The Latest in Longevity Medicine (2025 and forward)

Longevity science has entered an exciting era. In labs and clinics worldwide, researchers are pushing the boundaries of what is possible to extend healthy lifespan. From gene-editing therapies that reverse genetic aging markers to AI algorithms scouting for the next anti-aging drug, progress is accelerating. This review covers six key fronts in longevity medicine as of 2025: recent advances in gene therapy and epigenetic reprogramming, senolytics to purge “zombie” cells, AI-driven drug discovery, promising longevity pharmaceuticals, evidence on diet and fasting, and a critical look at popular social media fads. Let’s dive in.

Gene Therapy & Epigenetic Reprogramming

CRISPR and Genetic Reversal of Aging

Gene therapy is making headway in tackling aging at its roots – our DNA. One remarkable example is the use of CRISPR-based “base editing” to treat progeria, a rapid-aging disease. In a 2021 Nature study, scientists corrected a single DNA letter in mice with progeria using an adenine base editor, dramatically extending the animals’ lifespan. Treated progeria mice lived 2.5 times longer than untreated ones – a jump from ~7 months to ~1.5 years (approaching normal mouse old age) with a single treatment (In vivo base editing rescues Hutchinson–Gilford progeria syndrome in mice). David Liu, whose lab led the work, noted this degree of lifespan extension in a mammal is “unprecedented”.

While progeria is rare, the success fuels hope that editing DNA in normal aging could prevent or reverse some aging changes. Don’t order your DIY gene-editing kit yet, aging in humans is way more complex.

Researchers are also exploring CRISPR to boost longevity-associated genes (for example, delivering extra copies of youth-promoting genes like Klotho or FGF21 via viral vectors). Early mouse studies combining such gene therapies improved multiple age-related diseases simultaneously (A single combination gene therapy treats multiple age-related diseases - PMC), hinting that multi-gene interventions might extend healthspan. Though human trials purely aimed at “aging reversal” aren’t yet here, the first CRISPR therapies for age-related diseases (like genetic forms of blindness or cholesterol disorders) are in development, laying groundwork for broader anti-aging applications.

Epigenetic Reprogramming – Turning Back the Cellular Clock

Perhaps the most spectacular progress has come from partial cellular reprogramming, a technique that rejuvenates cells by briefly expressing embryonic genes. By transiently activating Yamanaka factors (a set of four genes used to create stem cells), scientists found they can reset a cell’s epigenetic age without erasing its identity. In lab dishes, old human cells treated with a short pulse of Yamanaka factors regain youthful patterns of DNA methylation and gene expression. Impressively, in living animals this approach has shown promise too. A landmark study showed that older mice regained youthful vision after an epigenetic reprogramming gene therapy: turning on three Yamanaka factors (OSK) in damaged retinal nerves reversed vision loss in a glaucoma model and even in naturally aged mice (Reprogramming to recover youthful epigenetic information and restore vision - PMC ).?

The treated old mice recovered retinal function, demonstrating that age-related deterioration could be undone at the cellular level.?

A 2023 review summarizes that partial reprogramming can rejuvenate multiple aging hallmarks – improving tissue regeneration, resetting epigenetic clocks, and even lengthening life in animal models ( Partial cellular reprogramming: A deep dive into an emerging rejuvenation technology - PMC ). These findings hint that cells retain a “backup copy” of youthful information that we might tap into to repair age damage.

This is all early-stage. Continuous reprogramming can cause tumors or other problems , so scientists are fine-tuning methods to get rejuvenation benefits safely. Nonetheless, the progress is exciting. Academic labs and new startups (e.g. Altos Labs and others) are racing to translate epigenetic reprogramming into therapies for age-related diseases. In the coming years, we may see clinical trials aiming to regenerate failing organs or reset certain aging biomarkers in humans. Gene therapy and epigenetic engineering have moved from science fiction to real lab results, making them one of the most pivotal fronts in longevity research.

Senolytics & Cellular Rejuvenation

Zombie Cells and Aging

As we age, certain cells in our bodies become senescent – they stop dividing but refuse to die. These stubborn “zombie” cells build up in tissues and secrete inflammatory factors that can harm neighboring cells. Senescent cells are now understood to be major drivers of aging and age-related conditions (from osteoarthritis to lung fibrosis).?

