It seems good in places but then in other places I'm baffled by his claims.
e.g. he claims HOMA-IR < 2.8 is fantastic (whereas anywhere else I've seen HOMA-IR > 2.0 is where you need to start getting concerned, i.e. mild IR...)
Yet he also claims fasting glucose >= 90 is cause for concern, and that ALT >= 25 is NAFLD...
Thoughts? Better Metabolic Health resources?
Hello, I (F 47) had my APOB tested for the first time about two months ago. It was 89. Since then, I have increased my cardio exercise frequency, as well as begun taken psyllium husk every day since then and doubled my omega 3 (algae) pills. I have an otherwise healthy diet and I always aim towards Mediterranean diet. My CRP has always been low, .02.
I retested after adding the psyllium husk and exercise increase and omega. Now the result is 93. I wonder if there’s any reason that it would actually be higher with these positive lifestyle changes? Or is that amount of difference and variability common within a one or two month time period? Or are temporary things like not drinking enough water before testing a factor? (Other cholesterol markers improved, only not Apob). I have one copy of Apoe4.
Hi everyone,
I wanted to share my journey thus far, in hopes that this may help at least one person. YMMV, and happy to discuss any of the below. AMA - will not be time bound and I’ll answer as much as I can in time, but could get delayed due to work and life.
I had my HA exactly 3 months ago while on vacation. Had 3 stents placed. Two in RCA, one in LAD. Funnily enough, I’m still fighting my insurance to get it reimbursed - they declined the claims because there wasn’t prior authorization (for an emergency procedure, but go figure)
Before my HA, I was a smoker for 20 plus years and diabetic for four years. Since the event, I’ve fully cleaned up my act - no smoking, no weed, barely any drinking. As I did a lot of research while on medical leave due to the HA, the main thing I learned is that this is a metabolic disease first, and it is insulin resistance that leads to fatty liver, visceral fat, and eventually plaque that gets unstable and ruptures. The few (big) changes that I made were:
Quit smoking (and marijuana) the day of the attack
Stopped eating processed foods
Cook and eat only whole foods that I cook
Healthy fats in good amounts - one avocado a day, olive oil for cooking(at least 2 tbsp), fatty fish (sardines and salmon) twice a week. Primary focus on monounsaturated fatty acids.
Huge impact - Time restricted feeding / intermittent fasting. Stop eating at 7 pm, first meal of the day at 12-1 PM (lunch) - total 18 hours fasting, 6 hour eating window. This is what allowed the metabolic switch (glucose to ketones for energy)
Huge impact - Bought a continuous glucose monitor - insurance doesn’t cover it, but doc prescribed it and it has made a big difference in helping me understand how food, exercise, sleep impact my blood glucose
Zone 2 cardio (slow jog) - 3 miles everyday;l15 miles / week. strength training 3X per week (not heavy, just resistance increasing progressively)
Sauna 4-5 times per week - helps a lot with keeping resting heart rate down
Meditation and Yoga - 1-2 times per week if I can
6- 7 hours of sleep
Therapy - once per week
ChatGPT as a second opinion provider, labs analyzer, research doer, advisor, emergency therapist when the urge to smoke comes thru a craving (ChatGPT prompt - urgent. Have a bad craving. Bring me off the ledge. 2 min talk track). See one of my older posts on how it helped save my life by diagnosing my HA while my buddies downplayed it as acidity. YMMV.
Medications: Brilinta 2X/day, 81 mg aspirin, Rosuvastatin (10mg), Ezetimbe (10mg), Losartan (25 mg), Metformin, Mounjaro (5mg, reduced to 2.5mg this month)
Supplements: COQ10, Omega 3 1000mg, Vit D3 (5000iu), Magnesium Glycinate (480mg), Calcium (Caltrate), Vit B12, One a day multivitamin.
