Kat K @RedKatBlue77

@JDVance Congratulations to you both! What a huge blessing! Welcome to the world little Alec Vance! You hit the jackpot being an American and having such loving parents! May God bless your life richly.

I'm a cardiologist. Today the FDA approved something I've been waiting two decades for: the first oral PCSK9 inhibitor in history. A once-daily pill — Lipfendra (enlicitide), from Merck — that lowers LDL as powerfully as the injections we've relied on. This is one of those days that quietly changes the trajectory of the disease that kills more people than anything else on earth. Let me tell you exactly why — and who should act on it this week. Start with the biology, because it's elegant. Your liver cells are covered in LDL receptors — molecular catcher's mitts that grab "bad" cholesterol out of your blood and pull it in for disposal. The more receptors you have working, the lower your LDL. But your body makes a protein called PCSK9 whose entire job is to find those receptors and drag them to the incinerator before they can be reused. PCSK9 is the saboteur. Block PCSK9, and the receptors survive. They get recycled back to the surface. They keep clearing LDL, over and over. Cholesterol plummets. It is one of the most powerful mechanisms we have ever discovered in cardiology. And until today, you could only access it through a needle. That needle was a bigger problem than most people realize. The injectables — Repatha, Praluent — are phenomenal drugs. But needle aversion, injection-site reactions, pharmacy logistics, and cost meant that millions of patients who desperately needed them simply said no. I have watched patients stay at heart-attack-level cholesterol for years because they wouldn't inject. The barrier was never the science. It was human. Now the trial data — from a program spanning over 19,000 participants — and it's genuinely impressive. Roughly 60% LDL reduction. A placebo-adjusted 56% in the main lipids trial, 59% in patients with inherited high cholesterol. On top of statins. That matches the injectable class in a daily tablet. But here's the detail that made me sit up as a cardiologist — the part most coverage is burying: enlicitide also significantly lowered ApoB and Lp(a). If you follow me, you know why that matters. Lp(a) is the genetic, inherited cholesterol particle that roughly one in five people carry at dangerous levels — the one that triples heart attack risk and that diet, exercise, and even statins barely touch. We've had almost nothing oral that moves it. A daily pill that lowers LDL, ApoB, AND Lp(a) simultaneously is a genuinely meaningful expansion of what we can do. Who should pay attention today: Anyone above their LDL goal despite maximum statins or ezetimibe. The roughly 9.8 million high-risk Americans still not at target. Anyone with familial hypercholesterolemia — the genetic condition that loads dangerously high LDL from birth and causes heart attacks in the 40s and 50s. These patients have avoided the injectables for years. Statin-intolerant patients who need powerful additional lowering. Anyone who's had a heart attack or stroke and needs to drive LDL far lower than a statin alone can manage. The price is notable too: about $315 a month, meaningfully below the injectables — though it'll still require insurance prior authorization, and formulary placement isn't set yet, so access won't be instant. Now the honest caveats, because I'm a physician, not a hype man: This approval is based on LDL lowering, not yet on proven outcomes. The big cardiovascular outcomes trial — CORALreef Outcomes, over 14,500 patients — is still running. We expect the heart-attack reduction to follow the LDL drop, because the link between lower LDL and fewer events is one of the most rock-solid relationships in all of medicine. But the definitive proof isn't in yet, and I'll tell you that honestly. And a pill isn't automatically right for everyone. Some patients love a shot they take twice a month and never think about again. This is a powerful new tool, not a mandate. But make no mistake about the size of this. For twenty years I've told patients that LDL is one of the most important numbers they will ever own — and that for the right person, lower is better, and lower earlier is better still. Today the tool to get there stopped requiring a needle. The medicine to protect your heart just got radically easier to take. And easier medicine is medicine people actually use. If you're on a statin and still not at goal — or high cholesterol runs in your family and you've been dodging the shots — this is the week to call your doctor and ask one question: "Is the new oral PCSK9 inhibitor right for me?" The needle was the wall. Today the wall came down. Know your numbers. The science to change them keeps winning.

