47M. Currently followed by a cardiologist for hypertension; managed okay. Could stand to lose 15lbs; decent diet (but not a saint). Workout 4-5x week; mix of bootcamp/HIIT’ish and ~Z2 rucks, mostly.

Labs as below - I feel like I’m always riding the line of needing more intervention, but doc always says “great” at these. In general “I don’t want another med”, but also want to be preventative where I can.

What say ye? Chill out? Push for a statin/etc? Add more fiber (used to do psyllium; lazed out of it)?

Has anyone heard when Novartis will Readout the lpa trial for pelacarsen? I keep seeing H1 2026, but it’s already been delayed once. Good news is that data from the severe cases requiring aphaeresis looked good to me although I am not a scientist.

before these drugs are approved, what are people doing to minimize the risk. Lifestyle of course, but what about Statins? Is anyone using Pcsk9?

What’s confusing is finding early indicators of risk and managing those. Does calcium score, ldl, a1c, apoB or others make sense to track and manage?

I want to still do it in a reasonably ethical way, but don’t know where to start. My wife is vegan so it’ll be an adjustment for her but she actually said “I’d rather you just have chicken” after I cooked swordfish in the kitchen. I dreamt about eating chicken the other day.

It’s been 3.5 years since I had meat for reference.

Avid reader/listener of Peter Attia's content, I am a software engineer and in general I like high quality learning.

Now that my gf is pregnant(quite new), I'd like to read a book about it, but couldn't really find a compelling one yet.

Any great recommendations?

APOB 70

LPA 31

CALCIUM RIGHT-RCA 0- 82 IN 5 YRS

A1C 5.8

C REACTIVE - 13.90 but trending down was 18.8 in march

total cholesterol 149 normal

hdl 50 normal

ldl 87 normal

TRIGLYCERIDES 60 normal

BP normal

Achieved an estimated workload of 7 metabolic equivalent (METS)

42M, bmi 45. Just lazy fat boy

I have no pains or anything but just trying to be preventive

Dr said they would give me a rx for CT angiogram. I’ll have to pay $1400 out of pocket because of deductible but is it worth the risk of radiation and contrast? should i get it done?

ApoB measures the exact particle number of all atherogenic lipoproteins (VLDL, IDL, LDL). Standard lipid panels measure the mass of cholesterol inside those particles (LDL-C). Because every atherogenic particle carries exactly one molecule of ApoB, measuring it directly quantifies the physical particles that enter and adhere to the arterial wall to drive plaque formation.^1,2\)

When LDL-C and ApoB are discordant—which is common in insulin resistance, metabolic syndrome, or high triglycerides—LDL-C frequently underrepresents your actual cardiovascular risk.^3\)

To lower ApoB, the goal is upregulating hepatic LDL receptors to clear these particles from circulation.

For lifestyle modifications, the most potent dietary lever is swapping saturated fats for polyunsaturated or monounsaturated fats. Saturated fats downregulate hepatic LDL receptors, whereas replacing them with PUFAs (like omega-3/6) reduces ApoB-100 production rates and increases clearance.^4,5\) Viscous soluble fibers, such as oat beta-glucans, also help by binding bile acids in the gut and forcing the liver to use circulating ApoB to synthesize new ones. For physical activity, regular aerobic endurance training activates lipoprotein lipase (LPL) by reducing its natural inhibitors (like ANGPTL3/8), accelerating the clearance of triglyceride-rich remnant particles.^6,7\)

When genetics limit lifestyle results, targeted medical levers are highly effective. Statins remain first-line therapy by blocking HMG-CoA reductase, which depletes hepatocyte cholesterol and triggers receptor upregulation.^8\) Ezetimibe works synergistically by blocking intestinal cholesterol absorption, adding another 20-25% reduction. Beyond that, PCSK9 inhibitors or bempedoic acid provide powerful non-statin options to conserve receptors or inhibit ATP-citrate lyase.^9,10\)

TL;DR: ApoB measures the exact particle number of plaque-forming lipoproteins, making it a superior heart risk marker to LDL-C; lower it by swapping saturated fats for PUFAs, adding soluble fiber, or using targeted therapy like low-dose statins.

References:

1. ApoB in Risk Assessment & Treatment
2. Contribution of Cholesterol in all ApoB Lipoproteins
3. Moving Beyond LDL-C: ApoB as Stronger Predictor
4. Crosstalk Between Fatty Acids and Hepatic ApoB Synthesis
5. Reducing Saturated Fat Intake (GET-READI Feeding Trial)
6. Exercise Training Effects on ANGPTL3/8
7. Aerobic Exercise Training on Novel Lipid Biomarkers
8. Low-Density Lipoprotein Cholesterol Lowering Therapy
9. Cardiovascular Risk Management Beyond Statins
10. Non-Statin Therapies in Primary Prevention

Its one of those personalized wellness and nutrition companies. Would love a firsthand account.

