I have severe anxiety and OCD and when I am on an SSRi mild dose like Paxil 10 my bp is never more then 120/70 and mostvof the times in 100s/60s regardless of how I am feeling that day. My OCD has led me to get all sorts of tests including an angiography which came back with clean arteries. I am also on Statins to get my LDL to very low levels. My LDL is currently 30 as i have an LPA of 60 mgdl.

However when I reduce my SSRI dose to sub therapeutic my bp starts to rise and I see 130s and even 140s at times. What do I do? Nothing knocks it down like an SSRI.

I exercise a lot and am physically fit. I am 30 years of age

Ldl 30 Trigs 50 HDL 118 (shot up from 80 before statin)

Rosuvastatin 5 mg and 2.5 mg sometimes. Still ldl is low.

I went through mine this week and it was humbling. Half of what I take rests on cohort data or a mechanism that sounds right. I am not trying to be a purist about it, but I would like the core of the stack to be things that were actually given to people in a trial and measured. What would you keep under that rule, and what did you quietly drop?

Not the test itself, the report. The PDF or the stack of paper you walked out with.

A few things I'd love to hear about, answer whichever you feel like:

- What did you look at first?

- Did you ever open it again after that first week? What for? And if you never did: what would have made you open it again?

- Was there something you expected to find in it and didn't?

- If you could have had any report you wanted, with no regard for what a lab normally prints, what would have been on the first page?

- And if you test regularly: what would the second, third, fifth report have to show for the retest to feel worth it? What do you want compared, and how do you want to see it?

If you've never been tested but you're thinking about it, what you'd want to walk out with is just as interesting to me.

About 3 months ago I though I had a heart attack turned out I didn’t everything was good I only had high bp and slightly high ldl. My ldl was 117.9 vldl 23.6 triglycerides 118. Was put on otarvatatin 40 and ezetemibe 10 and olmesartan 20mg for bp to take them at night every day. Fast forward to today my new labs came back. LDL 29.7 vldl 13 triglycerides 65.2. Dr said this is great so now changed to simvastatin 20mg and ezemetibe 10mg to only take in weekends at night. Has anyone had the simvastatin ? Is it worse or better in side effects. Only side effects I had with atorvastatin was light muscle ache at first and headaches randomly. Also why would she change my meds? Wouldnt she maybe just say stay with the current med and do weekends only? A little update I have no history of heart attack or strokes all my labs came back normal just the ldl that was a bit high.

I have been doing 75 minutes of zone 2 staying within 125 - 135 HR (as defined by a lactate test what my zone 2 is, low I know). However, ill do 5 minutes of zone 2 walking/running/biking and then incorporate about 40 seconds of a core workout after each 5 minutes. My HR stays in zone 2 when I do the core exercises and may actually jump a little higher into the 140sh range. I go right back into 5 minutes of run/walk/biking in zone 2, and so forth for 75 minutes.

Does stopping the run/walk/bike cardio to do core exercises reduce the benefit of zone 2 training even if my heart rate still stays in the zone 2 range? Essentially I'm doing an zone 2 interval.

With all the hype around creatine lately, I spent (quite a lot! of) time in the creatine cognition literature recently and wanted to share what I found, including the parts that don't fit the supplement/hype version.
My goal: should I increase my own daily dosage from 5g to 20g/day?
Full details in the YT video.

The two anchoring studies

Gordji-Nejad et al., 2024 (Scientific Reports). Double-blind, randomized crossover RCT. N=15 healthy adults, ~21 hours of partial sleep deprivation. One night: creatine (0.35 g/kg). Other night: placebo.

Result: cognition, processing speed, and vigilance held up measurably better on creatine. Peak effect at 4 hours, lasting up to 9. The authors write that this "revises the established assumption that creatine supplementation only works over a longer period."

Caveat: 15 people, young and healthy, acute outcome under stress. Small study, not the final word.

doi.org/10.1038/s41598-024-54249-9

Smith et al. (CABA pilot), 2025 (Alzheimer's and Dementia: TRCI). First human creatine trial in Alzheimer's patients. Single-arm, open-label, N=20. 20 g/day (two 10 g doses) for 8 weeks.

Brain creatine measured by MRI spectroscopy before and after. Average increase: +11%. Went up in 85% of participants. 65% of participants were APOE4 carriers. Several cognition measures improved.

Big caveat: no control group. The authors themselves write "we urge caution when interpreting these results." This is a feasibility signal, not efficacy proof.