Results: August 2025 vs April 14, 2026 (Advanced lipid panel has no past comparison, started post HA)
Weight: Down from 182lbs in August 2025 to 159.8 lbs
LDL - from 115 to 26
Triglycerides - from 165 to 47
HDL - from 39 to 59
Cholesterol - from 187 to 98
Cholesterol/HDLC ratio: from 4.2 to 1.7
Triglycerides / HDL (rough measure of insulin resistance): from 4.2 to 0.8
Non HDL Cholesterol: from 142 to 39
Apolipoprotein A1: 160
Apo B: 39
ApoB/A1 ratio: 0.24
HS CRP: <0.2
LP (a): <10
Fasting Glucose: from 105-110 to 85-90
HbA1c: From 6.3 to 5.7
Thankful for all the knowledge I have received on this forum. Happy to share more and answer any questions.

I have a 90% blockage according to PCCT Angio done recently in 1 coronary arter and 80% in another . Male 46 weight reduced and all parameters controlled over the last year. I read this article
https://pubmed.ncbi.nlm.nih.gov/31694019/ based on this i understand that if we have 0.8/kg of motsc for 4 weeks continuous - the calcification was reversed. This means if I am 75kgs = 60mg of MOTSC for 4 weeks. Wondering what 40mg taken daily could do as harm.
Already done it for a few days now but wanted to know if any one has done this daily at such a high dose. I have not experienced anything except elevated HR during workouts. Wondering what could happen if i target completing the 4 weeks daily SubQ of 40mg or more of MOTSC
33M, BMI 21.4. Non-smoker, regular cardio + weights, high-fiber diet (~55g/day). No medications, no known conditions. Posting my 2-year lipid trend — would love input from this community, especially anyone with experience with genetically-driven high HDL.
Between 2024→2026 I increased fiber from 25 to ~55g/day and reduced saturated fat (4-6x/week red meat down to ~2-3x). These changes should have stabilized or lowered HDL. Instead it jumped +46% in 2 years and the increase is accelerating (+18 in year 1, +24 in year 2). My total cholesterol rise (192→240) is almost entirely HDL-driven.
What concerns me:
After researching, the profile (high HDL + low LDL + low ApoB + low TG + elevated Lp(a)) fits CETP deficiency pattern well — reduced cholesterol transfer from HDL to LDL causes HDL accumulation. Also possibly SCARB1 variants (impaired hepatic HDL uptake).
My questions for this community:
Appreciate any insights from those who've gone down this rabbit hole.
Story seems a little biased against testing. Personally I think combining the more extensive testing with an assist from AI and a follow up with your doctor for an informed discussion is best.
I recently had a CPET (Cardiopulmonary Exercise Test) performed on a treadmill during my cardiac rehab. There was no warm-up, and I wasn't feeling at 100%, so the data should be taken with a grain of salt. Nevertheless, I hope the results are still useful, especially for defining my training zones. I am currently training for a marathon, running between 50–80 km per week.
According to the report, my VT2 (anaerobic threshold) was manually determined at ~173 bpm, which seems very high compared to my recorded max heart rate of 181 bpm. Is such a narrow margin realistic? My lactate was measured at the end of the test at 6.3 mmol/l, which seems rather low.
Is it possible to derive reliable training zones and a specific 'marathon pace zone' from this data?
Before and after 6 months 5mg rosuvastatin results as follows:
Total: 260 mg/dl > 173
LDL: 183 mg/dl > 103
Tris: 175 mg/dl > 116
HDL: 47 mg/dl > 49
My Apo(b) was INSANE last year at 167mg/dL. Slashed that down to 94.
All this with very modest lifestyle changes.
High LP(a) of 161 so I’m still going to ask my Dr about upping my dose and/or adding Ezetimibe (at r/ cholesterol advice). I was pretty pumped though to see how responsive my body was to such a small dose of the statin. I feel like I have a new body- I kind of spiraled after getting my results last year and was just accepting I’d die in my 50s.
I’m grateful I switched PCPs to someone who keeps up with this shit. If I stayed with my other dr I would have never heard of LPA or APOB nor probably had a conversation about a statin (my last drs advice for lowering cholesterol was grill rather than sauté meats).
