Masters in Nutrition Science & Bachelor of Science (Physio). Author and podcast host. Science over hyperbole. Tweets are educational only, not medical advice.
@lowcarbGP@I_mitochondria A minority of people lose weight and keep it off with keto. It’s doesn’t come close to GLP-1 drugs. And that should be celebrated by everyone … if the true focus is patient outcome not dietary dogma.
Had a great conversation yesterday with @DrMauinforma which will be on The Proof channels soon.
We had been talking about this episode for about eight years. Far too long … left the conversation grateful for the value that will be provided to our listeners but also regretting that it had taken so long to make this happen.
We focussed on metabolic health, cvd, and how medicine has changed over the past decade. I learned a lot.
Feeling extremely lucky to live in 2026 and have access to such incredible medicine and clinical research.
On the eve of my 40th I had my first dose (monthly injection) of a new treatment that I’m hopeful will prevent me from ever having a heart attack or stroke.
This drug will shift my physiology towards those who won the genetic lottery when it comes to atherosclerosis. I won’t get the benefit from birth but I’ll have it from here on out.
Why take this drug?
Well, full details to come in a series of YouTube which will also include my very own serial CTA angiogram results from the Lundquist Institute.
For now here’s some background information:
I had two scans done so I could see my baseline level of plaque and annualised plaque progression.
These scans were done under the supervision of @BudoffMd using the same machines/tech (Qangio and Heartflow analysis) as done in the latest Keto-CTA study (led by @realDaveFeldman) allowing for a reasonable comparison group (metabolically healthy individuals without a prior cvd event not on lipid lowering therapy). Yes I’m an n=1 and comparing myself to the mean has limitations but it’s helpful for me as an individual.
The main difference being that at age 29 I changed to a high fibre low saturated fat diet which lowered my LDL-C and ApoB to 70-90 mg/dl over the last decade.
In KETO-CTA 21% had a PAV annual change of 1% or higher by QAngio. That’s considered rapid progression. And total plaque grew by 18.7 mm3 per year on average (mean 18.7 mm3/median 6.6mm3).
I can also compare my results to Nature-CT - a great new study performed by @RonKarlsbergMD with annualised plaque progression for untreated (not on lipid lowering therapy) adults with average LDL-C of 111mg/dl. Over 5 years the group median non-calcified plaque nearly doubled. Total plaque grew by +6.7 mm3 per year (much less than KETO-CTA) despite 54% having a CAC of 0. Showing plaque progression in untreated adults with ‘normal’ cholesterol levels.
Episodes with CT imaging experts and clinicians will be found on my YouTube channel and made freely available so you can understand the science and decision making process here - and perhaps apply it to yourself with your own doctor.
Any guesses of what drug this is?
Hint: it’s thought to act peripherally - doesn’t cross the blood brain barrier. And it acts in circulation but its desired effect plays out at the liver (hepatocyte).
https://t.co/MVy8aiBIjN
👉This new Mendelian randomization study, including more than 425,000 participants from the UK Biobank, provides important insights into the specific causal effects of Lp(a) and its implications for future Lp(a)-lowering therapies.
☝️Top 5 Take-Home Messages
1️⃣ Lp(a) exerts a direct causal effect on coronary artery disease (CAD), independent of LDL-C. This reinforces that Lp(a) is not simply another LDL particle, but an independent driver of atherosclerosis.
2️⃣ Among 1,456 phenotypes analyzed, only CAD and HbA1c showed direct causal effects of Lp(a). Most other associations appear to be indirect or mediated through other pathways, highlighting the remarkable specificity of Lp(a).
3️⃣ Very low genetically determined Lp(a) levels were not associated with a higher risk of type 2 diabetes. These findings provide reassuring evidence for the long-term safety of profound Lp(a)-lowering therapies currently under development.
4️⃣ The optimal Lp(a) threshold for myocardial infarction risk discrimination was ~86 nmol/L in Europeans and ~93 nmol/L in Africans, suggesting that clinically relevant risk may begin at lower levels than the current 125 nmol/L cutoffs adopted by many guidelines.
