r/PeterAttia

A 2023 study followed 1,275 older adults for 8 years and compared their grip strength to three DNA-methylation aging clocks (tests that estimate your biological age from chemical markers on your DNA instead of your birthday).

Weaker grip lined up with faster aging on all three. And baseline grip predicted it years later, not just same day.

The methylation panels run $300–$500. A grip dynamometer is $30, a pickle jar in your pantry is basically free. They all point to the same thing.

How I interpret the results:

- Association, not causation. Grip doesn't cause aging. It reflects muscle, activity, inflammation, metabolic and neuro function. Grip is the readout, not the lever.

- Older cohort (avg ~70). Strongest evidence in that group.

- The mechanism is still unclear.

It's like the ApoB principle. One number that costs almost nothing and tells you where to dig. Not a diagnosis but a starting point.

That being said, how's everyone's grip holding up? Struggling to open the pickle jar?

(Peterson et al., J Cachexia Sarcopenia Muscle, 2023)

attached blood results, hdl is surprisingly low any suggestions to raise this? I eat well over 100g nuts (pecans, macadamia, walnut, almond, hazelnut and cashews) daily, cook all food in evoo, 3 eggs daily.

b12 is high also but I don’t supplement anything, how to lower this?

any other recommendations would be welcomed

background extremely active (12+ hours training for the last 3 months, usually around 8 per week), high vo2 max, good muscle mass etc, eat really healthy besides sugar consumption during hard training times (nothing major fig rolls for carbs etc)

I’m 32 and tracked my fiber for a week mostly out of curiosity.

I was getting like 12g a day.

The recommendation is 25–35g, which honestly explained a lot. I always had mid-afternoon crashes, bloating, and just random stomach stuff I never really thought about.

The tracking apps I tried didn’t really help either. MyFitnessPal tracks fiber, but it’s buried behind calories and macros. Cronometer felt way too detailed for what I wanted.

I basically just wanted an app that told me one thing:

Did I hit my fiber today or not?

So I built one.

It has a daily ring for your fiber goal, barcode scanner, 200+ USDA foods, and a plant diversity score. That last part was kind of surprising to me. A lot of gut health research points to variety per week, not just total grams.

A few honest surprises after using it for ~6 months:

• Getting to 30g isn’t that hard once you realize where fiber actually comes from. Beans, oats, raspberries, chia, avocado, etc.
• Plant diversity was harder for me than the actual fiber goal.
• A lot of packaged “high fiber” foods are not as useful as they make themselves sound.

Free, iOS only, on device, no account.

https://apps.apple.com/us/app/id6760719879

Would genuinely love feedback on the food database or anything that feels off.

I got both tests done not even a week apart from each other! Why does quest scores always go extremely high compared to labcorp?

Labcorp tested on 5-15-26
Quest tested on 5-8-26

This is been talked about everywhere on Reddit, so if you ever get tested from quest on a cardiac iq panel just know your results will be much higher.

Anyone know why this is the case. Also, I did my triglycerides and they were 134 on quest and 68 on labcorp 😂

How’s this even possible? A week apart from quest and labcorp. My triglycerides were 68 labcorp and 134 quest.

Quest shows 2070 for LDL-P and labcorp shows 1293.

I just had a very unusual and confusing meeting with a lipidologist. He said he was a fan of Dr. Attia's, but the first appointment went very strangely and confusingly. I'm curious to see what others think.

In particular, I am curious whether the following what others would expect from a meeting with a fan of Dr. Attia's. In the end, I didn't like this doctor, so I won't be seeing him again. But I'm curious if his practice was genuinely representative or typical for a fan of Dr. Attia's.

Background: late 30s male. Since about 3 years ago, I have been diagnosed with hypercholesterolemia. However, my other metabolic markers are generally good, and my PREVENT 30 year risk score remains low (5.5%). So I wanted to wait and see if I could improve my cholesterol through diet and lifestyle. In the end, my cholesterol did not improve, so now I am seeking appropriate pharmaceuticals.

I have no family history of CVD, but I have an extensive paternal family history of Alzheimer's disease.

TC: 227 mg/dL

non-HDL-C: 156 mg/dL

LDL-C: 140 mg/dL

HDL-C: 71 mg/dL

TG: 68 mg/dL

ApoB: 110 mg/dL

Lp(a): <8.4 nmol/L (off the chart, on the low end)

hs-CRP: 0.4 mg/L

HbA1c: 5.00%

LP-IR (lipoprotein insulin resistance score; 0-100, lower is better; less than 50 is insulin-sensitive): 20

BP: 110/70

Glucose (fasting): 78 mg/dL (guideline: 60-139)

Insulin (fasting): 6.5 uIU/mL (guideline: 2.6-24.9)

C-Peptide: 1.4 ng/mL (guideline: 1.1-4.4)

HOMA-IR: 1.3 (<1 is ideal)

ApoE 3/3; no E4. Father's genotype is unknown.

CAC: zero (but that's not very meaningful, since I am so young)

End of background.

-----

That was the background. Now, the meeting with the lipidologist:

At the lipidologist's office, my systolic blood pressure measured at 130. I was surprised, and I told him that it's usually 110/70, going back many years, consistently. Just a few week ago, I saw my primary care physician, and my BP was still 110/70. He replied that the general physician probably tested my right arm only once, while he tested my left arm thrice, so he was going with 130. Based on my blood pressure, he wanted to immediately start me on either a beta blocker or ACE inhibitor. I declined both for now, so he said okay, next time he sees me he'll prescribe one or the other. At the end of the visit, he asked me again if I wanted to take the B-blocker or ACEi now, and I again, I said no, not yet.

