Loved the blood pressure AMA! One question..
Hey Peter, I loved the blood pressure AMA. Your booking podcast have inspired me to start taking blood pressure more seriously. I would've loved a little bit more conversation about the variance within person in blood pressure with respect to caffeine. Standard home BP protocols say to measure before caffeine, and my physician wants my readings taken that way. But if I drink coffee every day and it raises my pressure for a few hours each time, isn't my true time-averaged exposure higher than my pre-coffee readings show? How should a regular coffee drinker weight pre-caffeine readings against post-caffeine readings or a 24-hour ambulatory average, and does the answer change for someone who sits near a threshold?
Blood pressure: how to measure, manage, and treat high blood pressure (AMA #48 rebroadcast)
Peter, I listened with great interest to your recent rebroadcast on blood pressure. I’m a physician-researcher with statistical training, and one issue in the discussion sent me back to the literature: age receives surprisingly little consideration in the evidence supporting treatment targets. You appropriately point out that hypertension becomes much more prevalent with age, and that younger adults potentially face decades of cumulative exposure. But when the discussion turns to the evidence for aggressive blood-pressure lowering, the principal randomized evidence comes from SPRINT, which deliberately enrolled a higher-risk population. While elevated blood pressure in younger adults is clearly associated with later cardiovascular disease, it is much less clear whether aggressively treating otherwise lower-risk younger adults produces the same benefit, particularly in terms of absolute risk reduction. The randomized evidence in adults under 60 is remarkably sparse, and the lifetime-exposure argument for early aggressive treatment, while biologically compelling, has not actually been tested in a randomized trial. Point estimates that trend toward benefit in underpowered subgroup analyses are often interpreted as supportive evidence, but a nonsignificant result cannot establish benefit; it leaves the question unresolved. There is also an interesting problem created by the low event rate itself. Because cardiovascular events occur predominantly later in life, trials capable of demonstrating treatment effects are necessarily enriched for older and higher-risk patients. Yet the low event rate that makes trials in younger adults difficult to power also means that the near-term absolute benefit available from treatment is necessarily small. The usual answer is that treatment matters because its effects accumulate over a lifetime, but that cumulative treatment benefit has not been demonstrated in randomized data, and recent evidence calls into question the assumption that benefit progressively amplifies with treatment duration. In that context, I think there is a legitimate question about how confidently results from older, higher-risk populations should be extrapolated to younger adults. This seems particularly relevant to your audience, many of whom may be younger, health-conscious adults deciding whether to begin lifelong antihypertensive therapy. Given your commitment to interrogating what the literature actually demonstrates, I thought the distinction between what we know, what we infer, and what remains untested might be of interest. Best, Kristan
Coronary Artery Disease Management Mastercalls
Hello, I think it might be useful for subscribers to get a masterclass on coronary artery disease management, particularly in the light of the new AI-enhanced CT angiograms that are available. Questions might include: - Is it worth doing a CT angiogram enhanced by AI? - If so, then what are the evidence-based courses of action to based on results? - We all know about the importance of managing APOB. What other management strategies should one use if one has plaque in the arteries, especially dangerous plaque? - What is the latest research on stenting and coronary artery bypass grafts for asymptomatic patients?
Exercise/Aerobics as One Ages
Are the same guidelines suggested for people as they age into their 60's and beyond, with the same amount of times, days per week and intensities as the general guidelines? Or are more rest days or lowered intensities suggested? Seems lowered heart rates are expected with age but how much of a factor should be considered with that?
OSA
I have OSA. I use CPaP machine daily. However I am still worried for my cardiovascular health as my HRV is pretty low. I think cpap machine is kind of adding to my fast breathing and maybe impacting my HRV. I have recently bought Morpheus and trying to leverage it to improve my cardiovascular health and HRV. What is the best way to use Morpheus to my advantage? How can I get rid of ISA and CPaP so that I can sleep peacefully? Additional details- I am 61 year old male with 205 lb and low activity. However since last 4 weeks I am doing 20 minutes of stationary bike 6 times a week and 3 strength training sessions a Last year my testosterone was 200 but my PCP is not in favor of HRT due to it’s stroke and heart attack risks as I had a TGA for 45 minutes . I also have insomnia which I am treating treat with sleep hygiene and 5 mg melatonin. I also had REM disorder ( talking during a dream usually a scary one) but since I take melatonin REM disorder is 95% solved. I also had PLMS ( moving my Hands and legs) due to low ferritin so I am taking regular iron supplement which is building my ferritin and solved my PLMS by 90%. I was taking statins but those gave me severe muscle weakness where I almost fell twice so I stopped it. I am taking ezetimibe 5mg to control my cholesterol which is little high. My abo(b) is high as well but lp(a) is fine.