5️⃣ The study supports treating LDL-C and Lp(a) as complementary but distinct cardiovascular risk factors. Even with optimal LDL-C control, elevated Lp(a) remains a causal contributor to coronary disease, emphasizing the need for dedicated Lp(a)-lowering strategies.
☝️Bottom line: Lp(a) appears to have a highly specific causal role in coronary atherosclerosis, independent of LDL-C, while concerns about diabetes risk from very low Lp(a) levels are not supported by this large Mendelian randomization analysis.
🔓🔗 https://t.co/hR9dfiOzrJ
@society_eas@nationallipid@JACCJournals
Most of the GLP-1 conversation is still about the drugs, not the biology they operate within. What are three types of hunger? What are the four phases of satiety? And what does "prehab" actually mean before starting medication?
In this episode, I sat down with Dr Federica Amati, Head Nutritionist at ZOE and author of The Appetite Reset, to unpack the science of appetite for everyone, on or off medication.
For the full show notes head to: https://t.co/ZsyQYSh7Cy
Some of my latest labs with @function
Note these lab tests are before commencing lipid lowering therapy (my baseline). Point being my goal is to get ApoB down from 75 mg/dl (where I sit with diet/lifestyle alone) to under 50 mg/dl.
Why? Details to come on YouTube
https://t.co/yDFoQqCqfU
Chat to a cardiologist. Note: side effects of statins are overblown on social media. They’re real but less common and severe than many make out. If you don’t want to take a statin there’s other options now to lower ApoB - ezetimibe, bempedoic acid and pcsk9 inhibitors. With the latter you get that Lp(a) down a fraction too.
@DrNadolsky Triumph cvd days will settle it.
retatrutide's point estimate for HR increase runs modestly higher than tirzepatide's in indirect comparisons, with a dose-dependent peak approx 24 weeks, but there's no head-to-head trial yet that I can find
Personally I'd say it's because its unsustainable and the initial benefits wear off. Similar to restrictive vegan diets.
Most diets have poor long term weight loss results. What's the point of restricting carbs if the weight is coming back on. Which is what happens to most people.
GLP-1's have provided a better solution.
Treat the Plaque. Not the Risk Factors.
For decades, preventive cardiology has largely operated under a simple assumption:
Measure risk factors.
- Estimate risk.
- Treat risk.
But there is a problem.
Many myocardial infarctions occur in patients who would never have qualified for aggressive prevention based on conventional risk scores alone. Meanwhile, many individuals with multiple risk factors will never experience a cardiovascular event.
Why?
Because risk factors are not the disease.
Atherosclerosis is the disease.
A patient does not suffer an MI because their SCORE2, PCE, LDL, ApoB, hsCRP, or Lp(a) is elevated.
They suffer an MI because they have developed coronary atherosclerosis.
Yet we continue to spend enormous effort measuring surrogates while often ignoring the organ that actually matters: the coronary arteries.
This review argues that coronary CT may allow a shift from population-based prevention toward disease-based prevention. Not by predicting who might develop atherosclerosis, but by directly visualizing who already has it.
Perhaps the most provocative observation is that, in large contemporary cohorts, total plaque burden and non-calcified plaque often outperform stenosis severity itself as predictors of future events.
That should make us pause.
For years we have been obsessed with narrowing.
Meanwhile, the disease was sitting in the vessel wall.
The future of prevention may not be:
👉 Treat the cholesterol.
👉 Treat the inflammation.
👉 Treat the risk score.
The future may be:
- Identify the plaque.
- Quantify the plaque.
- Track the plaque.
- Treat the plaque.
Everything else is a surrogate.
#CardiacCT #CCTA #Atherosclerosis #PreventiveCardiology #TreatThePlaque #CardiovascularImaging #PrecisionMedicine #PhotonCountingCT #PCCT
@SteAssent@BenBikmanPhD@cleanformnut Yep… that’s correct. It’s a little weird. I think people just want to have something unique to say that grabs attention.
@KenDBerryMD@Neuroscope_mp Not everything has to do with keto my friend. Unfortunately the reality is keto has failed to address poor health in America at a population level.