Ron Adler

@wolfejosh What does this mean for New York?

What happens? Sane people leave the party. And you are left with kookie hysteric whiny victim-Olympic leeches

@hubermanlab @bjpohl33 @MichaelAlbertMD Had the same issue. Figured out that a major filler/binder in Ezetimibe was lactose. (Unhelpful for those who are lactose intolerant). You can retrial a compounded lactose free version.

@bjpohl33 @MichaelAlbertMD No, was hoping for some insight from others as to whether this is a common occurrence (per real experience not product sheets). Could have been pure correlation with something else. Curious to learn more.

I'm 36. I'm a physician. I take a statin—and ezetimibe—every day. No symptoms. No cardiac history. Just an honest read of the evidence. Here's what I found—and why I stopped waiting for a reason to act.

@msuster The perfect word for the situation.

ngl. i loved this so much. verklempt.

@MLBgami What’s the market on the next scorigami?

FINAL: Reds 6, Red Sox 5 No scorigami. This score has happened 7,093 times in MLB history, most recently earlier today.

@wolfejosh Absolutely epic. Have a blast.

Nihi Sumba, Indonesia. 🇮🇩 🌊🏄‍♂️

@DarrenJMeenan The rideshare setup is also horrendous and needs improvement.

Unreal how many people are calling WFAN to complain about the traffic getting to/home from the game today. Are these casual Mets fans? Even in years without construction, traffic is horrendous. With what is going on now, what did you really expect? The team tried to warn you.

@TMTLongShort This is incredible. Makes it even easier to justify >$1T in Capex. Curing cancer would simply be a cherry on top.

We’re gonna need more GPUs 😭

@pmje73 importai.substack.com/p/import-ai-44…

What’s the best thing you’ve read, listened to or watched recently on AI?

@wolfejosh Your moves aren’t awful.

We are not great Bollywood dancers but we tried! ❤️🤣🇮🇳

@wolfejosh @altcap Isn't that special...

Me wearing incomparable Brad Gerstner’s iconic red glasses @altcap for a pic…👓 …but looking less like Brad and more like Church Lady from SNL🤣

Hey @JetBlue, my PBI>JFK flight tomorrow was canceled due to weather (miraculously the flight scheduled to arrive at LGA one minute later is still flying!? - thanks @flightaware) and there are NO rebooking options showing at all. The app isn’t working and I’ve been on hold for almost four hours. I urgently need to get home (as I’m sure many do post the break). Can someone please assist here ASAP - I’m at a loss. Thanks.

@AutismCapital 🤓

Where is the most beautiful place you've visited in the US?

Of course that's your contention. You're a first-time SaaS bear. You just got finished listening to some podcast, Dario on Dwarkesh, probably. Now you think it’s the end of white collar work and seat-based pricing is screwed. You're gonna be convinced of that til tomorrow when you get to “Something Big is Happening”. Then you’ll install ClawdBot on a Mac Mini, vibe code a dashboard on top of a postgres database and say we’re all just a couple ralph loops away from building a Salesforce competitor. That’s gonna last until next week when you discover context graphs, and then you're gonna be talking about how the systems of record will be disintermediated by an agentic layer and reposting OAI marketing graphics. “Well, as a matter of fact, I won't, because ultimately the application layer is just ….” The application layer is just business logic on top a CRUD database. You got that from Satya’s appearance on the BG2 pod, December 2024, right? Yeah, I saw that too. Were you gonna plagiarize the whole thing for us? Do you have any thoughts of your own on this matter? Or...is that your thing? You get into the replies of anyone posting a SaaS ticker. You watch some podcast and then pawn it off as your own idea just to impress some VCs and embarrass some anon who’s long SaaS? See the sad thing about a guy like you is in a couple years you're gonna start doing some thinking on your own and you're gonna come up with the fact that there are two certainties in life. One: don't do that. And two: you dropped thirty grand on Mac Minis and LLM API calls to come to the same conclusion you could’ve got for free by following a handful of VC accounts.

@lessin Except you’re not an em-dash guy. We are solidly in the double dash or ellipsis camp.

Moltbot is just crushing writing my linkedin comments for me... great ones (especially the gunpowder insight is fab!) ...

@martinonyc Congrats @martinonyc; well deserved.

It has always been a privilege to report on this team. The Mets have a special history and connection with fans, and I’m excited to tell their story in new ways. More to come…

Great thread, thanks for posting. Very clear framing of the LDL vs total cholesterol issue and the misconceptions around studies correlating with longevity… this is a critical clarification (and agree on the PCSK9 vs statin issues). Just because someone has a well-produced viewpoint doesn’t make them right; keep them honest.

