Knowledge hound 📖

Forever student. PICU doc, dad, husband . Manchester United fan. Views are my own and not my employer’s. Retweets are not endorsements. #PedsICU

[Dr Alo, DO, FACC @MohammedAlo]

🚨 Marijuana does not protect your heart. Daily users face a 6x higher risk of heart attack compared to non-users. The recreational drug millions consider harmless is quietly destroying cardiovascular health at a measurable, documented rate.

And no, they are not just older patients with preexisting disease.

🫀 Here is what the science actually says.

Cannabis triggers a surge in sympathetic nervous system activity. Heart rate climbs. Blood pressure spikes. Coronary artery spasm becomes a real and documented event. Platelet aggregation accelerates. And for the daily user, this is not a one-time insult. This is repeated, cumulative cardiovascular stress happening every single day.

💓 The numbers are not subtle.

Daily marijuana use is associated with a 6x increase in heart attack risk compared to non-users. Even weekly use carries measurable elevation in cardiovascular events. Young users are not exempt. Some of the most striking cases in the literature involve patients under 40 presenting with ST-elevation MI and a urine drug screen positive for THC. No other risk factors. No family history. Cannabis was the story.

🔬 The mechanisms are direct.

Cannabis activates CB1 receptors in cardiac tissue and vascular endothelium. This drives coronary vasospasm, impairs endothelial function, and accelerates atherosclerosis over time. THC increases carboxyhemoglobin when smoked, reducing oxygen delivery to myocardium. The combination of increased demand and reduced supply is exactly how you trigger an ischemic event.

⚠️ The cultural narrative is dangerous.

Millions of Americans treat marijuana as a wellness product. A stress reliever. A sleep aid. Something natural and therefore safe. The cardiovascular data does not support that framing. Natural does not mean cardioprotective. Arsenic is natural. The question is no longer whether marijuana feels harmless. The question is whether you are willing to accept a 6x increase in heart attack risk as the cost of daily use.

🩺 I see this in my practice. Young patients. No hypertension. No diabetes. No hyperlipidemia. Cannabis use is the only flag. And yet the coronary artery is in spasm on the cath table.

That is the real story.

❤️ Bottom line:

Marijuana is not a heart-safe drug. The data shows a 6x higher heart attack risk with daily use, and the mechanism is direct, not theoretical. If you use cannabis daily and you have not had a cardiovascular risk conversation with your doctor, that conversation is overdue. Stopping or significantly reducing use is a cardiovascular intervention with real benefit. The choice is yours. But make it with accurate information, not cultural mythology.

Are you willing to accept a 6x higher heart attack risk for a habit your doctor never warned you about?

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #MarijuanaAndHeart #CannabisRisk #CoronaryArteryDisease #HeartAttack #PreventiveCardiology #LifestyleMedicine

[Dr Alo, DO, FACC @MohammedAlo]

🚨 A Mendelian randomization study of over 1 million people just confirmed what the wellness industry does not want you to hear.

Every 38 mg/dL increase in your lifelong LDL cholesterol costs you 1.2 years of life.

But the data says otherwise when the gurus tell you low LDL is dangerous.

🔬 Here is what makes this study different from everything else the skeptics try to dismiss.

Most observational studies get attacked with one argument: reverse causality. Sick people have low cholesterol because they are already dying. Therefore low LDL looks dangerous. The wellness crowd runs with that talking point endlessly.

Mendelian randomization destroys that argument at the root.

Your genetic variants are assigned at conception. Before any disease. Before any medication. Before any lifestyle choice. This study used those genetic variants as a proxy for lifelong LDL exposure across more than 1 million people. The direction of causation runs one way only. Higher genetically determined LDL shortens lifespan. Period.

💓 The science is not subtle here.

Each 38 mg/dL increase in genetically determined LDL equals 1.2 fewer years of life. That is not a rounding error. That is a real, measurable, biologically determined cost you pay for carrying more LDL through your arteries across a lifetime.

This is cumulative exposure. Your arteries do not forget. Every year of elevated LDL adds to the plaque burden, the inflammatory load, and the vascular damage that eventually produces a heart attack or stroke.

🩺 I am a cardiologist. I treat patients with established cardiovascular disease every day. I watch people arrive in my clinic after decades of untreated high LDL, convinced by wellness content that their numbers were fine. The damage I see on their imaging tells a different story than the influencer they followed.

