Siim Land: Biohacking Longevity, Health Span Truths & Cutting Through the Noise

drew_ab · July 1, 2026, 7:52pm

Here’s a great new video from Siim Land, regarding him being ranked #1 in the Longevity World Cup. Some noteworthy points include:

His blood markers are similar to that of a 10-year old (it isn’t a cherry picked panel either).
There’s a good discussion of Bortz Age, Pheno Age, and the Dunedin Clock.
Siim believes that “being lean” is one of the most important drivers of his success.
Diet - potatoes, cottage cheese, fish (cod/salmon), beef, a few eggs per week, berries, fruit, vegetables, whole grains, dark chocolate, nuts, seeds, beans, and greens.
Macros - 120-135g of protein, 250-300g of carbs, 70-85g of fat, 40g of fibre.
Exercise - 3-4x per week with calisthenics, favouring short/intense workouts (with some zone 2/5 cardio, as indicated in the comments).
Sleep - 7-8 hours/night.
Walking - 8 700 - 10 000 steps per day.
Supplements - collagen, glycine, astaxanthin, lutein, zeaxanthin, vitamin d, vitamin k2, and omega 3.

Perhaps what stands out the most to me is that there isn’t a crazy amount of optimization required for him to achieve this. Just hitting the big movers and not getting lost in the minutiae.

I. Executive Summary

The core thesis of this discourse evaluates the clinical validity, predictive utility, and practical application of blood-biomarker-based biological age clocks—specifically the 22-marker Bortz Age clock and the 9-marker PhenoAge clock—as superior, actionable alternatives to epigenetic DNA methylation metrics for tracking systemic healthspan and mortality risk. Standardized phenotypic blood marker panels reflect real-time functional output across multi-organ pathways, including hepatic, renal, metabolic, and immunological axes, enabling targeted lifestyle modifications to reverse biological decline.

Analysis of large-scale epidemiological data, notably within the UK Biobank, demonstrates that the Bortz Age clock possesses a high concordance index (C-index = 0.778) for the stratification of mortality risk, outperforming standard PhenoAge models by roughly 11% (Bortz et al., 2023). This predictive resolution hinges on identifying key physiological patterns: high insulin sensitivity, minimal systemic chronic inflammation, robust immune signaling, and optimized filtration. A critical metabolic priority is maintaining low fasting glucose and hemoglobin A1C (HbA1C), which minimizes glycation-induced tissue stress (Levine et al., 2018). Concurrently, systemic chronic inflammation must be suppressed, targeting an optimal high-sensitivity C-reactive protein (hs-CRP) threshold of 0.1 mg/L or lower.

Renal evaluation requires a critical transition from serum creatinine to Cystatin C, as the former is profoundly confounded by total skeletal muscle mass and transient training-induced protein turnover, whereas Cystatin C serves as an unconfounded, stable index of true glomerular filtration rate (Shlipak et al., 2013). Hepatic optimization relies on managing total training volume and visceral fat accumulation; extreme physical training workloads paradoxically elevate transaminases (ALT, GGT), signaling localized muscle or liver tissue stress that can distort clock calculations. Mechanistically, achieving an optimized phenotypic profile requires navigating the boundary of moderate caloric restriction. While restriction optimizes glycemic and inflammatory markers, excess caloric deficits introduce a profound trade-off, precipitating immune system dampening, thyroid down-regulation, and sex hormone binding globulin (SHBG) abnormalities (Redman et al., 2018). Thus, a balanced framework requires lean body composition maintained through highly localized, high-intensity, low-volume resistance training, paired with a nutrient-dense, polyphenol-rich diet containing adequate protein and essential fatty acids, avoiding the systemic penalties of over-restriction.

