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The 2 Ages Your Body Rapidly Decays (And How to Stop It) | Michael Snyder | AFP 54

The following is based on a conversation with Michael Snyder, a Professor of Genetics at Stanford University.

What is the difference between linear aging and biological “ageotypes”?

Traditional models assume human aging is a steady, linear process. In reality, deep molecular profiling, measuring hundreds of thousands of biological indicators across the microbiome, urine, and blood, reveals that biological aging occurs in non-linear shifts or “spikes”. These major physiological transitions tend to cluster around specific life stages, notably the 40s and 60s.

In your 40s, biological changes occur alongside lifestyle factors like elevated stress, poor sleep, and reduced physical activity. In your 60s, biological mechanisms drive major declines in muscle mass (sarcopenia) and immune function. Furthermore, individuals do not age uniformly; each person exhibits a distinct pattern known as an ageotype. Depending on your primary metabolic or biological markers, you can be classified as a metabolic, cardio, kidney, or immune ager.

How do metabolic subphenotypes affect glucose spikes and prediabetes?

Type 2 diabetes and prediabetes are heterogeneous conditions. Through metabolic subtyping, individuals with glucose dysregulation can be divided into specific subphenotypes based on their underlying physiological defect:

  • Muscle insulin resistance: The muscles fail to respond properly to circulating insulin.
  • Hepatic insulin resistance: The liver fails to suppress glucose output effectively.
  • Beta-cell defect: The pancreas fails to secrete adequate amounts of insulin.
  • Incretin defect: Impaired GLP-1/incretin pathways.

These distinct subphenotypes dictate how an individual’s body responds to specific foods. For example, individuals with muscle insulin resistance or beta-cell defects tend to experience sharp glucose spikes when consuming starchy foods like potatoes or pasta. Understanding a person’s exact subphenotype, which can now be predicted using machine learning algorithms based on continuous glucose monitor (CGM) curve patterns, allows for targeted dietary interventions, such as consuming fiber or protein prior to carbohydrates to blunt glycemic spikes.

How can continuous physiological tracking and remote monitoring extend healthspan?

The modern healthcare system relies predominantly on reactive “sick care,” treating diseases only after clinical symptoms appear. Proactive health management utilizes non-invasive wearables (smartwatches, rings, continuous glucose monitors) combined with micro-sampling (mailing in a single drop of blood) to continuously establish a personalized biological baseline.

Wearable devices continuously track physiological signals such as resting heart rate, heart rate variability (HRV), blood oxygen saturation, and skin temperature. Because baseline shifts in these parameters occur prior to clinical symptoms, algorithms can detect early-stage infections (like COVID-19 or Lyme disease), cardiovascular events, or mental health disruptions days before a patient feels ill. Combining continuous wearable monitoring with regular metabolite tracking enables early, targeted interventions to extend “healthspan”, the period of life spent free from chronic disease.

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Cleaned Transcript

Jeroen Schreel: We always assume that our bodies age linearly with time, but that’s not always the case. Can you tell us a bit more about that?

Michael Snyder: Yeah, basically as we get older… backing up a little bit, we measure people incredibly deeply. We literally take hundreds of thousands of measurements on people. We take their blood, urine, and stool, and then we measure as many molecules as possible in their blood, quite a few in the urine, and their microbiome in the stool. From that, we see how they’re changing.

I can safely say that people definitely don’t age linearly, meaning some things happen more at certain times than others. It’s well known, for example, that as people hit their 60s, their immune system declines. That’s why they get vaccinated in their 60s—because they’re more prone to actually getting serious problems. Sarcopenia is another one. We also found that oxidative stress goes up as people get older. It goes up throughout your life, but it especially takes off later on.

There are other things that happen at different times, too. We believe changes occur in the 40s. It’s pretty well known that people often get injured as they hit their 40s, and we can see changes in muscle architecture occurring as well within our study group.

In the 60s, we know the biological basis: muscle mass declines, the immune system declines, and that leads to a lot of other problems. For the transitions happening in the 40s, we don’t know the exact answer, but we think it’s largely due to lifestyle changes. You’re very active in your teens and 20s, but in your 30s, you’re pushing your career and many people are starting families. I think that cuts into the things you should be doing, like exercising regularly and getting enough sleep. All those things get sacrificed in your 30s, and it probably catches up with you as you get a little older.

Jeroen Schreel: So, can we assume, maybe not with 100% confidence, that those mid-life differences are a result of changes in lifestyle?

Michael Snyder: I believe so. We haven’t proven that yet, but we’re currently correlating people’s lifestyles with their biochemical changes to see if keeping fit and active prevents those shifts.

We have other studies where we profile people deeply. I’m involved with a company called January AI / Iollo that does metabolic profiling. You send in a drop of blood, and they measure 650 metabolites. From that, they determine your biological age as well as what we call your ageotype—your personalized aging pattern.

