Luis A. Vegas Vicentini

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Racism, trickle-down economics, autocracy, ignorance, hate, grift, corruption, moral flexibility, lies, extremism, cultism, bullying, and treason have been rebuked by the vast majority of Americans. Congratulations on taking your country back from the few, the corrupt and the connected! Let this be the foundation for constructing a new, better America: A nation defined by fairness, driven by innovation, taxed equitably, and dedicated to giving every individual, regardless of ethnicity or social standing, the exact same power and tools to thrive. LAVV

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What a new heart study tells us about plaque, and whether it can shrink For a long time the working assumption in cardiology was that the plaque lining our coronary arteries, once built, could be slowed but not undone. A study published this week in JAMA Cardiology, drawn from a Danish trial called FLOWPROMOTE, offers a more hopeful picture, and it is worth understanding what it actually found. The researchers followed 104 adults, mostly men in their mid-sixties, who had just been diagnosed with stable coronary artery disease and had never taken a cholesterol-lowering medication. Each of them received detailed CT scans of their heart arteries at the start, again at nine months, and again at eighteen. Half were given a strong statin on its own, atorvastatin 40 mg. The other half received a more aggressive combination, rosuvastatin 40 mg together with ezetimibe, a second drug that blocks cholesterol absorption in the gut. The difference in blood results was striking. The statin-only group brought their LDL cholesterol, the fraction most tied to arterial disease, down by about 38 percent, to roughly 70 mg/dL. The combination group brought it down by about 65 percent, landing near 42 mg/dL. These are low numbers by any standard. What matters most is what the scans showed. In both groups the total volume of plaque in the arteries shrank over eighteen months, and the soft, uncalcified kind of plaque, the type most prone to rupture and cause a heart attack, shrank the most. But the group with the lower LDL saw clearly more regression: total plaque fell by about 21 percent compared with roughly 14 percent, and soft plaque fell by about 28 percent compared with 20 percent. Nearly every patient on the combination therapy, 98 percent of them, showed some shrinkage of soft plaque. The relationship was close to a straight line: the lower the LDL achieved, the more the plaque receded. Calcified plaque, the hardened kind, grew slightly in both groups, which researchers generally read as the arteries stabilizing rather than worsening. A few things deserve honest caution. This was a small trial, and plaque volume was a secondary measure rather than its main question. Eighteen months is a meaningful window but not a lifetime, and the study did not follow people long enough to count heart attacks or deaths, so it shows arteries changing on a scan rather than proving fewer events. The participants were overwhelmingly male and all had established disease, so the findings speak most directly to people in that situation, not to everyone concerned about prevention. Still, the direction is encouraging and consistent with what earlier, smaller imaging studies had hinted. Coronary plaque is not a one-way street. When LDL is driven low enough and kept there, the arteries appear able, at least in part, to clear some of what has accumulated. For anyone already living with a diagnosis, this is a reason to take lipid management seriously and to have a frank conversation with their cardiologist about how low their own target should be. LAVV Source: Mortensen MB et al., JAMA Cardiology, published online October 30, 2026, doi:10.1001/jamacardio.2026.4788. If you would like this as a shareable doc or a Spanish version, say so and I will prepare it.

I place a high priority on educating clients about gut microbiota and the vital role of gut health. A balanced microbiome supports a healthy symbiotic relationship between the gut and the enteric nervous system...a foundational driver of metabolic health and long-term lifespan.

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Calling Type 2 diabetes “100% genetic” defies foundational metabolic science and meta-analytic evidence. Twin and polygenic risk score data consistently demonstrate a complex gene-environment interaction, with lifestyle drivers being the primary determinant of phenotypic expression. If it were 100% genetic, monozygotic concordance would be absolute…yet large epidemiological cohorts tracked by the International Diabetes Federation and the European Association for the Study of Diabetes prove otherwise. Stop propagating absolutes that distort modern etiology.

Protein is elemental for life.

Your HOMA-IR is nothing more than a 7:00 AM snapshot of your liver at rest, so avoid reading it like a life sentence. Most men get a 2.4 back, panic, and immediately strip away every carbohydrate in sight. That isn't a sound strategy...thats just reactionary and it misses the biological reality of what’s happening inside your body. Here is the truth about the math, the metabolic machinery and why you don't need to fear real food: 1. It measures your liver at rest, not your capacity to burn carbs.HOMA-IR measures how much fasting insulin your liver requires to keep overnight glucose stable. It gives you insight into resting hepatic gluconeogenesis, but it tells you almost nothing about how efficiently your muscle mitochondria handle clean fuel after a workout. 2. Biological noise lies.A single HOMA-IR draw can swing by roughly 32% day-to-day. Poor sleep quality, elevated morning cortisol, or simple lab variance can falsely make a healthy, high-performing man look insulin resistant on a single morning. 3. Cutting carbs hides the signal and it doesn't fix the engine. Eliminating carbohydrates drops fasting insulin, so your score looks "better" on paper. But turning off the smoke alarm doesn't put out the fire. Extreme restriction often induces adaptive insulin resistance, elevates stress hormones, and impairs thyroid conversion (free T3) compromising your energy, recovery and long-term metabolic elasticity. 4. The reference targets: • Under 1.0: Optimal metabolic efficiency. • 1.0 – 2.0: The gray zone, time to look closer at the variables. • Over 2.0: An underlying driver exists, identify the mechanism, please don't guess. How to audit your data before making radical changes: • Standardize: 10–12 hr fast, draw between 7–9 AM, no heavy training or alcohol for 48 hrs, and prioritized sleep. • Cross-examine: Pair it with C-peptide, TG/HDL ratio, hsCRP, and Fructosamine. • Test real-world clearance: Run a home glucose curve with 75g of clean carbs (finger-prick at 0, 30, 60, 90, and 120 mins). You want to see efficient clearance back to baseline within two hours. Mastering your metabolic health isn't about fear or extreme elimination, it is really about objective data, understanding the underlying mechanism and building a resilient, adaptable biological system. So go ahead and test with precision, identify the true bottleneck and humbly aim to fix the root cause. LAVV