He urged me to buy a blood pressure tester for home. (I did so the day afterwards, and my systolic blood pressure has consistently tested between 105 and 120. My average reading is pretty close to the 110/70 I get at my primary care.)

Throughout the meeting, he repeatedly emphasized my high degree of insulin resistance. He said my high cholesterol is almost certainly due to insulin resistance, given that my HOMA-IR is above 1.0. He confidently stated my LDL pattern is likely to be pattern B. When I pointed out that lipoprotein fractionation actually showed pattern A, he changed the subject and didn't acknowledge his mistake. But throughout the meeting, he repeatedly and consistently mentioned my insulin resistance at almost any opportunity.

Then he wanted to start me on 20 mg rosuvastatin, to achieve ApoB < 60. He gave me the option of 5, 10 or 20 mg rosuvastatin, saying I'll almost certainly need 20, but I can start with 5 if I want.

I proposed ezetimibe monotherapy to start, see how I react, then add statin later. I said that regardless of which statin I do or don't tolerate, or how many statins it takes to find one I tolerate, and regardless of the efficacy of the statin, I'll probably want the ezetimibe anyway, since statins and ezetimibe are so complementary. Given that there is only one ezetimibe and many statins, I told him I thought it would be easier to make sure that I tolerate ezetimibe, and then I can cycle through as many statin varieties and doses as it takes to meet my target. Again, I said, I anticipated ending up taking both statins and ezetimibe together, so why not start with the simpler choice? I told him that given my own personality, I felt I would simply be more comfortable this way.

He responded indignantly and aggressively, "That is nonsense. You are hearing crazy nonsense on the internet. You want to be the doctor? No, that is not sound medicine. That is crazy. We don't start with ezetimibe and then add a statin later. The statin comes first."

I replied, okay, how about combination 5 mg rosuvastatin plus 10 mg ezetimibe. Again, I said, I'll almost certainly end up on the ezetimibe anyway, but we don't know for sure which statin I'll end up with or which dose, so why not include ezetimibe from the beginning? Furthermore, I said, why take 20 mg of rosuvastatin to reduce LDL-C by 55% when 5 mg of rosuvastatin plus 10 mg of ezetimibe will reduce LDL-C by 60%, and probably with fewer side effects, since two baby doses are likely tolerated better than one mega dose. He replied no, then if I have side effects, we don't know which drug will be responsible.

But he didn't explain why, then, he wanted to include an ACE inhibitor or beta blocker along with the statin. Wouldn't combining a statin plus an anti-hypertensive together at once also confound any side effects? I completely understand why he wouldn't want to start two drugs together at once, so that any side effects can be clearly attributed. But he contradicted himself.

Then I added that there is a recent observational study which finds that ezetimibe may reduce the risk of Alzheimer's 8-fold. (https://pubmed.ncbi.nlm.nih.gov/39263528/) I admitted that observational evidence is weak, but it's still something, and there's little potential downside of taking ezetimibe, so why not take it just in case it may perhaps reduce AD risk? I have zero family history of CVD, but I have an extensive family history of AD. So I liked the idea of starting with ezetimibe and adding the statin afterwards. He replied, "That is shit evidence. Show me the clinical RCT that ezetimibe reduces AD. Until then, that evidence is shit. But by contrast, there is evidence that statins reduce AD by 20 to 30%."

As far as I can tell, there is zero RCT evidence that statins reduce Alzheimer's risk. There is some evidence that statins may reduce the risk of AD, but it is observational data, not RCT: https://pmc.ncbi.nlm.nih.gov/articles/PMC11736423/.

He did call my attention to the pTau blood test, which I appreciated. He also told me to keep my eyes open for obicetrapib, because early evidence suggests obicetrapib may reduce AD risk. But so far, obicetrapib has only been found to reduce the pTau marker, meaning it reduces the surrogate marker but not necessarily the Alzheimer's endpoint. So that's not RCT evidence of reducing Alzheimer's risk either.

So strangely, he seems to demand RCT endpoint evidence for ezetimibe but he accepts observational and/or surrogate evidence for other drugs.

Then I showed him my Boston Cholesterol Balance test, which shows red for synthesis and yellow for absorption. So I am a heavy over-synthesizer and a mild over-absorber. My Boston lab results conclude, "Interpretation: Increased amounts of Lathosterol, Desmosterol and Beta-sitosterol may indicate an increased cellular production and intestinal absorption of cholesterol. Consideration: Consider lifestyle modification, statin and ezetimibe therapy if cholesterol lowering is indicated." I said, "See, I do over-synthesize, but I also over-absorb. So why not both statin and ezetimibe?" He said, "Ahh, see, this is evidence. It says you should take the statin. So why are you asking for ezetimibe? Take the statin, and then re-test your Boston test to see if it upregulates your absorption from yellow (mild over-absorption) to red (heavy over-absorption). I will only prescribe ezetimibe if you show red on the Boston Cholesterol Balance Test for absorption. Otherwise, I will double your rosuvastatin dose (from 5 to 10 to 20) before I ever consider prescribing ezetimibe."

I found it very strange that he preferred to first escalate to a maximal dose of statin before ever considering adding ezetimibe.

In the end, he struck me as eccentric in several ways. He wanted to immediately start anti-hypertensives based on a single aberrant BP reading, he was worried about confounding side effects of statins and ezetimibe together but not statins and anti-hypertensives together, and he had different standards of evidence (RCT vs observational, endpoint vs surrogate) for different drugs. He kept referring to my insulin resistance despite lack of unambiguous evidence of insulin resistance, and he assumed I had LDL pattern B and wasn't bothered when I refuted his assumption.