That deer is doing God's work

🚨 Ron DeSantis DESTROYS Dems over “Alligator Alcatraz” stunt: slams them for ignoring Angel moms and victims of illegal immigration while whining about cold ham sandwiches for illegal detainees 🔥

🚨New Paper: "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis: A Lean Mass Hyper-Responder Case Report" Link: doi.org/10.3390/diseases1405… For the past 7 years, I’ve been running what is essentially a natural experiment in cholesterol and heart health. During that time, I’ve largely lived with: 👉Total cholesterol around 700 mg/dl 👉LDL cholesterol between 500–600 mg/dL I recently underwent advanced coronary CT angiography imaging with AI-guided analysis. This is not a CAC. It measures all plaque (soft calcified), with expert interpretation and AI-guided analysis capable of quantifying plaque down to the cubic millimeter (mm3). Now, to address the obvious question: Am I too young for plaque? In brief: No. The clearest comparison is individuals with homozygous familial hypercholesterolemia, who often have similarly extreme LDL/ApoB levels and can develop advanced plaque as toddlers, and even heart attacks as early as age 8. Also, nutrition influencers in their 30s have publicly shared quantified plaque scores from these same imaging technologies. In one recent case, a plant-based influencer in his thirties was found to have 61.3 mm³ of plaque despite having far lower lifetime LDL exposure. (He can identify himself if he so chooses.) My case also isn’t a one-off. There are many individuals like me, including older individuals with similar LDL-C and ApoB without any plaque. The difference is that I’m an unusually well-characterized subject, with extensive metabolic data and health markers tracked over time. You can learn more at the newsletter or open-access paper, linked above. The science of heart health is not settled. And cholesterol is not a simple story. 🚨 If you want to help spread the word... Quote Tweet this post (or create an original post) including the article link with a thought. Academic papers are increasingly evaluated using attention metrics. Original posts from unique users are one way to increase these metrics and help ultimately increase its reach. 🚨 If you want to learn more, I'll include more learning resources below 👇

🚨 Breaking News 🚨 Experts warn that untreated Hantavirus may now progress into “Long Hanta™”… Symptoms include: • Changing your pronouns every 6 hours • Putting rotating non-US flags in every bio • Demanding a booster for a disease nobody has • Saying “trust the science” while ignoring actual science • Developing sudden intolerance to sunlight, steak, and mitochondria Fortunately, Pfizer is already developing a 14-dose vaccine subscription package with free virtue signaling tote bag and digital solidarity badge included. This will allow others to know your status for their safety and yours.

Florida being Florida

Do GLP-1 drugs reduce hunger by acting on satiety centers in the brain or by giving the brain more energy? This new article presents that idea (sciencedirect.com/science/ar…). At its simplest, they lay out a perspective that reduced hunger is a consequence of increased fuel availability for the brain.

Happy Tax Day, New York. We’re taxing the rich.

RFK Jr. says being on a carnivore diet helped him significantly reduce visceral fat. “I had a full-body MRI a year ago and I went to this doctor who said my organs were covered with visceral fat.” “I went on his diet, which is the carnivore diet.” “He said I can get rid of all that visceral fat within 90 days.” “Thirty days later I had lost 40% of it.” “The MRI I took this week, I was down to 1 percentile of visceral fat.” “About half the cabinet is on this same diet right now.”

I'll be very interested to see how Retatrutide affects glucose. The new ingredient is a glucagon analog, which can certainly facilitate fat burning. Of course, glucagon can also increase blood glucose. I wonder whether this will be more targeted specifically for weight loss, rather than diabetes.

Fixating on one variable with weak predictive power, instead of or even at the expense of more predictive and significant variables, is one of the most dumbfounding and careless behaviors of recent times. Folks who are already heavily medicated on lipid-lowering therapy believe that eating pasta, white rice, cereal, and oats is more beneficial to their health than red meat, fatty fish, and eggs. There is a reason why nearly every randomized trial has shown benefit when refined carbohydrates are removed from the intervention diet. This includes DASH studies, the PREDIMED trial, the CORDIOPREV study, and very low-carb trials. It’s not an Israel paradox or a French paradox or a Maasai paradox or an Inuit paradox or a Spanish paradox or a Tokelau paradox. It’s not the red wine either. What’s even more ironic is that people who push a plant-forward diet (a euphemism for a vegan or vegetarian diet), heavy in grains, even refined grains, are themselves on two medications to treat their cholesterol. They talk about the cholesterol-lowering benefits of their plant-forward diet, but still require multiple medications to keep their LDL-C low. Don’t be gaslit by this outdated nonsense.

The idea that red meat causes insulin resistance and diabetes is just crazy. We eat less red meat now than we have in over 100 years, and diabetes has climbed the entire time. Where does this idea come from?

Follow-up thoughts on version 1.0 of another physician who gets it! You’d have a hard time convincing me that an isolated, modest LDL (just above 100 mg/dL) is the primary driver of clinically significant ASCVD. Why? First, clinical observation. In practice, you see patterns over time. You start to recognize what actually shows up in stroke and cardiovascular clinics. Second, the data. Prospective cohorts like Framingham and multiple trials show that modest LDL in isolation has weak short- to intermediate-term predictive power. That changes completely when LDL is paired with markers of poor metabolic health: • low HDL • high triglycerides • elevated glucose • hypertension • central obesity • smoking Now risk rises sharply. This cluster is what Gerald Reaven described as Syndrome X, now known as insulin resistance or metabolic syndrome. This is the soil where clinically significant atherosclerosis develops. And you see it every day. Who shows up in stroke clinic? Patients with metabolic syndrome and its complications Smokers / substance-related vascular injury A small minority with genetic or structural causes That’s the reality at the bedside. This is a systems problem, not a single-variable problem. May 2020Pediatric Gastroenterology Hepatology & Nutrition 23(3):189 See the initial post below and the initial Cardiologist's post as well. 👇👇

Tom Dayspring is a fraud & statin shill: he advocates statins for people w/0 calcium score"just in case", equivalent to giving someone lung radiation therapy, although cancer free, "just in case" because his sister in law smokes. A lot of stat mistakes/base rate fallacies. youtu.be/gxIeRUbHauw?si=csWI… via @YouTube