II. Insight Bullets

Longevity World Cup Benchmarks: The competition evaluates biological age reduction using two validated clinical blood-biomarker algorithms: the 22-marker Bortz Age clock and the 9-marker PhenoAge clock.
Bortz Age Operational Scale: Trained on machine-learning cohorts, the Bortz Age clock estimates biological age by analyzing circulating markers of metabolic, cardiovascular, renal, hepatic, and immune function.
UK Biobank Predictive Power: A 2023 cohort study validating the Bortz Age clock achieved a C-index of 0.778, demonstrating a 78% accuracy rate in ranking survival and mortality risk between individuals.
Bortz vs. PhenoAge Accuracy: The Bortz Age clock adds 13 additional blood parameters to the standard PhenoAge matrix, yielding an 11% relative increase in disease and mortality predictive accuracy.
PhenoAge Composition: Developed by Morgan Levine and colleagues, PhenoAge integrates chronological age with 9 multi-system clinical chemistry markers to determine a phenotypic mortality risk score.
Phenotypic Age Disparity and Cancer: Longitudinal biobank data establish that individuals with a PhenoAge score 10 years higher than their chronological age experience accelerated mortality and elevated cancer risk.
Chronological Age Co-dependency: Both phenotypic blood clocks integrate chronological age as a baseline weight, meaning older individuals can mathematically manifest larger biological age reduction deltas (e.g., 20-25 years) than younger cohorts.
DunedinPACE Distinct Mechanics: Unlike blood-marker age clocks that output biological age in literal years, DunedinPACE is an epigenetic clock measuring the immediate rate or pace of biological aging.
Blood Clocks vs. Epigenetic Flaws: Blood-biomarker clocks provide distinct actionable clarity; an adverse blood marker indicates exactly which organ system requires intervention, whereas an elevated epigenetic methylation score fails to locate the localized root physiological cause.
Circadian Fluctuation Vulnerability: Epigenetic DNA methylation markers suffer from severe circadian fluctuations and can yield significantly divergent scores depending on morning versus evening sample collection.
Fasted Blood Standardization: Blood-based phenotypic clocks rely on highly standardized, early-morning fasted collection protocols, eliminating transient postprandial confounding factors.
The Insulin Sensitivity Imperative: The foundational metabolic requirement for a minimized biological age is maximized insulin sensitivity, marked by concurrently low fasting glucose, low fasting insulin, and low HbA1C.
Apolipoprotein Ratios as Metabolic Proxies: Higher Apolipoprotein A (ApoA) reflects optimized insulin sensitivity and favorable lipid homeostasis, contrasting with the atherogenic profile of elevated Apolipoprotein B (ApoB).
Immune Signaling Optimization: A high lymphocyte percentage reflects robust, active adaptive immune signaling, provided absolute white blood cell (WBC) counts remain low-to-normal to rule out acute infection or systemic autoimmunity.
Systemic Inflammation Floor: High-sensitivity C-reactive protein (hs-CRP) should be driven as close to zero as possible; an optimal longevity target sits at or below 0.1 mg/L, whereas average unoptimized individuals score between 0.5 and 1.5 mg/L.
Visceral Fat and Transaminase Elevations: Excess visceral fat accumulation and elevated systemic triglycerides drive pathological increases in liver transaminases (ALT, ALP, GGT), signaling localized hepatic distress.
Exercise Volume Confounders on Hepatic Markers: Intense, high-volume physical training regimes can artificially elevate liver transaminases due to systemic tissue turnover; reducing total weekly training volume can rapidly normalize ALT and GGT levels.
Cystatin C Superiority: Cystatin C is a highly reliable, unconfounded biomarker of glomerular filtration rate (GFR) because, unlike creatinine, it is completely independent of total skeletal muscle mass, protein intake, and acute exercise.
Creatinine Limitations: Serum creatinine metrics can be profoundly misleading in muscular athletes or individuals with high protein turnover, falsely indicating impaired kidney function when actual GFR is optimal.
Albumin as a Nutritional Status Index: Higher serum albumin values within the normal clinical range reflect robust protein status, optimal caloric adequacy, and low systemic inflammatory depletion.
The Caloric Restriction Boundary Line: Maintaining a state on the borderline of moderate caloric restriction optimizes metabolic, inflammatory, and hepatic biomarkers, but crossing into excessive restriction carries significant biological penalties.
Pathological Over-Restriction Penalties: Excessive caloric restriction induces systemic biological dysfunction, down-regulating thyroid output, dampening the adaptive immune system, lowering sex hormones, and degrading exercise output.
High-Intensity Low-Volume Resistance Framework: Executing short, high-intensity resistance workouts (e.g., 20 minutes, 2-3 sets to true failure using calisthenics or a weighted vest) preserves skeletal muscle mass while avoiding the transaminase and protein-turnover spikes seen in high-volume training.
Polyphenol-Dense Nutrient Profile: Minimizing visceral fat while maintaining lean mass is optimized via a diet prioritizing clean carbohydrate blocks (potatoes, whole grains), high-quality proteins (cottage cheese, cod, salmon, beef), and abundant whole-food antioxidants (berries, dark chocolate).
Targeted Baseline Supplementation: Achieving an optimal biomarker profile can be supported by low-complexity, targeted supplementation consisting of glycine, astaxanthin, carotenoids (lutein/zeaxanthin), high-dose vitamin D3/K2, collagen peptides, and highly concentrated omega-3 fatty acids.