I testified in front of the Senate today on the widespread fraud crisis in America. Since I exposed the fraud in Minnesota, it unleashed a war on fraud across the country. The fraudsters got away with it for so long they had literal “Learing Centers” that received millions of dollars from your taxes. When I first started making journalistic-style videos, I made it my mission to “show the world the reality of things as they really are.” Nothing was ever meant to be right or left, it was simply to show people what was happening from the source. Fraud affects every American because we all pay taxes, and the money being stolen comes from ALL of us, not a Republican or a Democrat. Hopefully people and politicians can realize that.

At ninety-eight, Fred Kummerow sued the Food and Drug Administration. He was a biochemist at the University of Illinois, born in Germany, and he had been trying to get someone to listen for a very long time. In 1957 he took samples from the arteries of people who had died of heart attacks and identified what was clogging them: trans fat, the artificial kind made by pumping hydrogen through cheap vegetable oil to turn it solid. The margarine and shortening the new dietary advice was busy recommending in place of butter and lard were full of it. He published the finding in Science. He fed the stuff to pigs and watched the lesions form in their arteries too. And he said so, plainly, for decades, while the food pyramid pointed the other way and the money stayed with the cheap solid fat that never went off on a shelf. The scale of it is worth stating plainly. By the time the ban finally arrived, artificial trans fats were being linked to something on the order of tens of thousands of American deaths a year. Kummerow was heckled by industry men at scientific conferences for daring to say so. Here was one biochemist, armed with a hospital's worth of diseased arteries and a lab full of pigs, up against an entire manufacturing sector whose cheapest and most convenient fat he was trying to condemn, and the sector had the ear of the regulator while he did not. They did not listen. The oil was profitable and convenient and the story had already been sold. So in 2009, aged ninety-four, he filed a formal petition asking the FDA to act. Three years passed and they did not answer it. So in 2013, a few weeks short of ninety-nine, he took the federal government to court for ignoring him. Two years later the FDA finally moved to ban artificial trans fats from the American food supply. Kummerow lived to see it. He died in 2017 at the age of a hundred and two, of the arteriosclerosis he had spent sixty years warning the country about. The fat he identified stayed in the food for another half century after he found it, because taking it out cost money and leaving it in did not. He was right in 1957. They agreed with him in 2015. Nobody has ever explained the years in between.

I just know those cheetos are hittin

With Senator Lindsey Graham’s passing, South Carolina Governor Henry McMaster will appoint an interim U.S. senator to fill the immediate vacancy. There is no legal deadline for him to make the appointment, but once he does, he has five days to formally call a special election. Because Senator Graham had already secured the Republican nomination in the June primary, there are now two separate processes underway: an interim appointment to fill the current Senate vacancy and a special Republican primary to choose a new GOP nominee for the November general election. (If necessary, a runoff would also be held.) Those are separate processes, so the interim appointee and the eventual Republican nominee could be the same person but they don’t have to be. Governor McMaster has long been one of President Trump’s earliest and strongest political allies, so this vacancy is not expected to change Republican control of the seat. Given that Senator Graham was a co-sponsor of the SAVE AMERICA ACT, McMaster will likely be looking for an interim appointee who supports Trump’s America First legislative priorities and can help maintain continuity in the Senate.

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Gov. Henry McMaster @henrymcmaster

a week ago

My statement on the passing of Senator Lindsey Graham:

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Senator Tim Scott was visibly emotional on CNN as he remembered his friend and fellow South Carolina Senator Lindsey Graham. SCOTT: “Well, Jake, gosh, America’s lost a true statesman.” “We don’t have many left. But he was a true statesman.” “But I’ve lost a friend. It is a morning of mourning for me.” “It’s a powerful reminder that life is fleeting, that we are not here very long.” “If I were to tell stories about Lindsey Graham, one of the most important stories is that when I was a new senator, he welcomed me in.” “He knew that my path was different. He understood the power of change in South Carolina and how much our state had changed. But he was one of the first folks in the Senate to welcome me in with open arms.” “And I will say that I do a South Carolina Prayer Breakfast every year in D.C. And I called Lindsey the first time, and Lindsey said, ‘Tim, if this thing starts before 10 A.M., I’m not coming because I’m not going—even if Jesus comes back before 10 A.M.’” “And I just laughed out loud. And of course, it started at 8:30. And who walked in the door at 8:31? Lindsey Graham.” “He was just the kind of committed person that you don’t really appreciate how committed he was to America.” “I can’t think of a more committed public servant to this country.”

RIP, Lindsey Graham. This moment in the Kavanaugh hearings was phenomenal.

