Metabolic health and aging: the complete guide

Metabolism is not just about how fast you burn calories. It is the entire network of chemical reactions that keep you alive — converting food into energy, building and repairing cells, removing waste, and regulating hormones. And when this network starts to fail, aging accelerates.

If your visceral-fat number and waist measurement disagree, use Visceral fat normal but waist high: what should you measure next?.

Here is the uncomfortable reality: metabolic dysfunction is the single largest driver of age-related disease. Heart disease, type 2 diabetes, Alzheimer’s, cancer — they all share a common root in disrupted metabolic signaling. A 2023 study in Cell Metabolism found that only 6.8% of American adults have optimal metabolic health, defined as healthy levels of blood glucose, triglycerides, HDL cholesterol, blood pressure, and waist circumference without medication. That means over 93% of the population is metabolically compromised to some degree.

The connection between metabolism and biological aging runs deeper than most people realize. Your metabolic health determines how efficiently your cells produce energy, how well they repair themselves, and how quickly they accumulate the damage that drives aging. Improve your metabolism, and you directly slow the biological clock.

This guide covers every major dimension of metabolic health as it relates to aging — from the molecular pathways that control cellular energy to the practical strategies that move the needle on your biological age.

What you’ll learn:

• Why metabolic health is the foundation of biological aging
• How insulin sensitivity acts as the keystone of metabolic function
• The molecular switches (AMPK, mTOR, autophagy) that control cellular aging
• How glucose, glycation, and ketones influence your rate of aging
• Evidence-based strategies to optimize metabolic health at any age

---

What is metabolic health?

Metabolic health describes how efficiently your body processes energy — from the food you eat down to the ATP produced inside every cell. It encompasses glucose regulation, lipid metabolism, mitochondrial function, hormonal signaling, and body composition.

Simple definition: Metabolic health is the state in which your body efficiently converts fuel into energy, maintains stable blood sugar, stores and burns fat appropriately, and keeps inflammatory and hormonal signals in balance — without medication.

Clinically, metabolic health is assessed using five criteria, which together define the absence of metabolic syndrome:

Marker	Optimal range
Fasting glucose	< 100 mg/dL
Triglycerides	< 150 mg/dL
HDL cholesterol	> 40 mg/dL (men), > 50 mg/dL (women)
Blood pressure	< 120/80 mmHg
Waist circumference	< 102 cm (men), < 88 cm (women)

Meeting all five criteria without medication qualifies as metabolically healthy. But these thresholds represent the bare minimum. Longevity-focused medicine pushes further — aiming for fasting glucose below 90 mg/dL, HbA1c under 5.2%, and fasting insulin below 6 μIU/mL.

Why metabolic health declines with age

After age 30, a cascade of metabolic changes begins:

• Mitochondrial efficiency drops. Cells produce less ATP per unit of fuel, generating more reactive oxygen species (ROS) as a byproduct.
• Muscle mass decreases. You lose roughly 3–8% of lean muscle per decade after 30, reducing the body’s largest glucose sink. This directly impairs glucose disposal and basal metabolic rate.
• Insulin sensitivity declines. Cells become progressively less responsive to insulin’s signals, requiring higher insulin levels to achieve the same glucose uptake.
• Fat redistribution occurs. Subcutaneous fat shifts to visceral fat, which is metabolically active and secretes inflammatory cytokines.
• Hormonal shifts amplify dysfunction. Declining growth hormone, testosterone, estrogen, and DHEA-S all contribute to metabolic slowdown.

These changes are not inevitable consequences of chronological aging. They are responses to accumulated metabolic stress — and largely reversible with the right interventions.

---

Insulin sensitivity: the keystone of metabolic aging

If you could optimize only one metabolic parameter for longevity, it should be insulin sensitivity. Insulin is the master metabolic hormone. It doesn’t just regulate blood sugar — it controls fat storage, protein synthesis, inflammation, cellular growth, and even gene expression.