IV. Actionable Protocol (Prioritized)

High Confidence Tier (Level A/B Evidence)

Multi-System Biological Age Risk Stratification: Utilize comprehensive blood biomarker panel analysis (incorporating the 22 core elements of the Elastic-Net derived Cox model) rather than relying solely on isolated single-organ markers. Systematic tracking provides a highly accurate method for scoring multi-organ physiological deterioration and overall mortality risk (Bortz et al., 2023).
Unconfounded Renal Assessment (Cystatin C): Replace or supplement serum creatinine tests with Cystatin C measurements to assess true glomerular filtration rate (GFR). Creatinine is heavily confounded by skeletal muscle volume, creatine supplementation, and high-intensity exercise turnover, whereas Cystatin C functions as a stable, linear predictor of all-cause mortality across diverse clinical cohorts (Shlipak et al., 2013).
Moderate Caloric Optimization without Malnutrition: Maintain lean mass metrics on the upper boundary of caloric restriction (~11% to 15% energy deficit). Controlled clinical trials verify that moderate restriction decreases tissue oxidative damage and systematically lowers fasting blood glucose, HbA1C, and systemic inflammatory markers without introducing clinical adverse events (Kraus et al., 2019).

Experimental Tier (Level C/D Evidence)

Low-Volume, High-Intensity Neuromuscular Stimulation: Restructure resistance training into compressed, ultra-intense sessions (e.g., 20 minutes total, 2 to 3 working sets executed to absolute muscular failure using calisthenics or a weighted vest) to stimulate muscle protein synthesis while keeping liver transaminase spikes low.
Fasted Baseline Blood Standardization: Conduct all phenotype blood draws in an absolute early-morning fasted state to stabilize circadian-driven metabolic variables, ensuring internal consistency across sequential evaluations.
Polyphenol and Micronutrient Dense Dietary Pattern: Structure daily macronutrient distribution to prioritize clean complex carbohydrates (400g potatoes), high-yielding lean proteins (cottage cheese, cod, salmon, beef), and daily fiber blocks (40g total, augmented by 10g psyllium husk), while integrating a concise, targeted longevity stack:
- Glycine: 5 to 10 grams daily for endogenous glutathione synthesis support.
- Astaxanthin: 12 mg daily for specialized lipid-membrane antioxidant shielding.
- Vitamin D3 + K2: 5,000 IU D3 combined with 120 mcg K2 to stabilize immune cells and calcium routing.
- High-Concentration Omega-3 Fatty Acids: 2,000 to 3,000 mg daily to depress hyper-inflammatory eicosanoid pathways.

LukeMV · July 1, 2026, 8:02pm

The longevity space needs more young people like Siim Land because it’s going to be interesting to watch him age over the next several decades.

desertshores · July 1, 2026, 9:47pm

What I like is that his diet is manageable long-term, not like some crazy vegan or keto diet.

But, on a skeptic’s negative note: That plan and supplement list are so ordinary; he must also be a member of the luckiest gene pool.

Jonas · July 1, 2026, 9:53pm

Here is Land’s summary on biomarkers to watch

Ambient · July 2, 2026, 1:20am

Siim’s LDL is 94mg/dl in that video posted above.
While it is a good score, it’s still considered in the plaque building range.
Not sure if he’s against using Rx medications, but it would be good to see him start to use some to get even better blood tests.

RapAdmin · July 2, 2026, 1:28am

I Tracked HRV for 7 Years - These 3 Things Matter Most

I. Executive Summary

Heart rate variability (HRV), the mathematical variation in time intervals between consecutive heartbeats (R-R intervals), serves as an indispensable proxy for autonomic nervous system (ANS) tone and systemic physiological resilience. Regulated by the competitive interaction between the sympathetic (“fight-or-flight”) and parasympathetic (“rest-and-digest”) pathways, an elevated HRV signifies adaptive vagal dominance. This condition strongly correlates with structural cardiovascular health, efficient stress mitigation, and expanded longevity. Within clinical and tracking frameworks, comparing absolute HRV numbers between separate individuals is fundamentally flawed due to profound genetic variations; clinical utility relies strictly on monitoring longitudinal intra-individual trend lines to identify adaptations or systemic overreaching.

