Hi everyone,
A few things from this week’s research stopped me in my tracks. A randomized trial showed that semaglutide, the same medicine sold as Ozempic, cut heavy drinking days far beyond placebo in adults with alcohol use disorder. A meta-analysis of nearly 3,800 adults pinned down 8,500 as the real daily step number for keeping weight off, not the famous 10,000 we have all been chasing. And a clean cycling study found that your favorite playlist boosts endurance by roughly 20 percent without making the work feel any harder.
On the podcast this week, I went deep on lipoprotein(a), the cardiovascular risk factor that around 1 in 4 adults globally carry at dangerous levels, and almost no one knows it. I have high LP(a) myself, and the conventional message is that it is a genetic bad hand. The biology tells a much more interesting story.
Let’s get into it.
This Week’s Podcast Spotlight
Episode 51: Lipoprotein(a): Genetic Risk, Seed Oils & 5 Steps to Protect Your Heart
I wanted to do this episode because lipoprotein(a), or LP(a), is something I personally carry at elevated levels, and frankly it took me a while to make peace with that number. LP(a) is a modified LDL particle with an extra protein attached, the apo(a) protein, that almost perfectly mimics plasminogen, your body’s clot-dissolving protein. That structural mimicry gives LP(a) two unique behaviors. It slows clot breakdown and helps wounds seal faster, and it acts as a magnet for oxidized fats in the bloodstream. The number itself is locked in by your DNA at 70 to 90 percent, so diet and exercise basically do not move it. About 20 to 25 percent of adults globally carry levels high enough to roughly double their lifetime risk of heart attack and stroke, and most never get tested because LP(a) is not on the standard lipid panel. You have to ask for it.
What I really want people to take from this episode is the reframe. If LP(a) were purely harmful, natural selection would have wiped it out a long time ago. It survived because it was useful. In the ancestral world, high LP(a) meant better wound sealing, fewer fatal childbirth hemorrhages, and faster recovery from animal attacks and battlefield injuries. The problem is what biologists call an evolutionary mismatch. In modern life, the injury never stops. Chronic hypertension shears the inside of your blood vessels, metabolic disease inflames those same walls, and smoking oxidizes them with every puff. LP(a) keeps showing up to repair, depositing cholesterol and oxidized fats from industrial seed oils, and that is what turns a survival gene into a plaque builder.
Three things that stood out from this episode:
- LP(a) levels are 70 to 90 percent determined by a single gene, the LPA gene, and stable from age five onward. Black and African populations run up to three times higher than European populations on average, South Asian populations also trend higher, and women run about 5 to 10 percent higher than men with levels climbing further at menopause. If your LP(a) is high, your first-degree relatives have a real chance of carrying it too, which is why family screening is one of the most practical things you can do with this information.
- The real lever is not the number on the lab report. It is removing the two conditions that let LP(a) cause harm: chronic endothelial injury and a bloodstream full of oxidized fats from industrial seed oils. Get seed oils out and cook with stable fats only, control blood pressure under 120 over 80, dial in metabolic health, stay physically active, and do not smoke. That is the framework I follow personally.
- The pharmacological pipeline is genuinely exciting. New siRNA therapies in late-stage trials are knocking LP(a) down by 70 to 90 percent with dosing every three to six months. PCSK9 inhibitors lower it about 20 to 25 percent as a secondary effect. Lipoprotein apheresis can drop it 60 to 90 percent acutely. But outcomes data on LP(a) reduction specifically is not in yet, and waiting for the drug is not a strategy when the lifestyle levers are sitting right in front of you.
We also got into why the Tokelauan islanders and the Masai of East Africa, two populations historically eating very high saturated fat diets, had remarkably low rates of atherosclerosis even in the context of heavy smoking. The answer points right back at oxidation. If your LP(a) is high, or if anyone in your family has had an unexpected heart event in their 40s or 50s, this episode is for you.
This Week in Health Science
Here is what stood out from the research this week. These studies fascinated me, and I think you will find them practically useful.
The Weight-Loss Shot That Also Quietly Cut Heavy Drinking
For years, patients on Ozempic and Wegovy have been telling their doctors something unexpected. Alcohol does not feel the same on these drugs. Many people say they simply lose interest in their evening glass of wine. This 26-week randomized trial of 108 adults with alcohol use disorder and obesity finally puts a hard number on that observation. Everyone in the trial got cognitive behavioural therapy. Half also got weekly semaglutide injections, half got placebo. By the end, heavy drinking days had dropped by 41.1 percentage points in the semaglutide group versus 26.4 points on placebo, a 13.7 point difference that was statistically rock solid. The drug also lowered cravings and improved liver biomarkers. The number needed to treat was 4.3, which compares favorably to naltrexone and acamprosate, the two medicines currently approved for alcohol use disorder, which sit around 7 or higher. The mechanism is fascinating. GLP-1 drugs act on receptors in the brain’s reward circuits, the same circuits that respond to food, alcohol, and other addictive substances, and they appear to turn down the dopamine response that makes alcohol feel rewarding. This is a single trial, the participants all had obesity, and we do not know how durable the effect is once the injections stop. But if a drug already sitting in millions of medicine cabinets also blunts the urge to drink, that could quietly become one of the most important public health stories of the decade.
Key finding: Weekly semaglutide cut heavy drinking days by 41.1 percentage points versus 26.4 points on placebo over 26 weeks, with a number needed to treat of 4.3, which beats every currently approved medication for alcohol use disorder.
