Cardiovascular Health 2026

Phred CAC history

The last one was a CCTA. I do seem to have plateaued after possibly backing it up a little in 2022. I did keto and a huge amount of exercise back then, getting my 2 mile down to about 15 minutes. I think it made my CAC worse, don’t know about my ACM. I started having injuries and really can’t run like that any more. Recently got PRP for my labrum and should be better in a couple months.

The only explanation I have is hugely unpopular here. I tested high for lead and used every form of chelation I could find. High heavy metal load causes heart disease. I think it helped several of my issues and I may be on the mend now for good. My LDL has not moved in the entire time. Always between 160 and 130. I tried statins, Repatha, ezetimbe (I use it now off and on and it works some), and now Leqvio but will soon quit it because it doesn’t work at all. I know I could get the LDL down with drugs if I put my mind to it. I’m not sure it needs to be lower and defer to the judgement of my ancestral DNA.

it is the test that is high sensitivity not the CRP.

Although obicetrapib has no effect on hs CRP, it is today given marketing approval in the EU
NewAmsterdam Pharma and Menarini Group Receive European Commission Approval for Ubeslo® (Obicetrapib Monotherapy) and Evlarco® (Obicetrapib Plus Ezetimibe Fixed-Dose Combination) — NewAmsterdam Pharma

3 Likes

The European Commission approval follows the positive opinion adopted by the European Medicines Agency’s Committee for Medicinal Products for Human Use (CHMP) and is supported by data from NewAmsterdam’s comprehensive clinical development program evaluating obicetrapib, including the Phase 3 BROADWAY, BROOKLYN and TANDEM trials, which demonstrated statistically significant LDL-C reductions of up to 40% with obicetrapib monotherapy versus placebo and approximately 50% with obicetrapib combined with ezetimibe versus placebo, with a tolerability profile comparable to placebo. NewAmsterdam and Menarini continue to advance the clinical development of obicetrapib through multiple ongoing Phase 3 trials, including PREVAIL, a cardiovascular outcomes trial, as well as REMBRANDT and RUBENS.

3 Likes

I walk daily, averaging 9000 + steps, and my hsCRP is 0.2 - could be connected to staying active.

3 Likes

It appears that low levels of hsCRP and IL-6 are not meaningfully protective against MACE. It remains the case that higher levels are worse, but low levels are not protective.

4 Likes

Lipoprotein(a) Management Simplified: The National Lipid Association Lipid Simplified Series

Highlights

  • This document aims to provide practical guidance on testing and management of Lp(a) for primary and secondary ASCVD risk management
  • There is a graded relationship between Lp(a) level and ASCVD risk
  • The 2026 ACC/AHA Multisociety Guideline on the Management of Dyslipidemia joins recommendations from the NLA and others for universal Lp(a) screening in adults at least one time
  • Lp(a) levels are mostly determined by genetic factors, but specific conditions may warrant repeat testing, especially for individuals with intermediate levels
  • Cascade screening of first-degree relatives is also recommended, especially with a family history of premature ASCVD
  • Strategies to reduce ASCVD risk, including lifestyle interventions and pharmacologic lipid-lowering therapies, may be intensified in adults who have high Lp(a)
  • Phase III cardiovascular outcomes trials, in both primary and secondary prevention settings, are in progress and the first of its kind trial is expected to report in 2026
1 Like

Interesting and informative clip: We Are Witnessing The End of Heart Attacks

Kind of makes sense, if you reduce/stop all risk factors that contribute/cause CVD’s then it makes sense there won’t be any heart attacks.

We Are Witnessing The End of Heart Attacks - YouTube

2 Likes

FWIW, not the greatest, but somewhat interesting.

Examining the Differences in Frequency of Whole Fruit or 100% Fruit Juice Intake among United States Adults With and Without Cardiovascular Disease Risk Factors: Analysis of 2019 Behavioral Risk Factor Surveillance System Data

https://cdn.nutrition.org/article/S2475-2991(26)01882-2/fulltext

Pop-sci article:

A survey of 371,000 adults links heart disease to eating whole fruit less often

3 Likes

Now they have put in more usage limits at OpenAI it takes about 30% of my 5 hour chatGPT Astra max subscription to do one paper review. I hope people find this useful. I find the reviews quite good and they find things that maybe should have been found in peer review.