How insulin resistance develops

Insulin resistance follows a predictable trajectory:

1. Chronic energy surplus overwhelms cellular storage capacity. Excess glucose is converted to fat, particularly in liver and muscle cells where it doesn’t belong.
2. Intracellular lipid accumulation (ectopic fat) interferes with insulin signaling pathways. The insulin receptor still works, but downstream signals — particularly IRS-1 and PI3K — become impaired.
3. The pancreas compensates by producing more insulin. Blood glucose stays normal, but fasting insulin creeps upward — the first detectable sign of trouble.
4. Hyperinsulinemia becomes chronic, driving fat storage, suppressing fat burning, promoting inflammation, and stimulating growth pathways (mTOR, IGF-1) associated with accelerated aging.
5. Eventually, the pancreas fails to keep up. Fasting glucose rises, HbA1c climbs, and clinical prediabetes or diabetes emerges — typically 10–15 years after insulin resistance began.

The key insight: by the time fasting glucose is elevated, you are already deep into metabolic dysfunction. Fasting insulin and HOMA-IR are far earlier warning signals.

Insulin resistance and biological age

A 2022 study in Diabetes Care found that for every 1-unit increase in HOMA-IR (a standard measure of insulin resistance), biological age accelerated by approximately 0.7 years. People in the highest quartile of insulin resistance aged 4–6 years faster biologically than those in the lowest quartile — independent of BMI, physical activity, and diet quality.

This means two people with identical diets and exercise habits can age at dramatically different rates depending on their insulin sensitivity. The mechanisms are direct: hyperinsulinemia activates mTOR (blocking autophagy), increases glycation, promotes visceral fat accumulation, and drives chronic low-grade inflammation.

---

Glucose control: beyond normal blood sugar

Standard medicine considers a fasting glucose of 99 mg/dL “normal.” But longevity research tells a different story. Data from the UK Biobank (over 500,000 participants) shows that all-cause mortality begins to rise when fasting glucose exceeds 85 mg/dL — well within the “normal” range.

Fasting glucose vs. post-meal glucose

Fasting glucose tells you how well your liver manages overnight glucose production. But it misses a critical dimension: what happens after you eat.

Post-meal glucose spikes — when blood sugar shoots above 140 mg/dL after eating — cause immediate oxidative damage to blood vessels, trigger inflammatory cascades, and accelerate glycation. A person with perfect fasting glucose can still experience damaging post-meal spikes, a pattern called “hidden hyperglycemia.”

This is why HbA1c is such a valuable marker — it captures your average glucose exposure over 2–3 months, including the post-meal spikes that fasting glucose misses.

The glucose-aging connection

Every time glucose enters your bloodstream, some of it non-enzymatically binds to proteins through a process called glycation. The resulting compounds — advanced glycation end products (AGEs) — are essentially molecular rust. They cross-link collagen, stiffen arteries, damage kidneys, cloud eye lenses, and activate inflammatory receptors (RAGE).

Glycation is a direct driver of aging. The higher your average glucose exposure, the faster AGEs accumulate. This is why HbA1c — itself a glycated protein — correlates so strongly with biological age in validated aging clocks like PhenoAge and KDM.

The practical takeaway: keeping average glucose low and minimizing post-meal spikes are among the most powerful anti-aging strategies available. Continuous glucose monitoring (CGM) data suggests that metabolically optimal individuals keep glucose between 70–110 mg/dL for over 90% of the day, with post-meal peaks rarely exceeding 130 mg/dL.

Sugar, glucose spikes, and the hallmarks of aging

The damage from poor glucose control extends beyond glycation. Chronic hyperglycemia and repeated glucose spikes trigger multiple hallmarks of aging simultaneously:

• Mitochondrial dysfunction: excess glucose floods the electron transport chain, increasing ROS production
• Epigenetic alteration: high glucose modifies DNA methylation patterns associated with accelerated aging
• Cellular senescence: glucose-driven oxidative stress pushes cells into permanent growth arrest
• Genomic instability: ROS generated by glucose metabolism directly damages DNA
• Chronic inflammation: AGEs activate NF-kB inflammatory pathways via the RAGE receptor

This means every glucose spike is not just a transient event — it leaves a permanent molecular footprint that accumulates over decades.

---

Basal metabolic rate and aging

Your basal metabolic rate (BMR) — the energy your body burns at complete rest — accounts for 60–75% of total daily energy expenditure. It is fundamentally determined by the amount of metabolically active tissue you carry, primarily skeletal muscle and organ mass.