Protein intake, Amino Acid Supplementation, and Creatine in ADPKD vs. standard CKD
Hi Peter and team, you frequently discuss the longevity trade-off between maximizing muscle mass (aiming for 1.6-2.0+ g/kg/day of protein) and mitigating hyper filtration or renal strain in chronic kidney disease (CKD). However, Autosomal Dominant Polycystic Kidney Disease (ADPKD) presents a unique cellular pathophysiology compared to diabetic or hypertensive CKD-specifically involving the hyper activation of the mTORC1 signaling cascade, metabolic inflexibilty (Warburg-like aerobic glycolysis), and sensitivity to circulating branched-chain amino acids (BCAAs). Could you do a deep dive addressing: 1. How does the cellular cyst proliferation mechanism in ADPKD alter standard renal protein guidelines (e.g., the historical MDRD findings vs. KDIGO targets)? 2. Does free amino acid supplementation ( such as EAAs or keto-analogues) pose a distinct risk of driving mTOR- mediated cyst expansion compared to whole intact proteins, especially regarding leucine intake? 3. Given that creatine supplementation causes an artificial rise in serum creatinine, is Cystatin C sufficiently reliable for monitoring eGFR in polycystic patients whose total muscle mass might be declining as kidneys enlarge? 4. What is your perspective on emerging metabolic therapies (such as ketogenic interventions and beta-hydroxybutyrate) being researched by labs like Thomas Weimbs to slow cyst growth while trying to avoid sarcopenia?
Fasting
I recently fasted for 4-5 days and on the fifth day my breathing became labored and my energy dropped and I felt sick. Was this ketoacidosis or something else? I am healthy, very active, eat like you do. My bro in law, who is none of those things, cruises through 6 day fast like nothing.
Vasectomy risks?
I'm 45 and my wife and I don't wish to have any more children. She is not going back to any form of birth control. Are there any long-term side effects I should be concerned about? I understand there may short-term complications from the procedure. I'm more concerned about things likesexual performance or hormone issues.
A Follow-Up Challenge on Your Recent Peptides Episodes
Hi Peter, I listened to your recent episodes on peptides. Across both, you really focused on BPC-157 and CJC-1295, rather than compounds like tesamorelin and others like Reta that are already widely used in the fitness world. You did touch on SS-31, but mostly in the context of Barth disease, when in reality, people are using it for broader mitochondrial repair, and there's already evidence out there supporting that use beyond the narrow disease indication. I am by no means a Physician, but I do hold a microbiology and cell science degree from the University of Florida, and I have spent the better part of thirty years studying research and new developments in the science and supplement world, along with valuing randomized controlled trials. You raised manufacturing controls as a reason to be cautious about gray market peptides, but that argument cuts both ways. A large share of FDA approved generic drugs, and the active ingredients in many brand name drugs, are already manufactured in China and India, often in facilities that could plausibly overlap with peptide production. Pointing to overseas manufacturing as a unique red flag for peptides is a bit of a stretch when it's already baked into a huge portion of the approved drug supply. On the purity question, saying a peptide has the same amino acid chain but might not be the same compound needs some unpacking, because identical sequence does mean identical primary structure chemically. Where real variation can creep in is in synthesis byproducts, truncated fragments, or folding differences that a purity certificate should be catching. That's worth clarifying in a future episode rather than leaving as a vague caveat. Beyond BPC-157 and CJC-1295, there are roughly seventy five peptides in active use across the fitness and longevity community. AOD-9604, retatrutide, tesmorelin, thymosin alpha-1, TB-500, GHK copper, MOTS-c, selank, semax, epithalon, and 5-amino-1MQ are mainstream examples people are using with a lot of reported success, and they got essentially zero airtime on the show. I understand these need to go through proper research channels to be fully validated, but the honest question is, how long is that going to take. We could be waiting a decade while millions of people are already using them and reporting real benefit. That gap is exactly why they deserve a hard, serious look now, not dismissal until the paperwork catches up. I'd also push back on the idea that something not prescribed by a clinician can't be trusted. If a peptide comes with a certificate of authenticity confirming it's tested and pure, that addresses the same core concern a prescription is meant to address, knowing what's actually in the vial. Plenty of well regarded supplements, like TRU NIAGEN, or urolithin A from Mitopure, are widely used and trusted without a prescription. On top of that, a lot of the dosing and timing protocols people are using now aren't guesswork, they're drawn from existing clinical trials, refined by many thousands of real-world users, a far larger sample than even a large Phase 3 trial. I've lived this dynamic before. I've dealt with psoriasis