At the end of a particularly thrilling and rollicking meeting in the Oval Office, Lindsey Graham turned to the room and said: “I’ve never had this much fun in my life.” I cannot describe to you how much joy President Trump’s leadership and friendship brought to Lindsey. Meetings with Graham at the White House were filled with camaraderie, kinship and uproarious laughter. As heartbreaking as his sudden passing is, I hope it will bring some measure of comfort to those who cherished him to know just how much he was living his dream every day. Very rarely in life do you get to be exactly where you want to be, when you want to be there, with who you want to be with, doing precisely what you want to do — that was every moment for Lindsey. When President Trump won in Nov 2024, Lindsey was exultant. Elated. And determined. He couldn’t wait to spearhead work, as the Budget Chairman, on the reconciliation bill that would cement President Trump’s most important campaign promises. I’ll never forget the senate lunch, when a couple Senators were a tad off the program, and Lindsey — in his inimitable way — made sure everyone was onside by the time we left. It was a glorious thing to witness. He knew how to move a room. Lindsey was a senator’s senator. The job was everything to him. Truly did he believe in the splendor of the office and the noble lineage behind it, of which he was the worthy heir. He was a senator in the mold of those who fashioned the institution, someone who still had the ability, in a heated exchange, to use rhetorical power to change the course of events. Which is why we will never forget his legendary Kavanaugh moment. We rarely think that we are out of time with our friends, so while there is a lot more I wish I could have said to Lindsey, I am glad that more than once I told him what that moment meant to the whole nation and why he was the only Senator who could have done it with such utter perfection. Most importantly, I had the chance to tell him on many occasions what his friendship meant to me and to us all. There was never once a time he didn’t answer a phone call and lend whatever assistance was required. It was never a question with Lindsey. He believed deeply in the code of friendship and loyalty. The fact that Lindsey started out as a political opponent only to become one the President’s most steadfast and faithful supporters underscores that Lindsey believed emphatically in the voice of the people. There is a lot more I would like to say. His passing, at a time when he had never been more dynamic, is as unexpected as it is shocking. In many respects, Lindsey was the last of a breed of American Senator whose like we may not yet see again for a long time. He lived every minute in the arena, a political gladiator to the very last. More than anything now, our thoughts are with his Sister, nieces and loved ones. We pray that God will ease their sorrow and heal their pain. Lindsey can never be replaced and will never be forgotten. Godspeed, my friend.

Just witnessed something at the Charlie Kirk assassination pre-trial in Utah that has NOT been made public yet and you need to hear about it... Erika Kirk asked for us to be here today. We sat inside the small courthouse in Provo with the family. The Judge told the media to turn off all cameras and allowed the full ENHANCED footage of the murder to play. Every movement of Tyler Robinson that day captured in full quality HD. Zoomed in. Some footage in 4K. Tracking all his movements. You can see crystal clear Tyler Robinson’s face, the license plate number on his vehicle, details on his clothing and his actions on the rooftop — and you can time every horrifying detail to the minute Charlie Kirk was murdered. What the public couldn’t see was the emotion in the courtroom. Charlie’s family sobbing uncontrollably, Erika in Mrs. Kirk's seniors arms. Charlie's father comforting them. Just feet away sat a pale, lifeless emaciated Tyler Robinson who stared at the floor with no remorse as he listened to the weeping. Robinson has never once looked at Erika this entire trial. The entire courthouse gasped when the video was over. Eventually this footage will be released. It was really tough to relive that day in such gruesome detail. This case is overwhelming. Please pray for a speedy trial. And to all the tormenters of the Kirk family, you can go to Hell where you belong. We pray for Justice for Charlie 🕊️

@MidwesternDoc Recent cardiologist lecture about statins. Cholesterol high since age 19. Current LDL 48 points above “normal“. Had recent “possible” heart attack scare. Scanned every artery in my body, including kidneys, abdomen, brain. All beautifully clear. Cardiologist still pushing statin.