I think this is the most important takeaway: it’s not how we age as a group, it’s how you age. We all age differently. We published a study showing that some people are metabolic agers, some are cardio agers, some are kidney agers, and some are immune agers. Once you see your profile, you can take action.

They take your metabolic data, combine it with scientific literature, and use AI to make very specific recommendations. It’s not just “exercise more” or “eat better”—it can tell you to eat specific foods you’ve never heard of. About 95% of people who follow those recommendations improve their biological markers. They may not be getting chronologically younger, but they definitely achieve a healthier profile. The same is true in our lab research: when people receive this information, they improve their lifestyle habits and their biological markers improve.

This is very actionable. We should all know how we’re aging so we can live a long, healthy life and then pass away quickly at the end. Currently, the difference between healthspan (the time you’re healthy) and lifespan is about 11 to 15 years. That means people are spending their last decade of life sick. By tracking this data, we can avoid that outcome.

Jeroen Schreel: I totally agree. I don’t want to just live longer if I’m unhealthy; I want my healthy years extended. Do you think personalized medicine is the actual future of extending healthspan?

Michael Snyder: Yes, we can go way beyond what we’re doing now. Let’s face it: most people don’t live a healthy lifestyle. They don’t exercise enough, and ultra-processed foods are absolutely terrible for us. When you’re young, you feel invincible—you eat cakes and muffins like it doesn’t matter, but that stuff is poison over time.

In the US, diabetes and obesity are continually rising. Right now, 11.6% of the US population is diabetic, and 38% are prediabetic. That means nearly half the population has broken glucose regulation, and 80% of prediabetics don’t even know it. We have a diabetes endemic that is far worse than the COVID pandemic.

This is where new technologies come in. We do a lot of research with continuous glucose monitors (CGMs). Wearing one will change the way you eat forever because it provides real-time visual feedback. CGMs measure glucose every five minutes, and you quickly learn that different people spike from completely different foods. Research by Eran Segal’s group in Israel and our own work showed that some people spike from potatoes, others from pasta, white bread, or rice.

When you wear a CGM, you identify your specific trigger foods and simply avoid them. If you drink a milkshake, you’ll watch your glucose shoot through the roof and think twice before doing it again. Or, if you do eat something high-glycemic, you can take a brisk 15-minute walk right afterward to suppress the spike.

Jeroen Schreel: In one of your papers, you divided participants into groups like “potato spikers” and “grape spikers”. Are all glucose spikes inherently bad?

Michael Snyder: Probably not all of them. If you do strength training, your body breaks down glycogen into glucose, causing a transient spike. That spike goes away quickly, aids muscle remodeling, and boosts health.

The spikes that stay elevated for long periods are the bad ones. Frequent, prolonged glucose spiking correlates strongly with diabetes, cardiovascular disease, and cancer. Even independent of diabetes, frequent glucose spiking is a risk factor for cardiovascular damage.

Our latest research focuses on subtyping diabetes and prediabetes. Traditionally, people classify diabetes as 10% Type 1 (autoimmune lack of insulin) and 90% Type 2. But Type 2 is incredibly heterogeneous. We perform tests to see if someone is:

  1. Muscle insulin resistant
  1. Hepatic (liver) insulin resistant
  1. Beta-cell deficient (insulin doesn’t release properly from the pancreas)
  1. Incretin deficient (defects in GLP-1 signaling)

I’m a thin guy, but I’m actually a Type 2 diabetic due to a genetic beta-cell defect. My pancreas doesn’t release enough insulin.

Your specific subtype determines what foods cause you to spike. If you have muscle insulin resistance or a beta-cell defect, you tend to spike from potatoes and pasta. Your subtype also dictates how you can suppress those spikes. You’ve probably heard advice to eat salad before french fries. Eating fiber, protein (like egg whites), or healthy fats before carbohydrates (like white rice) helps blunt the glucose spike for most people. However, if you have certain subphenotypes, that ordering trick won’t work as effectively.

We are developing AI algorithms that analyze the subtle shape of your glucose curve from a simple home CGM to identify your exact subtype and deliver personalized dietary rules.

Jeroen Schreel: Currently, medicine is reactive—we go to the doctor only when we’re already sick. How do we shift to proactive care, both for patients and reluctant doctors?

Michael Snyder: You hit the nail on the head. The primary hurdle is that financial incentives are completely misaligned. Doctors and systems get paid when you are sick, not when you stay healthy.

Countries with single-payer systems (like Canada or parts of Europe) have a structural advantage because the system retains the patient long-term, making preventive investments worthwhile. In the US, people switch health insurance providers every 18 months. An insurance company asks, “Why spend $10,000 keeping you healthy when you’ll be on someone else’s plan in two years?”

We need to align incentives. For example, the life insurance company John Hancock runs a “Vitality” program. They give policyholders financial credits for walking 10,000 steps daily or getting their genome sequenced. That works because when the customer lives longer, the life insurance company makes more money.

