Strokes are rising in younger adults, and the cause is still unclear

Between 1993 and 2020, first strokes among adults aged 20 to 54 in the Cincinnati area rose from 33.9 to 62.2 per 100,000 person-years. A person-year is one person followed for one year, so this is roughly a yearly rate per 100,000 people. Over the same decades, the rate in older adults fell, from 618.8 to 453.0.

Older adults still have far more strokes. But the two trends are moving in opposite directions.

Most of the increase came from ischemic strokes, the kind caused by a blocked blood vessel, which climbed from 23.8 to 47.3 per 100,000. Younger patients were also less likely to die within a month of their stroke: 9.4% in 2020, down from 11.7%.

The researchers looked at who these patients were. High blood pressure, diabetes and atrial fibrillation (an irregular heart rhythm) all became more common among young stroke patients. Substance use jumped from 4.6% of patients to 40.2%, mostly linked to marijuana.

That last figure is easy to over-read. The study counted risk factors only in people who had a stroke, with no comparison group of people who didn't, so it can't tell which change drove the rise. The data also come from a single five-county region that may not match national trends. Which of these shifts is doing the damage remains an open question.

If ultra-processed food raises colorectal cancer risk, a study of 461,682 people followed for a median of 18.8 years should be a good place to see it. Overall, it didn't show up. Among US adults aged 50 to 71 in the NIH-AARP study, the fifth who ate the most ultra-processed food had about the same rate of colorectal cancer as the fifth who ate the least, across 10,075 cases.

The label covers a lot of ground, from breakfast cereal to hot dogs. When the researchers split it apart, the pieces went different ways. Reconstituted meat and fish products were linked to about 10% higher risk. Breakfast cereals were linked to 16% lower risk, and bread to 9% lower. Fiber and calcium that came from ultra-processed sources also tracked with lower risk: 28% lower for every extra 10 grams of fiber a day and 23% lower for every 300 milligrams of calcium.

Overall diet quality mattered too. Compared with people who ate well and ate little ultra-processed food, people with poor diets had 22% higher risk in the top ultra-processed group and 28% higher risk in the second-lowest group. Poor diet quality carried extra risk even when processed intake was low.

There are real gaps. Diet was self-reported once, in 1995 and 1996, by mostly white, older Americans, and today's food supply is different. Labeling whole foods as ultra-processed can misclassify products, and additives couldn't be studied. With so many secondary comparisons, some of these splits could be chance. The results point toward what is in the food rather than how it was made, but an observational study like this can raise that idea without settling it.

There was no new drug and no wearable sensor. The eSTEPS trial tested a prompt in the electronic health record that sat on the doctor's screen without interrupting the visit. It made it easier to order strength and balance exercises tailored to the patient, refer them to physical therapy and hand over patient materials.

The analysis included 22 primary care practices in the Mass General Brigham system, assigned in matched pairs, and 11,945 adults aged 65 and older who had screened positive for fall risk. Follow-up ran 12 to 23 months. After statistical adjustment, the rate of patients with at least one recorded fall was 19.3 per 100 patient-years in practices with the prompt, compared with 21.2 in the other practices: about 9% lower. Fall injuries were also slightly lower, and death rates didn't differ.

The odd part is how few people the prompt reached. Only 22.1% of patients in the prompt practices were given an exercise prescription, and nobody knows how many did the exercises.

The counting is imperfect too. Falls were tallied from diagnosis codes, which miss many falls. The prompt practices differed from the others at the start, and before statistical adjustment only self-reported falls showed a significant drop. Everything happened in one health system using one record platform. The open question is what a change this small could do if far more than one in five patients actually got the prescription.

What is an ovary doing 25 years after menopause? The usual assumption is not much. Once eggs and hormone cycles are gone, the tissue is often treated as retired.

Researchers at Northwestern University and the Buck Institute looked more closely. They measured 5,812 groups of proteins in normal ovarian tissue from 28 postmenopausal women aged 50 to 75. Proteins do most of the work in tissue, so their mix is a rough readout of what the tissue is busy with.

The mix shifted with age. Ovaries from women in their 50s had more structural proteins, the scaffolding that holds tissue together. Ovaries from women 70 and older had more proteins tied to inflammation, immune activity and tissue breakdown. Some features resembled cellular senescence, a state in which aging cells stop dividing.

Some proteins previously linked to ovarian cancer were also more plentiful in the older ovaries, even though all of the tissue looked normal and cancer-free. The study doesn't show that aging ovaries cause cancer, and it says nothing about whether healthy ovaries should be removed during other surgery.

Twenty-eight samples is a small number, and each came from a different woman at a different age, so these are snapshots rather than one ovary followed through time. The study also can't tell whether this late remodeling helps the body or harms it.

Brown fat is the body's heater. Instead of storing energy, it burns energy to make heat. For a long time, adults were thought to have very little of it, and checking who does usually takes a dedicated scan. A team writing in Nature found another way: scans that already existed in a hospital archive.

Memorial Sloan Kettering Cancer Center uses PET-CT scans to look for tumors. The PET part relies on a tracer that shows where tissue is taking up sugar, and active brown fat takes it up too. The researchers assembled scan records from 101,243 patients. About 8.8% of them, or 8,897 people, had detectable brown fat; an AI-assisted method measured its activity in 8,709 of those patients.

Then they compared those scans with patients' medical records. After accounting for age, sex, body mass index, the outdoor temperature on the scan day and other factors, people with brown fat had less than half the odds of type 2 diabetes (an odds ratio of 0.42). Their odds of chronic ischemic heart disease, where narrowed arteries starve the heart of blood, were about half (0.53). The pattern extended to mental health: lower odds of depressive episodes (0.68) and anxiety disorders (0.78). Of 511 diagnoses tested, 98 stayed significant after adjustment, and 92 of those were less common in people with brown fat.

One unexpected lead came from the medication lists. People taking losartan, a common blood pressure drug, were more likely to have detectable brown fat. In cultured cells and in mice, losartan increased brown fat's heat-making activity. That is a reason to test the drug, not evidence that it does anything for brown fat in people. The mouse work used only males, and no human trial has been done.

The design has blind spots. Every patient came from one cancer center, and cancer or its treatment could shape both brown fat and other diagnoses. The scans weren't done after cold exposure, which normally wakes brown fat up, so many people with it were probably missed. The tracer tracks sugar uptake, which may not match how much heat the tissue can make. An outside researcher quoted in Nature's coverage said more work is needed to know whether brown fat causes any of these benefits. Healthier bodies might simply be more likely to keep active brown fat, and these scans can't tell the two possibilities apart.