The question is no longer whether LDL causes harm. The question is how many years you are willing to trade for the comfort of ignoring it.

❌ Low LDL will not kill you.
❌ Statins will not destroy your muscles or your brain.
❌ Cholesterol skepticism is not brave scientific thinking. It is dangerous misinformation with a body count.

❤️ Bottom line:

Low LDL does not shorten your life. Over 1 million people with genetic data prove the opposite.

Higher lifelong LDL exposure directly reduces lifespan by 1.2 years per 38 mg/dL increase. That is causal, not correlational.

Know your LDL. Know your ApoB. Talk to a cardiologist who reads the actual data. Do not manage your cardiovascular risk based on YouTube.

The wellness industry profits when you distrust the evidence. Your arteries pay the price.

Are you going to let a guru with a podcast cost you a year of your life?

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #LDLCholesterol #CholesterolMyths #MendelianRandomization #ApoB #PreventiveCardiology #MetabolicHealth

[Patty T @Patty3795B]

@Enezator Really makes you think about what is really important in this life

[Enezator @Enezator]

Hundreds of high school students filled the hallways of an Alabama hospital to say goodbye to their classmate Kimber Mills as she was taken into surgery to become an organ donor ❤️

[Pulm PEEPs @PulmPEEPs]

🚨❓When do you use steroids in sepsis? All patients? Only shock? Only shock with pressors at a certain level?

Listen to our new episode today on Steroids in Sepsis

https://t.co/kOgkCWcarh

Highlight video 👇

@CritCareTime @IM_Crit_ @EM_RESUS @PulmCrit @emcrit @COREIMpodcast

[Tony @UtdTony1]

🚨🔴 BREAKING NEWS:

Portugal head coach Roberto Martínez has reportedly held a private meeting with Cristiano Ronaldo regarding his role in the team's upcoming matches.

Sources close to the camp indicate that Martínez informed Ronaldo of his decision to start him from the bench in the next game as part of a tactical plan aimed at helping Portugal go further in the tournament.

Ronaldo is said to have accepted the decision professionally, making it clear that his priority is the success of the team and giving Portugal the best possible chance of winning the World Cup.

The Portuguese captain remains fully committed and ready to contribute whenever called upon. 🇵🇹🐐

[Knowledge hound 📖 @HoundKnowledge]

@Cooltalldave @Symply_rhoda1 Well he didn’t break his ankle. Perhaps, others now have permission to massage Messi’s ankles or jaw. 😎

[Dr Alo, DO, FACC @MohammedAlo]

🚨 1 in 5 people walking around right now carry a genetic cardiovascular time bomb in their blood. Their cholesterol looks fine. Their doctor never tested for it.

That particle is called Lipoprotein(a). And it is silently destroying arteries right now.

🔬 Here is what the science actually says.

Lipoprotein(a). also written as Lp(a). is a modified LDL particle with an extra protein called apolipoprotein(a) attached to it. That structural difference makes it uniquely dangerous. It does three things regular LDL does not. It promotes plaque buildup. It drives inflammation. It clogs clots by blocking the body's natural clot-dissolving system.

🫀 Your genetics set your Lp(a) level at birth. Diet will not lower it. Exercise will not lower it. Statins will not lower it. In some patients statins actually raise it. This is not a lifestyle problem. This is a molecular inheritance problem.

💓 The numbers are not small.

20% of the global population carries elevated Lp(a) above 50 mg/dL. That is roughly 1.4 billion people worldwide. Elevated Lp(a) increases the risk of heart attack by up to 3 times. It increases aortic valve disease risk independently of every other traditional risk factor. Most of these people have no idea.

🩺 I am a cardiologist. I test every single patient for Lp(a). Once. That is all you need because the number barely changes over a lifetime. One blood draw. One number that could reshape your entire prevention strategy.

A patient who discovers an Lp(a) of 180 nmol/L at age 40 and aggressively drives their LDL to below 55 mg/dL can change the trajectory of their disease before the first event ever occurs. That is the difference between a heart attack at 58 and arriving at 75 with a clean coronary CT.

⚠️ The question is no longer whether Lp(a) matters. The question is whether your doctor is testing it.

✅ HEART UK CONSENSUS (Lp(a)): Lp(a) testing recommended for all adults at least once in a lifetime.

✅ European Atherosclerosis Society Consensus: Lp(a) above 50 mg/dL classified as an independent causal risk factor for ASCVD.

