amount relative to their own placebo group. Leg press strength rose by roughly a third in the exercising creatine group, about double the gain from exercise alone, and bench press followed a similar pattern. Body fat percentage fell further when creatine was added.

There is an important asterisk. Creatine draws water into muscle cells, and DXA scanners count that water as lean tissue. Lean mass in the exercising creatine group peaked at six weeks and then slipped back, a pattern that fits early water loading at least as well as new muscle protein. The extra drop in body fat percentage partly reflects a larger denominator, since actual fat mass losses looked similar with or without creatine.

The brain findings warrant more caution. The researchers used a relatively high dose because only a small fraction of oral creatine reaches the brain, and they ran a large battery of memory, attention and reaction-time tests. Across eight cognitive tasks, none showed a significant overall difference between groups over time. The positive claims rest on individual comparisons, such as a temporary improvement in delayed word recall at six weeks, alongside results pointing the other way, including more attention errors and higher tension scores in some creatine groups. The authors themselves call these findings exploratory.

Blood work hinted that creatine without exercise lowered HbA1c, a marker of average blood sugar, by roughly a quarter of a percentage point versus placebo, with no change in fasting glucose. In people with normal glucose, that is a lead worth following, not a reason to treat creatine as a glucose-lowering therapy.

Context matters. The corresponding author chairs the scientific advisory board of AlzChem, which manufactured and donated the creatine, and he is also one of the journal’s editors-in-chief. That does not invalidate the data, but it raises the bar for independent replication.

The take-home is modest but useful: creatine appears to help middle-aged adults keep or build muscle and strength, including while dieting. Claims that it sharpens the healthy midlife brain remain unproven.

Actionable Insights

  • Muscle: 10 g/day (two 5 g doses) added about 1.1 to 1.3 kg of lean mass over 12 weeks versus placebo. That is roughly 2% of a typical participant’s lean mass, and some of it is water stored in muscle. The effect size is moderate to large (estimated Cohen’s d about 0.7 to 0.8).
  • Strength: Leg press 1RM rose about 33% with creatine plus training versus about 17% with training alone. A gap of that size is likely to matter for everyday function.
  • Dieting: Creatine appears to protect lean tissue during a calorie deficit. Expect the scale to read 1 to 2 kg higher than it otherwise would early on. That is water, not fat.
  • Memory: Do not take creatine expecting cognitive gains if you are healthy and well rested. No cognitive domain showed a reliable effect here.
  • Kidney labs: Serum creatinine rose (under 0.15 mg/dL) and calculated eGFR fell by up to 20% in exercising creatine users. This is a known measurement artifact, not kidney injury, but tell your physician and consider cystatin C for a cleaner reading.
  • Protein: Participants averaged only 0.94 g/kg/day, well below the 1.2 g/kg/day or more commonly advised for older adults who train.
  • Dose: 3 to 5 g/day is the established muscle dose. This trial did not test whether 10 g outperforms it.

Context and Source

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HeartRateHRVAging-2
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This single-author narrative review argues that resting heart rate and heart rate variability should be treated not merely as clinical vital signs but as accessible biomarkers of biological aging. It assembles three evidence streams: comparative biology showing that across mammals heart rate scales inversely with body mass and lifespan; large epidemiological cohorts, including a combined Taiwanese and Norwegian analysis of 692,217 adults, showing that elevated resting heart rate predicts cardiovascular and all-cause mortality; and clinical studies showing that reduced heart rate variability predicts adverse outcomes after myocardial infarction, in heart failure, and in diabetes. The proposed mechanisms are sympathetic overactivation, parasympathetic withdrawal, neuroendocrine stress activation, oxidative stress, inflammation, baroreflex failure, and structural remodeling. The review proposes wearables and machine learning as the route to individualized longitudinal tracking.

The pulse is the oldest diagnostic instrument in medicine and, on the evidence assembled here, one of the more underrated ones. This review makes the case that two numbers anyone with a cheap wrist device can read, resting heart rate and heart rate variability, carry real information about how fast a person is aging.

The comparative biology opening is the most quotable and the least useful. A shrew’s heart runs near a thousand beats a minute and the animal is dead within a couple of years. An elephant idles around forty and lives for decades. Across mammals, heart rate scales roughly as body mass to the minus one-quarter power, and the total number of heartbeats in a lifetime converges on something near a billion across many species. The review presents the old fixed-heartbeat hypothesis, then correctly labels it oversimplified, while still letting it set the tone.

The human epidemiology carries the argument. Across Framingham, the Chicago studies, NHANES, French and Finnish and Swedish and Chinese and Japanese and Korean cohorts, higher resting heart rate predicts cardiovascular and all-cause death after adjustment for the obvious confounders. The largest analysis, pooling the Taiwan MJ and Norwegian HUNT cohorts across 692,217 adults over 25 years, found that a resting pulse in the eighties and nineties cost measurable life expectancy, with the risk at 90 to 99 beats per minute comparable to carrying hypertension. That comparison is the single most striking line in the paper.