What do you think of the convos here?
Most longevity content treats natural compounds and pharmacological mTOR inhibition as separate conversations. This piece evaluates them together on the same evidentiary spectrum, which makes the comparison more honest and more useful.
The natural compound sections are handled honestly. The mechanisms are coherent but the bioavailability critique is fair and the authors do not oversell what the preclinical data can support.
ME/CFS that I found somewhat interesting. The autophagy biomarker data from that trial provides some of the most direct human evidence I have seen linking mTOR modulation to measurable cellular repair in living patients, not just animal models.
I don't know why they included circumin, Honokiol, and withaferin. I feel like they could have just tested it against berberine and fasting. The fasting section talks about a fasting mimicking diet and does not include data for a 72 hour fast, which could be more interesting
saw it come up a few times on here. home body comp scanner using BIA, marketed as a DEXA alternative. i know BIA is hydration-dependent and notoriously inconsistent device to device. they mention an accuracy report but haven't read it. anyone compared Hume Pod readings to actual DEXA or InBody?
Just curious with this current Lipid Panel how much Rosuvastatin should I be taking? Dr prescribed me 10mg but I’m thinking 5mg might be more appropriate.
Thanks for looking!
Dec 2025 got a 463 CAC focal to a single artery, distal RCA. Everything else clean.
Feb 2026 2x CCTA attempts failed due to elevated HR non responsive to beta blockers. CAC was repeated instead... ZERO score wut?
So of course cardiologist said that's impossible so now we know nothing. I'm now scheduled for the angiogram in 2 weeks.
35F. My LP(a) was measured at 190 nmol/L four weeks ago. I found this subreddit and implemented <10g saturated fat per day and >40g of fiber per day, aiming for high soluble fiber sources. Notably, I was already vegan before, but I cut out things like coconut milk and vegan cheese and ice cream. I added daily oatmeal with chia seeds and flax seeds and most days get one or two servings of beans. I also added 4 days per week of cardio (I was doing none prior).
After these 4 weeks of diet changes, my LDL dropped from 104 to 85 but ApoB is basically stable (from 76 to 78). I also measured hsCRP this time and it was 0.5 mg/L.
None of my parents or grandparents have had heart attacks; all grandparents lived until at least late 80s and two are still alive at late 80s/early 90s with no evidence of heart disease.
I'm looking for feedback from this sub:
would you go on statins with these numbers? I'm not opposed to medication but if I can afford to wait for LP(a)-specific ones, that would probably be my preference.
is ApoB likely to improve from these lifestyle changes but is just a lagging indicator? I was surprised that I achieved a drop in LDL but not ApoB. Since ApoB is the better risk indicator, it feels like the changes aren't effective.
is it likely a preventive cardiologist would see me? I have some social anxiety around how to even make an appointment when I don't currently have heart disease.
His podcasts give the best all-around medical info for me. Hope this Epstein thing just slides and he comes back like before.
San Millán is the exercise physiologist behind a lot of the Zone 2 and mitochondrial work this world cites. He trained Tadej Pogačar. He has been on every major health podcast in the space.
He just published a funny, sharp critique of where the longevity industry has ended up. Worth a read.
title says most of what I'm thinking kind of bummed out my calcium score wasn't a zero considering I've been eating a crap ton of fiber and trying to control my saturated fat as much as possible.
should I consider any other statin other than rosuvastatin at 5 mg?
I'm to start at that dose and then repeat labs in 3 to 6 months
any advice or should I be more aggressive?
I remember all the talk a few years back here and on Huberman about nicotine being a cognitive enhancer, and some folks even chewing nicotine gum while they worked.
I was recently reading about the painter Balthus and came across this quote which was before its time on the subject;
"I intuitively understood that smoking doubled my faculty of concentration, allowing me to be entirely within a canvas,"
I found the negative to outweigh the positive for me, but it’s interesting how many artists seemed to use nicotine as an enhancer before it was known.