❌ Niacin trials failed to reduce cardiovascular events despite lowering Lp(a).

✅ RNA-based therapies in active trials are reducing Lp(a) by 80% or more. The era of targeted Lp(a) therapy is coming.

❤️ Bottom line:

Lp(a) is not a specialty test. It is a basic cardiovascular literacy test. It is genetically determined, present from birth, and ignored by most standard lipid panels. One in 5 people carry it at dangerous levels and most will never know until they have their first event. Ask your doctor for an Lp(a) level today. Know your number. Build your prevention plan around the full picture, not just LDL. This is why every adult with any family history of early heart disease needs to pay attention right now.

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #Lpa #Lipoprotein #ApoB #LipidPanel #PreventiveCardiology #MetabolicHealth

[La Catrina Norteña @catrina_nortena]

🚨 YA EMPEZÓ EL ROBO DE LA FIFA

¿Y la roja? Bien, gracias...

[Knowledge hound 📖 @HoundKnowledge]

@Jdh06g @RyanRozbiani Agree. But how can you compete in a World Cup getting bussed in and out of 2 countries without adequate support staff. This will occur each day of each game. This is an absolute travesty. Really an insult to all true football fans and an injustice to their team

[Knowledge hound 📖 @HoundKnowledge]

@markkaplan20 Great job. I wish we all had your dedication and discipline.

[Knowledge hound 📖 @HoundKnowledge]

@feelgoodtale Respect 🫡

[FeelGoodTales @feelgoodtale]

Yesterday, during my father's funeral procession, led by the United States Marine Corps, my family noticed the man in this photograph standing at the side of the road. He held his hat in his hand and placed his hand on his heart as a sign of respect for my father and our family as we walked by.

His respectful gesture deeply touched my family and the entire train. Along the way, we encountered many other cars simply going about their day.

Since his license plate was visible in the photo, my daughter did some research and we found him!!!

His name is Ernest Boerlin and he is also a veteran of the United States Navy.

When I sent him a private message to thank him for honoring my father, he replied:

"It was an honor to show my respect for a comrade and his family." Please accept my prayers and condolences for you and your family in your loss. Fair winds and calm seas. God bless you.

Thank you, Ernest. Your gesture of kindness and respect deeply touched our family and friends, and we are grateful for it. May God bless you and your loved ones.

Let's thank Ernest for his service and show him our affection, folks!

[pushkar soni @pushkersoni72]

🚨 BREAKING: Claude can now map out your retirement better than most people charging $2,000 ever will.

Here are 6 prompts to figure out exactly when and how you can retire.

(Save this before it disappears).

[Dr Alo, DO, FACC @MohammedAlo]

🚨 Your doctor told you an LDL of 100 is fine.

The patients who actually reversed coronary plaque had LDL levels below 60.

The threshold you were given was never designed to reverse disease. It was designed to slow it down.

🫀 There is a difference between preventing a heart attack and actually shrinking the plaque sitting in your coronary arteries right now. Most physicians only aim for the first goal. The data demands we aim for the second.

Here is what the science actually says.

💓 The regression data is not subtle.

✅ ASTEROID (rosuvastatin): 40mg daily drove mean LDL to 60.8 mg/dL. Plaque volume regressed in the majority of patients. First trial to demonstrate definitive coronary atherosclerosis regression with statin therapy.

✅ REVERSAL (atorvastatin): Intensive therapy reduced LDL to 79 mg/dL versus 110 mg/dL in the moderate arm. Plaque progression stopped entirely in the intensive group.

✅ FOURIER (evolocumab): LDL reduced to 30 mg/dL. Major cardiovascular events fell 15%. The lower the LDL, the greater the clinical benefit. No floor effect was observed.

✅ ODYSSEY OUTCOMES (alirocumab): LDL driven to 40 mg/dL post-ACS. All-cause mortality dropped 15% in high-risk patients.

🔬 The biology is straightforward.

Atherosclerosis is driven by LDL particles penetrating the arterial wall and oxidizing.

Lower the particle burden aggressively enough and the arterial wall stops accumulating cholesterol.

Go low enough and the macrophages actually export cholesterol back out.

That process is called reverse cholesterol transport. It only activates when the concentration gradient favors it.

At LDL 100, you are fighting the gradient.

At LDL below 60, you are working with it.

🩺 I am a practicing cardiologist.

I have patients who completed serial coronary CT angiography showing measurable plaque regression after driving LDL below 55 mg/dL with combination therapy.

