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Welcome to Up for Debate. Each week, Conor Friedersdorf rounds up timely conversations and solicits reader responses to one thought-provoking question. Later, he publishes some thoughtful replies. Sign up for the newsletter here.

Last week, I asked readers what subject they would want to see debated and who the participants would be.

Replies have been edited for length and clarity.

J.E. wants a prominent current or former tech executive to face a critic:

I’d have Mark Zuckerberg or Sheryl Sandberg debate U.S. Surgeon General Vivek Murthy about the damaging effects of social media on the mental health and well-being of young people. I find it quite frustrating that Zuckerberg and Sandberg were so eager to engage with the media about the positive impact of Facebook (Bringing the world together!) or their confidence about creating change (Move fast and break things!). Now that it’s apparent that social media has caused serious problems, we don’t hear from them. Do they agree that children have been adversely affected? Can they offer any solutions to the problems their product caused? What is their response to Dr. Murthy’s report?

Chadd’s struggles with addiction inform the debate he wants to see:

As someone who went to drug-rehab centers all over the country, experienced the opioid crisis over a decade, watched a dozen or so of my friends die, and overdosed multiple times myself, I believe that an under-discussed issue is drug-rehab programs—not only drug rehab but the concept of the “disease of addiction” and the entire 12-step rehab regime that has basically had control of the alcohol and drug narrative for 100 years.

Having been to treatment something like 15 to 20 times (anything from seven-day detoxes to 90-day rehab programs), I’ve seen and experienced so many of these places that it’s embarrassing. But I did finally “recover” and have since been drug-free for more than 5 years.

With that in mind, I want people to understand that nearly every single one of these places offered nearly the exact same treatment program. Some were better than others; most were mostly bullshit. Some really did try, and had honest, kind, and compassionate staff that really cared. Some were full-on grifts, run by former (and current) addicts who took advantage of desperate parents and insurance companies to enrich themselves at the expense of these poor folks. Besides all that, the one thing they all had in common was that the absolute main aspect of the “treatment” was exposure to the 12 steps of Alcoholics Anonymous and Narcotics Anonymous. Sometimes it was very in-depth, with “therapists” who were essentially 12-step evangelists spreading the good word of AA. Some were credentialed and kind and talented. Almost all preached the 12 steps like it was pretty much the gold standard of treatment. Not only that, most would casually even make snide comments about other methods of treatment, dismissing them as if they were completely absurd and irrelevant. That mindset is highly prevalent in the 12-step ecosystem.

Why am I talking about all this? Because people talk about how difficult the “disease” of addiction is, and the dismal success rates of treatment. In my opinion, there are better, more effective, evidence-based treatments that are underutilized and disregarded, if not outright demonized. I have been attacked on social media for stating my views about the 12 steps by vicious AA evangelists, some of whom I used to consider friends. All because I said that I think the 12 steps don’t work and that we should be trying something else instead of the same thing over and over.

I just so happen to be one of those people for whom the 12 steps did not work. Over and over, I was told I “must not have been totally honest,” or “Maybe you’re just not done yet,” as if there is some magical “bottom” you have to hit before you’re ready to stop destroying yourself. None of that stuff ended up being true. What I was missing the entire time was direction and connection. And also medication-assisted treatment, or MAT.

MAT [incorporates] medications that a drug-dependent person can take to ease withdrawal symptoms and more easily reenter normal life. These drugs are heavily stigmatized and demonized in the 12-step community. When I left NA, one could not be considered “clean” if they were taking medication for this purpose. Because of this stigma and the general idea that MAT is just replacing one drug with another—and for that reason is doomed to fail—therapists, doctors, and families are generally pushed away from these treatments. Not only that, but to access them one typically must pay some cash [since insurance often does not offer full coverage]. This leads many users to go back to drugs like heroin and fentanyl, because it’s almost cheaper to continue to use heroin than to afford the doctor visit, travel expenses, and crazy-high prescription costs. These medications have been shown to be highly effective at stopping withdrawals, curbing craving, and preventing future use.