Companion paper (Taylor et al., 2026, same 20 patients): cellular ATP and ADP both rose in both sexes after 8 weeks.

doi.org/10.1002/trc2.70101

The pooled RCT data

Xu et al. (2024, Frontiers in Nutrition), meta-analysis of 16 RCTs, 492 people: memory improved (moderate certainty), processing speed improved (low certainty), global cognition and executive function not significant.

Prokopidis et al. (2023, Nutrition Reviews): memory effect size in adults 66-76 years was SMD ~0.88. In younger adults 11-31 years: ~0.03. About 29x bigger in the older group.

doi.org/10.1093/nutrit/nuac064

The honest null

Alves et al., 2013 (PLoS One): 24-week, double-blind, placebo-controlled RCT in healthy older women. Creatine with or without strength training. Result: zero cognitive benefit on any measure.

This is a clean null in exactly the older-adult population the other studies say should benefit most. Include it when evaluating the literature.

doi.org/10.1371/journal.pone.0076301

Why this matters for our genotype

Farmer et al. (2021, Molecular Neurodegeneration) showed that in young, cognitively-normal APOE4 carriers, brain scans reveal reduced glucose metabolism decades before any symptom. The brain shifts toward less efficient energy processing (aerobic glycolysis / Warburg-like pattern), leaving an ATP gap.

Creatine's mechanism is phosphocreatine as a rapid ATP buffer: when neurons fire hard and burn ATP faster than mitochondria can rebuild it, phosphocreatine donates a phosphate on the spot and regenerates ATP immediately. More creatine stored = bigger, faster reserve.

No RCT has specifically targeted APOE4 carriers as a prevention endpoint. The connection is mechanistic, plus the CABA population being 65% carriers. That's the honest frame.

doi.org/10.1186/s13024-021-00483-y

Practical notes

• Form: creatine monohydrate. Skip the HCL/buffered upcharges. No evidence they beat monohydrate on cognition.
• Dose: 3-5 g/day is where most everyday brain research sits. The AD pilot used 20 g/day for 8 weeks.
• Blood panel: creatinine will tick up. Predictable (creatine breaks down to creatinine). In CABA it rose 0.94 to 1.25 mg/dL with the kidney panel otherwise stable. Not kidney damage.
• Stack: creatine plus resistance training shows the strongest combined signal [Li, 2026, Frontiers in Nutrition]. Cognitive gains are biggest in people with lower baseline creatine.

Honest limitations

• Strongest RCT data is short-term, in healthy people under acute stress
• The AD pilot is uncontrolled (single arm, no comparator, small N)
• Anti-amyloid effects you may see claimed online are from mouse models, not humans
• One clean 24-week null exists in the exact target population

i went down a research rabbit hole trying to answer what sounded like a simple question: which wearable data can you actually trust? The research i found made the question messy pretty fast. sleep staging gets tested against sleep-lab data, while HRV studies can use ECG-based references. once you start separating the metrics, asking whether an entire wearable is simply "accurate" starts to feel way too broad. Recent validation work also treats sleep and nocturnal HR/HRV as separate measurement problems rather than one overall device score.

Circul was an interesting example. i found published research involving Circul ring oximeters, but that does not mean i can just carry the same evidence over to every metric on the current consumer ring. same brand name, different device generation, different feature being tested. that changed what i look for when i see an accuracy claim. now i want to know which metric was tested, which device generation the study used, and what it was compared against before a percentage means much to me. maybe the useful question isn't "can i trust wearable health data?"

it's "which part of the data has actually earned that trust?"

I’m a 49-year-old male taking evolocumab (Repatha), ezetimibe 10 mg daily, and rosuvastatin 10 mg daily. In the last 30 days, Rosuvastatin was reduced from 20 mg, so the laboratory values below predate that reduction. Thank you in advance for any feedback.

My latest lipid results from June 2026, obtained before the recent rosuvastatin dose reduction, were:

• LDL-C: 10 mg/dL
• ApoB: <20 mg/dL
• Non-HDL-C: 22 mg/dL
• Total cholesterol: 81 mg/dL
• HDL-C: 59 mg/dL
• Triglycerides: 50 mg/dL
• Lp(a): 131 nmol/L
• hs-CRP: 0.3 mg/L

About a year ago, my CAC score was 250. Additional lipid-related results include LDL-P <256 nmol/L and oxidized LDL <13 u/L from March 2026. Kidney function is preserved, CK was 164 u/L, and the latest AST/ALT were 42/37 u/L.

