#BlackFriday

These kind of purchases makes us happy:

1. Experiences: Trips, travel and activities.

2. Time-saving: Services like grocery delivery or cleaning services free up time.

3. Altruism: “Pro-social” spending, like gifts and donations to charities.

www.sciencedirect.com/science/chap...

Our takeaway is that the LMHR profile does not appear protective. Plaque grew fast—even with low inflammation, low TG, high HDL, and no metabolic syndrome.

13/14

In short, the KETO-CTA study raises several ethical concerns:
🔹 The primary outcome was never reported
🔹 Median change was shared on Twitter, not in the paper
🔹 Focus shifted to post hoc analyses
🔹 The study is called a "trial"—but it’s not

12/14

Moreover, increases in PAV can’t simply be blamed on statins.

Statins shift plaque toward calcification—they don’t raise unstable plaque.

Yet LMHRs (on no meds) had a PAV increase of 0.8%.
That’s not a statin artifact.

11/14

Some argue it’s unfair to compare LMHRs to high-risk groups—because those were often on statins. But LMHRs are often viewed as being “too healthy” to need meds.

10/14

PAV (Percentage Atheroma Volume) also increased by 0.8%.

This is:
– Higher than in many statin-treated patients
– Double the increase seen in low-risk untreated cohorts
– Close to the 0.93% threshold for increased CV risk

9/14

We eventually got one of the missing numbers via social media: A median increase in NCPV of 18.8 mm³ (~44% increase).

This is as fast or faster than what we see in diabetic and/or high-risk groups. That's despite these participants being “metabolically perfect”!

8/14

So what did the authors report instead? A post hoc analyses showing that ApoB did not correlate with plaque growth.

This is misuse of the data—and it's not acceptable in scientific publishing.

7/14

The primary outcome was not reported.
❌ No data in results
❌ Not in the abstract
❌ No statistical tests

6/14

The pre-registered primary outcome was a change in non-calcified coronary plaque volume (NCPV) over 1 year.

This type of plaque is soft and rupture-prone—the kind that causes heart attacks.

Here’s the problem 👇

5/14

The study enrolled 100 LMHRs who had:
– ≥2 years on keto
– No meds
– No smoking
– Normal HbA1c, glucose, BP, hsCRP
– LDL-C increase of ≥50% from baseline

A highly selected group—probably the “best case scenario” for testing this hypothesis.

4/14

LMHRs are defined by:
🔸 LDL-C ≥190 mg/dL
🔸 HDL-C ≥60 mg/dL
🔸 TG ≤80 mg/dL
They’re lean, insulin-sensitive, and otherwise healthy.

Many claim their LDL-C increase on keto is harmless or even protective of atherosclerosis. KETO-CTA was supposed to test that.

3/14

The study asked a good research question: Can extremely high LDL-C in healthy, keto-adapted people still promote atherosclerosis?

The lead author of the study is Adrian Soto-Mota, with co-authors Dave Feldman, Nick Norwitz, and Dr. Matthew Budoff.

2/14

We just published a critical review of the KETO-CTA study — the first study to examine coronary plaque progression in Lean Mass Hyper-Responders (LMHRs) on a ketogenic diet.

Here’s why we believe the study’s results have been seriously misrepresented.

1/14