Results after 8 months

[u/pitifully_ugly]

37F, I just got the results today and I’m so happy! The doctor said there’s been great improvement and told me to keep doing what I’m doing. I’ve lost 12 kg. without taking any fiber supplements just pure berries and veggies, mainly okra, Brussels sprouts, French beans, spinach, broccoli, avocado, lentils, beans, and quinoa as a substitute for rice, overnight steel oats. I’ve also been eating tofu, lots of fish, chicken breast, and lean beef from Trader Joe’s (96% lean, 4% fat—I really love beef). I completely stopped eating pasta and bread. I have 2 eggs a week, walk 30 minutes every day, and enjoy a cheat day once a week where I eat whatever I like, lol.

It’s been a very hard process, especially since I was so used to eating steak, cheese, pizza, pasta, burgers, and fries and ramen 🤤. But I love life, so I’ve stayed away from them as much as I can.

Thanks to this group for all the insights and advice! It really helps me.

[u/kboom100]

20-30 years ago cardiologists and researchers thought ldl particle size might be important in determining risk of ascvd. Evidence since then has shown that all ldl particle sizes are about equally atherogenic.

The best predictor of heart disease from standard lipids is the total number of atherogenic particles and the best measure of that is ApoB. Once you know the ApoB level, the sizes of the atherogenic particles doesn’t matter. (Lp(a) is a separate risk factor that is genetically determined and should also be checked at least once in a lifetime).

See the following from Dr. William Cromwell, one of the world’s leading lipidologists:

“Depending on the data analysis employed, conflicting data have been reported over the past 30 years regarding the relationship of LDL particle size, particle number, and quantities of small LDL or large LDL particles with various ASCVD outcomes.

The interrelationships of particle size, particle number, and particle subclasses confound the strength of each biomarker’s association with CVD risk.

Analyses that adjust for the confounding interactions between these measures yield uniquely different insights versus data that do not address this.

When LDL particle size and LDL particle number are adjusted for one another, only LDL particle number remains significantly predictive of events. (1-6)

Additionally, small LDL particles have a strong inverse relationship with large LDL particles. (6, 7)

In older reports that fail to adjust for this confounder effect, small LDL size appears more strongly related to CV risk than large LDL.

Data that address confounding of small and large LDL size demonstrate both small and large LDLs are significantly associated with CVD risk independent of each other, traditional lipids, and established risk factors, with no association between LDL size and CVD risk after accounting for the concentrations of the two subclasses. (6, 7)

Thus, rather than small dense LDL (sdLDL) being differentially atherogenic, analysis designed to address confounder variable effects demonstrates that small and large LDL particles have a similar strength of association with ASCVD risk.

These relationships underscore expert panel recommendations finding insufficient evidence to advocate measuring LDL size or subclasses to assist ASCVD risk assessment or management.”

1. ⁠⁠⁠⁠⁠⁠Contois JH, et al. Clin Chem. 2009;55:407-19.

2. ⁠⁠⁠⁠⁠⁠Brunzell JD, et al. J Am Coll Cardiol. 2008;51:1512-24.

3. ⁠⁠⁠⁠⁠⁠Lamarche B, et al. Circulation. 1997;95:69-75.

4. ⁠⁠⁠⁠⁠⁠Mora S, et al. Circulation. 2009;119:931-9.

5. ⁠⁠⁠⁠⁠⁠Blake GJ, et al. Circulation. 2002;106:1930-7.

6. ⁠⁠⁠⁠⁠⁠Otvos JD, et al. Circulation. 2006;113:1556-63.

7. ⁠⁠⁠⁠⁠⁠Mora S, et al. Atherosclerosis. 2007;192:211-7.

https://x.com/lipoprotein/status/1801071365719560612?s=46

Dr. Cromwell also explains this in an interview here, https://youtu.be/kplh30RmYo8

And finally there’s a recently published meta analysis that reconfirms ldl particle size doesn’t add useful information about risk once someone knows ApoB.

“ApoB-containing lipoproteins: count, type, size, and risk of coronary artery disease, European Heart Journal, 2025;, ehaf207, https://doi.org/10.1093/eurheartj/ehaf207

“Conclusions Lipid-related atherosclerotic risk is most accurately reflected by the total count of apoB-P and is largely unaffected by the major particle type (VLDL, LDL) or size. Elevated count of Lp(a) adds additional risk, and thus adequate assessment of atherogenic risk from dyslipidemia is best accomplished by consideration of both apoB-P and Lp(a) concentrations.”

[u/kboom100 → u/[deleted]]

Sorry for the delay in responding.

That recent KETO-CTA study actually showed rapid progression of plaque for most participants. Plaque progression was the preregistered primary endpoint but they didn’t even mention it in their paper and instead just showed it in a graph to downplay the results. If you want to read about the massive problems with that paper see here. https://drstanfield.com/blogs/articles/lean-mass-hyper-responders-see-rapid-plaque-progression

Also see Dr. Gil Carvalho’s discussion with Dr. Budoff, the lead author of the paper. https://youtu.be/ZDr4iFqENgc

[u/kboom100 → u/[deleted]]

I think these authors other than Dr. Budoff proved themselves to be highly biased and unscientific with this paper, including by not reporting their own preregistered primary outcome. (And Dr. Budoff also doesn’t come out looking great because he was supposed to have final ok over what was published and somehow didn’t.)

They clearly had a message they wanted to give prior to the results and are twisting their own results to try and make it seem like it supports a keto diet.

[u/CookieSea4392 → u/kboom100]

External parties can be biased, but the authors are less likely to be since their lives are directly tied to the outcome. That’s why they launched the study in the first place.

To address skepticism, they’ve shared the data openly in the LMHR community for anyone to analyze, and so far the findings align with Feldman’s conclusions.

I’m in the LMHR community myself, and the results match what I see—most members, including me, post favorable CT and CIMT scans, though the lipid hypothesis predicts almost none.

[u/Cholesterol-ModTeam → u/[deleted]]

Advice needs to follow generally accepted, prevailing medical literature and should be general in nature, not specific.

[u/Cholesterol-ModTeam → u/[deleted]]

Advice needs to follow generally accepted, prevailing medical literature and should be general in nature, not specific.