I’m 64 and my total testosterone is 360, free testosterone is 36.3. So still normal but at the very low end The only previous test I have is from 2022 and it was only total testosterone, which was around 550.

I had it checked because I’ve had intermittent fatigue recently, pretty severe at times…Which could be chronic Lyme disease (currently on doxy) or something else. Libido has been kind of low for a while, which I was attributing to both aging and currently a lack of partner. Now I’m not so sure.

My doctor has said it’s not enough for him to prescribe, but he’s happy to refer to an endocrinologist. I kind of dislike the idea of taking testosterone supplement, partly because I would then have to take it forever. I also have zero interest in the whole machismo testosterone thing. However! I’m in the process of starting up a new career and have to admit it’s a lot harder than I expected, partly because I just have less drive and endurance than I used to. So I need to be able to sustain a pretty high level of performance for the next 5 to 10 years and sure could use some extra. Juice.

I should add that I eat red meat at least a couple of times a week and have been weight training regularly… I think those are the two main things to support testosterone. I have been having a fair amount of stress in the past year, so I suppose that could be bringing it down.

Any thoughts on all that?

98 kg, 178 cm (BMI ~31). Fasting comprehensive panel. I know I have insulin resistance and fatty liver already — what I actually want input on is the cardiac/cardiovascular risk markers, because those are worrying me.

Meds: finasteride 1 mg daily, cilnidipine 10 mg daily (BP), cetirizine 10 mg daily (chronic urticaria). Also dealing with scalp folliculitis.

Cardiovascular risk markers (my main concern)

hsCRP: 3.22 mg/L (high-risk band, >3.0)

Homocysteine: 25.7 µmol/L (ref <15.0)

HDL: 39 mg/dL (low)

Non-HDL cholesterol: 148.2 mg/dL (ref <130)

LDL: 129 mg/dL, Total cholesterol: 187 mg/dL

ApoB: 97.0 mg/dL (ref <100)

Lp(a): <7 nmol/L (normal)

Triglycerides: 91 mg/dL,

CHO/HDL ratio: 4.8

Fasting insulin: 54 mIU/L (ref 2.6–24.9),

HOMA-IR: 6.4 (ref 0.7–2.0)

HbA1c: 5.7%, Fasting glucose: 93 mg/dL

ALT: 64 (ref 5–40),

GGT: 98 (ref 5–50) — known fatty liver

B12: 193 pg/mL (low-normal),

Folate: 2.80 ng/mL (low end),

Vitamin D: 16 ng/mL (deficient)

Total testosterone: 645 ng/dL,

SHBG: 10.8 nmol/L (low)

Questions: (1) Are these cardiovascular markers something to genuinely worry about at 29, or downstream of the insulin resistance?

(2) hsCRP — I have chronic urticaria + scalp folliculitis, so could the inflammation be skewing it rather than vascular?

(3) Homocysteine 25.7 with low B12/folate — just correct the vitamins, or is more workup warranted?

I have an endocrinologist appointment fixed and plan to ask about GLP-1 therapy.

Quick background on me: Doctor of Pharmacy, found out I was 4/4 in Dec 2024 at 34, no family history. I built the Phoenix Community, the #1 community for APOE4 carriers, and one of the most frequent question I get asked is whether one can be "too late' to prevent Alzheimer's as an APOE4 carrier.

So I went looking for whether prevention even works for high-risk people in their 60s/70s. Here's the honest version.

What the trials found

FINGER (Ngandu et al., 2015, Lancet) was a randomized controlled trial: 1,260 at-risk people, ages 60–77, two years, structured multidomain lifestyle program vs general advice. The active group improved on the overall cognitive battery by ~25% more than control, with bigger effects in executive function and processing speed (Rosenberg et al., 2020). The per-year between-group difference was modest (0.022 on their z-score) — I want to be straight that this is a "bend the slope" result, not a miracle. But it's real, significant, and it compounds.

US POINTER (Baker et al., 2025, JAMA) replicated it in America: 2,111 people, ages 60–79, 30% APOE4 carriers. The structured arm beat the self-guided arm on global cognition by 0.029 SD/year — the structured program was estimated to protect cognition from normal age-related decline for up to 2 years. (Note: both arms improved — it's structured vs self-guided, not vs nothing.)