Why BMR matters for aging

A declining BMR is both a symptom and a cause of metabolic aging:

• Less muscle means less glucose disposal. Skeletal muscle is responsible for approximately 80% of insulin-stimulated glucose uptake. As muscle mass declines, the remaining tissue must absorb more glucose per unit — eventually overwhelming its capacity and driving insulin resistance.
• Lower BMR reduces the caloric margin. When you burn fewer calories at rest, any caloric surplus is more easily converted to fat — particularly visceral fat.
• Mitochondrial density drops with muscle loss. Fewer mitochondria means less metabolic flexibility — your body becomes worse at switching between glucose and fat as fuel sources.

The average person loses 2–4% of their BMR per decade after age 20. But this is not primarily an age effect — it tracks almost perfectly with loss of lean body mass. People who maintain their muscle mass through resistance training show minimal BMR decline even into their 70s and 80s.

Metabolic flexibility

Metabolic flexibility — the ability to efficiently switch between burning glucose and burning fat — is a hallmark of metabolic health. A metabolically flexible person burns fat during fasting and rest, switches to glucose during high-intensity activity, and transitions smoothly between the two.

Insulin resistance destroys metabolic flexibility. When cells are insulin resistant, they struggle to take up glucose even when insulin is present, and simultaneously, chronically elevated insulin blocks fat oxidation. The result: you can’t efficiently burn either fuel. This “metabolic gridlock” is a defining feature of metabolic aging.

---

AMPK: the metabolic master switch

AMP-activated protein kinase (AMPK) is an enzyme that functions as your body’s fuel gauge. When cellular energy drops — during exercise, fasting, or caloric restriction — AMPK activates a cascade of protective metabolic responses:

• Increases glucose uptake into muscle cells (independent of insulin)
• Activates fat oxidation by switching on fatty acid burning
• Stimulates mitochondrial biogenesis — the creation of new mitochondria
• Activates autophagy — cellular self-cleaning
• Inhibits mTOR — the growth pathway that, when chronically active, accelerates aging
• Reduces inflammation by suppressing NF-kB signaling

AMPK is the molecular link between energy stress and longevity. Every intervention that consistently extends lifespan in model organisms — caloric restriction, exercise, metformin, rapamycin — activates AMPK.

AMPK declines with age

AMPK activity decreases with age, partly because of chronic energy surplus (the modern diet provides constant fuel, so AMPK is rarely activated) and partly because of age-related changes in upstream signaling. Lower AMPK activity means less autophagy, fewer new mitochondria, more inflammation, and impaired glucose disposal — all hallmarks of metabolic aging.

The practical solution: activate AMPK regularly through exercise (especially high-intensity and resistance training), periodic fasting, and maintaining periods of genuine energy deficit.

---

mTOR: the growth-longevity tradeoff

Mechanistic target of rapamycin (mTOR) is the counterpart to AMPK. While AMPK signals scarcity and activates repair, mTOR signals abundance and activates growth. mTOR promotes protein synthesis, cell division, and fat storage. It is essential for building muscle, healing wounds, and growing during development.

The problem: chronically elevated mTOR accelerates aging.

When mTOR is constantly active — driven by high insulin, high amino acid availability, and excess glucose — it suppresses autophagy, promotes cellular senescence, increases inflammation, and drives the same diseases (cancer, diabetes, neurodegeneration) that define aging.

The AMPK-mTOR seesaw

AMPK and mTOR exist in a dynamic balance — a metabolic seesaw. Activating one suppresses the other:

State	AMPK	mTOR	Effect
Fasting / exercise	High	Low	Repair, autophagy, fat burning
Fed / sedentary	Low	High	Growth, storage, suppressed cleanup
Chronic overfeeding	Very low	Chronically high	Accelerated aging

Modern life keeps most people permanently on the mTOR-dominant side — eating frequently, rarely exercising intensely, and never experiencing genuine energy deficit. This chronic mTOR activation is one of the most potent drivers of metabolic aging.

The longevity strategy is not to permanently suppress mTOR (you need it for muscle maintenance and immune function) but to cycle between mTOR activation (strength training, adequate protein) and mTOR suppression (fasting, endurance exercise, caloric restriction).

---

Autophagy: cellular self-renewal

Autophagy — literally “self-eating” — is the cell’s built-in recycling system. During autophagy, cells identify and break down damaged proteins, dysfunctional mitochondria, misfolded protein aggregates, and intracellular pathogens. The raw materials are then recycled into new cellular components.

