Ryan

6.1.21 One Day At A Time. #RaiderNation

[Dr Sudhir Kumar MD DM @hyderabaddoctor]

Take-home messages:
✅High homocysteine is associated with stroke, heart attack, CVST and depression.
✅Vitamin B12 and folate deficiencies are common causes.
✅Levels below 10 µmol/L are generally considered desirable.
✅Correcting nutritional deficiencies can substantially reduce homocysteine levels.
✅Do not ignore persistently elevated homocysteine, especially in younger individuals with vascular disease.

16/n (End)

(Disclaimer: The information provided here is general in nature. Consult your doctor for individual medical advice.)

Dr Sudhir Kumar @hyderabaddoctor

[Ábris Babicz | The Demi Cycle Protocol 🧬 @AbrisGains]

You're getting older, your metabolism is slowing down, and it's killing your fat loss.

Just eating less and moving more isn't enough anymore.

Here are 7 unconventional hacks to boost your metabolism and lose fat (bookmark this):🧵

1. Rucking

[Dr Sumit Sharma @dr_sumit_sharma]

Most people with insulin resistance don't need another advanced protocol.

They need the boring foundation their body has been quietly starving for.

Here's why I start every patient on the same handful of cheap supplements before anything clever:

[Mark Kaplan @markkaplan20]

Someone on here told me I give too many things to fix. They asked me to prioritize.

Fair point. Here are 4 steps. In order. Start at the top.

[Dr PARVEEN YOGRAJ @dr_yograj]

ApoB: The Silent Assassin in Your Lipid Panel – Why It Beats LDL for Heart Attack Prediction
—————————————————-
Answer: 3️⃣ Apolipoprotein B (ApoB). While many (including you) assume LDL-C is king, current evidence from discordance analyses and 2024–2026 guidelines shows ApoB is the superior predictor of future heart attack risk.
Why? LDL-C measures cholesterol content inside particles. ApoB counts the actual number of atherogenic particles (one ApoB per LDL, VLDL, or remnant). Small, dense LDL particles carry less cholesterol but are highly atherogenic—LDL-C underestimates risk here, while ApoB nails it. Triglycerides/HDL ratio flags metabolic issues well but misses particle count; total cholesterol is outdated.
Pathophysiology of LDL (ApoB particles) in MI: Excess ApoB-containing lipoproteins infiltrate the arterial wall’s subendothelial space. There, they undergo oxidation, triggering inflammation. Macrophages engulf oxidized LDL via scavenger receptors, forming foam cells—the core of fatty streaks. Cytokines recruit more immune cells, smooth-muscle proliferation creates a fibrous cap over the lipid core. Plaques grow, narrow arteries, and can rupture. A clot forms on the exposed core, blocking flow and causing myocardial infarction.
Bonus: Proven best fix? Lower ApoB aggressively. First-line: lifestyle (Mediterranean-style diet <7–10% saturated fat, 150+ min/week exercise, 5–10% weight loss) + high-intensity statins (20–45% ApoB drop). Add ezetimibe or PCSK9 inhibitors if needed. 2026 guidelines target ApoB <90 mg/dL (or lower by risk category)—this slashes events 20–30% per ~1 mmol/L LDL/ApoB reduction in trials.
We need to consult our doctor about adding ApoB to your next panel—it’s the clearest crystal ball for prevention.
#MedEd #MedX #MedTwitter @IhabFathiSulima

[Afshine Emrani MD FACC @afshineemrani]

I'm a cardiologist. I've held dying hearts in my hands in the cath lab at 3 AM. And I need to tell you something that changes everything about how we prevent heart attacks.

For decades, the entire field was built on one target: lower LDL cholesterol. Statins save lives — that's settled science. But too many of my patients did everything right — took their statins, hit their numbers, lived clean — and still ended up on my table with a ruptured artery.

We were treating the smoke while the fire kept burning.
The fire is inflammation. And the evidence is now overwhelming.

The CANTOS trial proved it first — lowering inflammation independent of cholesterol reduced cardiac events. But the newer data is what keeps me up at night.

AI-enhanced CT angiography can now detect inflamed arteries by measuring changes in the fat surrounding your coronary vessels — the perivascular fat attenuation index. Higher inflammation in the fat around even one artery independently predicts cardiac death. When multiple arteries show inflammation, the risk multiplies dramatically — even in patients whose cholesterol looks perfect.

This isn't theoretical. This is measurable. Right now. On a scan you can get this month.

Low-dose colchicine — a drug that's been around for centuries for gout — is now FDA-approved specifically for reducing cardiovascular events. It works by quieting the inflammatory cascade that destabilizes the plaque sitting in your arteries. A pill that costs pennies is saving lives the statins couldn't reach.