If I could have any two people debate, I would say Dr. Nora Volkow, the director of the National Institute on Drug Abuse (NIDA), versus either Dr. Carl Hart of Columbia University or Dr. Gabor Maté, a Canadian addiction and harm-reduction expert. The topic would be the merits of the entire disease concept, and the effectiveness of 12-step programs versus other, evidence-based modalities. I choose Dr. Hart or Maté because both are highly regarded in their fields and have written incredible books on relevant topics. Hart mainly focuses on neuroscientific aspects of addiction, while Maté mainly focuses on behaviors and things like past trauma. Both have talked about how the idea of addiction as a “disease” is highly questionable, and how many of the assumptions about drug use and addicts are totally wrong.

Volkow has been the head of NIDA for years, is also highly regarded in her field, and has been very vocal about her belief in the “disease of addiction” and access to 12-step programs.

I’d love to see them debate the topic of addiction as a lifelong, incurable disease and the effectiveness of the 12 steps. I believe that we have erred in accepting that heavy, dependent drug use is some kind of incurable disease and that once you have it, you'll never kick it, and you can never be the same again.

I’m living proof that this idea is nonsense.

M.’s suggestions raise a significant logistical challenge:

I would argue that the most important debate has already occurred and very few people noticed: John Maynard Keynes vs. F. A. Hayek. Although this version is a parody, the questions raised by these two individuals are still debated by governments throughout the world today. Another important debate resolution: “Is the U.S. federal administrative state in 2023 constitutional?” I’d nominate Woodrow Wilson to argue the affirmative and Alexander Hamilton to argue the negative. Because both support stronger federal governments, we would take Hayek as the moderator, giving him the moderator’s prerogative to ask questions throughout. For the past 100 years there has been a significant shift in the size and scope of both the federal and state governments, and in the responsibilities they claim. What is unclear today is where the limits are. Having a serious debate by “uninterested” (in this case, dead) parties might be useful in starting that conversation.

Adam believes his debate would turn out differently than I do:

What I think is dividing this country is a lost ability to have back-and-forth, unscripted conversation. What is the quickest way to win an argument these days? Don’t engage in one. The second quickest way? Dismiss the opponent’s position as a radical, fringe thought. Planned speeches with little Q&A are becoming more popular. Even more, any appearance of an adverse opinion is shunned instead of addressed. Our political leaders have adopted these methods, and as a result, the virtue of good-faith debate is fading.

My answer to the Question of the Week will thus focus less on the substantive issue and more on reviving spirited, rigorous, and professional debate. So here is what I would like to see (and why): Arthur Brooks debating Joe Biden on whether a hot dog is a sandwich.

One caveat: No notes or teleprompter allowed. This debate, I believe, would juxtapose a levelheaded, articulate, finely tuned oralist with our president. Hopefully this would remind Americans of how real leaders present themselves. The topic is, of course, silly and meaningless. But if it is plainly shown that our president cannot form coherent thoughts on something so simple, then Americans should be skeptical of how he performs behind closed doors with other world leaders. At bottom, what disheartens me most is that those who garner the most attention are either not sharp enough to engage in spontaneous speech or possibly so insecure in their beliefs that they resort to character attacks, leaving the merits of important issues unaddressed and unresolved.

Were I advising Joe Biden, I’d urge him to accept that debate and expect him to perform reasonably well in it––and I say that as someone with my own concerns about his advancing age, and as a fan of Arthur Brooks, who is a contributing writer here at The Atlantic.

Bob turns our attention to agriculture:

The proposition to debate would be: “Farmers and ranchers should be treated the same as other businesses with regard to the water pollution they generate.” I limited it to just water pollution because including all types of pollution would make the topic too broad for an effective debate. (If you want names of debaters, I suggest Carrie Vollmer-Sanders, sustainability director, U.S. Farmers and Ranchers in Action, versus Anne Schechinger, agricultural economist and Midwest director, Environmental Working Group.)

The debate premise would be: Currently, the damage to the general public that is done by agriculture-related groundwater and surface-water pollution is principally dealt with by education of farmers and ranchers regarding new practices, monetary incentives, and appealing to whatever environmental ethic they may have––in contrast to other businesses (paper mills are one example in my area) that are required by law to clean up their pollution to a certain level prior to discharge into waterways. Because there are readily available ways to reduce agricultural pollution, farmers and ranchers could be similarly required by law to do so. Any increased cost would be passed on to those consumers who choose to buy their product. This seems like a reasonable transition since the vast majority of farmers/ranchers impacted are now “businesses” in every sense of the word.