Enter senolytics: drugs or interventions that can selectively destroy senescent cells to rejuvenate tissues. In mouse studies, clearing senescent cells has yielded remarkable benefits. A 2016 experiment used a genetic “self-destruct” switch to periodically purge senescent cells in normal mice (yeah, I know, mice again). The result: the treated mice lived 17–35% longer than controls and stayed healthier, with delayed tumor formation and preserved organ function. Simply removing 30% of these bad actors was enough to significantly extend both lifespan and healthspan. This proof-of-concept sparked a new field of senolytic drug development.

Latest Research and Trials

Dozens of senolytic compounds have been identified, ranging from repurposed chemotherapy drugs to natural flavonoids. One combination, Dasatinib + Quercetin (D+Q), was shown in mice to clear senescent cells and improve cardiac and vascular function.?

Now, for the first time, D+Q has been tested in randomized human trials. In 2023, Mayo Clinic researchers reported the first placebo-controlled trial of senolytics in healthy older adults (Effects of intermittent senolytic therapy on bone metabolism in postmenopausal women: a phase 2 randomized controlled trial). Sixty women over 65 took D+Q or placebo for 20 weeks. The treatment was well-tolerated and showed target engagement – meaning it hit senescent cells – and even boosted markers of bone turnover and density in those who had high senescent cell burdens.?

Specifically, intermittent D+Q improved bone formation (and, in women with more senescent cells, increased wrist bone mineral density) compared to placebo. Other early trials in people with lung fibrosis and diabetic kidney disease (small pilot studies) have reported improved physical function and organ biomarkers after senolytic therapy, though larger controlled trials are needed.

That said, not all senolytic efforts have been smooth sailing. Unity Biotechnology, a pioneer in the field, saw mixed results – their senolytic drug for knee osteoarthritis failed to meet endpoints in a Phase II trial, reminding the field that translating mouse miracles to humans is challenging (Kneecapped by Aging: New and Scrutinized Science Suggests Why ...). Unity has since pivoted to eye diseases, where a senolytic approach (UBX1325) showed some encouraging signs in treating diabetic macular edema by improving vision for nearly a year with one injection (according to 2023 interim results). The broader lesson is that senolytics may need to be tailored to specific conditions or delivered at the right time to show full benefits.

Real-World Applications and Outlook

The concept of cleaning up senescent cells is powerful because it targets a root cause of aging. Imagine periodically taking a treatment that sweeps away toxic aged cells – a sort of “spring cleaning” for your tissues. This could theoretically prevent many diseases of aging at once. In mice, senolytics have already been shown to delay multiple age-related diseases simultaneously (e.g. improving cardiac function, atherosclerosis, and frailty in treated animals). Companies are developing improved senolytics, including PROTACs and gene therapies that seek out P16INK4a-positive senescent cells. Some labs are investigating “senomorphics,” drugs that suppress the harmful secretions of senescent cells without killing them, as a gentler alternative.

It’s also become clear that senolytics might not be a one-size-fits-all therapy. The recent Mayo Clinic trial found D+Q helped most in individuals who started out with higher senescent cell loads. Those with fewer “zombie cells” saw less benefit. This suggests that in the future, we may need to identify patients with high senescent cell burden (via biomarkers) to target with senolytics, and that timing and dosing will be critical. As senior author Dr. Sundeep Khosla cautioned, people should not rush to take over-the-counter senolytic supplements on their own.?

While compounds like quercetin and fisetin are being sold as longevity pills, we still don’t know the right dose or schedule in humans, and indiscriminate use could even be risky.

Ongoing clinical trials (for example, testing D+Q in Alzheimer’s disease, or a peptide senolytic in diabetic kidney patients) will shed more light in the next 1-2 years. If results stay positive, senolytics could become one of the first true anti-aging therapies to enter mainstream medicine – not by extending maximal lifespan dramatically, but by delaying the onset of multiple chronic diseases, thereby extending healthspan.

AI-Driven Drug Discovery

Artificial Intelligence as a Longevity Accelerator

I love AI, and this field is tailored for it: complex interactions and a huge feature space. The drug discovery process has traditionally been slow and expensive – it can take a decade and billions of dollars to find a single new drug. In longevity research, where we might need entirely new classes of drugs (so-called “geroprotectors”), this is a big bottleneck.?