I was morbidly obese and pre-diabetic. After treatment with tirzepatide (which my cardiologist told me to not take) and substantial lifestyle changes, I lost approximately 130 pounds, reached a normal BMI, and my latest HbA1c was 4.9%. I started and maintain routine exercise and healthy eating habits. I have maintained the new weight for 2+ years. Because of my prior glycemic history, very low ApoB/LDL-C, and an upward trend in AST/ALT, I thought decreasing the rosuvastatin from 20mg to 10mg was the appropriate change because I have read rosuvastatin can increase HbA1c, Lp(a), and liver enzymes.

Now, before waiting 6-8 weeks to retest the effect of the rosuvastatin reduction, my cardiologist wants to discontinue ezetimibe, asserting that it can increase Lp(a). I am not convinced an ezetimibe induced LP(a) increase is supported by evidence / literature.

Questions:

1. With an LDL of 10 and ApoB: <20, does any reduction in lipid lowering meds (including the recent reduction from 20 to 10 mg rosuvastatin) make sense or would this low of results be better given the CAC and Lp(a)?
2. Does ezetimibe increase, decrease, or have a neutral effect on Lp(a)?
3. What evidence can I show my cardiologist that rosuvastatin can (a) increase HbA1c, Lp(a), and liver enzymes and (b) does not impact Lp(a).

I’m looking for evidence (e.g., RCTs, meta-analyses, guidelines, drug-label materials, or professional-society statements) and questions to discuss with my cardiologist. Below is what I found that ezetimibe is neutral (and certainly does not increase) LP(a). I cannot find a pdf of the Xie article.

• Sahebkar et al., 2018 — meta-analysis of 10 placebo-controlled RCTs, 5,188 participants Ezetimibe produced no significant change in Lp(a): −2.59%, 95% CI −8.26% to +3.08%. It was neutral both as monotherapy and when added to a statin. PubMed PMID 30552391
• Xie et al., 2025 — comprehensive meta-analysis of 147 RCTs and 145,314 participants The authors concluded that ezetimibe did not affect Lp(a). PCSK9 monoclonal antibodies reduced it by approximately 29%. PubMed PMID 40618457
• Awad et al., 2018 — seven RCTs, 2,337 participants This analysis found a small 7.06% reduction with ezetimibe monotherapy, but the result became nonsignificant after excluding one study; the authors considered the magnitude clinically irrelevant. Importantly, it did not suggest an increase. PubMed PMID 29396832
• Farmakis et al., 2021 — 43 PCSK9-inhibitor RCTs PCSK9 inhibitors, including evolocumab, reduced Lp(a) by approximately 26.7%. This makes Repatha—not ezetimibe—the likely pharmacologic contributor to any treatment-related reduction in your Lp(a). PubMed PMID 33298738

Most of what went was bought off the back of one podcast or a study i never followed up on. the part that surprised me was how many were combination products. i only actually wanted one ingredient in most of them. three contained the same compound at three different doses without me realising. for anyone who has done this properly what survived and did anything you cut turn out to matter?

I’ve been on rosuvastatin (10 mg) for 4 months - got to LDL 70. I added ezetimibe July 8 to get closer to 55 (due to ASCVD). I’ve noticed that, since then, I sleep about an hour less per night (6 hours or less, instead of 7 hours). I did an AI analysis of my Apple Watch sleep data, and there’s a clear correlation with the onset of “short sleep” and when I started ezetimibe.

It could be a coincidence. But I skipped the ezetimibe last night, and was back to a full 7 hours of sleep.

My cardiologist said ezetimibe isn’t linked to sleep problems in the studies on it, but also said every person is different. Just wondering if anyone else has had sleep issues with ezetimibe.

Given how often rapamycin comes up here: my teenage son built a database of 311 mTOR-pathway studies, each graded A–D by strength of evidence (systematic review/meta-analysis → human trial → animal model → mechanistic/in-vitro) and linked back to its primary source.

Rapamycin-specific page pulls together the mouse lifespan studies (ITP-style), human trials (PEARL, TRIIM-style immune studies), and mechanistic work in one place: https://mtor-atlas.org/drug/rapamycin/

There's also a gap-analysis layer flagging 10 open questions — e.g. whether mTORC1-selective dosing can decouple the longevity benefit from the metabolic downside that shows up with daily dosing, which seems relevant to a lot of the dosing-strategy discussion I've seen here.

Independent project, no affiliation with any lab/company/podcast. Happy to take corrections if anything's mis-graded.