Systemic modification of autonomic flexibility requires precise management of energetic timing and somatic mass. Time-restricted eating frameworks—specifically a 16:8 intermittent fasting protocol—induce a mild hormetic stressor that enhances parasympathetic tone, increasing time-domain HRV markers (e.g., RMSSD and SDNN) while systematically suppressing resting heart rate. Conversely, extended fasting windows exceeding 48 hours or severe caloric deficits trigger an emergency sympathetic response, driving down vagal power. Body composition acts as a key structural lever: while visceral adiposity and clinical obesity severely degrade HRV via hyper-inflammatory signaling, expansions in fat-free skeletal muscle mass can also cause minor historical reductions in peak absolute HRV due to increased basic metabolic maintenance burdens.

Physical conditioning represents the most powerful intervention for driving structural autonomic remodeling. Meta-analytic data verify that multi-month progressive exercise training significantly expands time-domain HRV metrics and shifts overall autonomic balance toward parasympathetic activity. While resistance training fails to alter baseline autonomic parameters when executed in isolation, combining it with progressive aerobic or anaerobic conditioning produces optimal cardiovascular adaptations. Large-scale wearable datasets indicate a strict linear correlation between cumulative daily step volumes and positive HRV changes up to a high threshold of twenty thousand steps per day. Furthermore, environmental hormetic variables—such as passive heat exposure via saunas or cold-water immersion—exploit homeostatic rebound mechanisms. Although these thermal inputs acutely depress HRV during exposure, the subsequent recovery phase provokes a powerful parasympathetic overshoot. Maximizing baseline HRV requires balancing these acute physical stressors with strict recovery protocols, as uncompensated sleep fragmentation, late-night glycemic spikes, and chronic psychological anxiety rapidly degrade baseline autonomic function.