In the past few years, AI models have begun to design novel molecules, predict their effects, and identify new drug targets at a pace that was unimaginable before. For example, in 2022 the biotech company Insilico Medicine announced that an AI-designed compound (for fibrosis, a disease of aging) went from initial concept to Phase I human trial in under 30 months (From Start to Phase 1 in 30 Months | Insilico Medicine). This AI-discovered drug, now in clinical trials for idiopathic pulmonary fibrosis, validates that AI can drastically compress development timelines. Insilico’s AI platform not only found a brand-new biological target for fibrosis, but also generated a molecule to hit that target – all in about 2.5 years. Such speed is unprecedented in pharma and offers a blueprint for finding drugs to tackle complex aging processes.

Finding Geroprotectors with Big Data

Researchers are also using AI to comb through vast datasets from genomics, proteomics, and clinical records to find patterns – for instance, genes or pathways that are key drivers of aging, which could be targeted by drugs. Deep learning “aging clocks” can now predict biological age from DNA or blood biomarkers, helping test whether a drug actually slows aging rather than just treating a disease. New transformer-based AI models (akin to those that power ChatGPT, Claude and Gemini) are being adapted for biology.?

A 2024 study introduced PreciousGPT (P3GPT), a transformer trained on multi-species aging data that can suggest potential anti-aging compounds and targets (Deep learning and generative artificial intelligence in aging research and healthy longevity medicine | Aging).

In an experimental validation, P3GPT proposed 22 candidate molecules to test on senescent cells, of which 8 showed real anti-aging effects in cells – suppressing harmful senescent cell factors without killing the cells. Compounds like maslinic acid and dapsone emerged from the AI’s list as possible “senomorphics” that attenuate the bad effects of senescent cells. This showcases how AI can repurpose existing drugs or natural compounds for longevity applications that researchers might otherwise overlook.

Another AI approach is target repurposing – identifying proteins in the body that, if modulated, could affect aging. For instance, an AI system trained on scientific literature pinpointed CCR5 (an inflammation-linked receptor) and parathyroid hormone (PTH) as novel longevity targets.

These hadn’t been obvious targets for anti-aging therapy before, but evidence suggests they play roles in age-related inflammation and tissue maintenance. Such insights can direct new studies (or inspire using existing CCR5 blockers, for example, to see if they have geroprotective effects).

Impact on Longevity Research

The marriage of AI and longevity research is accelerating progress on multiple fronts:

• Drug Discovery

Several longevity biotech companies are now AI-powered. Notably, Calico (Google’s longevity venture), BioAge, and Insilico Medicine all have AI-discovered compounds in clinical trials. BioAge, for example, uses AI to analyze human aging databases (like blood analytes from people who live long lives) to find drug targets – they’ve advanced drugs into trials for muscle aging and immune aging based on those insights. As of 2025, at least 10 compounds identified with AI or data-driven methods are in human trials for age-related indications.

• Combination Therapies

Aging is multifactorial, and AI excels at finding combinations or multi-target approaches. Machine learning models have been used to predict synergistic effects of drug combinations that might hit multiple Hallmarks of Aging at once. For example, one can ask an AI to rank which pairs of existing drugs (say, an anti-inflammatory plus a metabolic booster) might together give an outsized benefit for lifespan. This could guide human trials combining, say, metformin + exercise mimetics or other polytherapy for longevity. (Don’t hang your running shoes up yet.)

• Biomarker Development

?AI is helping discover new biomarkers of aging (e.g. epigenetic clocks) that can rapidly tell if an intervention is working. Instead of waiting years to see if people live longer, researchers use AI-derived biomarkers (like DNA methylation age, transcriptomic age, etc.) as surrogate endpoints. This was evident in the CALERIE trial of caloric restriction, where an AI-derived DNA methylation metric (DunedinPACE) measured a slowing of aging – something we discuss in the Diet section.

Overall, AI acts as a force-multiplier. It doesn’t replace wet-lab science or clinical trials, but it supercharges hypothesis generation and optimization.?