Heart rate variability (HRV) tells a different story. Where resting heart rate reports how hard the autonomic system is leaning on the heart, variability reports how flexibly it can respond. In Framingham, a one standard deviation drop in a standard variability index was associated with roughly a 47 percent higher hazard of new cardiac events. In heart failure patients, the gradient is brutal: mortality ran 5.5 percent in those with the highest variability and 51.4 percent in those with the lowest.

The review also flags that the relationship is not monotonic. A Korean cohort of 31,697 adults found higher cardiovascular mortality both above 80 beats per minute and below 60. The Rotterdam Study found that unusually high variability also predicted cardiac death in older adults.

Actionable Insights

A hazard ratio is how much a person’s risk of an event multiplies relative to a comparison group. A hazard ratio of 1.5 means 50 percent higher risk. These are observational associations, not proof that changing the number changes the outcome.

Resting heart rate. Pulling the per-unit figures from the cohorts tabulated here: a Swedish cohort found about 3 percent higher all-cause mortality per additional beat per minute. FINRISK found 24 percent higher cardiovascular death in men and 32 percent in women per 15 beats. Working those back, roughly 15 to 25 percent lower mortality risk per 10 beats lower is a defensible central estimate, with one French cohort reporting a near doubling per 15 beats at the extreme end. In practical terms, 80 beats per minute is where the risk curve clearly steepens across multiple independent cohorts.

Heart rate variability. In Framingham, a one standard deviation drop in SDNN carried a hazard ratio of 1.47 for incident cardiac events and 1.38 for mortality in older adults. In heart failure, SDNN below 50 milliseconds marked a group with roughly nine times the mortality of those above 100.

Two cautions that matter. Lower is not uniformly better: one Korean cohort found elevated cardiovascular mortality below 60 beats per minute as well as above 80. And resting heart rate is heavily shaped by cardiorespiratory fitness, so these associations are partly measuring something else.

Context and Source

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ExerciseSnacks-2
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This systematic review and meta-analysis of 21 randomized controlled trials covering 921 adults asks whether exercise snacks, meaning multiple brief bouts of activity scattered through the day, deliver measurable physiological benefit. The answer splits cleanly. Cardiorespiratory fitness improved substantially, with maximal oxygen uptake showing a large pooled effect (Hedges’ g equals 1.04) and peak power output a moderate one (g equals 0.68), both rated moderate certainty. Body composition and blood lipids did not cooperate. Body fat percentage actually moved in the wrong direction (g equals 0.51 toward more fat, low certainty), and none of total cholesterol, HDL, LDL, or triglycerides shifted significantly overall. Age mattered: VO2max gains were clear in adults under 50 but statistically absent above 50, while peak power improved in every age band. Dose analyses pointed toward more bouts per day, four to five days per week, and seven to nine weeks of duration.

The World Health Organization counts roughly 1.8 billion adults who do not get enough physical activity, and the usual explanation is not ignorance but time. The exercise snack proposition is that the hour-long block was never the active ingredient. If you can accumulate the stimulus in one-minute and two-minute pieces, scattered across a workday, the physiology may not care how it arrived.

This review pulls together 21 randomized trials testing that idea, spanning 1994 to 2025 across ten countries, with 921 participants. The interventions are mostly unglamorous: climbing a public stairway at a brisk pace, thirty-second all-out cycle sprints, bodyweight resistance done at a desk.

The cardiorespiratory result is the strong one. Pooled across studies, maximal oxygen uptake improved with a Hedges’ g of 1.04, which sits firmly in large-effect territory and comfortably above the minimum important difference the authors set at 0.50. Peak power output improved with a g of 0.68. Both were graded moderate certainty. Given that VO2max is among the better single predictors of all-cause mortality, a real effect of this size from a few scattered minutes a day would be a meaningful finding.

Then the paper runs into its own data. Body fat percentage did not improve. It went the other way, with a pooled g of 0.51 toward higher body fat in the intervention arms, a result the authors report honestly and rate as low certainty. Heterogeneity for that outcome was 84 percent, meaning the included studies were measuring something that varied enormously between them. The entire signal came from the middle-aged stratum, where heterogeneity hit 92 percent and the confidence interval ran from 0.08 to 2.05. That is not a finding. That is noise with a p value attached, almost certainly driven by the mix of DXA, bioimpedance, and skinfold measurement across trials.

Blood lipids were flat. Total cholesterol, HDL, LDL, and triglycerides all produced confidence intervals straddling zero.

The age story is the most practically useful part. VO2max improved in adults under 25 and in the 25 to 50 band, but the over-50 estimate lost significance. Meta-regression confirmed the gradient, with study-level mean age explaining about half the variance in the VO2max effect. Peak power, by contrast, improved in all three age bands including the oldest. Older adults in this evidence base appear to gain muscular power from brief bouts even when aerobic capacity does not respond.

The caveat that governs everything above is publication bias. For VO2max, Egger’s test returned a p value below 0.001 and Begg’s test 0.006. That is an unambiguous funnel asymmetry on the paper’s flagship outcome, and it means the true pooled effect is probably meaningfully smaller than 1.04.

