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All the Carcinogens We Cannot See - The New Yorker   

In the nineteen-seventies, Bruce Ames, a biochemist at Berkeley, devised a way to test whether a chemical might cause cancer. Various tenets of cancer biology were already well established. Cancer resulted from genetic mutations—changes in a cell’s DNA sequence that typically cause the cell to divide uncontrollably. These mutations could be inherited, induced by viruses, or generated by random copying errors in dividing cells. They could also be produced by physical or chemical agents: radiation, ultraviolet light, benzene. One day, Ames had found himself reading the list of ingredients on a package of potato chips, and wondering how safe the chemicals used as preservatives really were.

But how to catch a carcinogen? You could expose a rodent to a suspect chemical and see if it developed cancer; toxicologists had done so for generations. But that approach was too slow and costly to deploy on a wide enough scale. Ames—a limber fellow who was partial to wide-lapel tweed jackets and unorthodox neckties—had an idea. If an agent caused DNA mutations in human cells, he reasoned, it was likely to cause mutations in bacterial cells. And Ames had a way of measuring the mutation rate in bacteria, using fast-growing, easy-to-culture strains of salmonella, which he had been studying for a couple of decades. With a few colleagues, he established the assay and published a paper outlining the method with a bold title: “Carcinogens Are Mutagens.” The so-called Ames test for mutagens remains the standard lab technique for screening substances that may cause cancer.

Scientists, including Ames, realized from the start that the test wasn’t a comprehensive method for catching carcinogens. Epidemiologists were learning, for instance, that exposure to certain estrogen-like chemicals, such as diethylstilbestrol (DES), increases the risk of vaginal, cervical, and breast cancer. (Toxicologists found similar results in mice and rats.) Yet DES wasn’t obviously mutagenic in cell cultures; its cancer-causing mechanism is still being explored, but probably involves driving the growth of hormone-responsive cells or changing the expression of cancer-linked genes. In time, additional classes of carcinogens were added to the list. One feature of cancer cells is that they avoid detection by the immune system. And so compounds that suppress the immune system, such as cyclosporine, were recognized as cancer-promoting chemicals, even though they don’t cause mutations in DNA.

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Biomilq and the New Science of Artificial Breast Milk - The New Yorker   

Not long ago, I suited up in a white coat and safety goggles and entered a quiet laboratory where an experiment at the frontiers of science and parenthood was under way. A young engineer with a tidy beard escorted me past rows of benches to a large freezer. He opened it to reveal an array of ice-caked steel drawers and, wearing blue Cryo-Gloves (reverse oven mitts, essentially), removed a small bottle from the chill, which measured minus eighty degrees Celsius. At the bottom of the bottle, two hundred and fifty millilitres of liquid had formed a shallow, colorless puck.

I was visiting Biomilq, a startup, founded by Leila Strickland and Michelle Egger, that is working to produce lab-grown breast milk. Biomilq’s headquarters are in North Carolina’s Research Triangle Park, a seven-thousand-acre wedge of pine forests and office complexes between Durham, Chapel Hill, and Raleigh. The bottle creaked as it began to adjust to the room’s warmth, and the engineer hastened to put it back in the freezer.

You could call the bottle’s contents Biomilq, or maybe just milk, or, as the engineer did—indicating a number of smaller bottles also stowed in the freezer—“our best shots to date.” The frozen puck represented a week and a half’s worth of output from a single line of lab-cultured human mammary cells. The company hopes to use these cells and others like them to re-create as closely as possible the process of making human milk. About three years before my visit, in February of 2020, Biomilq announced that it had successfully used cells to produce lactose and casein, a sugar and a protein found in breast milk. “Our opinion as a company—and most of us internally, too—is that breast-feeding, at the breast, has benefits that no one will ever be able to mimic,” Egger, a food scientist turned entrepreneur, told me. “If you can breast-feed—do it. Great. But the reality is, a majority of parents cannot exclusively breast-feed. . . . And that’s not for lack of trying.”

