Before You Take Your Next Statin, Watch THIS (New Research).

One in four adults over 40 takes a cholesterol pill every morning, a statin. A study published in 2024 found that statins also lower a key hormone in your body, GLP-1, the same hormone that hot new weight loss drugs like ozempic were built to copy. The reason has nothing to do with your liver, which is where the cholesterol pills are supposed to work. It has to do with the bacteria living in your gut and with a remedy that came from bear bile. In the next few minutes, you'll understand this issue better than most people who take that pill. And you'll walk away with one simple question to ask your doctor, if someone you love takes a cholesterol pill, please send them this video right now. I'm Neil K. Shaw, a Johns Hopkins and NIH-funded caregiving researcher and the CEO of CaryIA. I've helped thousands of families navigate aging, dementia, and serious illness. I'm not a clinician, but a leading researcher and innovator in caregiving. And one important note before we start, absolutely nothing in this video is a reason to stop taking a medication. Always consult with your doctor. I'm just going to lay out the numbers and walk you through why this matters. So now let's get into it. In a journal called Cell Metabolism in 2024, one of the best journals in the world for this kind of research, a team published about a simple study. They took 30 patients who were just starting a statin medication, a tour of a statin, 20 milligrams, very common dose. And then they took 10 more patients with the same cholesterol problems who had decided not to take the drug. They followed both groups for 16 weeks. Blood tests at the start, one week in, four weeks in, and 16 weeks in. Here's what they found that was surprising. The cholesterol result was great. Total cholesterol dropped. LDL dropped within one week. So the drugs did their job. But the blood sugar numbers went the other way. By week four, A1c levels had gone up. Now A1c is your three-month blood sugar average. That's a number that your doctor often checks for, you know, for diabetes. It went up at week four and it stayed up through week 16. Insulin went up. Insulin resistance went up. That's your body needing more and more insulin to do the same job. None of that happened in the group that was not taking the drug. And then one more measurement. A hormone called GLP-1 dropped significantly by week four and it just kept dropping throughout the end of the study. The line was still heading down when they stopped measuring at week 16. The paper says GLP-1 decreased significantly. The graph shows it falling by around half. You know, the half number comes from reading the chart, not from the text. And this was 30 people at one hospital and everyone knew, you know, who was getting the drug. Six of the 30 already had a history of diabetes. So these are real caveats and the authors say so themselves. So before we go into how any of this works, let me tell you what it actually means. It means this. For most people, the change is small and really small. On a standard dose, the average A1c went up by six hundredths of one percent. It's typically not a number that you'd feel. But it matters a lot for one group of people. If your blood sugar is already sitting right at the edge of the diabetes line, and millions of older people are, then even a tiny nudge can push you across the edge. Not because the drug itself created diabetes, but because you are already standing on the line and that change pushed you over the edge. So the practical takeaway here is not necessarily to avoid it, but it's this. If you're near the line, know your number and check it carefully if you do decide to start taking these drugs. I think that's a real action item. So now the real question of why does this impact happen? I think the why here is genuinely strange. To understand why a cholesterol pill would even touch your gut, you have to know where the pill came from. In 1971, a biochemist named Akira Endo worked at a drug company in Tokyo. He'd worked for two years in New York and came home convinced that Americans were eating themselves in heart attacks. He also grew up admiring Alexander Fleming, the man who had found penicillin growing in a mold. So Endo had an idea that most people thought was foolish. Molds make chemicals to kill off competing bacteria. Bacteria need certain building blocks to grow. Some of those building blocks are the same ones that your body uses to make cholesterol. So maybe, just maybe, some mold out there makes a chemical that shuts down your cholesterol production. So he started testing In July 1973, one hit. It came from a blue-green mold. The mold was recorded as coming from a rice sample taken from a grain shop in Kyoto. Same family of mold that gave Fleming penicillin. That was how the first statin drug was invented. Endo won the Lasker Award in 2008. He died in June 2024 at 90 years old. He never got rich from it. The fortunes from statins were made by other people and large pharmaceutical companies. But back to that detail. Molds evolved these chemicals to suppress bacteria. So now, what if you swallow that chemical? It travels through your gut, which holds trillions of bacteria. And after we started doing this, nobody checked what happened out there for the next 50 years. If this is the kind of thing you want more