The 10,000-Step Goal Was a Marketing Slogan. The Real Number Is Lower.
I have been telling patients for years that 10,000 steps a day is a marketing number, not a medical one. The famous target came from a 1960s Japanese pedometer campaign called manpo-kei, literally “ten thousand step meter.” There was never any clinical study behind it. This new meta-analysis of 14 randomized trials and 3,758 adults finally pins down the actual evidence-based threshold for keeping weight off, and it is closer to 8,500 a day. During the active weight-loss phase of the trials, participants climbed from a baseline near 7,200 steps to about 8,454, and lost roughly 4 percent of their body weight. The most important finding came from the maintenance phase. People who held around 8,500 steps a day kept the weight they had lost. People whose step counts drifted below that line tended to regain. The trials all combined steps with structured dietary changes, so this is not a case for walking replacing nutrition. What I love about this finding is that it makes the goal more reachable. Going from a typical baseline of 7,200 to 8,500 is roughly an extra fifteen minute walk, which is exactly the kind of small, sustainable change that people can actually keep up for years.
Key finding: A meta-analysis of 14 randomized trials and 3,758 adults found 8,500 daily steps, not the long-marketed 10,000, was the threshold most strongly tied to keeping lost weight off during the maintenance phase.
Your Own Playlist Boosted Endurance by Nearly 20 Percent
This study made me grin a little, because it takes something most of us already do without thinking and shows that it actually moves the needle. Researchers tested 29 recreationally active adults on a stationary bike at about 80 percent of peak power, which is a tough but doable intensity. Each person rode the same workout twice, once with their own favorite music and once in silence. The riders held that hard pace for an average of 35.6 minutes with music, compared to just 29.8 minutes in silence. That is a 20 percent gain in time to exhaustion. The most interesting detail was that ratings of perceived effort at the moment of quitting were essentially identical in both conditions. Music did not numb the pain or trick people into thinking they were working less hard. It seems to raise the threshold for how much sustained discomfort the brain is willing to accept before bailing out. The songs people picked clustered in the 120 to 140 beats per minute range, which lines up nicely with a strong, sustainable pedaling cadence. If a supplement company found these numbers, it would be on every podcast in the country. Build a workout playlist with songs you genuinely love and save it for the hardest sessions.
Key finding: Riders cycled an average of 35.6 minutes with their own favorite music versus 29.8 minutes in silence, a roughly 20 percent gain in endurance, with no change in how hard the effort felt at the point of exhaustion.
Eating Eggs Regularly Was Tied to a 27 Percent Lower Alzheimer’s Risk
Eggs spent decades on the medical naughty list over cholesterol concerns, and a lot of older adults are still skittish about them. This study from the Adventist Health Study-2 followed about 40,000 Seventh-day Adventists aged 65 and older for more than 15 years, matching their food habits with Medicare Alzheimer’s diagnoses. The pattern stepped up cleanly with intake. People who ate eggs one to three times a month had a 17 percent lower risk compared with rare consumers. Two to four times a week brought a 20 percent reduction. Five or more eggs a week brought a 27 percent lower risk. That kind of dose-response pattern makes the finding more believable, because it tracks the way a true biological effect should. The likely drivers are choline, which the brain uses to make acetylcholine, the same neurotransmitter that is depleted in Alzheimer’s disease, plus the carotenoids lutein and zeaxanthin, which build up in the brain and may lower oxidative stress. This is observational data, so we cannot fully untangle eggs from the rest of a healthy lifestyle. But a few eggs a week appears to fit comfortably into a brain-healthy eating pattern for most older adults, and the long fear of the yolk has not held up well to the evidence.
Key finding: In a 15-year study of 40,000 older adults, eating five or more eggs per week was tied to a 27 percent lower risk of Alzheimer’s disease compared with rare egg consumers, with a clean dose-response pattern starting at just one to three eggs per month.
Irregular Bedtimes Roughly Doubled the Risk of Major Heart Events
This is one of the cleanest signals on sleep and heart health I have read in a while. Researchers followed 3,231 adults from the Northern Finland Birth Cohort 1966, starting at age 46 and continuing for more than a decade. Each participant wore a wrist device for a week so the team could measure actual sleep timing, not just self-reports, and then tracked them through national health records for major adverse cardiac events: heart attacks, unstable chest pain, strokes, heart failure admissions, and cardiac death. In adults who slept less than eight hours, the most irregular bedtimes carried a 2.01-fold higher risk of a serious heart event compared with the most regular bedtimes. The signal held even after adjusting for body weight, blood pressure, blood sugar, cholesterol, employment, and total physical activity. The most striking detail for me is that wake-up time did not matter much. Bedtime did. Most of us cannot fully control when we get up because of work and kids, but we usually can control when we go to bed, and this study tells us that lever matters more than we thought. If you are already running short on sleep, anchoring your bedtime in the same 30 to 60 minute window every night, including weekends, may be one of the easiest heart-protective habits you can build.
Key finding: In short sleepers, the most irregular bedtimes carried a 2.01-fold higher risk of major heart events over 10 years compared with the most regular bedtimes, while irregular wake times did not show the same effect.
My book, 2mm, is almost here. It is the story of seven years inside the operating room, where every decision is measured in millimeters and every millimeter matters. If you want to be the first to know when it is available, leave your email at 2mmbook.com.
Stay curious. Stay skeptical. And stay healthy.
Dr Kumar