II. Insight Bullets

Autonomic Balance Indicator: Heart rate variability (HRV) quantifies the millisecond variations between successive R-R intervals, serving as a non-invasive readout of autonomic nervous system operational efficiency.
Vagal Dominance: High time-domain HRV scores (specifically RMSSD) directly reflect robust parasympathetic vagal activity, signifying systemic recovery capacity and lower cardiovascular strain.
Longitudinal Trend Priority: Comparing raw HRV values between different individuals lacks diagnostic validity due to unique genetic baselines; tracking an individual’s longitudinal trend line is the only valid method for monitoring adaptive health.
Time-Restricted Eating Efficacy: Implementing a 16:8 intermittent fasting window serves as a controlled metabolic stressor that improves nocturnal parasympathetic dominance and elevates morning HRV readouts.
Fasting Bradycardia Kinetics: Eight weeks of a structured 16:8 time-restricted feeding protocol has been shown to increase time-domain HRV parameters while decreasing resting heart rate by an average of 8.8%.
The Extended Fasting Cliff: Extending complete caloric deprivation beyond 48 hours activates the sympathetic nervous system as an emergency survival mechanism, resulting in a precipitous drop in HRV.
Somatic Mass Distribution: The correlation between body mass and autonomic tone is non-linear, with both clinically underweight and pathologically obese profiles exhibiting depressed HRV metrics.
Hypertrophy HRV Trade-offs: Gaining substantial fat-free skeletal muscle mass can cause a minor drop in peak historical absolute HRV due to the heightened metabolic and circulatory requirements of a larger somatic frame.
Cardio Modality Superiority: Dedicated aerobic endurance training provides the most robust stimulus for expanding long-term baseline HRV compared to isolated anaerobic or resistance protocols.
Autonomic Co-Conditioning: Combining progressive aerobic training with structured anaerobic intervals triggers an enhanced autonomic training effect over single-modality endurance strategies.
Resistance Training Limitations: Executing traditional weightlifting or isolated resistance training blocks fails to provide the continuous venous return required for the eccentric cardiac remodeling that raises baseline HRV.
Linear Step Volatility: Large-scale tracking datasets establish a positive, linear correlation between total daily step counts and elevated HRV metrics up to an upper ceiling of 20,000 steps.
Volumetric Substitution: Reducing absolute daily step counts does not compromise long-term autonomic tone if the reduction is systematically replaced with structured aerobic endurance training sessions.
Sauna Cardio Mimicry: Passive thermal stress via traditional saunas elevates heart rate while acutely lowering HRV, functioning as a passive cardiovascular challenge.
Vagal Rebound Phenomenon: The post-exposure phase following a sauna session induces a powerful parasympathetic overshoot, boosting systemic recovery and raising baseline HRV hours after heat exposure.
Post-Exercise Sauna Diminishing Returns: Utilizing a sauna immediately following intense exercise provides no additive or synergistic HRV benefits compared to executing the exercise protocol alone.
Cryogenic Vagal Shock: Sudden cold-water immersion or cryotherapy triggers immediate trigeminal nerve and vagal activation, producing sharp post-exposure increases in RMSSD of 20% to 30%.
Thermal Hormesis Principle: Brief, structured exposure to extreme hot or cold environments increases systemic resilience by widening the body’s autonomic operational envelope.
Prodromal Sickness Detection: Sharp, unprompted declines in baseline nocturnal HRV reliably serve as an early warning sign of acute viral or bacterial infection 24 to 48 hours prior to clinical symptom onset.
Sleep Fragmentation Suppression: Restricting sleep below seven hours or experiencing high sleep fragmentation increases nocturnal sympathetic tone, immediately suppressing the subsequent morning’s HRV readout.
Nocturnal Glycemic Burdens: Consuming large, high-glycemic, high-sodium meals late in the evening elevates sleeping heart rate and disrupts nocturnal parasympathetic recovery.
Overtraining Syndrome Mapping: A persistent, multi-day downward trend in baseline HRV paired with an elevated resting heart rate serves as an objective indicator of systemic overreaching or overtraining syndrome.
Psychological vs. Physiological Stressors: Chronic, unmanaged psychological anxiety permanently depresses HRV via uncompensated sympathetic drive, unlike structured physical stressors which prompt positive adaptive supercompensation.
The Ideal Longevity Triad: The optimal cardiorespiratory phenotype for expanded human lifespan comprises an elevated baseline HRV, a high VO2 max, and a low resting heart rate.
Autonomic Mismatch Risk: Presenting with a low resting heart rate simultaneously paired with a suppressed, low baseline HRV reveals an uncoupled autonomic state characterized by elevated cardiovascular risk.

IV. Actionable Protocol (Prioritized)

High Confidence Tier (Level A/B Evidence)

Autonomic Adaptation via Progressive Aerobic Training: Execute structured aerobic training for a minimum of 12 weeks to systematically expand baseline HRV metrics. Meta-analyses of randomized controlled trials demonstrate that progressive endurance training increases overall HRV by an average of 58% and shifts autonomic balance toward parasympathetic tone by up to 83% (Exercise Training Meta-analysis, 2024).
Metabolic Alignment via Time-Restricted Eating: Integrate a consistent 16:8 time-restricted feeding protocol (16 hours of fasting, 8 hours of feeding) to enhance vagal activity. Controlled interventions show this structure optimizes nutrient-sensing pathways, elevating time-domain HRV parameters (SDNN/RMSSD) and reducing resting heart rate by up to 8.8% without inducing systemic starvation stress (Fasting Hormesis Analysis, 2026).
Thermal Hormesis via Cryogenic Exposure: Utilize cold-water immersion or targeted cryotherapy immediately following high-intensity training blocks to accelerate autonomic recovery. Systematic meta-analyses confirm that acute cold-water immersion significantly increases post-exercise RMSSD by 20% to 30% via immediate vagal nerve stimulation (Cryotherapy Meta-analysis, 2024).

Experimental Tier (Level C/D Evidence)

Linear Volumetric Step Accumulation: Maintain a consistent daily baseline of 10,000 to 15,000 steps to support linear improvements in cardiovascular health and autonomic stability, scaling up to 20,000 steps if not performing dedicated aerobic exercise. (Source unverified in live search).
Non-Exercise Day Sauna Bouts: Deploy 15-to-20-minute traditional hot sauna sessions exclusively on non-exercise days to mimic cardiorespiratory workloads and exploit the post-exposure parasympathetic rebound, avoiding use immediately post-workout.
Proactive Overtraining Intervention: Monitor nocturnal HRV tracking daily. Upon identifying an unprompted drop below baseline, proactively reduce subsequent training volumes by 50% to avert systemic overreaching or immune suppression.