Russ gets right to his proposition:

Should Joe Biden stack the Supreme Court?

The debate opponents would be Elizabeth Warren (pro) and Mitt Romney (con). I picked them specifically for the following reasons: They are both current sitting senators but not the leaders of their party. They both have run for president, so there would be name recognition, and neither can truthfully claim to represent the majority of their respective parties any longer. They can both articulate a position fairly well. I am going to give credit early that both would equally wish to win the debate and therefore prepare accordingly.

Jaleelah would debate me:

Let’s assume that I could choose the format of the debate, pick a neutral moderator committed to enforcing time limits, and guarantee that the audience is randomly selected from a pool of all Americans. I have reservations about forcing figures I respect to participate in massively viewed debates. Not every smart person is a smart debater, and some people do not appreciate the possibility of being laughed at by millions of people. I would love to see Natalie Wynn debate Jordan Peterson on whether postmodern neo-Marxism is a real threat, but I would not want Wynn to face death threats from Peterson’s more extreme supporters.

I would choose myself as one of the debaters. I am a persuasive speaker, and I know I would be able to deal with the consequences of participating in such an event. I would make you debate me on the following question: “Are the principled pursuit of near-absolute freedom of speech and the practical pursuit of intelligent debate mutually exclusive?” Despite the fact that I sent you a very long email giving away many of my arguments last August, I am completely confident that I could win defending the proposition that the two cannot coexist. I think this debate would be fun, and it would probably force you to defend one over the other in future writing. There would be no good reason to refuse!

Statins—one of the most extensively studied drugs on the planet, taken by tens of millions of Americans alone—have long had a perplexing side effect. Many patients—some 5 percent in clinical trials, and up to 30 percent in observational studies—experience sore and achy muscles, especially in the upper arms and legs. A much smaller proportion, less than 1 percent, develop muscle weakness or myopathy severe enough that they find it hard to “climb stairs, get up from a sofa, get up from the toilet,” says Robert Rosenson, a cardiologist at Mount Sinai. He’s had patients fall on the street because they couldn’t lift their leg over a curb.

But why should an anticholesterol drug weaken muscles in the arms and legs? Recently, two groups of scientists stumbled upon an answer. They didn’t set out to study statins. They weren’t studying cholesterol at all. They were hunting for genes behind a rare disease called limb girdle muscle dystrophy, in which muscles of the upper arms and legs—sound familiar?—become weak and waste away. After both teams tracked the disease through a handful of families in the U.S. and a Bedouin family in Israel, their suspicions separately landed on mutations in a gene encoding a particularly intriguing enzyme.  

The enzyme is known as HMG-CoA reductase, and to doctors, it is not obscure. It is, in fact, the very enzyme that statins block in the process of halting cholesterol production. And so, the answers to two mysteries suddenly became clear at once: Dysfunction in this enzyme causes muscle weakness from both limb girdle muscular dystrophy and statins.

This connection between a rare disease and a common drug stunned the researchers. “It seemed too good to be true,” says Joel Morales-Rosado, a pathologist who worked on one of the studies as a postdoctoral researcher at the Mayo Clinic. “One of the first things you learn in medical school is association between statins and myopathy.” Now the answer as to why— along with a potential treatment for it—has emerged from the DNA of just a few patients living with a seemingly unrelated genetic disease.

The first patient the Mayo team studied had been showing signs of limb girdle muscular dystrophy since he was a child, and his symptoms worsened over time until he lost the ability to walk or breathe with ease. (The disease can also affect large muscles in the torso.) Now in his 30s, he wanted to know the genetic cause of his disease before having children and potentially passing it on to them. His two brothers had the disease as well. So the team looked for genes in which all three brothers had mutations in both copies, which is how they zeroed in on the gene for HMG-CoA reductase.

Six more patients from four other families confirmed the link. They too all had mutations in the same gene, and they too were all diagnosed with some degree of limb girdle muscular dystrophy. (Interestingly, for reasons we don’t entirely understand, they all have normal or low cholesterol.)

