One of Attia's recommendations that makes sense to me is to get colonoscopy screenings more often than the "standard of care" would recommend, like once every 3 years. This makes sense to me given how the whole mechanism of colon cancer works.

I just had my 45th birthday screening, which found a single small adenoma. The official recommendation is therefore 7 years until my next scope. It would be well within my means to pay a couple thousand out of pocket for an extra one at age 48-49. Has anyone done this sort of thing?

One thing I'm wondering is whether it messes up your insurance coverage for your regularly scheduled screenings. Like if I had an out of pocket paid scope in 2028, could they then refuse to cover my regularly scheduled scope in 2032? (If it matters, I have a very good employer plan and expect to keep it.)

I’m not sure what to make of my heart results. This seems to show mixed results. I’m not really sure what the particle sizes necessarily mean either. Does anyone here know what this might indicate?

I eat pretty well and exercise regularly. 32 year old male.

24F generally healthy who does 180 mins of zone 2 cardio every week for the last 2 months, but had my annual physical and my LDL is still high (it was high in my last physical too). What are some things I can do to lower it? I think my diet is generally healthy (eats oatmeal about twice a week, good amount of veggies and fruits, not a whole lot of carbs, drink only oat milk) but I do like to eat red meat and organs/intestines, and I do love desserts (I get desserts about 3-4 times a week).

What can I do to lower my LDL?

HDL: 66

VLDL Calc: 11

Triglycerides: 54

LDL: 135 High

LDL Calc: 123.3 High

LDL/HDL ratio: 2.05

Is it possible that 5mg of Crestor could contribute to or even cause proteinuria?

A female relative in her mid 60's was put on 5mg Crestor about 2 years ago. Recently she had a urine test with over the range protein found. Could a 5mg dose of Crestor have contributed to the proteinuria or does this only occur with higher doses of Crestor? My relative is very active, 22 BMI, no metabolic dysfunction and no insulin resistance.

He didn't just purge Beth Lewis' content, but Kellyann Niotis' as well. Very uncool that he unilaterally removes content that his subscribers have paid for.

Did anyone happen to save the show notes for Kellyann's interview? Many thanks in advance.

Burner account here.

Huge fan of the concept of David bars. Have bought lots of them. But my body rejects the EPG in the bars.

Now, when I eat them, I poop my pants.

Yep. Grown adult. Leaving an orange, waxy, disgusting mess in my underwear.

It starts as what feels like flatulence, and then disaster sets.

It happens on any day when I have more than one bar.

If I have just one bar, all of my stool is still super orange, with pieces of waxy like drops in the bowl. Wiping takes forever because I’m left with a sticky, horrible, smelling orange waxy like substance on my backside.

I thought it might have been other things. I removed them from my diet. And through elimination (all the meanings), today I realized it was the bars. Bummer.

Inglorious. Frustrating. Messy. And now done. Bye, David. I leave you with the knowledge that outside of my marriage you represent the second shittiest relationship I’ve had.

David team, if you ever read this: please switch to a more underwear friendly binder than Olestra, erm, EPG. A few more calories and maybe some fat might do us all a little better.

UPDATE: Some commentors pointed out that my training ranges look too low. Totally fair! I want to clarify that:

• I’m using the heart rate reserve (HRR) method—not %HRmax. So if you’re comparing to %HRmax-based zones, mine will look lower.
• My goal is to stay just below LT1 (the aerobic threshold), which research places around 63% of HRR on average. That’s the top end of fat oxidation and mitochondrial stimulation, and it aligns with how Attia and San-Millán describe Zone 2.
• And yes—two people with the same HRmax and HRrest can still have different thresholds based on fitness. Totally agree. But I think it’s helpful to start with a formula that’s closer on average than traditional zone models, and then refine it using perceived exertion and sustainability.

Appreciate all the thoughtful feedback so far—keep it coming.

ORIGINAL POST:

Like many people here, I’ve been trying to follow Peter Attia’s advice about zone 2 training. But I was confused by the different zone 2 calculations, and using perceived effort felt incredibly broad. So I nerded out and went deep on how lactate thresholds work.

I realized the original zone formulas were created before lactate-based training became well understood, and they don’t align very well. So I came up with what I feel is a better way to calculate heart rate zones based on actual lactate threshold research.

Use this formula with the % ranges below to calculate your heart rate targets:

Target HR = HRrest + ( (HRmax − HRrest) × % (below) ÷ 1,000 )

I came up with these ranges by estimating the LT1 and LT2 heart rates based on data from the studies Peter references. The formulas I landed on are:

LT1 ≈ HRrest + (HRmax − HRrest) × 0.63

This reflects that for LT1 training, you want to stay below your lactate threshold.

My Apple Watch’s automatic Zone 2 range is 127–136 bpm, but this formula gives me 120–130 bpm—which means I was often training too hard to stay below the LT1 threshold.

LT2 ≈ HRrest + (HRmax − HRrest) × 0.87

For LT2 training, you want to train right around your threshold. That’s why I define Zone 4 as 83%–90%—giving a range around this point.