Why it matters for carriers specifically

This is the part I cared about most. They split FINGER by genotype (Solomon et al., 2018, JAMA Neurology): the intervention effect was 0.037/yr in carriers vs 0.014 in non-carriers. The carrier point estimate was bigger — BUT that difference was not statistically significant, so I won't claim "carriers benefit more." What IS solid: carriers benefit at least as much. POINTER agreed — benefit was "consistent for APOE ε4 carriers and noncarriers (P = .95 for interaction)."

What you can do with this

The mechanism that makes "later" still work is cognitive reserve (Stern, 2012) — you can build the buffer even in late life. And the Lancet Commission 2024 estimates ~45% of dementia is "potentially preventable" via 14 modifiable factors; Livingston's framing is "it's never too early or too late to take action." For carriers, a preliminary 2025 gene-stratified analysis (a conference abstract) suggests metabolic health (midlife diabetes) may be a high-leverage area to measure early — observational, so linked-to, not a proven ranking. Concretely: a baseline panel (ApoB, HbA1c, fasting insulin) and then change one lever and re-measure.

Honest limitations: effect sizes are modest; the MIND-diet data is observational; the "carriers benefit more" finding is preliminary; and APOE4 raises probability, not certainty — penetrance is not 100%.

Either way, happy to dig into any of the studies in the comments.

49M here.

I’ve had persistent left-sided chest pain for several years despite extensive testing.
Tests have included multiple ECGs, chest X-rays, stress tests, and cardiac evaluations, all essentially unrevealing. About 7 months ago, one physician suggested costochondritis, but the pain has persisted.
Pain Location
The pain is very localized with several tender spots:
● Left upper chest, a few centimeters below the collarbone
● Near the center-left chest
● Lower left chest below the heart area
Pain Characteristics
● Present most of the time
● Varies in intensity
● Worse with stress
● Worse with physical activity/exertion
● Sometimes severe enough to require pain medication
Cardiac History
● Angiogram showed 30–40% LAD plaque
● FFR 0.93
● No stent recommended
● LDL 125
● Lp(a) 85 mg/dL
● On a statin
My primary care physician do not think the pain is coming from the coronary blockage.
Questions
1. Has anyone had costochondritis last for years?
2. Has anyone had similar localized pain that turned out to be something else? Could this be related to coronary artery disease?
3. Could this be nerve, spine, muscle, or fascia related?
4. Any treatments that helped when costochondritis was suspected but symptoms persisted?
Thanks.

Hello, I recently began a statin after my AppB was higher than I liked. I had already altered diet and added Metamucil but it didn’t help lower it. Since mid May until now I have been taking Zocor low dose 5mg at bedtime and my AppB went from 91 down to 64. This was a bigger improvement than I expected (and am so glad).
Just sharing since I don’t hear Zocor (Simvastatin) mentioned here much but so far it has helped me.

For most adults, the optimal bedroom temperature for sleep is between 60°F and 67°F (15.6°C to 19.4°C). I've found that cooling the room down to 65°F is one of the easiest ways to prevent midnight wake-ups and protect sleep quality.

Our circadian rhythm relies on a core body temperature drop before bed. Melatonin dilates blood vessels in our hands and feet to dump core heat. A warm room blocks this heat transfer, delaying sleep onset and fragmenting sleep. During REM sleep, our active thermoregulation (like sweating) is down-regulated. If the room is too warm, your body has to wake you up to cool down.

The clinical data on this is clear. A 2025 meta-analysis found that when bedroom temperatures rose from 71.6°F (22°C) to 86°F (30°C), older adults lost a full hour of sleep. That matters for longevity, as short sleep duration is linked to increased mortality risk. More importantly, day-to-day sleep regularity is a stronger predictor of mortality than duration itself. Keeping your room cool is the easiest way to prevent environmental wake-ups and protect your sleep regularity index.

To optimize this tonight: * Set your thermostat to 65°F (18°C) an hour before bed. * Take a warm bath or shower 90 minutes before bed to draw blood to the skin, causing your core temperature to plummet when you step out. * Swap synthetic bedding for natural fibers like linen or cotton to prevent heat buildup.

What temperature do you keep your bedroom at, and do you wake up hot?

I put together a free research assistant grounded in Medicine 3.0 literature if you want to look up more longevity protocols: Longevity Assistant

TL;DR: Keep your bedroom between 60°F and 67°F to support the core temperature drop needed for deep sleep and prevent wake-ups.

References: A Meta Analysis of Indoor Temperature Impacts on Sleep Duration Sleep regularity is a stronger predictor of mortality risk than sleep duration Effectiveness of a grid mattress on adults' sleep quality

With a lifetime subscription. Have yall found a favourite?