And the next wave is already in Phase 3 trials. Ziltivekimab — an IL-6 inhibitor — targets the central inflammatory pathway driving atherosclerosis. Phase 2 data showed a 90% reduction in hsCRP. The ZEUS cardiovascular outcomes trial is enrolling now, with results expected late 2026 into 2027. If positive, anti-inflammatory therapy will become standard in managing heart disease alongside lipid-lowering. The era of inflammation-targeted cardiology is arriving.
But it goes deeper than drugs. AI is now predicting heart failure and cardiac events 5+ years before symptoms — integrating CT imaging, electronic health records, and genetic data with accuracy that jumps far beyond traditional risk calculators.

And polygenic risk scores — a simple genetic test that flags inherited cardiovascular risk — are now formally recognized as a risk-enhancing factor in the 2026 ACC/AHA guidelines. A single blood draw can reveal risk that's been silently building since birth. Decades before the first chest pain.

Here's what this means for you right now — today:
Ask your doctor for a high-sensitivity CRP test. It's cheap, routine, and measures the systemic inflammation that standard cholesterol panels completely miss. You can have perfect LDL and inflamed arteries that are quietly preparing to rupture.
If your hsCRP is elevated, discuss low-dose colchicine with your physician. It's FDA-approved for exactly this.
Push for a coronary CT angiography with AI plaque and inflammation analysis if you have risk factors. This isn't the stress test your parents got. This is 3D visualization of your actual arteries — with AI quantifying not just how much plaque you have, but what kind it is and whether the surrounding tissue is inflamed.
Consider polygenic risk score testing — especially with a family history of early heart disease. It's now guideline-supported.

And the foundation that never changes: move daily, eat real food, sleep 7-9 hours, manage stress, and know your numbers — ApoB, Lp(a), hsCRP, fasting insulin.
I left Iran as a child with nothing. I rebuilt everything in a country that gave me the freedom to become a physician. I've spent twenty years watching patients get second chances.

The ones who haunt me aren't the ones who died on my table. They're the ones who survived but never acted on what the science was telling them — years before the event that didn't have to happen.

You can have perfect cholesterol and still have a heart attack. Inflammation plus genetics can drive plaque rupture in arteries that look "fine" on a standard panel.
The myth that normal cholesterol means you're safe has cost more lives than I can count.

We now have the tools to detect the fire — not just the smoke. AI to see it. Genetics to predict it. Drugs to quiet it. And the ancient basics — movement, real food, sleep, purpose — to prevent it from starting.

Prevention is the new cure. And the science to make it real is no longer coming.
It's here.

[Dan Go @CoachDanGo]

Your doctor says your bloodwork is "normal" but that word has probably cost more years of healthy life than any disease.

Normal doesn't mean optimal.

Here are 8 blood markers that predict your future better than your waistline (most doctors don't track #2):

[Bret Scher, MD @bschermd]

Cardiology calls statins miracle drugs. Social media calls them poison.

Both sides cite published scientific papers. How can they be looking at the same evidence and reaching opposite conclusions?

As a cardiologist, I think both sides are are on to something. Let me explain. 🧵

[Dr. Priyam Bordoloi @DocPriyamMD]

A patient asked me today: "Why do I always wake up at exactly 3:30AM with my heart racing, wide awake, and unable to go back to sleep?"

This is actually one of the most misunderstood physiological alarms in the human body.

[J∅kër Kîng 👑 @j0ker937]

Man, this guy is 100% correct.
You CAN eat healthy, and it's cheaper than you think.

[BowTiedYukon @BowTiedYukon]

I saw Charles Glass teaching a guy these DB lateral raises on IG. I’ve been doing them for a few weeks and am a big fan

[Fitness Freak @fitdaddy_]

How To Grow Bigger Arms Using Dumbbells Only 🦾

[Ken LaCorte @KenLaCorte]

Here's what they don't teach kids about American Indians.

If you were taught the kinder, gentler version of Native Americans, you're in for a shock. And we don't honor them by pretending they were eternal victims.

0:00 - Introduction
1:46 - America Before Columbus
5:35 - Clashing War Codes
9:25 - The Comanche
14:43 - Blood on Both Sides
18:10 - Conclusion

[Soulful Sprinter @SoulfulSprinter]

If You Do 60...

[Sport boy @Sp_bo1]

تمارين الصدر للمبتدئين بأستخدام الدمبل

[FitWithPurpose @FitWithPurposeX]

Build strength with diamond &amp; Shoulder pushups✅️👇

[Metabolic Alpha @MetabolicAlpha]

Stop useless workouts. Do this instead

[Cary Kelly @CaryKelly11]

A coworker wanted to know why I was fasting for two days.

I told him I could feel some inflammation had crept into my body and this was my reset button.

But you’ll die of hunger, he said.

So I found this video to show him how my hormones will reward me and what really happens when we go more than a day without eating.

Source: https://t.co/LY7amLyf5W.human (IG)

[🎈 @freakdaleaks]

🎈