1/ A new RCT in @JAMACardio found that vitamin K2, specifically MK7, slowed coronary artery calcification progression compared to placebo in 180 adults over two years.

Promising finding. But it raises a fascinating question about how we measure cardiovascular disease. 🧵 2/ And the finding makes sense. Vitamin K2 activates proteins that direct calcium away from arteries and toward bone where it belongs. Sounds like a good thing. But does it help heart and vascular health?

A new study called NATURE-CT gives us something genuinely valuable: a look at how coronary plaque progresses naturally in relatively “low-risk” adults on no lipid-lowering therapy.

But the way some people are using it online concerns me. Let's talk about what the data actually shows and how it relates, or does not, to ketogenic therapy. 🧵 205 adults, mean age 55, no prior cardiac events, no lipid-lowering therapy, all with a baseline CAC under 100, had plaque analysis by CTA five years apart.

Total plaque volume roughly doubled.

Non-calcified plaque grew fastest. Even low attenuation plaque, the most dangerous kind, increased.

Genuinely useful reference data.

And worth noting: mean baseline LDL was only 111 mg/dL. Plaque still progressed. That should prompt us to look beyond LDL as the sole driver.

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. 🧵 The mainstream cardiology position: LDL and plaque cause heart disease/attacks, statins lower LDL and stabalize plaque, therefore statins prevent heart attacks and save lives. For preventing heart attacks, the trials are numerous and the guidelines are clear. (for saving lives, the data is weaker, but the guidelines remain clear.)

The social media position: statins are overprescribed, LDL is protective, and the side effect burden is being systematically underreported.

Here is the uncomfortable truth. Neither position is entirely wrong.

And as a caveat, yes, we have many other ways to lower LDL, but statins are often the “poster child” for this, so I will use them as the focus in this discussion.

I'm at the @APApsychiatric conference, and there is a conversation happening here that deserves a much wider audience.

Psychiatric medication deprescription. When to taper, how to taper, and who should be making that call. It is one of the most underserved questions in mental health care. 🧵 The administration has called for greater discussion about deprescribing psych meds. That has created real controversy here.

APA leaders openly acknowledge overprescription is a problem, especially with antidepressants. But these medications are also genuinely necessary and life-changing for many people. Both things are true.

In metabolic health, the most dangerous words a clinician can say are 'the science is settled.'

Here are six debates that are very much not settled, and that affect every patient I see. 🧵 Controversy #1: The Lipid “Paradox”

Is elevated LDL/ApoB inherently causative of heart disease for everyone?

Or is it one of many contributing factors that is less “causal” if your:
→ BP is normal
→ TGs are low
→ HDL is high
→ Inflammation is near zero?

Should we be studying this more?

Your veins and arteries carry the same blood. Same LDL. Same ApoB. Same everything. Yet veins almost never get plaque. Arteries constantly do.

Maybe you've seen the recent discussions about this. It's an interesting question that provides clues in cardiovascular science, and could challenge how we think about LDL and ApoB. 🧵 If ApoB-containing lipoproteins were "sufficient" to cause the disease, we should see plaque everywhere.

But we don't.

We only see it in the high-pressure, high-turbulence environment of the arterial system.

The real "experiment" happens during bypass surgery (CABG).

When a surgeon takes a pristine vein and grafts it into the arterial circulation, something changes.

Subjected to arterial pressure, that vein suddenly becomes susceptible to atherosclerosis.

Lowering TGs with pemafibrate doesnt lower CV events. Does that mean we can ignore TGs? No! A brief thread nejm.org/doi/full/10.10… Changing a lab value with a drug has NOTHING to do with changing it with a lifestyle approach Just look at HDL and CETP inhibitors.

1/ As medical director at @DietDoctor, it's my responsibility to ensure our material is accurate and trustworthy according to the latest science. Our veg oil guide has received a lot of attention lately, so I want to make sure we have objectively relayed the evidence 2/ So we will have one of our experts on our medical review board thoroughly review the guide to help us in our mission of being objective and helpful with our information. I appreciate those of you who provided constructive feedback to our guide.