By sifting through the noise of complex biological data, AI can highlight the most promising levers to tweak aging. It’s telling that both academia and industry are embracing these tools: even the National Institute on Aging is funding AI projects to map cellular changes in aging.?

Longevity Pharmaceuticals (Metformin, Rapamycin, NAD+ Boosters, etc.)

A number of existing drugs have caught the spotlight for their potential to extend lifespan or healthspan. Unlike gene or cell therapies, these pharmaceuticals could be taken as pills – making them attractive for widespread use if proven effective. Here we review the latest on a few leading contenders:

• Metformin - Diabetes Drug Turned Geroprotector?

Metformin, a safe and cheap diabetes medication, is perhaps the most famous “longevity pill” candidate.?

Epidemiological studies about a decade ago raised eyebrows when they showed that diabetics on metformin outlived even healthy people without diabetes. In one large study from the U.K., patients with type 2 diabetes taking metformin had about a 15% longer median survival than non-diabetics of the same age (Can people with type 2 diabetes live longer than those without? A comparison of mortality in people initiated with metformin or sulphonylurea monotherapy and matched, non-diabetic controls - PubMed)?

The results (metformin users lived longer than those without the disease) implied metformin might confer general anti-aging benefits, not just manage diabetes. Metformin has since been shown in animals like mice and worms to extend lifespan under certain conditions, likely by improving metabolic and inflammatory profiles. It appears to act as a mild calorie restriction mimetic, activating cellular stress defenses (AMPK pathway, for example) and reducing insulin levels. As we dug deeper, things changed a little.

The longevity field has eagerly awaited the start of the TAME Trial (Targeting Aging with Metformin), a large randomized trial intended to see if metformin can delay chronic diseases in older adults. As of 2025, TAME has not fully launched (funding hurdles slowed it), but smaller trials have reported insights. The MILES trial found metformin induced some “youthful” changes in gene expression in older non-diabetic adults (A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan - PubMed). Recent critical review of the evidence concluded that while metformin is promising, it’s still unclear if it truly extends lifespan in healthy humans.?

Metformin definitely improves healthspan for those with metabolic syndrome or pre-diabetes – e.g. reducing rates of cardiovascular disease, cognitive decline, and cancer in diabetics – which indirectly extends healthy life.

But whether it helps already healthy, lean individuals.. That’s probably not the case.?

The upcoming trials should clarify which populations benefit most. In the absence of any hint of insulin resistance, I do not think it is worth it.

• Rapamycin - The Current Star of Anti-Aging Research

If one drug had to be picked as the most compelling pharmacological anti-aging candidate right now, most geroscientists would point to rapamycin.?

Rapamycin (an mTOR inhibitor) has consistently extended lifespan in lab animals – mice live ~10–25% longer when given rapamycin, even if treatment starts in mid or late life ( Rapamycin, the only drug that consistently demonstrated to increase mammalian longevity. An update - PMC ). Notably, the NIH’s Intervention Testing Program found rapamycin increased both median and maximal lifespan in genetically diverse mice, effectively resetting the paradigm that pharmacological aging interventions are possible. No other drug has shown such reproducible longevity effects across multiple studies and in both male and female animals as rapamycin.?

It works by mimicking calorie restriction at the cellular level – inhibiting the nutrient-sensing mTOR pathway, which in turn triggers autophagy (cellular cleanup) and shifts metabolism to a more youthful state. Beyond mice, rapamycin extends lifespan in organisms from yeast to flies, and improves healthspan (e.g. mobility, cognition) in mice and even pet dogs. Human Evidence and Trials

Rapamycin is already FDA-approved (for organ transplant rejection and certain cancers) but at doses and schedules very different from those thought to promote longevity. Chronic daily high-dose rapamycin can cause side effects (e.g. high blood sugar, high lipids, immune suppression) ( Blazing a trail for the clinical use of rapamycin as a geroprotecTOR - PMC ), which is why the anti-aging community is exploring intermittent dosing (e.g. once weekly) to get benefits without significant side effect.

Early human studies hint at positive effects: a small trial in older adults found a rapamycin analog (everolimus) given once weekly for 6 weeks enhanced immune function, improving the response to a flu vaccine by ~20%. This suggests rapamycin can rejuvenate aspects of the aging immune system. However, higher doses (20 mg/week) weren’t tolerable long-term, so finding the sweet spot is key.?