This is a large descriptive study with modest novelty. It finds that adults reporting several cardiovascular conditions eat whole fruit slightly less frequently, while the findings for fruit juice are mixed. It cannot establish whether either dietary pattern caused disease. Two reporting errors also warrant attention.

The paper is by Kesler and colleagues: Examining the Differences in Frequency of Whole Fruit or 100% Fruit Juice Intake among United States Adults With and Without Cardiovascular Disease Risk Factors , published in Current Developments in Nutrition in 2026. PIIS2475299126018822(1)

The study compares dietary frequency between people with and without reported cardiovascular diagnoses. It analyses 371,038 adults from the 2019 US Behavioral Risk Factor Surveillance System, a telephone survey.

Participants reported how often they consumed whole fruit and 100% fruit juice, and whether a health professional had ever diagnosed:

  • High blood pressure.
  • High cholesterol.
  • Heart attack.
  • Angina or coronary heart disease.
  • Stroke.

The researchers used survey weights and accounted for the sampling design. Adjusted analyses included age, education, income and smoking. The methods also mention race and ethnicity, although the table footnotes omit them.

Crucially, the dietary measure was consumption occasions, not portion size, grams of fruit or millilitres of juice . Average reported frequency was 1.06 occasions per day for whole fruit and 0.30 for juice.

The adjusted results were as follows. Differences compare participants reporting each condition with those not reporting it; negative numbers mean less frequent consumption.

Reported condition Whole-fruit difference, occasions/day Adjusted p-value Juice difference, occasions/day Adjusted p-value
High blood pressure -0.087 <0.0001 +0.002 1.000
High cholesterol -0.081 <0.0001 -0.023 <0.0001
Heart attack -0.062 <0.0001 +0.043 0.0187
Angina or coronary heart disease -0.053 0.0034 +0.005 1.000
Stroke -0.037 0.1343 +0.029 0.0700

The p-values incorporate the authors’ Bonferroni correction for five cardiovascular comparisons. Figures are rounded from the detailed results accompanying Tables 6 and 7.

Whole-fruit consumption remained significantly lower for four of the five conditions. For juice, only two associations remained significant: lower frequency with high cholesterol and higher frequency with a history of heart attack . The adjusted stroke associations were not statistically significant for either fruit or juice.

The novelty is primarily the scale and specific US population comparison. The paper supplies a large set of estimates describing fruit and juice consumption among people with different cardiovascular histories.

However, separating whole fruit from juice in cardiovascular research is already established. The earlier EPIC-NL study followed 34,560 participants for an average of 14.6 years and examined both exposures against subsequent cardiovascular events. It reported favourable associations for moderate juice consumption, although residual confounding remained possible. Cambridge Core

A subsequent EPIC-NL analysis also explicitly modelled substituting juice for whole fruit or sugar-sweetened beverages. Substitution of juice for fruit showed no statistically significant association with cardiovascular disease after adjustment. That does not establish equivalence, but demonstrates that more directly comparative analyses already existed. Cambridge Core

The authors emphasise their approach of treating cardiovascular status as the predictor and dietary frequency as the outcome. That changes the descriptive question being asked, but reversing the regression direction does not establish which came first . There is no new biological mechanism, intervention or causal method here.

The study has useful strengths. Its large sample provides precise estimates of average differences. The analysis incorporates survey weights, clustering and stratification, separates juice from whole fruit, and corrects for multiple comparisons. The authors also acknowledge many limitations and use publicly available data.

My main criticisms concern interpretation, measurement and reporting.

