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  • Everything I Thought I Knew About Nasal Congestion Is Wrong

    Everything I Thought I Knew About Nasal Congestion Is Wrong

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    Having caught a cold every month since my kid started day care, I’ve devoted a lot of time recently to the indignity of unclogging my nose. I’m blowing, always. I have also struck up an intimate acquaintance with neti pots and a great variety of decongestants. (Ask for the stuff that actually works, squirreled away behind the counter.) And on sleepless nights, I’ve spent hours turning side to side, trying to clear one nostril and then the other.

    Nasal congestion, I’ve learned in all this, is far weirder than I ever thought. For starters, the nose is actually two noses, which work in an alternating cycle that is somehow connected to our armpits.

    The argument that humans have two noses was first put to me by Ronald Eccles, a nose expert who ran the Common Cold Centre at Cardiff University, in Wales, until his retirement a few years ago. This sounds absurd, I know, but consider what your nose—or noses—looks like on the inside: Each nostril opens into its own nasal cavity, which does not connect with the other directly. They are two separate organs, as separate as your two eyes or your two ears.

    And far from being a passive tube, the nose’s hidden inner anatomy is constantly changing. It’s lined with venous erectile tissue that has a ”similar structure to the erectile tissue in the penis,” Eccles said, and can become engorged with blood. Infection or allergies amplify the swelling, so much so that the nasal passages become completely blocked. This swelling, not mucus, is the primary cause of a stuffy nose, which is why expelling snot never quite fixes congestion entirely. “You can blow your nose until the cows come home and you’re not blowing that swollen tissue out,” says Timothy Smith, an otolaryngologist at the Oregon Health & Science University’s Sinus Center. Gently blowing your nose works fine for any mucus that may be adding to the stuffiness, he told me. But decongestants such as Sudafed and Afrin work by causing blood vessels in the nose to shrink, opening the nasal passages for temporary relief.

    In healthy noses, the swelling and unswelling of nasal tissue usually follows a predictable pattern called the nasal cycle. Every few hours, one side of the nose becomes partially congested while the other opens. Then they switch, going back and forth, back and forth. The exact pattern and duration vary from person to person, but we rarely notice these changes inside our noses. “When I tell people about the nasal cycle, most people are not aware of it at all,” says Guilherme Garcia, a biomedical engineer at the Medical College of Wisconsin. I certainly wasn’t, and I have been breathing through my nose only my entire life. But the idea made sense as soon as I consciously thought about it: When I’m sick, and extra swelling has turned partial congestion into complete congestion, I do tend to feel more blocked on one side than the other.

    Once you’re aware of the nasal cycle, you can control it—to some extent. In fact, when I was turning from side to side during my sleepless nights, I was unknowingly activating receptors under my arm, which open the opposite side of the nose. This could be an age-old survival reflex: When we lie down on our right side, our left nostril is farther from the ground and likely less obstructed. Yogis have learned to take advantage of this, using a small crutch under the arm, called a yoga danda, to direct breathing to one nostril or the other. And an online hack for stuffy noses suggests squeezing a bottle under the opposite arm. The effect is not instantaneous, though. When I tried this recently, my arm got tired before my nose unclogged. And when I tried again with an old crutch I had from a knee injury, it took several minutes, by which time I’d already reached for a tissue out of impatience and habit.

    No one knows exactly why humans have a nasal cycle, but cats, pigs, rabbits, dogs, and rats all have one too, according to Eccles. One hypothesis proposes that this cycle helps guard against pathogens. When the venous erectile tissue shrinks, antibody-rich plasma is squeezed out onto the inner lining of the nose. Each cycle might replenish the nose’s defense. Eccles also pointed out that upper-respiratory viruses seem to prefer temperatures just below body temperature; when one side of the nose becomes partially congested, it might warm up enough to ward off viruses. Or, he said, the cycle allows one half of the nose to rest at time. Unlike our eyes, ears, and mouths, noses have to function 24 hours a day, every day, constantly filtering and warming air for the delicate tissue of our lungs. The nose’s job might not sound that hard, but consider what it has to do: The air we breathe is maybe 70 degrees Fahrenheit and 35 percent humidity, Smith said. “By the time that air goes in my nose and gets back to my nasopharynx—which is, what, maybe three to four inches—it is 98.7 degrees Fahrenheit and 100 percent humidity.” The nose is quite the powerful little HVAC system.

