William B. Funk, MD

05/18/2026

05/18/2026

05/18/2026

Another bluff?

President Donald Trump on Monday afternoon called off a plan to begin attacking Iran again.

Iranian leaders did not immediately confirm Trump’s apparent pending deal. Throughout the war, the president has cited imminent pacts with Iran only to have his words shot down publicly by Tehran.

📸: Alex WROBLEWSKI / AFP via Getty Images

05/18/2026

05/18/2026

About right

05/18/2026

Same for smoking and likely Vapes and inhaled pot

A 39-year longitudinal study just published in Mechanisms of Ageing and Development did something most air pollution research hasn't. It asked not just whether breathing dirty air kills people. It asked how.

The team pooled data from two large European cohorts. The UK Biobank gave them 309,467 adults aged 37 to 73. The Lifelines cohort from the Netherlands added 29,146 adults aged 18 to 93. They estimated each person's long-term residential exposure to three pollutants using land-use regression and dispersion models. Fine particles under 2.5 microns. Coarser particles under 10 microns. Nitrogen dioxide.

Then they measured biological age. Not chronological age, the number on your driver's license. Biological age, the number your body actually runs on. They used three independent composite measures built from blood biomarkers and clinical data. The Klemera-Doubal Method. PhenoAge. The frailty index. These are validated tools used widely in the longevity literature, and crucially they were measured at one point in time and tracked forward against mortality and hospitalization outcomes.

Two findings.

Higher exposure to air pollution was associated with accelerated biological aging across all three clocks. Not just slightly. Measurably and consistently across cohorts and pollutants.

The second finding is the one most coverage of air pollution misses. Mediation analysis quantified how much of the pollution-to-death and pollution-to-hospitalization relationship runs through that accelerated biological aging. In the UK Biobank, biological aging mediated between 11.5 and 25.4% of the pollution-hospitalization link and between 11.5 and 52.3% of the pollution-mortality link, depending on which pollutant and which aging clock was used. In Lifelines, fine particulate exposure was associated with frailty, and there was evidence of mediation through PhenoAge for the coarser particles.

In plain language, accelerated biological aging is a major part of how air pollution kills you. Not the only part. The remainder is the direct organ-level damage everyone already knows about, lung inflammation, plaque destabilization, oxidative stress in the cardiovascular system. But up to half of the death signal goes through a slower, system-wide process where every organ ages faster than it should.

Three things make this matter.

The mechanism is system-wide. The standard mental model for air pollution is that it damages specific organs. Lungs get COPD. Hearts get strokes. This paper says that picture is incomplete. Pollution accelerates aging on independent measures built from biomarkers across the whole body. The lungs are the entry point. The damage radiates outward through the bloodstream.

The exposure levels are not high. These were European pollution concentrations, well below the levels seen in heavily polluted cities in the United States, India, China, or Southeast Asia. The mediation effect was visible at relatively low ambient exposure. Whatever is happening biologically is not a megacity-only phenomenon.

The mediator is something you can theoretically intervene on. Direct lung damage from particulate exposure is hard to reverse. Biological aging acceleration is in principle modifiable through interventions that slow aging across organs: cardiometabolic control, sleep, physical activity, avoiding additional inflammatory exposures, possibly future senolytic or metabolic therapies. The paper does not test any intervention. It just shows that there is a pathway worth intervening on.

A few caveats this paper deserves to have spoken aloud.

This is observational data. Mediation analysis cannot prove causation, only show a pattern consistent with one. Long-term residential pollution exposure is correlated with income, neighborhood quality, occupational exposures, and healthcare access. The authors adjusted for demographic and socioeconomic factors but adjustment is not the same as randomization.

The aging clocks themselves are not perfect. KDM, PhenoAge, and the frailty index are validated against mortality, which means they will tend to mediate mortality findings by construction. They are not measuring some abstract truth called biological age. They are measuring weighted combinations of biomarkers that predict aging outcomes. That is useful but worth holding loosely.

The mediation percentages have a wide range, from about 11% to about 52%, because the answer depends on the pollutant and the clock and the outcome. The single sharp number does not exist. The right framing is that aging-mediated mortality is a substantial, not a negligible, fraction of the total.

What this changes in practice. If you live in a city with measurable air pollution, indoor air filtration sized for your living space and a HEPA filter in the bedroom are the highest-evidence personal interventions. PM2.5 enters indoor air at 70 to 100% of outdoor concentrations in homes without filtration. A properly sized HEPA unit cuts that substantially. N95 masks during peak pollution days, especially during wildfire season or commuter traffic exposure, are similarly evidence-supported. None of these are sold to you as longevity interventions, but the data here suggests they functionally are.

The bigger picture. Air pollution research has spent decades documenting which organs get damaged. This paper says the more interesting question may be how fast pollution makes you biologically older. And the answer is fast enough to account for up to half of the early deaths.