What survives scrutiny is modest and still useful: brief, repeated, vigorous bouts improve fitness in working-age adults, improve power at any age, and will not reshape your body composition or your lipid panel on their own.

Actionable Insights

Hedges’ g expresses a difference in standard deviation units, corrected for small samples. Roughly, 0.2 is small, 0.5 moderate, 0.8 large.

The VO2max result (g equals 1.04) means the average person doing exercise snacks ended up fitter than about 85 percent of the control group. Put differently, pick one exerciser and one control at random and the exerciser improved more about 77 percent of the time. The authors set a minimum important difference at 0.50, and both the point estimate and the entire confidence interval (0.68 to 1.39) clear it. Peak power (g equals 0.68) clears the threshold at the point estimate but its lower bound of 0.25 does not, so clinical relevance there is less secure.

The practical dosing signal: at least three bouts per day, with the largest VO2max effect in studies using more than five bouts daily (g equals 1.74, though with a very wide interval); four to five days per week; seven to nine weeks before expecting meaningful change. Sessions of one to two minutes performed hard are sufficient.

Set expectations honestly. Do not expect fat loss, and do not expect lipid improvement, from this alone. And discount the fitness numbers somewhat, because the publication bias on that outcome is real and significant.

Context and Source

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SleepDeclineAging-2
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This pooled analysis of 149 healthy men aged 16 to 83 shows that age-related sleep deterioration happens in two distinct waves, each tied to a different hormonal system. Deep slow wave sleep collapses early, falling roughly five-fold between early adulthood and midlife, and this collapse runs in parallel with a near 75 percent drop in 24-hour growth hormone secretion. Critically, when the authors modeled growth hormone against age and slow wave sleep together, slow wave sleep carried the statistical weight and age by itself did not. The second wave arrives after about age 50: sleep becomes fragmented, REM sleep declines, total sleep time falls by roughly 27 minutes per decade, and evening cortisol begins climbing by about 19 nmol/L per decade. The study is cross-sectional, male-only, and observational, so it establishes chronology and association rather than causation. But it reframes the somatopause as a sleep-architecture problem beginning in young adulthood rather than a geriatric one.

For most of the last half century, the decline of growth hormone with age has been filed under geriatrics. Clinics sell recombinant growth hormone and secretagogues to men in their sixties and seventies on the premise that this is when the deficiency bites. This paper, assembled from 149 healthy men studied across four sleep laboratories between 1985 and 1999, says that premise has the timing badly wrong.

The researchers took 24-hour blood sampling at 15 to 30 minute intervals, paired with overnight polysomnography, and sorted the results by age band rather than the usual young-versus-old split. What emerged was not one curve but two, separated by decades.

The first wave is the loss of deep sleep. Between the 16 to 25 band and the 36 to 50 band, slow wave sleep fell from about 19 percent of the night to about 3 percent. The lost deep sleep was not replaced by wakefulness. It was replaced by light stage 1 and 2 sleep. Total time asleep barely moved. A man of 45 in this cohort was sleeping about as long as a man of 20, but in a structurally different and far shallower way.

Growth hormone tracked that curve almost exactly, falling close to 75 percent over the same interval. The interesting part is what happened when age and slow wave sleep were entered into the same model. Slow wave sleep explained the variance. Age, on its own, explained essentially nothing. Deep sleep was not a marker of hormonal aging in these men so much as a proxy for the mechanism.

The second wave begins around the fifth decade and has nothing to do with growth hormone. Here sleep starts breaking apart. Time awake in bed rose by roughly 28 minutes per decade, REM sleep by then had fallen by about half compared with young adulthood, and evening cortisol, which had been flat for thirty years, began a steady climb. Morning cortisol peaks did not change. What changed was the body’s ability to switch the stress axis off at night.

That matters because the evening trough is where glucocorticoid excess does its damage, and chronically elevated evening cortisol has been linked to insulin resistance and memory impairment. The authors frame it as accumulating allostatic load: the wear from a stress system that no longer stands down.

The limits are significant. This is cross-sectional data pooled from studies not designed to answer this question, combining two different growth hormone assay methods, in men only, who slept in a laboratory with a catheter in one arm and at least eight hours of enforced darkness. Nothing here was randomized. Nobody’s sleep was manipulated and nobody’s hormones were measured afterward.

What it does deliver is a map with timing on it. If slow wave sleep is the lever on the growth hormone axis, the window to pull it opens in your twenties and is mostly closed by 50. If sleep continuity and REM are the levers on evening cortisol, that window opens later. Two targets, two clocks, and interventions aimed at the wrong decade.

Actionable Insights

Effect size is simply how large a difference is relative to the natural spread in the data. A Cohen’s d of 0.2 is small, 0.5 is moderate, 0.8 is large. Anything above 2.0 means the two groups barely overlap.