    But it’s fallible, too. Our noses don’t measure airflow directly; instead, they rely on cold receptors that are activated when cool air passes by. These cold receptors can be tricked by, say, menthol. Eccles has found that people given menthol lozenges can hold their breath longer, possibly because the minty coolness fools them into thinking they are still getting air. And it’s why Vicks VapoRub might make congestion feel better, despite having no positive effect on the opening of the nasal passages. The opposite may happen in a baffling condition called empty-nose syndrome, in which a very small proportion of patients who have surgery to improve airflow in their noses end up feeling completely clogged—possibly because of damage to cold receptors and other changes in sensation. The lack of a feeling of airflow can be so disturbing that these patients feel like they’re suffocating, even though their noses are perfectly unobstructed.

    To a lesser extent, we are all unreliable narrators of our nasal congestion. When patients go to be examined, a doctor might see that one side of their nose is clearly more swollen than the other—but it’s not necessarily the same side that the patient feels is more congested. “This still baffles clinicians,” Smith told me. Other factors, such as temperature, must play a role. The inner workings of the nose are complicated and still mysterious. I’ll be thinking about all of this the next time I’m lying awake at night, once again sick, once again congested.

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    Sarah Zhang

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  • We Have No Drugs to Treat the Deadliest Eating Disorder

    We Have No Drugs to Treat the Deadliest Eating Disorder

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    In the 1970s, they tried lithium. Then it was zinc and THC. Anti-anxiety drugs had their turn. So did Prozac and SSRIs and atypical antidepressants. Nothing worked. Patients with anorexia were still unable to bring themselves to eat, still stuck in rigid thought patterns, still chillingly underweight.

    A few years ago, a group led by Evelyn Attia, the director of the Center for Eating Disorders at New York Presbyterian Hospital and the New York State Psychiatric Institute, tried giving patients an antipsychotic drug called olanzapine, normally used to treat schizophrenia and bipolar disorder, and known to cause weight gain as a side effect. Those patients in her study who were on olanzapine increased their BMI a bit more than others who were taking a placebo, but the two groups showed no difference in their cognitive and psychological symptoms. This was the only medication trial for treating anorexia that has shown any positive effect at all, Attia told me, and even then, the effects were “very modest.”

    Despite nearly half a century of attempts, no pill or shot has been identified to effectively treat anorexia nervosa. Anorexia is well known to be the deadliest eating disorder; the only psychiatric diagnosis with a higher death rate is opioid-use disorder. A 2020 review found people who have been hospitalized for the disease are more than five times likelier to die than their peers without it. The National Institutes of Health has devoted more than $100 million over the past decade to studying anorexia, yet researchers have not found a single compound that reliably helps people with the disorder.

    Other eating disorders aren’t nearly so resistant to treatment. The FDA has approved fluoxetine (a.k.a. Prozac) to treat bulimia nervosa and binge-eating disorder (BED); doctors prescribe additional SSRIs off-label to treat both conditions, with a fair rate of success. An ADHD drug, Vyvanse, was approved for BED within two years of the disorder’s official recognition. But when it comes to anorexia, “we’ve tried, I don’t know, eight or 10 fundamentally different kinds of approaches without much in the way of success,” says Scott Crow, an adjunct psychology professor at the University of Minnesota and the vice president of psychiatry for Accanto Health.