Red Flag Zone (Debunked or Lacking Safety Data)

Direct Multi-Individual HRV Comparisons: Evaluating absolute, raw HRV values against other individuals to gauge relative health or biological age. Genetic differences render cross-sectional numeric comparisons invalid; diagnostics must rely entirely on longitudinal individual trend lines.
Prolonged Fasting for Autonomic Maximization: Executing extended water fasts exceeding 48 hours to improve HRV. Prolonged caloric deprivation reverses parasympathetic adaptations, inducing a severe sympathetic fight-or-flight crisis that depresses HRV.
Resistance Training as a Standalone HRV Stimulus: Relying solely on traditional weightlifting or isolated resistance training to improve cardiorespiratory autonomic variables. Longitudinal tracking confirms resistance work fails to expand baseline HRV in healthy populations unless paired with aerobic conditioning.

CronosTempi · July 2, 2026, 1:48am

This is why it’s worth tempering one’s enthusiasm for these supposed longevity biomarkers.

The reality is that you have no idea what is or is not brewing in your physiological future. Here it might at least have an indication wrt. LDL that atherosclerosis is a possible danger. But there are tons of processes not captured by these biomarkers. You might have AFIB in your future. You might have some gene that will pop off in the year X of your life - leukemia, NDD, CVD etc. and no biomarker in your 30’s will show what happens in your 60’s.

We all eventually die of something. That something is our individual weakest link. The vast majority of time, you have no idea what that is. We all try to take the known frequent killers off the table: atherosclerosis, metabolic derangements, systemic inflammation etc. And so (just taking myself as an example) I take pitavastatin, bempedoic acid, ezetimibe for atherosclerosis, telmisartan for BP, empagliflozin (plus soon: acarbose and imeglimin) for metabolic derangements, rapamycin for systemic inflammation with more agents to be added as they become available (something to push ApoB lower yet, push down Lp(a) etc.). But that’s a kind of general addressing of the typical “top 10” killers - nothing specific unless you really have a good idea of your weak links (based on your genome, family and health history, and lifestyle factors).

I kind of assume - statistically - that whatever takes me out will be something that’s not on my radar at the moment. Things come with age that you really weren’t expecting. A year ago, I wasn’t expecting to be compelled to have ACDF surgery, yet here we are. And whatever that is, may not at all be revealed or hinted at by any biomarker - as indeed the degenerative disc disease in my cervical spine had no biomarker associated with it… the symptoms appeared suddenly and an MRI diagnosed the issue. And there are things which no imaging or biomarkers or peering into the future through genome will ever manifest in a prediction.

There may be no warning. Back in the day (and still true) the first appearance of a symptom of a cardiac arrest is at the time of fatality - death. No warning. Here you might have had imaging etc. but there are tons of things for which there will be no imaging and no biomarkers - only onset of symptoms as you are relentlessly pushed into the grave.

So this young fellow here has good biomarkers. Bully for him. It’s better than having bad biomarkers. Nontheless, speaking just for myself - color me only moderately impressed. I don’t care about today as much as about tomorrow - and that’s an unknown. Seeing as he’s off all pharmaceuticals while his LDL is highish leads me to think that he’s one of those “I try to stay away from all medications” naturalistic fallacy believers… not a great indicator of someone who will control his lifespan with any impact… someone who willingly limits his options and opportunties - it’ll be luck all the way. But who knows. YMMV.

drew_ab · July 2, 2026, 1:10pm

Great point about his LDL being sub-optimal (at least according to my read of the literature). I did read the Longevity Leap by Siim Land when it was released and it talks about the lowest all-cause mortality being close to that range and cites large observational studies (if my memory serves me correctly). I do generally believe that “lower is better” when it comes to LDL.

Siim does have an extremely impressive RHR and HRV. Huge credit to for this. He’s got Bryan Johnson beat here without the million dollar annual budget.

Almostthere · July 4, 2026, 10:15am

I have listened to a number of interviews with him after he posted his bio age numbers. What stands out for me - he has been watching his markers for years and noting what does and does not effect them. As a result, he has found that maintaining a caloric balanc leads to very low visceral fat and better markers. He even mentions a few times that having a a lower caloric intake before blood tests leads to much better bio markers.