The headline difference here is enormous. Slow wave sleep falling from 18.9 percent to 3.4 percent of the night between young adulthood and midlife works out to a Cohen’s d of roughly 2.1. That is not a subtle aging effect. It is the near-total disappearance of a sleep stage. Light sleep rising from 51 to 67 percent gives a d of about 1.8.

The more useful number for anyone deciding what to do is the matched comparison the authors ran. They took men of the same age and same BMI and split them by how much deep sleep they actually got. The high deep sleep group secreted roughly 65 to 70 percent more growth hormone during sleep than the low group, a moderate-to-large effect of around d equals 0.7. Same age, same body composition, different sleep, meaningfully different hormone output.

Practical takeaways: deep sleep is worth defending aggressively starting in your twenties and thirties, but perhaps less so at 60. Higher BMI was associated with less deep sleep in men under 44 but not over, so weight management is a sleep-architecture lever that appears to work only while the window is open. After 50, the target shifts to sleep continuity and REM, which the data tie to evening cortisol.

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Context and Source

  • Paywalled Paper: Age-Related Changes in Slow Wave Sleep and REM Sleep and Relationship With Growth Hormone and Cortisol Levels in Healthy Men, Published Aug. 16, 2000.
  • Institution: Department of Medicine, University of Chicago, Chicago, Illinois. Contributing data sets came from the University of Pittsburgh, the University of California Los Angeles, and Pennsylvania State University at Hershey.
  • Country: United States
  • Journal: JAMA (The Journal of the American Medical Association), 2000.
  • Impact evaluation: The impact score of this journal is 65.4, evaluated against a typical high-end range of 0 to 60+ for top general science and medicine, therefore this is an Elite impact journal.

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FGF21inHealthandAging-2
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This narrative review from the University of Cincinnati and the National and Kapodistrian University of Athens examines fibroblast growth factor 21 across healthy aging and age-related disease. FGF21 is a liver-derived hormone that also acts as an adipokine, myokine, and cardiomyokine, signaling through FGFR1c paired with the co-receptor beta-Klotho to activate ERK, PI3K-AKT, and AMPK-SIRT1 pathways. The review’s organizing problem is a genuine paradox: higher circulating FGF21 predicts mortality and frailty in older humans and is lower in disease-free centenarians, while FGF21 overexpression extends lifespan in mice. The authors propose that effects depend on duration of exposure, tissue of origin, and which receptor complex forms, with beta-Klotho-dependent signaling protective and FGFR4 signaling driving cardiac hypertrophy.

The same hormone looks protective in mice and lethal in humans, and this review is an attempt to work out why.

FGF21 is a starvation signal. The liver makes it when nutrients are short, and it tells the body to burn fat, improve insulin sensitivity, and shift into a conservation mode. It is also what is called a mitokine, a molecule released when mitochondria are under stress, which puts it in the same family as GDF15. Levels climb steadily in human blood from age 5 to 80 regardless of body composition.

On the human side the picture is bleak. In the Polsenior2 study of 3,512 Polish adults over 60, people in the top third of FGF21 had roughly double the death rate of the bottom third over four years. FGF21 tracks with frailty, with insulin resistance, with cachexia in people over 60, with lower bone mineral density, and with weaker grip strength. Disease-free centenarians have less of it circulating than healthy people in their seventies. Every human association points one direction.

On the mouse side the opposite. Transgenic mice overexpressing FGF21 in the liver live substantially longer. Mice given the gene in fat tissue while eating a high-fat diet live longer than their littermates. A single dose of gene therapy delivered to muscle in old mice extended life expectancy by about a fifth. Protein restriction extends mouse lifespan and stops working if you delete FGF21.

The authors’ resolution has three parts and it is the most useful thing in the paper.

Duration matters. Acute FGF21, the kind you get from a hard workout or a short fast, drives mitochondrial adaptation. Chronic elevation, the kind you get from aging or persistent mitochondrial damage, drives muscle atrophy. In cardiac tissue the authors put a number on it: benefit for about two weeks and not after.

Tissue of origin matters independently of the level in blood. Liver and fat overexpression extends lifespan. Cardiomyocyte-derived FGF21 promotes hypertrophy even when circulating levels are unchanged.

And the receptor matters most. FGF21 needs a co-receptor called beta-Klotho to signal through FGFR1c, and that pairing is the protective route. When beta-Klotho is scarce, FGF21 signals instead through FGFR4, which drives the heart toward thickening. Aging and metabolic stress both reduce beta-Klotho, partly through a protease called ADAM-10 that chews it up. So aging does not stop FGF21 signaling. It reroutes it down the harmful path.

That framework makes a sharp prediction. High endogenous FGF21 in an older person is a stress alarm firing in a body that has lost the receptor needed to respond to it usefully. Giving a drug version is a different act entirely, which is why FGF21 analogues clear liver fibrosis in trials while natural elevation predicts death.

The review reports two mouse lifespan figures incorrectly, and both errors run in the same direction.

Actionable Insights

Read your own FGF21, if you ever measure it, as an alarm rather than a cause. Nothing in this literature supports trying to raise it.