in the past, and it was actually eliminated through my own routine. Along the way, I was the one researching the pipeline of upcoming drugs and treatments, and bringing specific options to my doctor to try, not the other way around. That experience taught me that patients can be capable, informed advocates for their own care, and I'm applying that same approach to peptides now. I can offer my own results as data. I plateaued around 180 lbs for a year or two despite consistent training and a healthy diet. After adding retatrutide and then tesamorelin 6 weeks later, I lost nearly fifteen pounds, increased lean muscle mass, and dropped body fat by over five percentage points within 3 months. My hypothesis was straightforward and falsifiable by your own standard. I predicted that adding retatrutide and tesamorelin would break my plateau and produce measurable fat loss and muscle gain. That's exactly what happened. It wasn't a vague feeling, it was a testable prediction that turned out to be correct. One more nuance: response to these compounds varies by baseline fitness. Someone already well trained and lean might only see a five to ten percent benefit, but dismissing that as minimal misses the point, since that margin is often exactly what people are chasing. I agree that regulation matters and anecdote isn't proof. But when millions of Americans are already using these compounds and the medical establishment's stance is largely wait for approval, that gap between real-world use and formal validation is itself worth more airtime, not less. Creatine is a good example. I've taken it since I was seventeen, long before the science and mainstream medical opinion fully caught up to what athletes already knew worked. I'd be genuinely interested in a future episode that goes deeper on tesamorelin, retatrutide, and this wider list, beyond the general framework. Thanks for the work you do translating complex science for a general audience. Roman Rudzik 407-970-6243 nycroman@msn.com
Sedation during colonoscopy (re: episode on colorectal cancer screening)
In your episode on colorectal cancer screening, you mentioned receiving sedation during your colonoscopy. I had a colonoscopy a few years ago while fully awake, without sedation or pain medication, and experienced no pain. Does the absence of sedation affect the quality or completeness of the examination—for example, the endoscopist’s ability to reach the cecum, spend sufficient time inspecting the colon, or detect adenomas—or is sedation primarily a matter of patient comfort? Assuming the procedure was completed and bowel preparation was adequate, is there any reason to question the quality of an unsedated colonoscopy?
peptides
Can you describe what these items do? They are currently available online from china but do not specify what they are for. Seems like a lot of peptides coming out: Adamax CBL-514 Dermorphin Thymosin Alpha-1 hCG (Human Chorionic Gonadotropin) GHRP-6 Acetate IGF-DES SS-31 (Elamipretide) MT-1 (Melanotan I) Mazdutide Glow (BPC-157 + GHK-Cu + TB500) Glow50 (GHK-Cu + TB500 + BPC-157) Cagrilintide + Semaglutide Bacteriostatic Water (BAC Water) CJC-1295 (Without DAC) CJC-1295 (With DAC) Ara-290 Cerebrolysin Thymalin LL-37 Survodutide Pinealon PNC27 (5 mg) PNC27 (10 mg) G610 Oxytocin Acetate HIAG CU50 + TB10 + BC10 + KPV10 Blend BPC-157 TB500 (Thymosin Beta-4 Acetate) Ipamorelin Sermorelin Acetate NAD+ BPC-157 + TB500 Blend (10 mg) BPC-157 + TB500 Blend (20 mg) Kisspeptin-10 AOD-9604 5-Amino-1MQ CJC-1295 (Without DAC) + Ipamorelin Vitamin B12 (HKB12 formulation) HGH 191AA (Somatropin) Super Human Blend Healthy Hair, Skin & Nails Blend Relaxation PM AA Acetic Acid Water Adipotide ACE031
Benefits of the Galleri test
Have had a long history (I am 81) of low PSA (1.07) and high free PSA and see a urologist 3 times a year. Obviously not high risk for prostate cancer. The Galleri test said otherwise and sure enough after my biopsy I had a Gleason score of 8. Very possible that the Galleri test will save my life.
Does food choice move inflammation — or is the "no benefit" verdict measuring the wrong variable?
In your "Should you choose organic food?" piece, you set the final gate at terminal outcomes — cancer, IQ, neurodegeneration — where dietary-exposure signals nearly vanish under long latency and confounding. But I battle chronic inflammation, and inflammation is the intermediate mechanism sitting upstream of at least three of the Four Horsemen. It would register long before any hard endpoint does. So would you tell me the foods I choose don't impact my inflammation? Or is "no measurable health benefit" partly an artifact — testing for the finished disease instead of the upstream inflammatory mediator, with an instrument like hs-CRP too noisy to catch a small chronic-exposure effect? Is the gate set at the wrong altitude, with too blunt a tool?
Bernoulli's Fallacy
I've recently finished listening to an audio book called Bernoulli's Fallacy by somebody called Aubrey Clayton, who claims that the current model of null hypothesis significance testing is logically incoherent because it ignores the prior probability of the truth of the hypothesis. He further goes on to claim that this is creating significant problems for medical research. We'd be really interested to get Peter's views on this in an AMA.