ModernHealthspan

Thanks to Dr. JoAnn Manson for a great talk about a landmark VITAL trial discovery: 2,000 IU of Vit D daily slowed telomere loss by 3 years compared to placebo over a 4-year period. We also discussed the 39% reduction in autoimmune risk. youtu.be/XvtI-Ts0tWA

What you do in private always shows in public, and this is such good news. Your diet shows in your energy. Your diet shows in your skin. Your diet shows in your confidence. Your diet shows in your results. The whole foods you eat when no one’s watching…the vegetables, the healthy fats, the clean proteins, they don’t just disappear. They become the clarity you feel at 2pm instead of brain fog. They become the natural glow people notice. They become steady energy that lasts all day, not the crash-and-burn cycle of processed foods and sugar. You can’t fake real nourishment. Your body tells the truth. Feed it real food, and it shows. Skip the nutrients it needs, and that shows too. You are what you cultivate when no one is watching. And every single meal is either building you up or breaking you down. Choose foods that serve you.

GLP-1s are more than a just weight loss. Dr. Mikhail Kolonin’s 2025/2026 data shows these molecules induce adipocyte browning and activate telomerase (TERT) in adipose tissue, even without weight loss. We're shifting from appetite control to active metabolic re-programming.

You don't magically become healthy. You practice it. You notice you're making a bad choice and correct it, over and over again until the good one becomes automatic. The people who figured this out aren't special. They just decided to take it seriously one day and never stopped.

Big thank you to @nirbarzilai for joining us and ranking 4 FDA-approved drugs as potential longevity medicines and you've probably heard of them. Metformin, GLP-1 agonists, SGLT2 inhibitors and bisphosphonates. youtu.be/YJIAekRlPjk

Kobe Bryant once said: “I have nothing in common with lazy people who blame others for their lack of success. Great things come from hard work and perseverance. No excuses.”

Most electrolyte products are missing something fundamental. You can take all the potassium you want — but without enough magnesium, it won't stay where it needs to be. Magnesium activates ATP, and ATP powers the pump that actually moves minerals into your cells. Skip magnesium, and the whole system stalls. This is basic physiology that most products ignore. If you've ever wondered why you're still exhausted, still cramping, still thirsty no matter what you take — this video is going to change how you think about hydration completely.

Mitochondrial Transplant Reverses Disease Scientists just transplanted healthy mitochondria into diseased cells -- and reversed Parkinson's, Leigh syndrome, and mtDNA depletion. In Cell. As a medical school professor, I can tell you this is one of the most important papers of 2026. Chinese researchers solved the delivery problem that's challenged mitochondrial medicine for decades. The breakthrough: wrapping healthy mitochondria in red blood cell membranes. Delivery efficiency jumped from under 5% to 80%. The results: - Rescued mitochondrial defects in patient-derived cells - Reversed mtDNA depletion syndrome in mice - Extended survival in Leigh syndrome mice - Prevented neuron loss and restored motor function in a Parkinson's model Tested in both mice and monkeys. This is what I wrote about in "Lies I Taught in Medical School" -- we treated mitochondrial diseases as untreatable because we couldn't fix the powerhouse. Now we can replace it entirely. "Organelle therapy" is no longer theoretical. It's here. Full breakdown coming on the Health Longevity Secrets podcast. Source: cell.com/cell/abstract/… #Mitochondria #Parkinsons #RegenerativeMedicine #CellTherapy #Longevity

Thanks to @ProfValterLongo for a fascinating conversation on his new book Fasting Cancer. Key insight: While on an FMD healthy cells enter a protected mode while cancer cells can't, making them more vulnerable to therapy. Full interview:

Grateful to Dr. Luigi Ferrucci from @theNIAgov for sharing his insights from 60 years of Baltimore Longitudinal Study. We talked about how they measure the pace of aging, how it relates to healthspan and how mitochondria could be the source of all aging. youtu.be/NS-VxoHltdw

At NIH, we’re accelerating the future of medical research, advancing innovation and repurposing existing drugs to deliver new treatments faster for the American people🔬🇺🇸

I don't know where Dr Eades would put me on the continuum of properly understanding a paper but I agree with his point!