Unbeknownst to the Mayo team, a group of researchers halfway around the world was already studying a large Bedouin family with a history of limb girdle muscular dystrophy. This family also carried mutations in the gene encoding HMG-CoA reductase. Those afflicted began experiencing minor symptoms in their 30s, such as muscle cramps, that worsened over time. The oldest family members, in their late 40s or 50s, had lost all movement in their arms and legs. One bedridden woman had to be ventilated full-time through a hole in her windpipe. Another had died in their mid-50s, Ohad Birk, a geneticist and doctor at Ben-Gurion University of the Negev, in Israel, told me. When his team saw that this family had the mutations in HMG-CoA reductase, they too immediately recognized the potential link to statins.

This pair of studies in the U.S. and Israel “really strongly suggests” that statins cause muscle damage via the same HMG-CoA reductase pathway, says Andrew Mammen, a neurologist at the National Institutes of Health who was not involved in either study. The enzyme’s role had been suspected, he told me, but “it had never been proven, especially in humans.” (Questions still remain, however. The enzyme, for example, is found in tissues throughout the body, so why do these common side effects show up in muscles specifically?) Rosenson, at Mount Sinai, wondered if variations in this gene could explain why statins don’t affect everyone the same. Perhaps patients who suffer particularly severe muscle side effects already have less functional versions of the enzyme, which becomes problematic only when they start taking statins, which reduce its function even further. This research might end up concretely improving the life of at least some of the patients most severely affected by statins.

That’s because Birk’s team in Israel did not stop at simply identifying the mutation. For two decades, he and his colleagues have been studying genetic disorders in this Bedouin community in the Negev and developing genetic tests so parents can avoid passing them on to their children. (Cousin marriages are traditional there, and when two parents are related, they are more likely to carry and pass on the same mutation to a child.) With limb girdle muscular dystrophy, his team went one step further than usual: They found a drug to treat it.

This drug, called mevalonolactone, allows muscle cells to function more normally even without the HMG-CoA reductase enzyme. Birk’s team first tested it in mice given doses of statins high enough to weaken their limbs; those also given mevalonolactone continued to crawl and even hang upside down on a wire just fine. They seemed to suffer no ill effects. When that experimental drug was given to the Bedouin woman bedridden with limb girdle muscular dystrophy, she also started regaining control of her arms and legs. She could eventually lift her arm, sit up by herself, raise her knees, and even feed her grandchild on her own. It was a dramatic improvement. Birk told me he has since heard about dozens of patients with limb girdle muscular dystrophy around the world who may benefit from this experimental drug.

Mammen and others think the drug could help a small subset of patients who take statins as well. However, the majority of patients—those with relatively minor pains or weaknesses that go away after they switch statins or have their dosage reduced—probably don’t need this new treatment. It probably even undermines the whole point of taking statins: Mevalonolactone eventually gets turned into cholesterol in the body, so “you’re basically supplying the building blocks for making more cholesterol,” Mammen said. But for some people, numbering in the thousands, severe muscle weakness does not go away even after they stop taking statins. These patients have developed antibodies to HMG-CoA reductase, which Mammen suspects continue to bind and disable the enzyme.

Mammen is eager for these patients to try mevalonolactone, and he’s been in touch with Birk, who unfortunately doesn’t have enough of the drug to share. In fact, he doesn’t even have enough to treat all of the other family members in Israel who are clamoring for it. “We’re not a factory. We’re a research lab,” Birk told me. Mevalonolactone is available as a research chemical, but that’s not pure and safe enough for human consumption. Birk’s graduate student Yuval Yogev had to manufacture the drug himself by genetically engineering bacteria to make mevalonolactone, which he then painstakingly purified. Making a drug to this standard is a huge amount of work, even for commercial labs. Birk is looking for a pharmaceutical company that could manufacture the drug at scale—for both patients with limb girdle muscular dystrophy and those with the most severe forms of statin-associated muscle damage.

Back in 1980, the very first person to receive an experimental dose of statins suffered muscle weakness so severe, she could not walk. (She had been given an extremely high dose.) Forty years later, muscle pain and weakness are still common reasons patients quit these very effective drugs. This recent breakthrough is finally pointing researchers toward a better understanding of statins’ toll on muscles, even if they still can’t fix it for everyone.

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