Definitely do not stop statins, and preventative LDL-cholesterole lowering therapies in general, based on these arguments, as they clearly misrepresent the facts. The AMORIS study only showed that extremely low total cholesterol was negatively associated with the chance of becoming a centenarian (reaching 100 years of age) (observational association; not causal, and low total cholesterol can also reflect underlying illness in older adults). Total cholesterol is different from LDL. Statins specifically lower LDL in the blood by increasing LDL receptor expression in the liver. The points made here perpetuate a common misconception, often propagated by health influencers, which is mixing up the beneficial functions of a molecule (nearly all naturally occurring biological molecules have legitimate functions in cells, tissues, and organs) with the level of these molecules in the blood, abnormally high levels do not mean a particular molecule is doing its job better, for a simple example, think of glucose, it fuels the brain, too much would not cause your brain to function more, the contrary as it causes metabolic disease, diabetes, and even increases cognitive decline risk. Cholesterol, and even LDL, have their legitimate functions, but these functions do not improve when the molecules are abnormally high in the blood. In fact, elevated LDL in the blood is often an outcome of defective liver uptake, frequently due to metabolic disease, and in rarer cases, solely due to genetics (familial hypercholesterolemia). LDL is causally linked to cardiovascular disease, and lowering it reduces heart attack risks in patients with existing plaque. Mendelian randomization studies also show that lifelong exposure to lower LDL levels reduces coronary artery disease risk; a 38.7 mg/dL reduction correlates to over a 55% reduction in coronary artery disease risk. Moreover, loss-of-function mutations in PCSK9 lead to a 28% reduction in LDL and correlate to an 88% reduction in coronary heart disease. The genetic variants with lower cholesterol share a similar mechanism with statin or PCSK9 treatments, in that they mainly lower LDL by increasing liver clearance. The U-shaped relationship between LDL-cholesterol levels and all-cause mortality at a population level is likely driven by reverse rather than actual causation, since many aging and chronic disease drivers, including inflammation, malnutrition, cancer, and liver disease, can all contribute to lowered levels of lipoprotein. Contrary to the observational data, a large meta-analysis showed that more intensive statin regimens and further reductions in LDL cholesterol produced further reductions in heart disease events and death risk. 20% reduction in coronary heart disease death and 10% reduction in all-cause mortality per 1 mmol/L (38.7 mg/dL) LDL-C reduction across trials. With that said, you might want to reconsider statins in the following cases: A severely lowered LDL coupled with partially increased blood glucose can be a sign of cholesterol "overmedication." The same mechanism that leads to increased clearance by liver uptake also works to increase LDL uptake by pancreatic islet cells. Preclinical evidence shows that overmedication to lower blood LDL can lead to disrupted pancreatic islet functions and insulin secretion, and increased blood glucose (In humans, statins are associated with a modest increase in diabetes risk overall; this is not reliably diagnosed by “LDL too low,” and risk is most evident in predisposed individuals). Consider swapping to PCSK9 inhibitors. This is a well-established injectable (once every month or every two weeks) class of biologics (recombinant monoclonal antibodies targeting PCSK9 and preventing its effect in degrading the LDL receptors in the liver). PCSK9 inhibitors have shown added protective effects in lowering cardiovascular disease risk even in patients already on statins. They also have a speculative anti-aging mechanism since circulating PCSK9 has been shown to increase with aging. While they can also plausibly interfere with the pancreatic islets and cause similar disruption seen with statins, there is no evidence yet to date of PCSK9 inhibitors increasing diabetes risk, such as evidence exists for statins (major outcomes trials have not shown a significant increase in new-onset diabetes over ~2–3 years of follow-up). If your HDL is too low, you need to pursue strategies to increase it, including exercise, healthy diets rich in MUFA and Omega-3 fats and fibers, avoiding added sugar and refined carbs, and abstaining (or seriously cutting down) on alcohol. If you are experiencing muscle ache and discomfort with statins, this is also a strong reason to switch. While the more acute form of muscle degeneration is very rare and would have been detected earlier as you began your statin therapy, lower-grade muscle aches are common in statin users. Changing to PCSK9 inhibitors, or other medications like ezetimibe (a cholesterol absorption blocker), can also help. Personally, I am currently on Repatha, a PCSK9 inhibitor, as I replaced statins after noticing they slightly increased my blood glucose.

.@bryan_johnson should I stop my statin?!?!

A moment for Kreids 💙❤️

Charlie Hicks ate his lunch and dinner at the Shrimp Basket in Pensacola, Florida, every day for 10 years. When he suddenly stopped showing up, the chef went looking for him – ultimately saving his life. @SteveHartmanCBS is On the Road.

Oracle has nearly round tripped its huge post-earnings spike from Sept, as clear a sign as any that the market is growing increasingly skeptical about the AI data center construction boom

if you could change the outcome of a single game in baseball history, which game would you choose?