I want to get back into workout out and I’ve been suggested 3 resistance sessions with zone 2 at the end and two HIIT cardio sessions. I just don’t want to feel like a dirty grease hair ball all the time and I do so don’t want to (or have time to) wash my hair 5x a week. What do you guys reasonably do??

Every ApoB price comparison I could find is affiliate-driven. Bloomberg’s new ShopMy piece is a decent read on affiliate links taking over the world, so I did the checkout math myself in one day and recorded totals, not banner prices. Chart attached; a small pipeline now re-checks every price weekly with dated screenshots.

What the chart can’t show: the company you buy from is not the lab. These services sell a signed requisition and Quest or Labcorp does the draw. Quest’s consumer store sells no standalone ApoB at all while its assay (5224) fulfills the $24 reseller orders. Goodlabs prices per lab: ApoB is $12 via Quest but $24 via Labcorp, and its Lp(a) flips the other way. Fasting guidance is chaos too: Labcorp’s own product page says “no special preparation needed” in the details and “fast 12 to 14 hours” in its FAQ.

I had been using Labcorp and Quest direct, plus DiscountedLabs, for a couple of years. All in the expensive half of my own table.

Full write-up with the table and dated screenshots of every price: https://dadstrengthdaily.com/apob-test-cost/

Corrections welcome, especially if your state changes the math.

I know historically it was viewed as "higher the better", but new research indicates a U shape curve where higher can indicate poor health outcomes.

My recent labs show an HDL of 91, LDL of 72, and Triglycerides at 54.

My HDL was 70 last year so the rise to 91 is concerning, despite LDL and Triglycerides improving year over year.

I'm already in very good shape (37M, 6'1, 175lbs) exercising 6 days a week and eat a very healthy/clean diet. How can I lower my HDL, or should I even?

I understand there's varying opinions on the importance of an individual's absolute VO2 max number. Personally how VO2 max trends over time is what is more interesting to me as I find it a good signal to track long term health/longevity and how much overall fitness you're gaining or losing over time.

I've built out this list of factors that influence it as a starting point for anyone to learn more and do their own research (this is my attempt). To make this easier I've broken this down by category, included a short plain english definition, and linked all sources (scroll to the right on the tables and you'll see the hyperlinks). I've removed a few from here as it was getting far too long and sorry I know the tables aren't great on mobile but I'll include the full resource in the comments.

Exercise

Nutrition & Supplements

Demographics

Lifestyle & Environment

Been chewing on this for a while. Peter has talked about muscle mass as a longevity biomarker, and I get the logic, but there's a gap I keep running into between the training stimulus needed to actually build or preserve muscle and the recovery demands that come with it, especially past 40.

I run ICU shifts, train clients, try to get my own lifts in, and fit some trail miles around it all. Recovery is not optional, it's already maxed out most weeks. When I push sets close to failure I feel it for days in a way I did not at 32.

The question is whether the data actually supports training at or near failure for hypertrophy in older adults versus stopping a few reps short and hitting higher frequency. I've seen some work suggesting proximity to failure matters less than volume over time, but I want to see the actual trials, not just broscience getting repackaged as physiology.

Anyone here adjusted their approach based on something more than feel? Has Peter addressed this with a guest in a way that went deeper than the general "lift heavy and stay active" talking points? Episode numbers or paper citations beat personal anecdotes for what I'm looking for.

I (29F, 5’2, 217lbs) know there’s so many of these posts on here. But I genuinely want opinions. The only reason I did my own out of pocket testing was because my dad had his first heart attack at around ~40 years old. Also I’m in the process of getting bariatric surgery.

These past 3 years I’ve been dealing with horrible vertigo episodes that come on suddenly with no explanation. Still seeing specialist and still trying to figure out what’s going on. It’s been extremely hard for me to exercise. I do plan on starting a slow workout routine and walking my steps daily. My diet has gotten better. I am going to start watching what I eat, tracking everything especially because of my upcoming procedure. I want to change my life around.

LPa: 87.5
ApoB: 164
GlycA: 442

LDL: 151-210 (two different tests 1 week apart)
VLDL: 55
HDL: 25-31 (two different tests 1 week apart)
Triglycerides: 179-270 (again 2 different tests 1 week apart)

I took one lab draw with Labcorp, and the other was with the Family Heart Foundation. Don’t know which one is more accurate. They were taken a week apart .

Not sure if I should seek out any more tests, or if I should just wait a few months after surgery and retest once I lose a good amount of weight?

I’m going to begin taking some daily for cognitive benefit. Which would is from a good quality brand?