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How an HIV/AIDS tragedy spurred human evolution

Researchers show that a type of AI known as a large language model often outperformed physicians at diagnosing complex and potentially life-threatening conditions, including decreased blood flow to the heart, even in the fast-moving stages of real ER care when information is limited.

In early ER cases, the model identified the correct or a very close diagnosis in about 67% of cases, compared with roughly 50% to 55% for physicians. And the technology is only getting better.


Before antiretroviral (ARV) drugs started to become widely available in KwaZulu-Natal in 2005, there was “kind of the perfect storm,” with several unusual factors coalescing to drive a devastating epidemic, says Philip Goulder, an immunologist at the University of Oxford who led the study, which appears today in the Proceedings of the National Academy of Sciences. HIV had made few inroads into South Africa until the early 1990s, when an epidemic exploded in the heterosexual population, infecting about 40% of pregnant women in KwaZulu-Natal. (That astonishingly high prevalence persists today.) Because of a mix of genetics, limited health care, and possibly the viral subtype in circulation, infected people developed AIDS—when the destruction of the immune system threatens survival—exceptionally quickly, within about 4.5 years versus 10 years in North America.

Other studies have shown how infectious diseases, including malaria and tuberculosis, have altered the human genome. But those changes took thousands of years. “That’s what is quite exciting about this: You can see how rapidly evolution actually can occur,” Goulder says.

Similar evolutionary forces may have been at work in North America and Europe, but they are more difficult to see—and less likely to affect future generations. HIV prevalence in those regions is below 1%, and the hardest-hit group is men who have sex with men. “They are generally not a population that’s leaving behind as many offspring,” Worobey notes.

Neutrophils manufacture schizophrenia-linked protein, according to new research

The most common white blood cells in your body—immune cells called neutrophils—can make a protein nobody knew they were making, Stanford Medicine investigators have discovered. That unexpected sighting joins a growing list of hints tying schizophrenia, a disorder of the brain, to events occurring elsewhere in our bodies. The findings are summarized in a paper published in Proceedings of the National Academy of Science.

The newly noticed neutrophil nexus, as a source of the protein called C4A, links a long list of other observations that are somewhat puzzling when looked at in isolation: For example, large-scale population-genetic studies have identified C4A, already known to be produced mainly in the liver, as a pronounced risk factor in schizophrenia. People with schizophrenia tend to have increased numbers of neutrophils in their blood. And the most effective medication for schizophrenia inhibits neutrophils.

Schizophrenia affects one in every 100 persons globally almost without variation by geography or ethnicity. Its most noticeable symptoms are hallucinations, delusions and fixations. A fundamental feature of the disease is cognitive impairment: inability to think clearly, reduced working memory, disorganized thinking and behavior.

A DNA-organizing protein offers new insight into infertility, IVF and generational health

The causes of male infertility can be hard to diagnose, with many tests failing to detect genetic defects. Sometimes, infertility doesn’t even involve the genes themselves. It can arise from improper folding of the father’s DNA in the sperm. If a couple conceives, this mispackaged DNA can damage the lifelong health of the child.

“Paternal health is critical to sperm quality and the health of the offspring,” said Satoshi Namekawa, a professor of microbiology and molecular genetics. “Understanding the packing and folding of DNA in sperm cells is a fundamental question in modern biology.”

Namekawa and Ph.D. student Yu-Han Yeh have now unveiled an important new piece of this puzzle. They have identified a protein, called DAXX, that guides how sperm DNA is organized. DAXX silences thousands of genes so they don’t interfere with reproduction. It also keeps a handful of crucial genes turned on—shaping the delicate, early stages of embryonic development. The work was published recently in Genes & Development.

Dietary fats shape pancreatic cancer risk via ferroptosis

For decades, the relationship between fat and cancer has been treated as a question of quantity: Eat less fat, reduce your risk of developing cancer. But new research published April 29 in Cancer Discovery shows that for pancreatic cancer, the type of fat you consume matters more than the amount.

“It’s really the type of fat that you’re consuming, not just total fat content,” says Christian Felipe Ruiz, Ph.D., an associate research scientist in YSM’s Department of Genetics and lead author of the study. “Depending on the type of fat that you consume, it can go completely different ways. We found that some fats promote cancer, as we would expect, while other fats are really good at suppressing cancer.”

One fat in particular—oleic acid, the primary fatty acid in olive oil—may be accelerating tumor growth in ways scientists never anticipated. The result was surprising given oleic acid’s reputation in medicine. “It’s traditionally been considered a healthy type of fat for cardiovascular health,” Ruiz says.

Small Study Shows One-time Cell Therapy Can Control HIV Infection

Unlike previous HIV “cures” involving cancer patients given bone marrow stem cells from a donor with a rare genetic mutation that resists HIV infection, researchers said CAR-T could be used by a much broader patient population. The Phase 1 trial involved CAR-T, a one-time therapy in which a patient’s T-cells are extracted, altered and multiplied in a lab and infused back into ⁠their body. In this case, the CAR-T targeted the CD4 and CCR5 binding sites of the HIV.

Of three trial patients ‌treated with a standard CAR-T dose, researchers said two maintained undetectable to ‌very low levels of HIV after stopping antiretroviral therapy — one for over two years so far and another for nearly a year. “The two that have ‌been off (HIV drugs) the longest and doing well were importantly diagnosed pretty quickly and put on therapy pretty quickly,” said Dr. Steven Deeks, professor of medicine at the University of California, San Francisco and the study’s lead investigator.

Currently, CAR-T ‌treatments are available for several types of blood cancer, and are being developed for autoimmune diseases like lupus and scleroderma. Tap the link to learn more about the recent study.


Re-engineering an HIV patient’s own immune cells to find and destroy the virus succeeded in controlling the infection in a small first-in-human study, but researchers said work is needed to confirm ⁠the findings and determine which patients are most likely to benefit.

Why Some People Have Endless Energy (And Others Never Will)

From the article:

To put this in quantitative terms: consider an individual at the 5th percentile of genetic vitality. Even with an impeccable lifestyle, such a person might only reach the 25th percentile of vitality (energy levels, mood, motivation). Now consider someone at the 95th percentile of genetic vitality. Even with a mediocre or actively harmful lifestyle, this person might still operate at the 75th percentile or above. The gap between these two individuals, after both have optimized (or neglected) every modifiable factor, is entirely genetic.

The single most effective thing one can do to guarantee great energy, mood, motivation, metabolism, cognition, physique, and longevity is to pick the right parents.

This is not to say that lifestyle, hormones, and pharmaceuticals are unimportant. They clearly matter, often enormously. Rather, the point is that these interventions operate within a window whose size, position, and ceiling are defined by inherited genetic variation.


Vitality is affected by many things which I extensively discuss on my blog. These include metabolic health, hormones, inflammation, diet, exercise, and sleep, among other things. Each of these domains is important, and each is modifiable to varying degrees through lifestyle choices, pharmaceutical interventions, or behavioral change.

However, every one of these discussions has implicitly assumed a background variable that I have largely unaddressed: genetics.

Blood Test #2 In 2026: Biological Age, CVD Risk, Correlations With Diet

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