The human mortality numbers. In 3,512 adults over 60 followed 4.19 years with 664 deaths, each standard deviation of higher FGF21 carried a 34 percent higher death rate unadjusted and 24 percent after age adjustment. Comparing the top third to the bottom third, the hazard ratio was 2.56 unadjusted, 1.94 age-adjusted, and 1.53 after full adjustment for comorbidity. The middle third was not significantly different from the bottom after full adjustment, so this looks like a top-end threshold rather than a smooth gradient, and the drop from 2.56 to 1.53 means much of the raw association was comorbidity.

What lowers it, with numbers. Long-term exercise training of four weeks or more reduces circulating FGF21 while increasing FGF receptor and beta-Klotho expression in muscle, liver, and fat. In adults aged 62 to 70, resistance training increased muscle mass and decreased plasma FGF21. In elderly people with and without type 2 diabetes, resistance training significantly reduced FGF21 in both groups. Acute exercise raises it transiently, which is the adaptive signal; training lowers the chronic level. One study found the response depends on metabolic status: 10 weeks of resistance exercise lowered FGF21 in women with metabolic syndrome and raised it in women without.

What the drugs do, for context. Pegozafermin in 222 patients with MASH over 24 weeks produced fibrosis improvement in 22 to 27 percent against 7 percent on placebo, and MASH resolution in 23 to 37 percent against 2 percent. Those are large effects. One FGF21 analogue also raised systolic and diastolic blood pressure dose-dependently in humans.

The practical read: train for strength, which raises FGF21 acutely and lowers it chronically, and treat a high resting level as information about mitochondrial and metabolic stress rather than a target to push.

Context and Source

  • Open Access Paper: Fibroblast growth factor 21 (FGF21) in healthy aging and aging-related diseases., published October 26, 2026.
  • Institutions: First Department of Cardiology, National and Kapodistrian University of Athens, Greece; Metabolic Biology Laboratory, Cardiovascular Center, Department of Biomedical Sciences, University of Cincinnati College of Medicine.
  • Countries: Greece and the United States.
  • Journal: Geromedicine, volume 3
  • Impact evaluation: this journal has no impact factor. Geromedicine launched in May 2025 under Science Exploration Press, a Singapore-headquartered publisher that is a regular member of the STM Association and lists 14 journals. Two mitigating facts should be weighed against that. The editor-in-chief is Guido Kroemer, with Andrea Maier and Hans Meij as deputy editors, which is a serious geroscience board, and the author list here includes the leadership of LonGenity, BLSA, and the Stanford organ-clock group. This is credible work placed in a venue with no track record.

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PlasmaProteinsMortalityRisks-2
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This prospective cohort study from Barzilai’s group at Albert Einstein measured 4,265 plasma proteins in 1,025 community-dwelling Ashkenazi Jewish adults aged 65 and over from the LonGenity study, then tested each against all-cause mortality over a mean 8.05 years of follow-up during which 258 participants died. Seventeen protein measurements reached significance after false-discovery-rate correction, of which eleven replicated in 1,124 participants from the Baltimore Longitudinal Study of Aging. GDF15, HE4, NT-proBNP, IGFBP-2, SVEP1, thrombospondin-2, and osteopontin predicted higher mortality; EGFR, ANTXR2, NOTUM, growth hormone receptor, GDF11/8, and others predicted lower mortality. The authors then correlated these proteins with proteomic organ-specific aging clocks. They state plainly that the proteins are biomarkers rather than demonstrated mediators.

The protein that came out on top of this analysis was not the one that predicted death. It was the one that predicted survival, and it is a protein most people associate with cancer.

Epidermal growth factor receptor, usually written EGFR and here labeled ERBB1, is the target of a whole class of oncology drugs built to shut it down. In this cohort of adults aged 65 and older, higher circulating levels of it were associated with a 34 percent lower rate of death per standard deviation, the single strongest association among 4,265 proteins tested. It also tracked with younger biological age in every organ system the authors examined, most strongly the liver and brain. It replicated in an independent cohort.

That is either a real and important finding about what keeps older bodies functioning, or it is an artifact of measuring a membrane receptor’s soluble fragment with an aptamer. The honest answer is that nobody yet knows, and the paper says this.

The structure of the study is straightforward. Take a cohort, measure everything in plasma, wait, count deaths, run a Cox model per protein, correct for multiple testing. Seventeen measurements survived. Then check them against an independent cohort, and against a third published study of 22,913 Icelanders in which GDF15 had also been the top mortality protein out of 4,684.

What emerges is less a list than a set of three biological themes. Several of the proteins are extracellular matrix molecules: thrombospondin-2, osteopontin, angiostatin, hyaluronidase-1, SVEP1, ANTXR2. Several are growth factor signaling components: EGFR, growth hormone receptor, GDF11/8, IGFBP-2. And three are stress signals: GDF15, HE4, NT-proBNP. So dying, on this reading, is not a single failing pathway. It is matrix turnover, signaling capacity, and systemic stress moving together.