of, by the way, real research, explained honestly, no sponsors, no products, please subscribe and follow along. I love breaking these things down so that people can better understand important health topics. And please share with others. That's the only way these messages can get out there and reach people. So back to the researchers in that cell metabolism paper. They asked the obvious question, how does this happen? They tested stool samples and blood samples. And the biggest change they found wasn't in the cholesterol at all. It was in something called bile acids. Here's how that works in plain terms. Your liver makes bile. Bile helps you digest fat. But bile also acts like a set of signals in your body. Your liver makes one kind of bile acid. Then certain gut bacteria take that bile acid and change it into a different one. Think of it like a factory floor. Your liver makes the raw materials. The bacteria do the finishing work. The finished product is called UDCA. And remember that name because it'll come back later. In the patients on statins, that raw part went up and the finished part went down week after week. The factory was just totally getting backed up. Why? Because the workers were disappearing. The bacteria that are doing that conversion are a group called clostridium. In the statin patients, they started dropping after just one week and kept dropping for the whole 16 weeks. And remember where statins came from, a mold that evolved to suppress bacteria. The researchers grew these gut bacteria in a dish, added the statin, and watched the growth slow down. More drug, less bacterial growth directly. So the chain looks like this. Drug suppresses bacteria. Fewer bacteria means less UDCA. Less UDCA means less GLP-1, which brings us to that hormone because you've probably heard of it even if you don't know it directly. GLP-1 hormone is made by the cells in your intestine when food shows up. It tells your pancreas to release insulin, but only when your blood sugar is actually high. It also slows your stomach down. It tells your brain that you've eaten enough. It's the hormone that today's super popular weight loss drugs like Ozempic and Wegovy were designed to imitate. And the way we found that out is one of my favorite stories in healthcare. In the early 1990s, a doctor named John Eng worked at a VA hospital in the Bronx. He got curious about the gila monster. That's a fat, orange, and black lizard from the Arizona desert. Because it can go for months between meals with steady blood sugar the whole time. So Dr. Eng ordered dried gila monster venom from a reptile facility in Utah. His colleague used to drive up the test tubes from Brooklyn in his Toyota Camry. In 1992, they pulled out a compound they named Xendin-4. It looked about half like human GLP-1, but with one key difference. Human GLP-1 gets chopped up and destroyed within minutes. The version from the lizard doesn't. It lasts for hours. The VA didn't want to patent it, so Eng patented it himself. Then he spent about three years trying to get a drug company interested and got nowhere. A diabetes drug from lizard spit sounded like a total joke. In 1996, he stood next to a research poster at a conference in San Francisco and pitched anyone who would stop. One person slowed down. The decade later, the first GLP-1 drug was approved in 2005. Every GLP-1 medication you've heard about traces back to that story. So when a common cholesterol pill like statins lowers that same hormone, I think it's worth a closer look. Now, a pattern in the 30 people in this study in cell metabolism doesn't convincingly prove that anything caused anything. So the researchers went to mice. Mice, given the statin, developed the same problem. Blood sugar trouble, GLP-1 levels went down. Then they repeated it in mice whose gut bacteria had been wiped out with antibiotics first. Nothing happened. No blood sugar problems at all. So if you take away the gut bacteria and the effect disappears, that's a strong argument that the bacteria are the actual cause of the change. Then they went even further. They took stool from long-term human statin users and transplanted it into ordinary mice. Those mice then developed insulin resistance. Then they reversed it in two different ways. Put the directly, everything recovers. So that's the result I promised you, the one buried in the back of the paper that nobody quoted. Also, all of these mice were eating a high-fat diet. When researchers ran the same experiment on mice eating a high-fiber diet, the blood sugar problem never showed up at all. Think about why that might be. Fiber is food for the exact bacteria that the Now, this is just a mouse result. It has not been tested in this way in people, so it should be a big caveat. But I think it's one of the most interesting findings in that paper, and it went totally unreported. So if low UDCA is the problem, could you just give people UDCA? Now that question has a 1,300-year history. Dried bear bile shows up in traditional Chinese medicine going back centuries. The clearest early descriptions are dated to the Tang Dynasty around the year 659. It was used for liver and gallbladder problems. Then in 1902, a Swedish professor named Olaf Hammerstein got hold of gallbladders from polar bears. He found a substance nobody had ever described. Chemistry wasn't advanced enough for him to say what it was, so he just named it after the animal. 