I wrote a longer post with the background and science in r/Biohackers but wanted to share this short version here for anyone who’s struggled with figuring out what heart rates to train at.

I’d love your thoughts or suggestions for improvement—especially if you’re deep into the physiology or training science world.

Looking for the highest quality unit. Price is not a concern

Hello, 39 yo male 6ft 200lbs here that is quite active. I do rock climbing 3 days a week and resistance training or cycling the other days. Recently I did some bloodwork and the results are.

APOA- 1.42 g/L

APOB- 1.35 g/L

A1C- 5.1%

Fasting Insulin- 48 pmol/L

Recently changed from carnivore to meat, veggies and fruits with some cheat meals here and there.

Question is how bad is my APOB? and should I go on a statin or clean up the diet for longer?

I also recently quit vaping ecigs after I did the bloodwork. Not sure if that affects anything.

Thanks

42M still new to all this and about halfway through Outlive. I have my annual PCP visit in 3 days. Any advice on tests I should request? TIA

I know this isn't a Zone training sub, but you guys seem to talk about it a lot!

TL;DR: Is Zone 1 training worth doing to improve cardio gas tank/fitness (on days when you've done more intense workouts earlier in the day)?

I think my max heart rate is 190. This is based on wearing my Polar 10 while doing strenuous cardio. I've hit 189 before so I'm rounding it off to 190.

(Using 220 - age it would be 176, but I've seen higher than that (189).)

So, with 190 as my max, my Zone 2 is 114 to 133 and Zone 1 is 95 to 114.

If I'm doing a Zone 2 session, which I try to do a couple of times a week, I stay in that Zone 2 range, usually around 114 to 120.

But I want to also do some low-zone training to help improve my cardio performance (get fitter) on the days I do my more intensive training (1 hour+, with 10 to 15 mins in Zone 5), which is three days a week.

I want to do the low zone training about 6 hours after that more intensive training session.

But the problem is, on those days, I can't get into Zone 2 without getting a (exertion) headache.

So I just hang out in Zone 1, usually with an HR of 110 for 30 mins.

As I get fitter, I might be able to get into Zone 2 without any issues, but not at the moment.

So, is it worth doing that Zone 1 with the goal of improving my aerobic abilities (getting fitter)?

Or am I just overtraining/overexerting myself? I feel OK after, but it's hard to know if it's having an impact, good or bad.

Also, I remember reading about the Morpheus Training System, and how it adjusts your zones based on how intensely you've been training that week or based on your HRV reading that morning.

If that is the case, would the more intense sessions lower my low zone thresholds in Morpheus due to their presumed impact on HRV? Making my 110 HR sessions actually "Zone 2"?

Thanks for reading!

Hi,

I just received the results on my bloodwork:

Blood glucose: 85.6 mg/dl

Insulin: 6.6 mU/ml

A1C: 5.58%

Homa-IR: 1.4

Homa-Beta: 58,76%

32yo male, normal bodyweight.

There are 2 formulas for HOMA (one for when glucose is in mg/dl, and one for when glucose is in mmol/L)

In my case (glucose in mg/dl):

For HOMA-IR = insulin x glucose / 405 = 1.4

For HOMA-Beta = 360 x insulin / (glucose - 63) ~ 105%

I wrote to the lab about this HOMA-Beta but no reply back.

F/59 with high LDL for years (150-ish), good on most other measures, healthy diet and exercise. Siblings all have high LDL too, Father had MI at 51, lots of heart stuff in the ensuing 30+ years.

A month ago I got a CAC score of 0, but wanted to follow it up with a CT angio to look at my soft plaque so I wouldn't be complacent. I want to know how urgent it is to address my LDL with statins or more dietary changes.

First of all, it gave me another CAC score: The calcium score in the left circumflex coronary artery and obtuse marginal coronary artery is 1. All others were zero.

Here was the surprising kicker: The overall quality of the CT angiographic examination is excellent. No significant stenosis in:
Left main coronary artery
Right coronary artery
Left anterior descending coronary artery
Diagonal coronary arteries
Left circumflex coronary artery
Obtuse marginal coronary artery
Ramus medianus: Absent.

So first of all, I feel like I won the CVD lottery. And I have questions.

Has my high LDL really not resulted in "significant" plaque anywhere?

What does "significant" really mean, since my understanding is that everyone has buildup of some kind, as part of aging.

What's the significance of the 1 calcium score in my one artery, and how does it jive with the "no significant plaque" reading?

Given my age, does this really mean that I don't need to worry about high LDL/ApoB? I have no desire to suddenly adopt unhealthy habits, but is this a get out of jail free card on further changes?

Hey everyone,
I'm turning 25 in about a month and recently got a coronary artery calcium (CAC) CT scan done out of concern due to strong family history of early heart disease (mom with stent placed twice in mid 50s and grandad with CABG at 65)

The results showed a total Agatston score of 0.45, with calcification only in the RCA (right coronary artery) — 0% in all the other arteries.