To sell statins, we're told cholesterol damages arteries—in reality, it repairs arterial injury. Statins hence don't prevent death and give 20% of users muscle, liver or nerve damage Here I show what doctors never tell you about statins and heart disease midwesterndoctor.com/p/the-great-ch…

This is where the truth got hijacked. In 1958, a physiologist named Ancel Keys published what would become one of the most influential and most damaging studies in the history of medicine. He had data from 22 countries. Fat intake and heart disease mortality. If you plot all 22, there is no clear correlation. The dots are scattered. The data does not support the thesis. So he used 7. He selected the 7 countries that showed a clean upward line between fat consumption and heart disease. He left out the 15 that did not. And he published it as evidence that dietary fat causes heart disease. Look at this chart. The 7 red dots form a line. The 15 gray dots do not. One man chose which data points to show the world. And the world built an entire medical paradigm on his selection. What followed was a cascade that changed everything. 1961.The American Heart Association adopts the diet-heart hypothesis and recommends Americans eat less fat. 1962.The US government issues the first Dietary Guidelines for Americans. Low fat. High carbohydrate. The food pyramid is born. Grains at the base. Fat at the top. 1963.The food industry reformulates everything. Remove the fat. Replace it with sugar and seed oils to make it taste good. Ultra-processed food explodes. 1964.Time Magazine puts a frowning face made of eggs and bacon on its cover. Cholesterol is officially the enemy. 1965.The pharmaceutical industry sees the opportunity. If cholesterol causes heart disease, a drug that lowers cholesterol is worth billions. One cherry-picked study. One hypothesis treated as fact. Decades of dietary guidelines built on selected data. An entire population told to eat less fat and more carbohydrates. And a $26 billion drug industry built on the back of it. The 15 countries he left out told a different story. France had high fat intake and low heart disease. The data did not fit. So it was excluded. The science was not settled. It was selected. And we have been living with the consequences for 67 years.

@end3of6days9 If you learned fractions in school, you can read measure. Maybe it just looks intimidating to you in that format?

Jenny Johnson, CEO of Franklin Templeton on @TrumpAccounts: "If you invest $1,000 a year for 10 years at age 20, when you retire... you will have more money than a person who starts to invest at age 30 and invests the same amount per year for 30 years—that's the power of compounding—and so if you look at @TrumpAccounts, we're now starting at birth and being able to compound. I think it's incredibly powerful."

Women lose a critical brain growth factor during menopause that men maintain well into their 70s. That sex-specific drop in BDNF creates a cognitive vulnerability window during the exact years when Alzheimer's pathology starts accumulating. Brain-derived neurotrophic factor supports neurogenesis, synaptic plasticity, and non-amyloidogenic APP processing, the pathway that prevents amyloid accumulation. The BDNF gene contains an estrogen response element, meaning estrogen directly upregulates BDNF expression. When estrogen falls at menopause, BDNF falls with it. This isn't a gradual age-related decline that affects both sexes equally. It's a sex-specific drop tied to a hormonal transition that occurs during the fifth decade for most women. Men don't experience this decline at the same age. The result is a postmenopausal vulnerability window where synaptic support decreases, protein clearance becomes less efficient, and susceptibility to proteotoxic stress increases during the exact decades when amyloid pathology begins to accumulate. Women have a 67% higher lifetime risk of developing Alzheimer's compared to men, and while longevity explains part of that gap, the estrogen-BDNF cliff creates a distinct biological mechanism. Exercise produces a compensatory mechanism through irisin, a muscle-derived exerkine that crosses the blood-brain barrier and directly stimulates BDNF expression. Animal models show that irisin-deficient mice display impaired memory and elevated amyloid-beta, while irisin supplementation reverses both effects. What researchers recently quantified is that women generate substantially larger irisin responses to high-intensity endurance exercise than men. During maximal cycling tests, women produce acute irisin spikes two to three times higher than men performing the same relative workload. This heightened irisin-BDNF signaling may explain why postmenopausal women often derive greater cognitive benefits from aerobic training. In a cohort with mild cognitive impairment, six months of exercise at 75 to 85% heart rate reserve improved executive function more in women than men. A meta-analysis covering 33,816 adults found that physical activity offered significantly greater cognitive protection for women over one to twelve years of follow-up. Higher daily step counts correlated with larger hippocampal volumes in older women but not men, a structural signature of enhanced neuroplasticity. The amyloid data shows the same pattern. Physically active women reduced their amyloid burden to 8.94 ng/mg, compared to 12.69 ng/mg in sedentary women, a 42% difference that brought active women's levels down to match men's baseline. Sedentary women carried the highest amyloid load of any group. Exercise didn't just slow accumulation. It reversed it. But the mechanism isn't uniform across sexes. Women appear to benefit through irisin-driven BDNF restoration that compensates for estrogen loss. Men benefit more through enhanced Nrf2-mediated antioxidant defenses and Tau clearance pathways. Exercise reduces Alzheimer's risk by 45% across the population, an effect size that rivals or exceeds most pharmacologic interventions under development. But the timing matters because the BDNF decline is tied to menopause, not gradual aging. If exercise intervention begins during or shortly after this transition, the irisin-BDNF axis can be activated before synaptic support erodes. Waiting until cognitive symptoms appear in the seventh or eighth decade means intervening after pathology is already established. The estrogen-BDNF cliff creates a vulnerability window during the fifth and sixth decades. The decisions made during that window about exercise intensity and consistency may determine whether BDNF levels are maintained or allowed to fall unchecked. Current exercise guidelines recommend 150 minutes per week of moderate aerobic activity for general health, a threshold associated with reduced neurodegenerative risk in observational studies. But the guidelines don't account for sex-specific mechanisms, hormonal transitions, or the intensity required to generate meaningful irisin responses in postmenopausal women. High-intensity exercise, not moderate-intensity walking, produces the irisin spikes that drive BDNF expression. The difference between 60% and 85% heart rate reserve isn't just cardiovascular conditioning. It's the difference between triggering a neuroprotective signaling cascade and missing it entirely. The estrogen-BDNF cliff creates a distinct vulnerability period for women. Irisin-driven BDNF restoration through high-intensity exercise offers a compensatory mechanism. But only if the intervention happens during the window when estrogen falls and BDNF levels are still responsive to exercise-induced signaling, not decades later when the pathology is already compounding.