The growth hormone result deserves attention because it points the opposite way from a well-known story. In mice, worms, and flies, dialing down growth hormone and IGF-1 signaling extends lifespan, and that trade-off between growth and longevity is close to canonical. Here, in humans past 65, higher growth hormone receptor was associated with lower mortality. The authors’ interpretation is that what protects a young organism from growing too fast is not what protects an old one from frailty and sarcopenia.

Which brings up the thing the study did not do. LonGenity exists specifically to study longevity: roughly half its participants have a parent who lived past 95. That parental longevity was entered into every model as a covariate, meaning it was statistically removed. The paper’s title promises implications for longevity, and the one longevity contrast the cohort uniquely offers was treated as noise.

Insights

These are biomarkers with no intervention attached, and the authors say outright that the proteins are “best interpreted as reflecting the cumulative physiological consequences of biological aging” rather than as causes.

What the numbers mean in absolute terms. Hazard ratios here are per one standard deviation of protein level, which is a statistician’s unit, so here is the translation. Over the mean 8-year follow-up, 258 of 1,014 participants died, an absolute risk of about 25 percent. Being one standard deviation above average on GDF15, hazard ratio 1.38, shifts that 8-year risk from roughly 25 percent to roughly 33 percent. Being one standard deviation above average on EGFR, hazard ratio 0.66, shifts it from roughly 25 percent down to roughly 18 percent. Real, but not destiny, and these are the two largest effects in the paper.

The strongest associations, all per standard deviation: EGFR 0.66 (0.57 to 0.77), ANTXR2 0.72 (0.63 to 0.83), SVEP1 1.41 (1.23 to 1.63), GDF15 1.38 (1.18 to 1.62), HE4 1.37 (1.17 to 1.59), IGFBP-2 1.33 (1.15 to 1.54), NT-proBNP 1.33 (1.15 to 1.53).

The one finding with a practical edge. Of all the clinical phenotypes tested, the frailty index correlated with the most mortality proteins, 13 of 17. Depression correlated with the fewest, 5. Frailty is also the phenotype on that list most responsive to resistance training, protein intake, and activity. If you want one thing from this paper, it is that frailty appears to sit closest to whatever the mortality proteome is measuring, and frailty is modifiable in a way that GDF15 is not.

A caution on buying tests. The paper reports no C-statistic, no area under the curve, and no reclassification metric, so there is no evidence here that measuring any of these proteins adds anything to knowing someone’s age and sex.

Context and Source

  • Open Access Paper: Exploring mortality-linked proteins: Understanding their association with biological aging, disease phenotypes, signaling pathways, and their implications for longevity.
  • Authors: Nicholas Garvey, Sanish Sathyan (corresponding), Toshiko Tanaka, Cassandra Joynes, Hamilton Se-Hwee Oh, Tina Gao, Keenan A. Walker, Tony Wyss-Coray, Joe Verghese, Luigi Ferrucci, Sofiya Milman, Nir Barzilai (corresponding).
  • Institutions: Institute for Aging Research and Department of Genetics, Albert Einstein College of Medicine, Bronx; Renaissance School of Medicine, Stony Brook University; Kannur University, Kerala; Translational Gerontology Branch and Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore; Stanford University School of Medicine and the Phil and Penny Knight Initiative for Brain Resilience.
  • Countries: United States, with one Indian affiliation.
  • Journal: Geromedicine, volume 3, published October 9, 2026.
  • Impact evaluation: this journal has no impact factor. Geromedicine launched in May 2025 under Science Exploration Press, a Singapore-headquartered publisher that is a regular member of the STM Association and lists 14 journals. Two mitigating facts should be weighed against that. The editor-in-chief is Guido Kroemer, with Andrea Maier and Hans Meij as deputy editors, which is a serious geroscience board, and the author list here includes the leadership of LonGenity, BLSA, and the Stanford organ-clock group. This is credible work placed in a venue with no track record.

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ErgothionineReview-2
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This is a critical narrative review from two authors at the University of Rzeszow in Poland examining whether ergothioneine, a thiol antioxidant obtained almost entirely from mushrooms, prevents neurodegeneration. The authors survey the compound’s chemistry, dietary sources, bioavailability, and OCTN1-dependent transport, then assess cellular, animal, epidemiological, and human interventional evidence across Alzheimer’s and Parkinson’s disease. They conclude that the mechanism is probably Nrf2 activation and signaling modulation rather than direct radical scavenging. The review’s most useful contribution is its catalog of contradictory findings, including one study where higher serum ergothioneine was a risk factor for Alzheimer’s disease.

Ergothioneine has the cleanest story in the antioxidant field, and that is both why it is interesting and why it should be read carefully.