Currently, there is a groundswell of clinical research: the PEARL trial is underway, enrolling 150 adults ages 50–85 to receive either placebo or rapamycin (5 or 10 mg weekly) for one year to see if it improves markers of aging (primary endpoint: change in visceral body fat)

Other trials like REACH are testing rapamycin in early Alzheimer’s disease, given its neuroprotective effects in animal models. There’s also a trial named VIBRANT looking at rapamycin’s effect on ovarian aging in women. These studies will inform how rapamycin might be used clinically to target aging or specific age-related diseases. Meanwhile, hundreds of enthusiasts aren’t waiting – anecdotal reports suggest over 2000 people in the US are already taking off-label rapamycin for “anti-aging” purposes. Preliminary observational data from these users (compared to non-users) indicate that side effects at weekly doses are manageable (mostly mild mouth ulcers).?

Of course, without controlled trials, it’s unclear if these individuals are gaining any longevity benefit. The fervor around rapamycin has also spawned derivatives (like RTB101) and epigenetic clocks to measure its impact. As of 2025, rapamycin remains the most robust lifespan-extending drug in animals and is the focus of multiple human trials – by around 2026–2027 we should have much harder data on its efficacy in people. If successful, rapamycin or its next-generation analogs could become a geroprotector pill taken in midlife to stave off diseases of aging.

• NAD+ Boosters (NR and NMN) – Boosting Cellular Energy Molecules

NAD+ is a molecule found in every cell, needed for metabolism and DNA repair. Its levels decline with age, which has been linked to fatigue, metabolic decline, and weaker cell repair mechanisms.?

This led to the rise of NAD+ boosters like Nicotinamide Riboside (NR) and Nicotinamide Mononucleotide (NMN), often sold as supplements promising to “recharge your cells.”?

In mice, giving NR or NMN can raise NAD+ levels and has shown benefits such as improved muscle function, better insulin sensitivity, and enhanced DNA repair – essentially making older mice’s cells behave more youthfully. But what about humans? Current Evidence

Over the past 5 years, multiple clinical trials have tested NR and NMN in adults, and the results have been a bit mixed. On the bright side, these compounds do appear to increase NAD+ levels in humans ( Dietary Supplementation With NAD+-Boosting Compounds in Humans: Current Knowledge and Future Directions - PMC ). Studies in middle-aged and older adults (typically using 300–1000 mg/day of NR or NMN) show that blood NAD+ metabolite levels rise significantly.?

They are generally well tolerated with minimal side effects. One trial found NR supplementation led to a slight drop in systolic blood pressure and arterial stiffness in older adults with higher baseline blood pressure, but none of those changes were statistically significant. There is a lot of financial interest in pushing those but honestly, there is no juice to squeeze out of this one.?

Another recent placebo-controlled study in healthy older men found NMN (250 mg/day for 12 weeks) raised NAD+ levels ~70% but did not significantly change muscle strength, gait speed, or other functional measures.

Overall, the consensus from several trials is that short-term NAD boosters in generally healthy adults have limited to no observable benefits. Could be because the studies are too small and don’t last long enough, could be because there is nothing more to this target. There was also a slight signal towards more cancer in the NAD boosted mice, but again, who knows what that means.

So far, we have proof of mechanism (NAD goes up) but not yet proof of significant clinical benefit. Consumers should also be aware that as supplements, these are unregulated – and in late 2022 the FDA actually ruled NMN cannot be sold as a supplement anymore (because it’s being investigated as a drug).?

The bottom line: NAD+ boosters were promising in theory, but so far, no evidence supports its use. As always, maintaining healthy lifestyle factors (exercise, diet) also raises NAD+ naturally by activating the same pathways (and many others equally if not more beneficial). Get on your bike or grab your dumbbells and move.