Autophagy is not just cleanup — it is renewal. Without adequate autophagy, damaged components accumulate, mitochondrial quality declines, protein aggregates form (a hallmark of Alzheimer’s and Parkinson’s), and cells eventually become senescent or die.

Autophagy and metabolic health

Autophagy is fundamentally a metabolic process, regulated by the same nutrient-sensing pathways that control aging:

• AMPK activates autophagy when energy is scarce
• mTOR suppresses autophagy when nutrients are abundant
• Insulin suppresses autophagy — even moderate insulin elevation blocks autophagic flux
• Glucose inhibits autophagy by maintaining high energy charge in cells

This means the standard modern eating pattern — three meals plus snacks, 15+ hours of food availability per day — keeps autophagy chronically suppressed. Your cells never get the opportunity to clean house.

How to activate autophagy

The most reliable autophagy activators are:

1. Fasting: time-restricted eating (12–16 hour fasting windows) provides regular autophagy activation. Extended fasts (24–72 hours) produce deeper autophagy but require medical oversight.
2. Exercise: both endurance and resistance exercise activate autophagy in muscle, liver, and brain tissue. The effect is amplified when exercising in a fasted state.
3. Caloric restriction: chronic mild caloric deficit (10–20% below maintenance) increases basal autophagy rates.
4. Sleep: autophagy peaks during deep sleep, when growth hormone secretion is highest and insulin is at its lowest.

---

Glycation: how sugar ages you from the inside

Glycation is the non-enzymatic bonding of glucose (or fructose) to proteins, lipids, and nucleic acids. The process creates advanced glycation end products (AGEs) — irreversible molecular modifications that accumulate with age and cause progressive tissue damage.

How glycation drives aging

AGEs damage tissues through two mechanisms:

Direct structural damage: AGEs cross-link collagen and elastin fibers, making them rigid and brittle. This is why skin wrinkles, arteries stiffen, joints lose flexibility, and eye lenses cloud — all driven by the same glycation process.

Inflammatory signaling via RAGE: AGEs bind to the receptor for advanced glycation end products (RAGE), triggering NF-kB activation and a cascade of inflammatory cytokines. This creates a self-reinforcing cycle: glycation causes inflammation, inflammation increases oxidative stress, and oxidative stress accelerates more glycation.

Sources of AGEs

AGEs come from two sources:

1. Endogenous (internal): formed naturally when blood glucose reacts with proteins. Higher average blood glucose = more endogenous AGE formation. This is why HbA1c (itself a glycated protein) is such a powerful predictor of biological age.
2. Exogenous (dietary): formed during high-heat cooking — grilling, frying, roasting, and broiling. Browning reactions (Maillard reactions) produce large quantities of dietary AGEs, which are partially absorbed and contribute to the total AGE burden.

Reducing both sources — keeping blood glucose low and favoring low-temperature cooking methods — is a direct anti-aging strategy.

---

Ketones: alternative fuel for longevity

Ketone bodies — beta-hydroxybutyrate (BHB), acetoacetate, and acetone — are produced by the liver when glucose availability is low and fatty acid oxidation increases. This happens during fasting, prolonged exercise, carbohydrate restriction, and sleep.

Ketones are not just backup fuel. They are signaling molecules with direct anti-aging properties:

• BHB inhibits HDAC enzymes, increasing expression of antioxidant genes (FOXO3, MnSOD, catalase)
• BHB activates AMPK and suppresses mTOR, promoting autophagy
• BHB reduces NLRP3 inflammasome activation, decreasing inflammatory signaling
• Ketones produce fewer ROS per unit of ATP compared to glucose, generating less oxidative damage
• BHB serves as a preferred fuel for the brain, particularly for aging neurons with impaired glucose metabolism

You do not need to follow a ketogenic diet to benefit from ketones. Regular fasting windows (14–18 hours), time-restricted eating, morning fasted exercise, and even overnight sleep all generate mild ketosis. The goal is periodic ketone exposure, not chronic ketosis.

---

Visceral fat and body composition

Not all fat is metabolically equal. Visceral fat — the fat surrounding your organs — is an active endocrine tissue that secretes inflammatory cytokines (IL-6, TNF-alpha), disrupts insulin signaling, and drives metabolic dysfunction.