25 years later in 1927, a Japanese scientist named Masato Shoda pulled the same substance out of black bear bile and gave it a permanent name, ursodeoxycholic acid. By the way, ursus is Latin for bear. By 1936, the structure was worked out, which meant it could be made in a lab. No bear was needed ever again. Today, it's a prescription drug in the United States. It's called ursodiol. It's approved for a liver condition, and it's been used well in people for decades. We know it well. So the research team ran the obvious test. Five patients, all on statins for more than six months, all with A1C levels that had crept up. They added UDCA, 500 milligrams a day, and kept the statins going. Two months later, A1C levels down, insulin down, insulin resistance down, liver enzymes down. So what matters the most in that is the cholesterol benefits stayed, LDL unchanged, HDL actually improved. Five people, there was no comparison group, nothing was double blind. So this is a hint but not a definitive answer, you know, so we need to hold it loosely. The real answer is coming. There is a proper trial running right now, randomized placebo-controlled six months, adults 40 to 75. That trial will either confirm this or not. That's how this is supposed to work. Then in May 2024, a research group at Oxford published the biggest analysis ever done on statins and blood sugar. Not just 30 people like in the cell metabolism study, but 123,000 people, 19 trials where nobody, not even the doctors or the patients, knew who got the real pill. They were followed for more than four years and they confirmed the effect is real. Then they measured how big it is. On a standard dose, average A1C levels rose by six hundredths of one percent. On the highest dose, eight hundredths. And most of the new diabetes diagnoses happen in people who are already sitting right there at the edge of the line. So they said the thing that settles it. You know, those same trials counted heart attacks and strokes, so whatever harm comes from that small blood sugar shift, it's already included in the benefit that those trials found. Both were measured in the same people at the same time. And what was that benefit? The statins lowered the LDL by about 39 points and cut the risk of heart attacks and strokes by 22%. So put another way, there was roughly one extra case of diabetes per 1,000 people per year against roughly five heart attacks or strokes prevented. And one more thing why this is timely. This March, the American Heart Association, the American College of Cardiology and 10 other groups put out a new cholesterol guideline. They changed the risk calculator. They widened the age range from 40 through 75 to now be ages 30 through 79. An analysis published in July put real numbers on what that means. 87.5 million American adults now qualify for a statin. 21.5 million of them didn't qualify before. And by age, 85% of adults in their 60s, 93% of adults in their 70s. So if you're over 60, this conversation is either already happening or it's about to happen, which is why I think it's worth understanding exactly the gut side of it. Not as a reason to say no, but just as a reason to ask better and more thoughtful questions. So three questions, you might want to write these down. One, for me personally, how much does this pill actually lower my risk? Two, what is my A1C level right now? And should we check again in a few weeks or a few months? The Oxford researcher said routine checking isn't needed for everyone, but if you're near the line, that's exactly who this might matter for. Three, is there anything worth about my diet that's worth changing alongside all this? The fiber finding in the studies came from mice, not people, but fiber is good for you, you know, for a dozen different reasons that don't depend on the study. And also clearly on UDCA, I'm not telling you to take anything by yourself. The real version requires a prescription. There are sometimes supplements sold online with similar names, but they're different, unapproved products. That's not what was tested. So bring these up with your doctor or your pharmacist. These are thoughtful, real conversations you should have with providers that know you personally and your medical history. If cost or coverage is a problem, your state health insurance assistance program gives free Medicare help with no sales pitch. The scientist Akira Endo tested 6,000 molds because he had a hunch that a fungus was hiding something. And he was right. Since then, hundreds of millions of people have lowered their cholesterol because of the discovery. But a mold that evolved to kill bacteria was never going to pass through the human gut without touching anything or having side effects. It took 50 years for someone to check. And when they finally did and published it in a leading journal, it just sat there without much media coverage. So the answer to a question that millions of people have been asking can sometimes be published and still never reach the person that's holding the bottle. Now I hope the message has reached you. Take it to your doctor as a question, not as a verdict, and please send this to a person you know out there that could benefit from this information. That's the only way this travels. I'm Neil K. Shah. Let's take care of each other, and I'll see you in the next one. Thank you.