I want to share a crucial update on our study, KETO-CTA. (The video for this article is in the next tweet) Our study recruited 100 participants, each undergoing two high-resolution heart scans, known as CT angiograms, one year apart. (For more background on this study design, see preprint in the following tweet) There are now four analyses of those same 200 scans. But one of those analyses stands out — and I have some new developments to report. For a quick background, the first quantitative analysis was from an AI company, Cleerly. We published their analysis of our scans last year. After the paper was published, the Citizen Science Foundation was free to look at the raw Cleerly data, and we found a number of patterns that appeared different from what is typically seen in other coronary plaque studies. For example, in Cleerly's analysis, not one of the participants showed lower plaque levels at follow-up — even though CTA scans typically show some natural variation in both directions, especially in people who start with very little plaque. For another example within their data, people with no detectable calcium in their scans appeared to have several times more plaque progression than those who already had some calcium present. This runs counter to what many in cardiology call the "power of zero" — the well-established finding that having no coronary calcium is typically associated with lower risk and slower disease progression. Another major development: shortly after publication, we learned that the scans Cleerly was analyzing were not fully blinded. In studies like this, the order of scans is typically kept unknown to the analyst to help prevent any potential for bias. But in this case, the chronological order was available in the scans. We therefore asked Cleerly to repeat their analysis using a properly blinded set of scans, which is standard practice in longitudinal studies. Cleerly declined to perform a blinded reanalysis. Because of this, we commissioned an additional, independent analysis from Heartflow. Heartflow has been a leader in this space and is the most extensively validated AI platform for coronary CTA analysis. The Heartflow analysis was conducted with full operational blinding and completed right before the prespecified third, and final quantitative analysis, which uses Medis QAngio. These two independent platforms were consistent with each other, yet both differed substantially from the Cleerly results. As these independent results became available, we shared them privately with Cleerly and again requested a blinded reanalysis of their original work. We offered to cover any costs involved just in case this was the barrier to reanalysis. Cleerly again declined. However, a new development emerged. Several participants requested their scans from the study and submitted them directly through their own, personal cardiologist. Any cardiologist with a proper Cleerly account can appropriately submit scans on their patient's behalf. So in a sense, our participants themselves were able to provide a portion of the blinded analysis we were originally requesting. This was then shared with me on behalf of the Citizen Science Foundation. In total, there are 19 of these individual submissions — about 10% of the total scans in our study so far. Individual Submissions vs. Study Data We focused on the 8 participants who have both a baseline and a follow-up individual submission of their scans (the other 3 submissions are unpaired). [Please Note: These data are preliminary] Figure 1 compares the change in soft plaque (Non-Calcified Plaque Volume or NCPV) reported by the original Cleerly study analysis against the results from each participant's individual submission. [See Figure 1] Of the 8 participants, four showed an increase in soft plaque in both datasets — but in three of those four cases, the individual submissions reported substantially less progression than the study data. The remaining four participants all showed progression in the study data, yet every one of their individual submissions showed a decrease — a complete reversal of direction. The largest discrepancy was a single participant whose study data reported an increase of 32 mm³, while their individual submission showed a decrease of 48 mm³ — a reversal of approximately 80 mm³. The median change in soft plaque for these 8 participants was +20.6 mm³ (a 31% increase) in the original study data, compared to just +0.7 mm³ (about a 2% increase) from their individual submissions (Figure 2). The mean average is even more pronounced: the study data shows an average increase of +20.9 mm³ (42% from baseline), while the individual submissions show an average decrease of 5.1 mm³ (an 8% decline). In other words, the study data says plaque went up; the individual submissions say it went down (Figure 3). Direction of Change Across Platforms To put these individual submissions in broader context, Figure 4 compares the direction of soft plaque change across three analyses of these same scans. On the left is the original Cleerly study analysis — 99 participants after excluding one who had a procedure between scans. 98% showed an increase in soft plaque. Only 2 showed no change. Zero showed regression. In the middle are the 8 individual submissions, split right down the middle: 50% showing progression and 50% showing regression. On the right is the full Heartflow analysis across 95 participants. While 8 is a small sample size, the direction-of-change in these individual submissions is far closer to the Heartflow analysis than the original Cleerly analysis. It is worth emphasizing: 4 out of the 8 participants — fully half — received individual submission results showing less plaque in their second scan than their first. But after accounting for the single exclusion mentioned above, not one of the 99 participants in the original Cleerly study analysis showed plaque regression. We are not sure what happened with the original Cleerly analysis. We just know the other analyses are largely consistent with each other — and now, that includes these individual submissions to Cleerly as well. Next Steps We have already taken steps regarding last year's paper that contained the original Cleerly analysis. We are working with the journal on that now, and we expect news on this very soon. In the meantime, the preprint of our current paper with both Heartflow and QAngio results is available at the link below. Importantly, the two principal findings reported in the original paper have been reproduced in both the Heartflow and QAngio analyses: (1) baseline plaque strongly predicts future plaque progression, and (2) ApoB was not associated with plaque progression I want to once again thank Dr. Budoff and the Lundquist team for providing these scans to study participants who request them. If you are a participant in our study and interested in sending in your scans through your cardiologist, we now have a budget to help cover the cost of that submission. You can contact us at info@citizensciencefoundation.org for more details. Thank you again to everyone for your support. 🙏 cc @nicknorwitz @AdrianSotoMota