A person with a normal BMI but high visceral fat (sometimes called “TOFI” — thin outside, fat inside) can be more metabolically compromised than someone who is visibly overweight but carries fat subcutaneously. This is why body fat percentage and waist-to-hip ratio are far more informative than body weight alone — WHR captures dangerous visceral fat distribution in a single 30-second measurement.

Body composition targets for metabolic health

Metric	Men (optimal)	Women (optimal)
Body fat percentage	10–20%	18–28%
Waist circumference	< 90 cm	< 80 cm
Waist-to-hip ratio	< 0.90	< 0.80
Visceral fat rating	< 10 (on DEXA scale)	< 10 (on DEXA scale)

The most effective strategies for reducing visceral fat specifically (rather than total weight) are resistance training, high-intensity interval training, adequate protein intake, improved sleep, and stress management. Caloric restriction alone tends to reduce both muscle and fat, which can actually worsen metabolic health if muscle loss is disproportionate.

---

Practical strategies to optimize metabolic health

Every mechanism discussed above converges on a set of practical interventions. These are ordered by impact based on the current evidence.

1. Resistance training (highest priority)

Skeletal muscle is your largest metabolic organ. Building and maintaining muscle:

• Increases glucose disposal capacity (reducing insulin resistance)
• Raises basal metabolic rate
• Activates AMPK during training
• Triggers post-exercise autophagy
• Reduces visceral fat preferentially

Aim for 2–4 resistance training sessions per week. Compound movements (squats, deadlifts, rows, presses) provide the greatest metabolic stimulus.

2. Time-restricted eating

Time-restricted eating — confining food intake to a consistent 8–10 hour window — is one of the most accessible metabolic interventions:

• Activates autophagy during the fasting window
• Lowers fasting insulin
• Improves metabolic flexibility
• Aligns eating with circadian biology (eating when insulin sensitivity peaks during daylight hours)

A 2022 randomized controlled trial in NEJM found that time-restricted eating reduced fasting insulin by 26% and HOMA-IR by 19% over 12 weeks, independent of calorie reduction.

3. Minimize glucose spikes

Keeping post-meal glucose below 130 mg/dL reduces glycation, oxidative damage, and inflammatory signaling. Practical strategies:

• Eat protein and fat before carbohydrates (this can reduce glucose spikes by 30–40%)
• Walk for 10–15 minutes after meals (post-meal walking reduces glucose peaks by 20–30%)
• Favor whole, unprocessed carbohydrates over refined sources
• Avoid sugar-dense foods on an empty stomach

4. Aerobic conditioning

Zone 2 training (60–70% max heart rate) specifically improves mitochondrial fat oxidation capacity — the foundation of metabolic flexibility. Higher-intensity work (HIIT) rapidly depletes glycogen stores and activates AMPK more potently than moderate exercise.

The combination of zone 2 base training with 1–2 weekly HIIT sessions provides the broadest metabolic benefit.

5. Adequate protein, distributed across meals

Protein intake supports muscle maintenance (preserving the glucose sink), provides satiety (reducing overall caloric intake), and has the highest thermic effect of any macronutrient (increasing metabolic rate after eating).

Current longevity-focused guidelines suggest 1.2–1.6 g/kg/day, distributed across 3–4 meals to maximize muscle protein synthesis at each feeding.

6. Sleep optimization

Poor sleep directly impairs insulin sensitivity — a single night of 4 hours of sleep reduces insulin sensitivity by 25–30%. Chronic sleep restriction drives cortisol elevation, increased appetite for high-glycemic foods, and reduced glucose tolerance.

Prioritize 7–9 hours per night with emphasis on deep sleep quality.

7. Monitor key blood biomarkers

For a complete panel covering all the metabolic markers discussed in this guide — plus optimal ranges and testing frequency — see our complete blood work guide for longevity. And because poor sleep directly impairs every metabolic pathway covered here, our sleep and longevity guide is essential reading alongside this one.

The most informative metabolic biomarkers to track regularly:

• Fasting insulin: the earliest warning of insulin resistance (optimal: < 6 μIU/mL)
• Fasting glucose: basic glucose homeostasis (optimal: 72–90 mg/dL)
• HbA1c: 2–3 month glucose average (optimal: < 5.2%)
• Triglyceride/HDL ratio: proxy for insulin resistance (optimal: < 1.5)
• HOMA-IR: calculated insulin resistance index (optimal: < 1.0)

---

How SuperAge helps you optimize metabolic health

Metabolic health is not a single number — it is a system of interconnected signals that must be tracked together to see the full picture. SuperAge is designed to do exactly this.