That is not theoretical. That is documented in their imaging files.

⚠️ The standard target of LDL below 100 mg/dL came from population-level risk reduction trials.

It was never calibrated for regression.

It was calibrated to reduce the rate of first events in broadly defined populations.

If you already have plaque, that target is not aggressive enough.

🔸 Achieving LDL below 60 typically requires high-intensity statin therapy plus a PCSK9 inhibitor, ezetimibe, or both.

🔸 The safety data at LDL levels of 20 to 40 mg/dL now spans over 5 years across major outcomes trials. No signal for harm.

The question is no longer whether low LDL is dangerous. The question is whether your current LDL is low enough to reverse the damage already done.

❤️ Bottom line:

LDL of 100 is not a regression target. It is a compromise target borrowed from prevention trials.

Plaque regression data now spans tens of thousands of patients across multiple randomized trials.

Know your actual LDL number. Know your plaque burden. Ask your cardiologist about regression-level targets specifically. Demand serial imaging if you have known coronary disease.

A patient who drives LDL below 60 with combination therapy and sustains it for 24 months can achieve measurable plaque regression on repeat imaging.

That is the difference between managing your disease and actually reversing it.

Are you aiming to slow your heart disease down, or are you aiming to reverse it?

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #LDLCholesterol #Statins #PCSK9Inhibitors #PlaquRegression #PreventiveCardiology #MetabolicHealth

[Mouin Rabbani @MouinRabbani]

Posted by former US Congressman @AdamKinzinger on Facebook. Beautifully written, in both form and substance:

Hey everyone, happy Sunday. Are you ready for some good news? I know I am.

We are told, over and over, that America has gone cold on the rest of the world. That we have decided the people on the other side of the ocean are a threat to be kept out. That the welcome mat got rolled up and put away for good.

Then a soccer team from the North African nation of Algeria showed up in Lawrence, Kansas, and within a week the whole town was wearing green.

For today's Good News Sunday, I want to tell you about one of the best things happening in this country right now. It is happening at a soccer tournament, and it has almost nothing to do with soccer.

The World Cup is here, 48 teams playing across the United States, Canada, and Mexico. Each team in the tournament picks a base camp, one town to live and train in between matches. Germany set up shop in Winston-Salem, North Carolina. Spain is training in Chattanooga, Tennessee. And Algeria, playing two of its games up the road at Arrowhead, picked Lawrence and made it home for the summer.

What the people of Lawrence did with that is the part I can't stop thinking about.

It started small, with a whole town of people who had never given Algeria much thought deciding, more or less overnight, that this was their team now. Flags went up in shop windows. Folks pulled on the green jerseys. People drove over just to catch a glimpse of the players. And then a local news crew stopped an older gentleman on a Lawrence sidewalk, standing in front of a storefront draped in a whole row of Algerian flags he had clearly just gone out of his way to find.

They asked him what he actually knew about the country whose colors he was flying. He grinned, paused for a beat, and said something along the lines of: not much yet — but we want to welcome you here. There is no agenda in that man. Nothing performative. Just a neighbor, thrilled to his bones that these strangers chose his town, and perfectly at ease with the fact that he has a lot left to learn about them.

The welcome only got bigger from there.

The University of Kansas, the state's flagship school that calls Lawrence home, sent its marching band out to the training ground. They had spent the previous days learning Algeria's national anthem, note for note, and they played it as the players walked out for practice. Think about what that means for a moment.

These men are thousands of miles from their families, living out of a hotel in the American Midwest, preparing for the biggest sporting event of their professional lives. And the first thing they hear when they step onto the grass is the sound of their own country's song, played by a hundred American college kids in red and blue who learned it just for them. Several of the players stopped walking. A few of them looked like they weren't sure what to do with themselves.

Algeria did its part, too. The team opened a training session to the public and spent the afternoon out on the grass with neighborhood kids, walking them through drills, signing autographs, posing for pictures. There are children from small-town America who are going to be telling the story of the day they trained with a World Cup team for the rest of their lives. And the Algerians have spent the last week calling themselves honorary Kansans, falling hard for a corner of a state most of them could not have found on a map two months ago.

But it's not just Lawrence.

This is happening all over the country, in towns you would never expect.