Diet & Fasting – The Role of Nutrition in Longevity

One of the most profound levers on lifespan across species is dietary intake. Caloric restriction and intermittent fasting are two approaches that have consistently shown longevity benefits in lab organisms. Here’s what science says about these strategies and how they might (or might not) work in humans:

• Caloric Restriction (CR)

This refers to a sustained reduction in calorie intake (typically 20–40% less than ad libitum, without malnutrition). For over 80 years, studies have shown that CR extends lifespan in organisms ranging from yeast and worms to mice. In rodents, lifelong CR can increase lifespan by up to 30-50%, and even starting in mid-life still yields significant extension (Intermittent and periodic fasting, longevity and disease - PMC ).?

Importantly, CR also delays the onset of age-related diseases – CR mice have lower incidence of cancer, heart disease, and neurodegeneration.?

Research in non-human primates (rhesus monkeys) gave more nuanced results: two long-term monkey studies (one at University of Wisconsin and one at NIH) initially had conflicting outcomes on lifespan, but re-analysis showed that moderate CR (with a healthy diet) did improve monkey survival and healthspan, whereas overly severe CR or certain diets did not. Essentially, monkeys on a nutrient-rich, 30% calorie-reduced diet had a lower risk of diabetes, cancer, and cardiovascular disease and tended to live longer than control-fed monkeys. Human Data on CR

We can’t feasibly run a 50-year human trial of CR, but shorter studies give insight. Notably, the NIH sponsored the CALERIE trial, a 2-year experiment in which young and middle-aged adults (non-obese) were asked to cut ~15% of their calories and were compared to a control group eating normally.?

Results, published in 2022-2023, showed that even this moderate CR led to significant improvements in health markers: lower cholesterol, blood pressure, inflammation, etc. Most intriguingly, it slowed measures of biological aging. Using DNA methylation “aging clock” analysis, researchers found the CR group’s pace of aging was about 2–3% slower than the control group.?

That might sound small, but it’s estimated to correspond to a 10–15% reduction in mortality risk – similar to the longevity benefit one might get from quitting smoking. In other words, caloric restriction actually decelerated the participants’ biological aging. This provides some of the first direct evidence in humans that CR could extend healthy lifespan. On the downside, participants did experience some negative effects (e.g. loss of muscle mass in a few cases, increased sensitivity to cold, and unsurprisingly, hunger/moodiness).?

Long-term CR in humans can also lead to reductions in bone density and libido and is impractical for most people. It’s also not advised for anyone who is already lean or with health conditions. Still, these findings are scientifically important: they validate that the human body responds to calorie restriction in a way that mirrors animals, by shifting into a more preservation-focused physiology that may slow aging processes.

• Intermittent Fasting (IF) and Time-Restricted Feeding

In recent years, approaches that focus on when you eat, rather than how much, have gained popularity. Intermittent fasting encompasses diets like 16:8 (16 hours fasting, 8-hour eating window each day), 5:2 (two days a week of severe calorie cut, five days normal eating), or alternate-day fasting (eat one day, very little the next, and so on). Animal studies show many IF regimens can extend lifespan almost as effectively as continuous calorie restriction. Part of the reason is that fasting triggers beneficial stress responses – like autophagy (cellular cleanup) and improved insulin sensitivity – similar to CR. In mice, even without reducing total weekly calories, just extending the daily fasting period has been shown to improve metabolic health and lifespan. Human Evidence on Fasting

While long-term data is still accruing, short-term human trials of intermittent fasting have shown improvements in metabolic health markers. For example, studies of alternate-day fasting (ADF) in overweight adults found it can produce weight loss, lower LDL (“bad”) cholesterol and triglycerides, reduced insulin levels, and improved insulin sensitivity.?

In fact, one trial reported that 6 months of ADF was about as effective as standard calorie restriction for weight loss and metabolic benefits – and ADF had even stronger effects on cholesterol profile (raising HDL and lowering LDL more) than daily calorie restriction. Other fasting studies (e.g. 5:2 diet trials) similarly show reductions in blood pressure and markers of oxidative stress. A recent review by Longo and Mattson noted that intermittent fasting can engage the same longevity pathways (like lowering IGF-1, enhancing insulin sensitivity) that CR does, but with potentially more easily adoptable patterns. They also pointed out that fasting’s benefits come during the refeeding period as well – when the body, after being in a stressed state, rebuilds cells and tissues more resiliently. It’s important to mention that human fasting studies are still in their infancy regarding longevity outcomes. We don’t yet know if people who practice intermittent fasting for decades actually live longer, because such studies would need to run for a long time. But many indirect signs are positive: better cardiovascular metrics, lower inflammation, improved autophagy, and fat loss (especially visceral fat loss, which is linked to longer life). All these changes would be expected to reduce disease risk. Ongoing trials are examining whether intermittent fasting can improve specific age-related conditions like cognitive function or manage diseases like diabetes in a way that also prolongs healthspan. For now though, the benefits mainly stem from the caloric deficit they induce more than anything else. Fasting Cautions & Individualization