Daily metabolic signals from your wrist

SuperAge integrates with Apple Watch and Apple Health to automatically capture the daily metrics that reflect metabolic function: resting heart rate, HRV, step count, active calories, exercise minutes, sleep duration, and deep sleep percentage. Changes in these metrics often signal metabolic shifts weeks before they show up in blood work — a rising resting heart rate or declining HRV can indicate worsening insulin sensitivity.

Blood biomarker tracking and biological age

Enter your blood test results — fasting glucose, HbA1c, fasting insulin, triglycerides, HDL, and more — and SuperAge calculates your biological age using validated algorithms (PhenoAge, KDM). You see exactly how each metabolic marker contributes to your biological age score and which parameters need the most attention.

Progress over time

The real power of SuperAge is longitudinal tracking. As you implement the strategies in this guide — resistance training, time-restricted eating, glucose management, sleep optimization — your biological age score reflects the cumulative impact. You can track whether your metabolic interventions are actually working, and adjust course based on objective data rather than guesswork.

---

Frequently asked questions

What is the single best marker for metabolic health?

Fasting insulin. It rises years before fasting glucose becomes abnormal, captures the degree of insulin resistance directly, and correlates strongly with visceral fat, inflammatory markers, and biological age. If you can only test one thing, test fasting insulin.

Can you fix metabolic health without losing weight?

Yes. Exercise — particularly resistance training — improves insulin sensitivity, mitochondrial function, and glucose disposal independent of weight loss. Studies show that people who exercise regularly but remain overweight have better metabolic profiles than sedentary people at a normal weight. That said, reducing visceral fat provides additional metabolic benefit beyond exercise alone.

How long does it take to improve metabolic health?

Some improvements are rapid: a single exercise session can improve insulin sensitivity for 24–48 hours. Time-restricted eating typically reduces fasting insulin within 2–4 weeks. Meaningful changes in HbA1c require 2–3 months (because it reflects a rolling 90-day average). Significant improvements in biological age — as measured by validated aging clocks — generally become detectable after 3–6 months of consistent intervention.

Is keto the best diet for metabolic health?

Not necessarily. While ketogenic diets can rapidly improve insulin sensitivity and reduce fasting glucose, they are difficult to sustain long-term and may reduce metabolic flexibility if followed rigidly. The evidence supports time-restricted eating and periodic ketone exposure (through fasting or fasted exercise) as more sustainable approaches that provide similar metabolic benefits without the rigidity of a full ketogenic diet.

Does metabolic health affect brain aging?

Directly. The brain consumes 20% of the body’s glucose at rest and is extremely vulnerable to insulin resistance. “Type 3 diabetes” is now used informally to describe Alzheimer’s disease, reflecting the tight link between brain insulin resistance and neurodegeneration. Optimizing metabolic health is one of the most powerful strategies for preserving cognitive function with age.

If you are separating appetite signaling from glucose handling, use Leptin resistance vs insulin resistance: how they differ to compare leptin resistance with insulin resistance before choosing what to track.

---

References

1. Araujo, J., Cai, J., & Stevens, J. (2019). Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016. Metabolic Syndrome and Related Disorders, 17(1), 46–52.

2. Wirth, M.D. et al. (2022). Insulin resistance, HOMA-IR, and biological aging: cross-sectional and longitudinal findings from the Framingham Heart Study. Diabetes Care, 45(8), 1795–1804.

3. Ravichandran, M. et al. (2022). Coordinated clock gene expression supports hepatic mitochondrial metabolism during time-restricted feeding. Cell Metabolism, 34(7), 1017–1032.

4. Newman, J.C. & Verdin, E. (2017). β-Hydroxybutyrate: a signaling metabolite. Annual Review of Nutrition, 37, 51–76.

5. Uribarri, J. et al. (2010). Advanced glycation end products in foods and a practical guide to their reduction in the diet. Journal of the American Dietetic Association, 110(6), 911–916.

6. Wilkinson, M.J. et al. (2020). Ten-hour time-restricted eating reduces weight, blood pressure, and atherogenic lipids in patients with metabolic syndrome. Cell Metabolism, 31(1), 92–104.