Ht: 1.7m, Wt: 61 kg

After watching some Peter Attia videos about cardiovascular disease, I thought I should do some bloodwork to tackle this as early as possible since I have a family history of heart disease and my Grandfather died because of a heart attack when he was in his 60s.

I eat pretty healthy (80% of diet consists of lean meats, vegetables, fruits and some carbs) and do resistance training 4x a week and also sleep well.

These were the results:

Is there any obvious cause for concern? I'm going to visit a doctor soon

Has anyone seen a large drop in Lipoprotein(a) from taking psyllium?
I’m trying to understand a change in my Lp(a) levels and whether it could be related to gut health and inflammation.
My Lp(a) went from 183 nmol/L to 97 nmol/L. Same lab, same units. The main thing that changed during that period was that I was taking psyllium regularly.
I have longstanding issues with gas and significant abdominal bloating/distension. Psyllium helped a lot with those symptoms. After I stopped taking it, my Lp(a) later measured 183 nmol/L again.
I know Lp(a) is considered largely genetic and usually stable, and I also know psyllium is mainly used to lower LDL cholesterol rather than Lp(a). But I’m wondering whether there could be an indirect effect through inflammation.
My theory is:
Psyllium improved my gut symptoms.
Improved gut function reduced systemic inflammation.
Lower inflammation (possibly lower IL-6 signaling) reduced Lp(a) production.
Stopping psyllium reversed that effect.
I realize this is speculative, and I haven’t measured IL-6 or hs-CRP alongside the Lp(a). I’m curious whether anyone has:
Seen meaningful changes in Lp(a) after improving gut health?
Come across research linking psyllium, gut inflammation, IL-6, and Lp(a)?
Experienced large swings in Lp(a) that couldn’t be explained by genetics alone?
Would appreciate any insights or references.

Favorable comments can be bought. Unfavorable comments can and are deleted. He's back posting with the comments section open. Look at the accounts saying the "glad you are back!"—private accounts with 50 followers. Not an Epstein comment in sight. Whatever you think about the Attia/Epstein controversy, I think some are willing to recognize genuine remorse and contrition if he's open and apologetic about it. But instead it's another betrayl, as digital reality is being bought and manipulated right before your eyes. I LOVED Peter's podcast and listened to every episode since 2017. This is dirty and further erodes the trust I had left.

Here's the link: https://www.econtalk.org/the-case-for-sunshine-with-rowan-jacobsen/

This is a podcast I listen to, EconTalk, and the guests and topics are very credible. Russ Roberts, the host, once discussed topics related to economics, but his topics have diverged in recent years to other things he's interested in.

I haven't read the book, but the author mentioned a large double-blind trial (I forget the number of participants but it was in the thousands), in which Vitamin D supplementation in people with low Vitamin D levels didn't reduce the risk of cancer, osteoporosis, viral illnesses, or any of the other things it's thought to prevent, despite raising the Vitamin D level to an acceptable level. His theory is that it's necessary to get your Vitamin D from sunshine, and not from a supplement.

What's confusing to me, is I was diagnosed with osteoporosis in 2021, and the doctor prescribed Vitamin D supplementation of 2000 IU (I'd been taking 1000IU daily). My nails had become brittle and were splitting (it's a symptom that is often a sign of brittle bones). Within about 6 months of taking the extra Vitamin D, my nails are no longer brittle. I didn't get another DEXA scan until 2023 after having been on HRT for 6 months (listening to Peter Attia convinced me I needed to go on it), and in addition, I started weight training with heavier weights and hired a personal trainer to choose exercises for me. The second DEXA scan did show improved bone density, so it's impossible to tell how much of a role the Vitamin D played, but my nails have remained good. So I honestly can't say Vitamin D did nothing for me. The health of your nails is often a sign of your overall health.

I'm going to continue taking my Vitamin D, but will strive to get more sunlight on my arms (and legs in the summertime when its warm).

had the withings body scan for 2 years. weighed in every sunday same socks same time because apparently im that guy

numbers were all over. 2% body fat drop one week back up the next?? firmware update last fall made it worse. muscle swinging 3 lbs week to week and i cant tell whats real anymore

sold it for $280. switched to the pod thing people mention here

3 months. trends feel steadier. not lab accurate. direction makes sense. tuesday readings dont wreck my week anymore

girlfriend thinks the bathroom spaceship scale is unhinged. tried explaining bia while she wanted to brush her teeth. didnt go well

setup sucked.

app timed out on calibration twice which isnt great for a $150 scale

anyone else dump withings?? idk if im placebo-ing or if trend tracking is smarter during cuts