The basics are genuinely unusual. Humans cannot make it. Fungi and some bacteria can, which makes mushrooms the dominant dietary source, accounting for roughly 95 percent of intake in a typical European diet. The body treats it as something worth keeping: there is a dedicated transporter, OCTN1, that concentrates it into cells; the kidney reabsorbs it so that under 4 percent of an oral dose appears in urine; and blood levels keep climbing for at least 28 days of supplementation without saturating. A compound that has a transporter, a retention mechanism, and no endogenous synthesis is a compound the body is acquiring on purpose. That is the observation behind calling it a vitamin-like molecule.

The epidemiology is consistent in direction. People with mild cognitive impairment have lower blood levels than age-matched controls. People with dementia have lower levels than people with cognitive impairment, who have lower levels than the cognitively intact. In an analysis screening 991 blood metabolites against cognition, ergothioneine came out at the top. Two longitudinal cohorts, one of 470 people and one of 1,344 Japanese adults followed a median of 11.2 years, found that low baseline levels preceded faster decline and predicted incident dementia.

Then the review does something most reviews in this genre do not. It lays out the findings that do not fit. Plasma levels did not differ between Alzheimer’s and vascular dementia, which is odd if the mechanism is specifically neurodegenerative. Levels did not differ between elderly people with low and high brain amyloid burden. And one study found higher serum ergothioneine to be a risk factor for Alzheimer’s disease, the opposite of everything else.

They also name the right precedent. When they ask whether the evidence justifies recommending supplementation, they answer that it would first require large randomized trials of the kind run for beta-carotene. That is a pointed comparison. Beta-carotene had excellent observational data and then increased lung cancer in smokers in two large trials. It is the standard case for why antioxidant epidemiology does not survive contact with randomization.

Which makes the ending hard to explain. Two sections after invoking that precedent, the conclusions state that supplementation can be broadly recommended for the general population, especially older adults. The abstract hedges differently again, saying the recommendation is not yet adequately supported. Three positions, one paper.

The human trial data are where this matters. Across the interventions the review cites, no randomized trial has shown a cognitive benefit over placebo. The largest, 147 adults on 10 or 25 milligrams for 16 weeks, reported a memory improvement at week 4 that was not sustained and no clear between-group result on its primary outcome. The one thing that replicated was subjective sleep quality, in two trials, by questionnaire.

Insights

What the human numbers actually are. No randomized trial has beaten placebo on a cognitive endpoint. The largest, 147 adults aged 55 to 79 on 10 or 25 milligrams daily for 16 weeks, found a composite memory gain at week 4 in the higher-dose arm that was a within-group change only and had disappeared by week 16. An earlier trial of 5 or 25 milligrams for up to 35 days found only non-significant downward trends in oxidative and inflammatory markers. A one-year trial in mild cognitive impairment enrolled 19 people, 11 on treatment and 8 on placebo, performed no between-group comparison, and its own authors stated the sample precludes conclusions.

The one finding that replicated is subjective sleep. Two trials, 8 milligrams for 16 weeks and 20 milligrams for 4 weeks, reported improved self-reported sleep. Neither measured sleep objectively.

The observational numbers worth knowing. In 2,203 middle-aged and older Chinese adults, each additional 10 grams of mushroom per day was associated with 12 percent lower odds of mild cognitive impairment, cross-sectionally. In the Alzheimer’s Disease Neuroimaging Initiative cohort, lower blood ergothioneine in people with mild cognitive impairment was associated with a 12 percent higher rate of progression to Alzheimer’s over two years. Both are associations.

A dose gap nobody flags. Human trials used 5 to 30 milligrams daily. Rodent efficacy studies mostly used 8 to 100 milligrams per kilogram, which on body surface area normalization corresponds to roughly 45 to 570 milligrams daily for a 70 kilogram adult. The doses that worked in mice are two to twenty times what has been tested in people.

Dietary intake for reference: about 1.1 milligrams daily in the United States, 1.3 to 4.6 across four European countries.

Context and Source

  • Open Access Paper: Ergothioneine: A Natural Antioxidant Claimed to Prevent Neurodegeneration., Published: 8 November 2026.
  • Institution: Laboratory of Analytical Biochemistry, Institute of Food Technology and Nutrition, Faculty of Technology and Life Sciences, University of Rzeszow, Poland. Single institution, two authors.
  • Country: Poland.
  • Journal: Nutrients, volume 18, article 3708, 2026. Published by MDPI.
  • Impact evaluation: The impact score of this journal is 5.8, evaluated against a typical high-end range of 0 to 60+ for top general science, therefore this is a Medium impact journal.

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VanadylSulfateSenolytic-2
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Researchers have identified that vanadyl sulfate, an inexpensive dietary supplement, functions as a potent senolytic agent capable of selectively destroying senescent cells while preserving healthy tissue. During aging, senescent cells develop a unique redox environment characterized by diminished glutathione reductase activity and an accumulation of oxidized glutathione. To survive and continually release inflammatory factors, these cells rely heavily on endoplasmic reticulum protein-folding machinery. Administering vanadyl sulfate selectively oxidizes reactive cysteines within these folding enzymes, inducing catastrophic protein aggregation and triggering autophagic cell death specifically in senescent cells. In aged male mice, a ninety-day oral regimen improved muscle endurance, lowered visceral fat, reversed hepatic and renal decline, and extended median post-treatment lifespan by nearly seventeen percent. These therapeutic improvements persisted even after treatment withdrawal, suggesting that periodic dosing protocols could offer substantial longevity and metabolic advantages.