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Why Are We So Bad at Getting Better? - The New Yorker   

Four and a half years ago, in the heat of an N.B.A. playoff game against the Houston Rockets, Kevin Durant, the superstar forward of the Golden State Warriors, dodged a defender, dribbled once, and sank a two-point jump shot. When he turned to run upcourt, however, he bounced off his right foot and felt something tear. He managed to hop to mid-court, clutching his leg, but then doubled over in pain. After Durant limped out of the game, an MRI showed that he had ripped the muscle fibres in his calf; a prior injury, along with a sharp increase in playing time, probably placed him at increased risk. For the next few weeks, as the Warriors advanced to the N.B.A. Finals, Durant tried to recover. But when his teammates found themselves down three games to one, facing elimination, some of them reportedly complained about his absence.

Durant decided to return for Game Five against the Toronto Raptors. Fifteen minutes into the game, he dribbled across half-court, crossed over between his legs, and stopped abruptly, letting the ball roll away. This time, he limped to the sideline, fell to the ground, and grabbed his right leg with a resigned look on his face. He left the arena in a gray walking boot, crutches under both armpits, with a ruptured Achilles tendon.

The Warriors ultimately lost the series, and Durant lost a full season of play in the prime of his career. In the years that followed, he counselled other players not to rush their recoveries. “I wish I had made a different decision,” he has said.

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The Case That Being Poor and Black Is Bad for Your Health - The New Yorker   

It was the nineteen-eighties, the height of a certain panic. Reaganism reigned, but even Democrats agreed upon scapegoating America’s Blacks as the source of the country’s ills. The Black family, that old chestnut, was as topical as ever, and of special prurient interest was the so-called blight of teen pregnancy. “Babies having babies,” as community leaders and politicians of various stripes put it, became emblematic of dreams deferred, a testament to the failings of a cultural, social, and political order. It was taken for gospel that, for mothers and their babies alike, teen pregnancy spelled doom: for mothers, low grades in school; for their babies, low birth weights; for both, no future but cyclical poverty. Everybody knew it.

Arline T. Geronimus, a young public-health researcher, had doubts. As an undergraduate working in Princeton’s Office of Population Research, in the late seventies, she’d watched the grim-faced poster child of teen motherhood morph from white to Black, and the media in turn cotton to the notion that young, undereducated Black moms were to blame for poverty and for bad health in the ghetto. But at the women’s clinic situated in the nearby, very Black city of Trenton, New Jersey, Geronimus met young women who were well versed in contraceptive methods and ecstatic about their pregnancies, who had the support of family networks—in short, who looked nothing like the Black teen mother as she existed in the public imagination.

This theory made Geronimus unpopular among those concerned with the supposed plight of Black teen mothers. A representative from the Children’s Defense Fund called her work “perverse.” Rosann Wisman, at the time the executive director of Planned Parenthood of Metropolitan Washington, D.C., wrote in the Washington Post that Geronimus was “incredibly presumptuous . . . to assume that it is desirable and or affordable for the ‘extended family network’ to provide for the teen mother and her child.” People complained to the University of Michigan and sent death threats; colleagues dissuaded students from taking Geronimus’s courses. Her work was called racist. But, in the decades since, the idea of weathering has caught on within a range of academic fields, including public health and literary studies, to help explain health disparities that can not be convincingly attributed to matters of life style or genetics. The American ethos of personal responsibility still guides our medical system, as illustrated by the national response to the pandemic, in which community health initiatives were soon jettisoned in favor of individualist choice. (Per the M.T.A.’s mask policy, revised this past fall: “You do you.”) At the same time, these past few years have forced a new awareness of the structural and systemic forces shaping American life. In 2021, Anthony Fauci refuted the view that the health conditions associated with severe cases of COVID-19 (such as hypertension and diabetes, which African Americans are more likely to develop) were racially determined, emphasizing instead the “disadvantageous conditions that some people of color find themselves in from birth regarding the availability of an adequate diet, access to health care, and the undeniable effects of racism in our society.” What he was describing sounds a lot like weathering.

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