Every health plan should give members a smartwatch and a CGM upon joining. Preventing chronic disease via continuous monitoring will save the entire healthcare system massive amounts of money in the long run.

Jeroen Schreel: How could scientists theoretical engineer someone to extend lifespan far beyond normal limits?

Michael Snyder: If you want to speculate on extreme longevity, you need to solve three core biological issues:

  1. Mitochondrial Transfer: Mitochondria produce energy, but they also generate reactive oxygen species that damage mitochondrial DNA over time, leading to cellular fatigue. Cells naturally swap mitochondria. In the future, we could inject billions of fresh, functional mitochondria into the body to replace damaged ones.
  1. Senolytics: As we age, some cells become senescent—often called “zombie cells”. They stop dividing, refuse to die, and secrete inflammatory signals that damage surrounding tissue. Companies are developing senolytic compounds to target and destroy these cells.
  1. Stem Cell Rejuvenation: This is the hardest piece because stem cell niches exist across all organs, including the brain. Rejuvenating or re-infusing stem cells safely—without triggering cancer—could replenish tissue regeneration.

Jeroen Schreel: How close are those therapies, and what interventions are available right now?

Michael Snyder: Mitochondrial transfer and senolytic clinical trials are actively running now. Skin-focused stem cell trials are also underway, as skin is an accessible test organ.

Beyond speculative therapies, GLP-1 receptor agonists (like Ozempic and Mounjaro) are showing powerful longevity effects. I take them for my diabetic beta-cell defect, and they work remarkably well. Beyond weight loss and glycemic control, GLP-1s appear to reduce risk in cardiovascular disease, kidney disease, and cognitive decline. Many longevity researchers are currently experimenting with GLP-1 microdosing to capture these systemic benefits.

Jeroen Schreel: What is your opinion on popular longevity supplements like NMN or Vitamin D3?

Michael Snyder: The clinical evidence for supplements is mixed. Vitamin D3 (taken with K2 for proper absorption) and Vitamin B12 have clear benefit profiles for people who are deficient.

For compounds like NMN (nicotinamide mononucleotide), the biological mechanisms make complete sense—NMN boosts NAD+ levels to fuel declining mitochondrial function. However, large-scale human clinical trials are still lacking.

We launched a citizen-science initiative called My Supple Hub to track real-world supplement use, self-reported outcomes, and biological markers to help design better clinical trials.

Personally, I take about 10 supplements daily based on my family history and scientific plausibility:

  • NMN: For cellular energy support.
  • Beetroot Extract / Nitric Oxide Boosters: For endothelial function and blood flow.
  • Vitamin D3 + K2: For systemic health and calcium metabolism.
  • Fish Oil (Omega-3s): For cardiovascular and brain health.
  • Magnesium Threonate & Glycinate: Taken at night for muscle relaxation and sleep support.
  • Baby Aspirin: Taken in the evening due to strong family history of early cardiovascular disease.
  • Milk Thistle & Saw Palmetto: For liver detox pathways and prostate health.

I caution everyone to consider timing—some supplements belong in the morning, while others are best taken at night.

Jeroen Schreel: It’s also worth noting that nutritional interventions like the ketogenic diet are gaining clinical traction.

Michael Snyder: Absolutely. Ketogenic diets are becoming a primary metabolic therapy for bipolar disorder, and anecdotal evidence points to benefits in depression and schizophrenia.

In daily life, simple behavior adjustments make a massive difference. Avoiding ultra-processed foods, prioritizing whole fruits over starchy processed carbohydrates, eating your largest meal earlier in the day rather than late at night, and prioritizing 7 to 8 hours of sleep all directly lower baseline glucose and inflammation.

Jeroen Schreel: You mentioned wearing multiple devices. How many wearables do you wear, and what do they track?

Michael Snyder: Right now, I am wearing four smartwatches, two smart rings, and continuous-sensing hearing aids.

You don’t need four watches—I wear them simultaneously to compare research data. These sensors continuously track resting heart rate, heart rate variability (HRV), blood oxygen, skin temperature, and electrodermal activity.

In 2017, our lab proved that consumer smartwatches can detect early illness pre-symptomatically. I picked up my own early Lyme disease infection when my smartwatch flagged an elevated resting heart rate and dropped blood oxygen levels before I felt sick. During COVID-19, we analyzed smartwatch data from thousands of participants and showed we could alert individuals to an active viral infection up to four days before symptom onset.

Continuous tracking acts like a real-time dashboard for the human body. You track your car’s fuel, oil, and engine health continuously; your body deserves the exact same level of insight.

Jeroen Schreel: Do you have a final take-home message for our listeners?

Michael Snyder: Start building these health habits early. I wish I knew 40 years ago what I know today. While you cannot change your genetics, taking control of your daily choices—prioritizing strength training to preserve muscle mass, tracking your metabolic markers, avoiding processed foods, prioritizing sleep, and staying socially active—will compound over time to maximize your healthspan.

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