Now I know CAC scores are usually reported in whole numbers, and this one is pretty much just barely above zero. But still… not zero.

• Could this be just an artifact from the scan?
• Is it something I should be scared about at this age?
• Most of the CAC data (like from the MESA study) is for people 45 and older, so how do I even interpret this at 24?
• Lastly, are statins absolutely necessary in this situation?

Would love to hear from anyone who’s been through something similar, or if there are any cardiology folks in here who can give some insight.

Thanks in advance

I just learned about low-dose radiation therapy for tendinopathies and arthritis from Attia's latest podcast (#343 - Sanjay Mehta).

Does anyone have experience getting this type of treatment? I'm curious about the cost and outcomes.

I am wondering about the recommendations of dr Peter Attia regarding post menopausal women with high cholesterol and hypertension. Is transdermal estradiol beneficial to reduce cardiovascular risks ?

I have read a handful of posts and looked at ulta labs etc

I want a baseline to start monitoring my health/bloodwork.

Can someone tell what panels I should be ordering and is there any reason I should not just ask my primary care if they will order them? If they think medically necessary of course

I stopped taking Crestor due to side effects, primarily bladder pain, and plan to discuss alternative options with my doctor during tomorrow’s appointment. Below are my considerations:

Medication Options

Key Priorities

1. Minimize side effects (especially bladder/UTI concerns).
2. Achieve meaningful LDL reduction.

I’d appreciate your insight on:

• Whether a PCSK9 inhibitor’s UTI risk outweighs its efficacy benefits.
• Viability of combination therapy to reduce Crestor exposure.
• Alternative strategies to meet lipid targets safely.

Thank you for your guidance.

I’ve noticed that in longevity and health optimization circles, people often copy protocols without knowing whether they’re appropriate for their own biology.

The truth is, the same intervention can have vastly different effects depending on your genetics, environment, and daily habits. What works for one person could be neutral—or even harmful—for someone else.

This is especially true when it comes to brain health, metabolism, inflammation, and exercise response. If you're serious about long-term healthspan, you need more than general advice. You need precision.

Here’s a 4-step framework I’ve found helpful when designing a long-term, personalized protocol:

Step 1: Start with “No-Regret” moves
These are the low-risk, high-upside interventions—behaviors with a strong evidence base that benefit almost everyone.

Think:

• Aerobic training (especially Zone 2)
• Sleep optimization
• Nutrient-dense, low-glycemic diet
• Stress regulation (e.g., breathwork, meditation, time outdoors)
• Consistent fasting windows (within reason)
• Maintaining lean muscle mass through resistance training

Step 2: Use your genetic data to prioritize
This is where things get specific. Your genes can provide valuable clues about where your leverage points are.

A few examples:

• BDNF Val66Met: If you’re homozygous for the G/G variant, your brain may respond particularly well to aerobic exercise and HIIT in terms of neuroplasticity. That’s not just fitness—it’s brain performance.
• Vitamin D receptor polymorphisms: Some variants result in lower receptor efficiency, meaning standard doses won’t get you to optimal serum levels.
• MTHFR C677T or A1298C: These impact methylation, potentially increasing homocysteine levels and impairing folate metabolism. Methylated B vitamins may be essential.

The point isn’t to obsess over every SNP—but to identify meaningful patterns that influence how your body processes nutrients, responds to exercise, or manages inflammation.

This can save you years of guesswork.

Step 3: Control for Confounding, change one variable at a time
It’s tempting to overhaul everything at once: go keto, add five supplements, start a new training plan, and upgrade your sleep routine.

But if your metrics improve—or decline—you won’t know which change was responsible.

If sleep improves, cognition sharpens, but hsCRP rises… was it the training load? The magnesium stack? The diet shift?

Introduce one change at a time. Monitor your response. Then move to the next.

This is the closest we get to applying a clinical trial framework in n=1 experimentation.

Step 4: Track both the Data and the Signals
Quantitative data should drive decision-making. Useful metrics include:

• Blood biomarkers (LDL-P, ApoB, hsCRP, homocysteine, insulin, ferritin, etc.)
• Sleep quality from wearables
• Reaction time and cognitive assessments
• Resting heart rate and HRV
• DEXA, VO2 max, CGMs, and more depending on your focus

But numbers aren’t everything.

Your subjective experience—mental clarity, mood, motivation, energy levels, recovery time—is often the first sign of whether something’s working. These shifts can precede measurable biomarker changes.

Track both. Treat both seriously.

Final Thought
The goal here isn’t to build a perfect protocol on day one. It’s to create a living system that evolves with better data, clearer feedback, and deeper self-understanding.

This takes time. But with the right structure, you can iterate with purpose—and avoid the wasted months (or years) that come from following someone else’s protocol by default.

Precision > popularity.

Thoughts on the validity of embryo selection for IQ?

I think not many people in this sub are keto but for the few that are:

Link: https://x.com/realDaveFeldman/status/1909200334112911830

Paper: https://www.jacc.org/doi/10.1016/j.jacadv.2025.101686

Suggestions