A team of investigators at the University of Chicago has uncovered an unexpected biological vulnerability that could transform how we eliminate senescent cells. As cells age, they often enter senescence, a state of irreversible growth arrest where they refuse to die, instead churning out inflammatory proteins that degrade neighboring tissues and drive systemic decline. Researchers screening a library of circulating blood nutrients discovered that vanadyl sulfate, an over-the-counter mineral supplement commonly used for blood sugar control, selectively triggers the death of senescent human cells while leaving healthy counterparts unharmed.

The discovery hinges on a peculiar metabolic defect found within senescent cells. Healthy cells maintain an optimal balance of reduced glutathione to buffer against oxidative stress. Senescent cells, however, experience an accumulation of oxidized glutathione disulfide because of the downregulation of the recycling enzyme glutathione reductase.Simultaneously, these damaged cells dramatically upregulate their endoplasmic reticulum protein-folding machinery,particularly protein disulfide isomerases and endoplasmic oxidoreductin 1 alpha. This enhanced protein-folding infrastructure is necessary for senescent cells to manufacture and secrete high volumes of toxic inflammatory cytokines without succumbing to internal stress.

This protective infrastructure doubles as an Achilles heel. When vanadyl sulfate enters a senescent cell, its oxidized vanadyl ions interact with the abnormal redox environment. The compound attacks reactive cysteine residues on the overworked endoplasmic reticulum folding enzymes, forcing inappropriate disulfide bonds to form. This reaction causes widespread protein misfolding and massive protein clumping within the cell. While senescent cells attempt to rescue themselves by ramping up autophagy and lysosomal clearance, the volume of aggregated protein rapidly overwhelms their digestive capacity, ultimately killing the cell. Healthy cells, which retain normal antioxidant defenses and balanced protein synthesis, tolerate the compound without distress.

To evaluate practical outcomes, researchers administered vanadyl sulfate in the drinking water of aged male mice for three months, starting at approximately seventeen months of age, which corresponds to late middle age in humans. The intervention produced striking physical and systemic benefits. Treated animals doubled their hanging grip endurance, lost significant visceral fat mass, and exhibited sharp reductions in markers of liver and kidney damage. Blood glucose regulation and insulin responsiveness were restored to levels approaching those of young animals. Most importantly, the treatment extended median survival from 886.5 days in control animals to 952 days in the treated group.

Remarkably, these functional improvements persisted weeks after the supplement was removed from the water, and blood vanadium levels returned to baseline. This durability demonstrates a hit-and-run senolytic mechanism: once the toxic senescent cells are eradicated, tissues remain rejuvenated until new senescent cells accumulate over time. The findings indicate that pulse-dosing this accessible trace mineral may provide a viable therapeutic pathway for mitigating age-related decline.

Actionable Insights

Vanadyl sulfate demonstrates genuine senolytic activity in preclinical models, offering a potential nutritional tool for targeting cellular senescence. In the study, aged mice given vanadyl sulfate for three months experienced an absolute median lifespan gain of 65.5 days, which represents an extension of their remaining lifespan after treatment by 16.9 percent. In physical performance, treated animals demonstrated a 100 percent improvement in muscle hanging endurance relative to untreated controls. Metabolic biomarkers displayed similarly dramatic shifts: serum urea dropped by approximately 66 percent, serum liver damage markers fell by 47 percent, and brown adipose tissue lipid congestion was reduced by roughly 45 percent.

Caution: Vanadium exhibits a narrow therapeutic window. Chronic excessive exposure to oxidized vanadium compounds can cause severe pulmonary and renal toxicity. In the mouse trial, the effective drinking water concentration equated to roughly 51 milligrams per kilogram of body weight in mice, which translates to a human equivalent dose of approximately 4.1 milligrams per kilogram, or roughly 290 to 330 milligrams daily for an average adult. Over-the-counter supplements typically supply 10 to 30 milligrams. The research strongly suggests that if vanadyl sulfate is deployed clinically, it should follow an intermittent, pulse-dosing protocol, such as two to four weeks on followed by several months off, rather than continuous daily consumption.

Context and Source

  • Open Access Paper: Altered protein cysteine reactivity in senescent cells is a vulnerability for senolysis to ameliorate aging, Nov. 6, 2026.
  • Institutions: Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, Illinois,USA; UT Southwestern Medical Center, Dallas, Texas, USA; City of Hope, Duarte, California, USA; University of Utah, Salt Lake City, Utah, USA; Buck Institute for Research on Aging, Novato, California, USA
  • Country: United States of America
  • Journal: Nature Aging
  • Journal Impact Factor: The impact score of this journal is 16.6, evaluated against a typical high-end range of 0 to 60+ for top general science, therefore this is a High impact journal.

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