Thank you Sec. Kennedy & President Trump. I will work hard to help make the @cdc the best public health agency in the world, following gold standards science and restoring public trust in public health.

Latest video: @Healthformance explains the dosing protocol that preserves cognitive performance under sleep deprivation and aging, including reaction time, working memory & decision-making. youtu.be/IxyRlcr86Jo

Grateful to Dr. Allen Taylor from @TuftsUniversity for this deep dive on vision and nutrition: high glycemic foods damage your eyes as much as smoking does. The good news? Switching to low glycemic eating protects your vision AND your heart. youtu.be/2GTTcGl_7vc

Just interviewed @DrGoodenowe on plasmalogens, brain lipids that decline after 60. His trial: 41% of Alzheimer's patients improved cognition. Not just slowed, improved. Why it works: His precursors cross the blood-brain barrier where plasmalogens can't. youtu.be/SMMiWvi38X0

But so difficult to do.....

The practical answer is what @Madam_Mito said - think of how much money has gone into biochemistry and molecular biology over the last 50+ years; I don't know the exact numbers but the investment in bioelectricity has to have been << 0.1% of that. The scientific answer is that biochemistry and genetics can be done on dead tissue: take cells, fractionate them, sequence everything, etc., the information is still there. Bioelectricity is much harder - it only exists as long as the cell is alive. It's gone the moment you kill, preserve, freeze, or fractionate cells. The technology to read and write that kind of physiological information in the living state is relatively new. The first noninvasive imaging of non-neural voltage patterns, and the first use of molecular biology to manipulate those patterns, was only in 2002. If you can't slice organs into pieces without losing the info (cell voltage changes if you separate them from their microenvironment), it mean you have to image voltage fluorescence *through* tons of other cells. That's difficult. Think of how long it's been since the first complete gene sequence was read - 1972 or so? Bioelectricity is an emerging field, but it's definitely moving forward. A number of commercial efforts are working on human stem cells, mouse regeneration, and electroceuticals for human cancer etc. It's coming but it needs a lot of tool development up-front to get to the exponential rise tipping point.