Bowe et al., Lancet Planet Health, 2018
Boogaard et al., Environ Health Perspect, 2024
Klemera & Doubal, Mech Ageing Dev, 2006
Levine et al., Aging, 2018
Mechanisms of Ageing and Development, 2026 (UK Biobank + Lifelines mediation paper)

05/18/2026

The U.S. Centers for Disease Control and Prevention confirmed May 18 that one American has tested positive for Ebola who was exposed as part of their work in the Democratic Republic of Congo.

The individual developed symptoms over the weekend and tested positive late Sunday, May 17. The CDC is working with the Department of State to move the American to Germany for treatment, along with six other high-risk contacts for monitoring.

📸: Arlette Bashizi/Reuters

05/18/2026

Useful information on how long it takes to recover from surgery or injury

Your muscle rebuilds in about three months. Your tendons and cartilage take roughly a year and a half. Your bone, up to two years. Adding 40 grams of whey daily for two weeks doesn't change any of those timelines.

That's the finding from a study published this month in the American Journal of Clinical Nutrition. The team measured rebuild rates across more than a dozen knee tissues in living older adults using a safe heavy-water tracer. Tissues sampled during routine knee replacement surgery. Half the participants kept their habitual diet. Half added 40 grams of whey daily for 14 days. At the end, the rebuild rates of every tissue were the same in both groups.

The hierarchy was dramatic.
Muscle rebuilt at about 1.2 percent per day. At that rate, your quadriceps theoretically turn over in roughly three months. Synovium, the membrane that lines the joint capsule, rebuilt at 0.8 percent per day. The fat pad behind your kneecap, about 0.5 percent. The cruciate ligaments deep in the knee, about 0.45 percent. The patellar tendon, the femoral cartilage, and the menisci all rebuilt at 0.18 to 0.21 percent per day, putting their full-pool turnover at roughly 1.3 to 1.5 years. Bone rebuilt at 0.12 to 0.21 percent per day across five sites, with the slowest taking up to 2.3 years for a complete cycle.

What this does and does not say.
It does not say protein doesn't build connective tissue. It does. Every tissue in your body depends on dietary amino acids as substrate, and the synthesis rates measured here confirm that all of these tissues are actively turning over. Bone is a living tissue that constantly remodels. Cartilage maintains itself, slowly. Tendons repair from training and from daily mechanical load, slowly.
What the study shows is that for these older adults on their normal diets, adding 40 grams of whey on top for two weeks did not accelerate the rebuild rate of any tissue measured. It is one trial. It is small and short. It cannot rule out effects in people with inadequate baseline intake, or effects that might appear with longer supplementation. What it does establish is that connective tissue synthesis rates are dramatically slower than muscle, and a two-week protein bump does not compress those rates.

That has direct implications for what protein supplementation is and isn't doing.
Protein supplementation is a tool for closing intake gaps and for hitting the per-meal threshold that maximizes muscle protein synthesis after training. It's effective at those goals. People who are not eating enough total protein, or who are not getting enough per meal to drive muscle protein synthesis in older muscle that has lost some sensitivity to amino acids, benefit from supplementation. That's well established and not in dispute.

Protein supplementation is not a connective tissue repair accelerator. Cartilage damage from running mileage, tendon overuse injuries, bone density loss in postmenopausal women, ACL rehabilitation timelines: none of these can be hurried with whey. The biology runs at its own clock speed regardless of how much you put in.

What this means in practice.
For training and recovery, the protein protocol that has actually been shown to work is unchanged. Roughly 1.6 grams per kilogram of body weight per day, spread across three or four meals, each meal hitting at least 0.4 grams per kilogram. Training stimulus and adequate sleep do the heavy lifting on muscle adaptation. Supplemental protein at the meal level helps people hit those thresholds, especially for older adults, vegetarians, and anyone with a small appetite.

For connective tissue, the levers are different. Mechanical load through progressive training is the dominant signal for tendon and ligament adaptation. Resistance training drives bone density gains. Cartilage health responds to weight management and joint loading more than to nutrition. Collagen and vitamin C combined before training has interesting data for tendon collagen synthesis, but the effect sizes are modest. None of these tissues respond meaningfully to a protein bolus in a two-week window the way muscle does after a single training session.

The bigger reframe.
We have been treating tissue protein synthesis like a single dial. The reality is that your body runs many tissue clocks at very different speeds. Muscle is the fast one. Most of what we call "tissue building" outside of muscle takes 1 to 2 years per cycle, not days. When you injure a tendon at 55, the rehab timeline is set by how fast that tendon can lay down new collagen. Mechanical load and time do the work. Adequate protein supports it but doesn't compress the timeline.

Muscle responds to protein on a short timescale. Everything else responds on a long one. The two are not interchangeable.

Houtvast et al., Am J Clin Nutr, 2026
Moore et al., J Gerontol A, 2015
Morton et al., Br J Sports Med, 2018
Bauer et al., J Am Med Dir Assoc, 2013
Shaw et al., Am J Clin Nutr, 2017

05/18/2026

A question for you this Monday morning.

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