    The discrepancy is puzzling to anorexia specialists and researchers. “We don’t fully understand why medications work so differently in this group, and boy, do they ever work differently,” Attia told me. Still, experts have some ideas. Over the past few decades, they have been learning about the changes in brain activity that accompany anorexia. For example, Walter Kaye, the founder and executive director of the Eating Disorders Program at UC San Diego, told me that the neurotransmitters serotonin and dopamine, both of which are involved in the brain’s reward system, seem to act differently in anorexia patients.

    Perhaps some underlying differences in brain chemistry and function play a role in anorexia patients’ extreme aversion to eating. Or perhaps, the experts I spoke with suggested, these brain changes are at least in part a result of patients’ malnourishment. People with anorexia suffer from many effects of malnutrition: Their bones are more brittle; their brain is smaller; their heart beats slower; their breath comes shorter; their wounds fail to heal. Maybe their neurons respond differently to psychoactive drugs too.

    Psychiatrists have found that many patients with anorexia don’t improve with treatment even when medicines are prescribed for conditions other than their eating disorder. If an anorexia patient also has anxiety, for example, taking an anti-anxiety drug would likely fail to relieve either set of symptoms, Attia told me. “Time and again, investigators have found very little or no difference between active medication and placebo in randomized controlled trials,” she said. The fact that fluoxetine seems to help anorexia patients avoid relapse—but only when it’s given after they’ve regained a healthy weight—also supports the notion that malnourished brains don’t respond so well to psychoactive medication. (In that case, the effect might be especially acute for people with anorexia nervosa, because they tend to have lower BMIs than people with other eating disorders.)

    Why exactly this would be true remains a mystery. Attia noted that proteins and certain fats have been shown to be crucial for brain function; get too little of either, and the brain might not metabolize drugs in expected ways. Both she and Kaye suggested a possible role for tryptophan, an amino acid that humans get only from food. Tryptophan is converted into serotonin (among other things) when we release insulin after a meal, Kaye said, but in anorexia patients, whose insulin levels tend to be low, that process could end up off-kilter. “We suspect that that might be the reason why [SSRIs] don’t work very well,” he said, though he emphasized that the theory is very speculative.

    In the absence of meaningful pharmacologic intervention, doctors who treat anorexia rely on methods such as nutrition counseling and psychotherapy. But even non-pharmaceutical interventions, such as cognitive behavioral therapy, are more effective at treating bulimia and binge-eating disorder than anorexia. Studies from around the world have shown that as many as half of people with anorexia relapse.

    Colleen Clarkin Schreyer, a clinical psychologist at Johns Hopkins University, sees both patients with anorexia nervosa and those with bulimia nervosa, and told me that the former can be more difficult to treat—“but not just because of the fact that we don’t have any medication to help us along. I often find that patients with anorexia nervosa are more ambivalent about making behavior change.” Bulimia patients, she said, tend to feel shame about their condition, because binge eating is stigmatized and, well, no one likes vomit. But anorexia patients might be praised for skipping meals or rapidly losing weight, despite the fact that their behaviors can be just as dangerous over the long term as binging and vomiting.

    Researchers are still trying to find substances that can help anorexia patients. Crow told me that case studies testing a synthetic version of leptin, a naturally occurring human hormone, have produced interesting data. Meanwhile, some early research into using psychedelics, including ketamine, psilocybin, and ayahuasca, suggests that they may relieve some symptoms in some cases. But until randomized, controlled trials are conducted, we won’t know whether or how well any psychedelic really works. Kaye is currently recruiting participants for such a study of psilocybin, which is planned to have multiple sites in the U.S. and Europe.

    Pharmaceutical companies just don’t seem that enthusiastic about testing treatments for anorexia, Crow said. “I think that drug makers have taken to heart the message that the mortality is high” among anorexia patients, he told me, and thus avoid the risk of having deaths occur during their clinical trials. And drug development isn’t the only area where the study of anorexia has fallen short. Research on eating disorders tends to be underfunded on the whole, Crow said. That stems, in part, from “a widely prevailing belief that this is something that people could or should just stop … I wish that were how it works, frankly. But it’s not.”

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    Rachel Gutman-Wei

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