  1. **The timing of diet and disease is unresolved.**Current reported eating habits are compared with diagnoses that could have occurred years earlier. Participants might have changed their diet after a heart attack or cholesterol diagnosis. Disease, disability or changes in appetite could also affect food choices.Consequently, the findings are compatible with diet influencing disease, disease influencing diet, or other factors influencing both. They do not estimate the effect of fruit consumption on future cardiovascular risk.The discussion suggests that a health scare might explain some findings. That is plausible, but the disappearance of an association after adjustment does not demonstrate a post-diagnosis change in behaviour.
  2. **Frequency is a weak measure of dietary exposure.**Someone drinking a small glass of juice once daily and someone drinking a large glass once daily receive the same frequency score.Without quantities, the study cannot establish a dose-response relationship, distinguish moderate from high-volume juice intake, or quantify sugar, energy, fibre or polyphenol exposure.It also cannot determine whether juice replaced whole fruit, another beverage or nothing. Participants could consume both fruit and juice, so these are not mutually exclusive dietary groups.
  3. **The absolute differences are small, despite very low p-values.**The statistically significant adjusted whole-fruit differences correspond to approximately 0.37 to 0.61 fewer consumption occasions per week .For juice, the heart-attack association corresponds to approximately 0.30 additional occasions per week , and the cholesterol association to 0.16 fewer occasions per week .These differences may have descriptive population value, but their clinical significance is unknown. A very large sample can make small differences statistically convincing without showing that they meaningfully affect health. The study provides no estimate of cardiovascular risk reduction or increase attributable to these differences.
  4. **Adjustment leaves substantial scope for confounding.**Sex is absent from the reported adjustment set. Physical activity, BMI, broader dietary patterns and sugar-sweetened beverage consumption were also not controlled; the authors acknowledge these latter omissions.Whole-fruit consumption could therefore be acting partly as a marker of other behaviours or circumstances. The appropriate adjustment strategy would depend on a clearly specified causal question, which this descriptive analysis does not resolve.Reporting is also inconsistent about whether race and ethnicity were included. A complete model specification and analysis code would improve reproducibility.
  5. **Self-reported diagnoses and selection limit interpretation.**Reporting that a clinician has diagnosed high cholesterol is different from having a measured current LDL cholesterol concentration. It depends on testing, access to care, recall and treatment history. Some people in the comparison group may have undiagnosed conditions.The study also concerns surviving, noninstitutionalised survey respondents. It cannot capture people who died from cardiovascular disease, and missing dietary responses led to substantial exclusions. Survey weighting helps address known sampling differences but cannot guarantee elimination of selection bias.
  6. **The proposed mechanisms were not tested.**The discussion places considerable emphasis on fibre, polyphenols and differences in their bioavailability between fruit and juice.These are reasonable hypotheses, but the study measured none of those exposures directly. It did not measure relevant metabolites, microbiome changes or physiological responses. It therefore cannot identify which constituent, if any, explains the associations.

There are also specific reporting problems that should be corrected:

Location Problem
Abstract States that lower whole-fruit frequency remained significant for all five conditions after adjustment. For stroke, Table 7 reports p = 0.1343, which is not significant.
Discussion, page 7 One sentence says both high cholesterol and heart attack were associated with greater juice frequency. The cholesterol association was actually with lower frequency.
Titles of Tables 6 and 7 Describe the “impact” of intake on cardiovascular risk factors, although the stated models predict intake frequency from cardiovascular status. This misstates the model direction and implies more causality than the design supports.

These discrepancies do not by themselves invalidate the numerical analyses, but they can materially mislead readers relying on the abstract or discussion.

The paper discloses that the first author was employed by VDF FutureCeuticals and received tuition reimbursement from the company. USDA funding is also reported. This is relevant context for assessing interpretation, although it is not evidence that the results are biased.

A stronger follow-up would measure food and juice quantities repeatedly before and after diagnosis, validate cardiovascular outcomes, and explicitly examine dietary substitutions. Testing the proposed mechanisms would additionally require measured nutrient exposures and biological responses.