IF isn’t for everyone – some people (particularly lean individuals or those with certain medical conditions) can experience fatigue, irritability, or nutrient deficiencies if fasting is not done carefully. The consensus at this point: modest fasting windows (e.g. 14 hours fasting overnight) are generally safe and can be part of a healthy lifestyle, but extreme fasting or prolonged water-only fasts should be done under medical supervision and for a very specific goal. Also, what you eat when you’re not fasting still matters – fasting is not a license to binge on junk food during eating windows.

In addition to CR and IF, there’s interest in specific dietary compositions. Plant-heavy diets (Mediterranean diet, etc.) correlate with longevity in epidemiological studies. There’s also research into protein restriction or amino acid restriction (like methionine restriction) which in animals can extend lifespan by altering growth pathways. These are areas of active investigation to see if certain diet tweaks can give some of the longevity benefits without full-on CR.

In summary, the pillars of nutrition for longevity remain: eat a diverse, nutrient dense food. Focus on including good food instead of restricting. These habits have the strongest evidence for improving healthspan.

Debunking Social Media Fads and Pseudoscience

The growing popularity of longevity has unfortunately been accompanied by a lot of hype and pseudoscientific “hacks” on social media. It’s common to see influencers promoting extreme diets or miracle supplements claimed to add years to your life – without any credible evidence. They are good at sounding convincing though, I will give them that. Whenever I hear a reel starting with “Gary Brecka” or “My morning routine starts with…” showing someone ridiculously young living in a mansion with a green juice in one hand on their way to their cold plunge, I scroll up. Jealousy? Maybe. But honestly, if you have time to do that every morning - good for you. For the rest of us let’s debunk a few trending fads you shouldn’t waste time and money in.?

• “Detox” Cleanses and Superfood Hype

A persistent myth is that you need special juice cleanses, detox teas, or superfood regimens to “flush toxins” and stay young. In reality, there is no scientific evidence that short-term cleanses remove any toxins or have lasting effects on aging. Our liver and kidneys are already highly effective at detoxing the body; no lemonade-cayenne cleanse will enhance that. Similarly, while foods like blueberries, kale, or acai berries are healthy, the term “superfood” is mostly a marketing gimmick – longevity comes from a balanced diet, not overloading on one supposed magic food. For example, antioxidant-rich foods are generally good, but taking them to an extreme can backfire.

• Mega-Dose Antioxidant Supplements

Decades ago, researchers thought consuming lots of antioxidants (like vitamins A, C, E, beta-carotene) would slow aging by neutralizing free radicals. This idea has not panned out; in fact, clinical trials suggest harm from overdoing it. Large meta-analyses have found that high-dose antioxidant supplements do not extend life or prevent disease, and in some cases may increase mortality. One comprehensive review concluded that beta-carotene and vitamin E supplements in doses above the RDA significantly increase risk of death (Meta-Regression Analyses, Meta-Analyses, and Trial Sequential Analyses of the Effects of Supplementation with Beta-Carotene, Vitamin A, and Vitamin E Singly or in Different Combinations on All-Cause Mortality: Do We Have Evidence for Lack of Harm? | PLOS ONE). (Vitamin A also trended toward higher mortality in excess)

The likely reason is that oxidative stress is only one part of aging, and our bodies need a balance of reactive species for normal signaling – flooding the system with antioxidants can disrupt this balance and even impair some of the beneficial stress responses (like exercise-induced adaptations).?

The takeaway: getting antioxidants from a diet rich in fruits and veggies is great, but popping high-dose antioxidant pills is not an anti-aging shortcut and might do more harm than good.