I'm a cardiologist. You've been told the golden rule of sleep is eight hours. New data says you've been optimizing the wrong number. It's not how long you sleep. It's how consistently. Researchers strapped accelerometers on 60,977 adults and tracked over 10 million hours of sleep for six years. They scored each person on sleep regularity — how closely their bed and wake times matched from one day to the next. The result should change your entire approach to rest: The most consistent sleepers had a 20 to 48% lower risk of dying from any cause than the most chaotic ones. 16 to 39% lower cancer mortality. 22 to 57% lower cardiometabolic mortality — the heart disease and stroke I treat every day. And here's the part that overturns conventional wisdom: sleep regularity predicted survival better than sleep duration. The clock you keep mattered more than the hours you logged. Dr. Ryan McCormick captured it perfectly: a consistent, good-quality 6.5 hours a night — same bedtime, same wake time — probably carries less risk than a fragmented, anxious 8-hour routine, or a pattern where your sleep swings wildly night to night. Read that again. A steady 6.5 may beat a chaotic 8. Here's why, as a cardiologist. Your entire body runs on a circadian clock. Blood pressure, heart rhythm, hormone release, glucose metabolism, cellular repair — all timed to a 24-hour rhythm anchored by when you sleep and wake. When that timing is consistent, every system synchronizes. When it swings — late Friday, early Monday, 2 AM one night and 10 PM the next — you inflict "social jet lag" on your body. Your heart never gets its stable nightly recovery. Metabolism destabilizes. Inflammation rises. The chaos is the damage. Not the hours. There's also a warning buried in this — one I see more and more in practice. Orthosomnia: anxiety about achieving perfect sleep, usually driven by obsessively tracking a wearable. People lie awake stressed that they didn't hit their eight hours or their deep-sleep target — and the stress itself wrecks the sleep. Chasing the perfect number can be worse than the imperfect sleep you're chasing it away from. So stop white-knuckling the duration. Here's what actually moves the needle: Pick a bedtime and a wake time. Hold them within about an hour — including weekends. Consistency is the lever, and it's the one you can actually control. You can't always dictate how long you sleep. Stress, kids, work, and biology don't negotiate. But you can almost always control when you lie down and when you get up. That's the finding that matters: the most powerful sleep intervention isn't a longer night. It's a regular one. Same bedtime. Same wake time. Every day. Your heart keeps time whether you tell it to or not. Give it a rhythm it can count on. nytimes.com/2026/07/05/opi…

@DC_Draino @KurtSchlichter Wow

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