3 Likes

Full writeup here:

4 Likes

I mean, I’m happy he turned around and found a more evidence based path, and respect for being able to publicly change his mind, so I’m not going to criticize him, but… I can’t help but be dismayed how he fell into the denialist camp in the first place. Seriously - this is your health, your one and only body - this is not like arguing which oil is best for your car engine, if wrong, you can always get another car. If this was some unclear case, I could understand - but the evidence was there all along, all you had to do is read the damn papers and look at the bloody evidence! Like, before you decide to take or not any medication, don’t you do tons of research to make sure you understand all the risk/benefit and applicability scenarios?? It takes me months/years, to get on any med, or even switch between classes of statins from atorvastatin to pitavastatin. And regardless of how much I learn, I guess I’m just not bold enough to then start “teaching” whatever I think is the truth, become an “influencer” or whatnot - participating on a site like this is as far as I’ll go. Yet there he was, actually teaching that wrong-headed stuff that he gleaned from dogdy doctors, misinformation and a complete lack of basic analytical skills. If you ever step up to actually teaching people, I imagine you’d move heaven and earth before you dared to open your mouth, because it’s a huge responsibility when you are dealing with life and death and health issues. I don’t think I would ever feel I’ve studied enough to be so bold. I’m content to implement my research in my own life, and at best share opinions on a board like rapamycin.news., frequently with the disclaimer and caveat YMMV.

Almost all the papers he cites were there before he fell into the denialist camp. He could have read them. Why is he listening to anyone telling him what to do with his health based on someone’s “authority” - is that part of the conservative tendency to worship authority? It can’t even be that, because the consensus of establishment was firmly in the lipid and statin corner. Perhaps it’s another tendency - to follow charismatic personalities, to believ that some person is the “holder of truth”, and you then rely on their word without questioning. I don’t even know why we need to bring politics into this - as he did - because it doesn’t matter if you are a lefty or rightwinger, you can read a study just as well - politics is not an excuse! You have a brain, regardless of your politics, use it.

The problem is in not carefully looking at the evidence in the first place. Unless he really learned his lesson, he could fall into another dogma again just as easily.

4 Likes

Another look, not new, but worth revisiting. The STAREE trial was discussed in this thread above back at the end of August.

Atorvastatin, Cardiovascular Events, and Disability-free Survival in Older Adults

https://www.nejm.org/doi/full/10.1056/NEJMoa2607314

"RESULTS

A total of 9971 participants were enrolled: 4984 were assigned to receive atorvastatin and 4987 to receive placebo. The mean (±SD) age of the participants was 74.7±4.5 years, and 51.9% were women. After a median of 5.9 years, a primary cardiovascular event had occurred in 297 participants (10.9 events per 1000 person-years) in the atorvastatin group and in 412 participants (15.5 events per 1000 person-years) in the placebo group (hazard ratio, 0.70; 95% confidence interval [CI], 0.61 to 0.82; P<0.001). Death from any cause, dementia, or persistent physical disability occurred in 637 participants (21.6 events per 1000 person-years) in the atorvastatin group and in 676 participants (23.0 events per 1000 person-years) in the placebo group (hazard ratio, 0.94; 95% CI, 0.84 to 1.05; P=0.25). Serious adverse events occurred in 131 participants (2.7%) in the atorvastatin group and in 129 (2.7%) in the placebo group, with musculoskeletal, hepatobiliary, and diabetes-related adverse events occurring more commonly in the atorvastatin group.

CONCLUSIONS

Treatment with atorvastatin led to a lower risk of major cardiovascular events than placebo at a median of 5.9 years but did not result in longer disability-free survival among community-dwelling older adults without clinical cardiovascular disease.(Funded by the National Health and Medical Research Council and others; STAREE ClinicalTrials.gov number, NCT02099123.)"

3 Likes

Serial Changes in Epicardial Adipose Tissue Attenuation Identify Residual Atherosclerotic Risk Independent of LDL Lowering

https://www.jacc.org/doi/10.1016/j.jcmg.2026.05.014

This study is about what drives coronary plaque progression, even after LDL is lowered. Participants were stratified into three target LDL cholesterol groups, and more than half of the participants in every single group experienced an increase in noncalcified plaque percent atheroma volume. The LDL groups were:

  • LDL <1.4 mmol/L (<55 mg/dL): Plaque progression was observed in 52.2% of participants (12 out of 23).
  • LDL 1.4–1.8 mmol/L (55–70 mg/dL): Plaque progression was observed in 50.0% of participants (22 out of 44).
  • LDL >1.8 mmol/L (>70 mg/dL): Plaque progression was observed in 57.1% of participants (133 out of 233)

What drives plaque progression:

  • Adipose tissue composition and inflammatory activity , rather than total fat volume , drive ongoing noncalcified plaque remodeling
  • Epicardial adipose tissue (EAT) attenuation serves as a marker for residual inflammatory risk, driving ongoing atherosclerotic plaque progression even when LDL cholesterol goals are met.
  • Regional epicardial fat inflammation likely influences coronary plaques via localized pericoronary adipose tissue (PCAT) signaling pathways

So even when patients achieve aggressive lipid targets (<1.4 mmol/L or <55 mg/dL), standard lipid-lowering therapy alone does not fully arrest plaque progression. Ongoing noncalcified plaque remodeling in these patients was driven by non-lipid pathways—specifically residual inflammatory activity captured by changes in epicardial and pericoronary adipose tissue attenuation.

1 Like


Nice

6 Likes

Well, as I’ve posted before there are tons of studies addressing this - here’s a few (I’ll cross-link in the other thread).

SGLT2 inhibitors are associated with reductions in epicardial adipose tissue volume and thickness: a meta-analysis

https://www.nature.com/articles/s41366-026-02110-6

Empagliflozin Suppresses the Differentiation/Maturation of Human Epicardial Preadipocytes and Improves Paracrine Secretome Profile

The article:

Empagliflozin significantly reduced epicardial adipose tissue, subcutaneous adipose tissue, myocardial extracellular volume, matrix volume, cardiomyocyte volume, aortic stiffness and several inflammatory biomarkers, compared to placebo in nondiabetic patients with HFrEF.

And the above referenced in full:

Mechanistic Insights of Empagliflozin in Nondiabetic Patients With HFrEF: From the EMPA-TROPISM Study

https://www.jacc.org/doi/10.1016/j.jchf.2021.04.014

Effect of empagliflozin on ectopic fat stores and myocardial energetics in type 2 diabetes: the EMPACEF study

Effect of SGLT2-Inhibitors on Epicardial Adipose Tissue: A Meta-Analysis

https://www.mdpi.com/2073-4409/10/8/2150

High released lactate by epicardial fat from coronary artery disease patients is reduced by dapagliflozin treatment

https://pubmed.ncbi.nlm.nih.gov/31783199/

Effects of Empagliflozin on Carotid Intima-Media Thickness and Epicardial Fat Tissue Volume in Patients with Type-2 Diabetes Mellitus

3 Likes

Yep, both SLGT2i and GLP1s reduce epicardial fat volume and inflamation

3 Likes

It is actually very easy to fall into that trap. For the longest time, I used to get influenced by that space and didn’t know any better. I just didn’t see any “evidence based” doctors with any sort of platform so it was mostly those people running free. I was taking about 30-40 supplements and no statin thinking it was bad. I never fell for the LDL is good trap though because I would see the number clearly go up if I started eating worse and knew that eating worse wasn’t healthy.

Once the more evidence based folks starting actually addressing each of their points and debunking them with evidence, I started to realize there was another side to the story. I credit Layne Norton with really being one of the firsts to do this and now it’s become widespread (Gil and Stanfield come to mind).

I give this guy a lot of credit for admitting his wrongs. Sure, it’s easy to say he should have known better in the first place but at least he arrived in the right spot in the end. Hopefully, it encourages others to admit their wrongs as well.

I will also add that most of my friends tend to be more conservative so I hear them say a lot of crazy things when it comes to health. I am more independent and aligned with them on other topics in general, but they are taking every peptide you can imagine, NAD injections, megadosing vitamin d, no statins, think seed oils are the worst thing ever, etc. I’ll help them if they ask but it is a waste of time to correct them all.

5 Likes

Aren’t we living in interesting times that what you think about science is commonly dependent on your political beliefs.

PS, I always admire you for admitting your past mistakes and making a better path forward for yourself.

3 Likes

People tend to be tribal in their thinking. Hence even policy viewpoints can depend on the tribe that people associate with rather than people associating with a political tribe because they agree with the policies.

People tend to disassociate with a tribe when the leaders of the tribe do things that they dislike normally because it causes them problems (or people close to them).

Sadly, but not surprisingly necessarily, this goes as far as scientific views.

4 Likes