The city of Alexandria, Virginia threw a street festival with an evening of Croatian food and music, and wrapped a city bus in the team's red and white. After crowds in Spokane, Washington flocked to watch Egyptian superstar Mohamed Salah, a brand-new Egyptian restaurant in town suddenly had locals lining up for food most of them had never tasted. All told, 19 American communities that are not hosting a single match still raised their hand to take in a national team and call them neighbors for a month.

There is a story we get told constantly about who we have become. That Americans have soured on outsiders. That we have decided the rest of the world is a threat. That we look at people who do not talk like us or pray like us or come from where we come from and see a problem instead of a person.

And then a college town in Kansas goes and learns every note of a North African country's national anthem, just so a group of strangers feel at home for a few weeks. An old local stands in front of a row of its flags and tells them, in so many words: we don't know much about you yet, but we are awfully glad you came.

That is who we actually are when nobody is telling us to be afraid. The band on the field, playing somebody else's song as if it were their own. The neighbor who knows next to nothing about you and waves you in anyway. We forget it sometimes. The good news is that it takes about one afternoon to remember.

That, my friends, is good news for your Sunday.
— Adam

[Rafael Sirera @ProfSirera]

ESR tells you that inflammation has left a slow systemic footprint.
CRP tells you that the liver is actively responding to cytokines
Procalcitonin tells you that the inflammatory programme may be bacterial or septic in nature.
They are not interchangeable clocks.
They are different biological readouts.

[Dr Alo, DO, FACC @MohammedAlo]

🚨 A viral keto study just claimed high LDL on a ketogenic diet is harmless. The researchers buried the data that proved the opposite. But the science says otherwise.

This is not a debate about dietary preference. This is about deception dressed up as research.

🔬 Here is what the KETO-CTA study actually showed.

The researchers recruited lean, metabolically healthy individuals following a ketogenic diet. Many had LDL cholesterol levels above 190 mg/dL. Some exceeded 300 mg/dL. The study used coronary CT angiography to assess plaque burden.

The headline claim circulating online: high LDL in keto dieters is benign.

That is not what the data showed.

💓 What the researchers did not lead with:

✅ Participants with the highest LDL levels had measurably higher coronary plaque volumes compared to the lower LDL subgroups.

✅ Atherosclerosis does not announce itself. It builds silently over 10 to 20 years before the first heart attack.

✅ ApoB, the direct measure of atherogenic particle number, was elevated in the high-LDL keto group. ApoB is the metric that predicts cardiovascular events better than LDL-C alone.

❌ The study had no long-term follow-up. Zero outcome data. No heart attacks tracked. No deaths recorded.

❌ The sample size was too small to draw the conclusions the authors and influencers drew from it.

❌ Calling elevated coronary plaque "not statistically significant" in a short-term study does not mean it is safe over a lifetime of exposure.

🩺 I am a board-certified cardiologist. I have seen what 20 years of elevated ApoB does to coronary arteries. No short-term imaging study reverses that biological reality.

The LDL hypothesis is not a hypothesis anymore. It is settled mechanistic science confirmed across hundreds of randomized controlled trials and Mendelian randomization studies involving millions of patients.

⚠️ Here is what happens when influencers run with cherry-picked data:

🔸 People with genetically elevated LDL stop their statins.

🔸 Young patients with familial hypercholesterolemia believe they are protected because they eat clean.

🔸 Cardiologists spend clinic visits undoing the damage of a single viral post.

That matters because plaque does not regress on its own once it forms. The window for prevention closes.

🫀 The question is no longer whether dietary fat raises LDL. The question is whether sustained elevation of atherogenic particles causes vascular injury over decades. And every line of evidence says yes.

No imaging study with no outcome data changes that answer.

❤️ Bottom line:

The KETO-CTA study did not prove high LDL is safe on a ketogenic diet. It proved that researchers can frame data to support a predetermined conclusion and that the internet will amplify it immediately.

If your LDL is above 190 mg/dL, your ApoB is elevated, and you have coronary plaque on imaging, you are not metabolically protected. You are a cardiovascular event in progress.

Get your ApoB measured. Get a coronary calcium score or CTA. Talk to a cardiologist who reads the full paper, not the press release.

That is the real story.

#Cardiology #HeartDisease #HeartHealth #CardiovascularHealth #LDL #ApoB #KetoDiet #FamilialHypercholesterolemia #PreventiveCardiology #MetabolicHealth

[Knowledge hound 📖 @HoundKnowledge]

@MohammedAlo What are your targets for ApoB, LPa