• Over-the-Counter “Longevity” Supplements (Senolytics, NAD boosters, etc.)

As discussed, there is exciting research on things like senolytics and NAD boosters – but some people have jumped the gun. Supplements like quercetin, fisetin, NMN, resveratrol and others are being marketed with strong anti-aging claims that outrun the evidence. A Mayo Clinic gerontologist recently warned that many folks are taking senolytic combos (D+Q or fisetin) on their own, “without knowing if they have high enough senescent cell numbers to benefit, or what dose…is needed to be effective yet safe.” In other words, self-experimenting with these is risky – the science is still working out who should take them and how.?

Always approach such supplements with skepticism and consult healthcare professionals. The best supplement for you is the one you are deficient in, and this my friends, if often vitamin E, but as E for Exercise.

• Young Blood Transfusions and Other Extreme “Biohacks”

A few years ago, startups offered young blood plasma infusions to older clients, based on mouse parabiosis studies. The FDA swiftly issued a warning – stating that there is no evidence young blood infusions combat aging or memory loss, and such procedures carry serious risks (NBC News: 'Young blood' company Ambrosia halts patient treatments after FDA warning | Stanford Health Care). Those companies have since shut down their controversial trials.?

Another fad is hyperbaric oxygen therapy for longevity: a small study in 2020 claimed that daily hyperbaric oxygen over 60 days increased telomere length by ~20% in older adults. While interesting, this was not a lifespan study and telomere length alone is not a simple proxy for aging. Until we have outcomes data, spending thousands on hyperbaric chambers or young plasma is not justified.

• Miscellaneous Wellness Hacks

Social media is rife with other dubious advice – from drinking alkaline water to grounding earthing rituals – typically with zero credible research behind them. Many such practices are harmless but also useless for lifespan. Some can be harmful: e.g., excessive raw water consumption (risking infections) or strict all-fruit diets (causing nutrient deficiencies) in the name of longevity.?

In navigating longevity advice, consider the source. Peer-reviewed studies and clinical trials should carry more weight than a marketing ad. Often the real science is more nuanced – for instance, cold exposure (like ice baths) might have health benefits, but claims that it “doubles your lifespan” are unfounded. Be especially wary of anyone selling expensive products or requiring large payments up front (some anti-aging clinics charge tens of thousands for unproven therapies).

The pursuit of longevity is entering a more rigorous, evidence-based phase – moving from snake oil to science. Legitimate research is rapidly expanding our toolkit for extending healthspan. But with that comes a responsibility to stay grounded in data and avoid hype.

The bottom line

Longevity medicine in 2025 stands at a thrilling frontier. We have gene therapies that reprogram the clock of life in cells, drugs that kill toxic senescent cells and rejuvenate tissues, and AI guiding us to the next breakthroughs at blazing speed. Fasting and caloric restriction show that even simple lifestyle tweaks can nudge our biology toward longer life, while new pharmaceuticals like rapamycin and metformin hint at a future where aging itself is treated like a condition. At the same time, it’s critical to remain discerning – embracing innovation but staying skeptical of claims that aren’t backed by solid evidence. Not every “anti-aging” pill or practice will pan out, and some may be outright fads.

What’s remarkable is how quickly science is progressing. Five years ago, the idea of age reversal was on the fringes; now it’s published in top journals. As research continues, we might soon redefine what “old age” means, pushing diseases like cancer, dementia, and frailty further into our 80s and 90s or beyond. The goal many emphasize is not immortality, but healthspan – maximizing the years of life that we live in good health. The breakthroughs reviewed here all serve that goal: keeping cells and systems youthful for longer, so that more of us can enjoy vitality in our later decades.

The coming years will see pivotal clinical trial results (from TAME, PEARL, and others) that will tell us which interventions are ready for prime time. It’s an era of great hope, where aging is no longer seen as an untouchable fact of life but as a malleable process we can understand and influence. By combining advanced biotechnologies, pharmaceuticals, and proven lifestyle interventions, the dream of adding “life to years, not just years to life” is closer than ever. We will need to carefully validate each breakthrough and ensure equitable access to any longevity therapies. If we do so, the advances in longevity medicine promise not just longer lives, but longer, healthier lives, for millions of people in the generations to come.

See ya,

Julien