Hard things, explained simply.

Short explainers on how your body actually works: sleep, blood sugar, muscle, aging, the chemicals in everyday products, and the weight loss series. Each one builds on the last, every claim is cited on screen, and nothing here is a sales pitch. They work with the sound off.

21 videos, one to two minutes each
Vertical for your phone, wide for your laptop
Sources shown on screen and listed below each video
Free to download and share

The weight loss series

The order Laird lost nearly 100 pounds in, and the order he coaches in. Start here.

Why you cannot exercise your way to weight loss

I lost nearly 100 pounds. Exercise was the last thing I fixed.

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Exercise is wonderful for your heart, brain, bones and mood. But with 30, 50 or 100 pounds to lose it is not the first lever: the body compensates, appetite rises, and high insulin keeps fat locked in. The hierarchy Laird lost nearly 100 pounds with puts exercise near the top on purpose.

What you will learn

Your body compensates: the Hadza walk miles every day and burn about the same daily calories as office workers. Exercise programs alone average a few pounds in a year.
Exercise makes many people hungrier, and the earned meal can erase the deficit.
When glucose spikes all day, insulin stays high, and high insulin keeps fat locked inside fat cells no matter what the treadmill burns.
The hierarchy, bottom to top: diet, metabolic health, sleep and stress, movement and walking, fasting, exercise, supplementation and peptides. Nothing above holds without the base.
What moved Laird's weight: diet dialed in, long daily walks, the occasional water fast, then exercise once the bulk was off. 280 to 180 pounds over about three years, after cancer.
Just starting? Walk, eat real food, get curious about your body. You do not need a gym yet.

Sources

Pontzer H, et al. Hunter-gatherer energetics and human obesity. PLoS ONE. 2012;7:e40503.
Pontzer H, et al. Constrained total energy expenditure and metabolic adaptation to physical activity in adult humans. Current Biology. 2016;26:410-417.
Thorogood A, et al. Isolated aerobic exercise and weight loss: a systematic review and meta-analysis of randomized controlled trials. American Journal of Medicine. 2011;124:747-755.
King NA, et al. Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss. British Journal of Sports Medicine. 2007 (published online); International Journal of Obesity. 2008;32:177-184.
Saltiel AR, Kahn CR. Insulin signalling and the regulation of glucose and lipid metabolism. Nature. 2001;414:799-806.
Laird Doman, Why You Can't Exercise Your Way to Weight Loss, domanhealth.com: his own experience, not a promise of results. Check with your physician before fasting.

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Three things I will never let back in

Sugar, sugar substitutes, and food in a health-food costume.

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For decades the goal was weight loss and nothing stuck. The goal that worked was metabolic health, with the weight as a side effect. If you do nothing else, cut three things: sugar, sugar substitutes, and ultra-processed food in a health-food costume.

What you will learn

Drop 15 pounds, plateau, rebound, start over: decades of that. Chasing metabolic health instead took 30 pounds off in three months.
Sugar hides behind 60+ names. If one is in the first three ingredients, it is a sugar product. Put it back.
Sugar substitutes: in 120 healthy adults, two weeks of saccharin or sucralose impaired glycemic responses, with changes in the gut microbiome. Laird treats them like sugar.
Sugar-free, diet and light foods are industrial food in a health-food costume. On an ultra-processed diet people ate about 500 more calories a day and gained about 2 pounds in two weeks.
If it did not exist a hundred years ago, be skeptical.
Read the first three ingredients, skip the costume, build the engine.

Sources

Suez J, et al. Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance. Cell. 2022;185:3307-3328.
Hall KD, et al. Ultra-processed diets cause excess calorie intake and weight gain: an inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism. 2019;30:67-77.
Laird Doman, Food Is Fuel. Food Is Medicine., domanhealth.com: his own experience, not a promise of results.

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The three phases of weight loss

The diet that gets the weight off is not the one that keeps it off.

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Most people find one diet that works and try to stay on it forever; the phase changes and they do not. Laird's playbook in three phases: Attack (strict clean keto, a reset), Stabilize (low carb, more variety, the guardrails stay) and Perform (strategic carbs around hard training), with ketosis, the keto flu and food noise explained on the way.

What you will learn

Two fuels: glucose and fat. Eat very few carbs and in 3 to 10 days your body burns fat and makes ketones; insulin stays low, which unlocks fat stores and quiets cravings.
The first days can feel rough (the keto flu); salt, magnesium and potassium help. Then the food noise, the constant chatter about eating, goes quiet.
Clean keto means whole foods, not bacon-and-butter keto, lab-made keto snacks, seed oils or artificial sweeteners (a little allulose or stevia is okay).
Phase 1, Attack: strict clean keto, about three months for Laird, 30 pounds down. A reset, not a forever diet.
Phase 2, Stabilize: low carb with more variety (fermented foods, A2 yogurt); the guardrails stay: no sugar, grains, alcohol or sugar substitutes. Phase 3, Perform: strategic carbs around hard training, for muscle and performance.
What breaks people: attacking too long and burning out, never attacking hard enough, or hitting goal and drifting back. Find your phase, eat for that phase, and talk with your physician before keto or fasting.

Sources

Laird Doman, How to Actually Eat Through the Phases of Weight Loss, domanhealth.com: his own experience, not a prescription.
Paoli A, et al. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition. 2013;67:789-796.
Volek JS, Phinney SD. The Art and Science of Low Carbohydrate Living. Beyond Obesity LLC, 2011 (keto-adaptation).

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The meal is only half the story

Same meal. Two different bodies. The difference was 15 minutes.

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What happens around a meal matters almost as much as what is on the plate. A gentle curve versus a spike and crash, why A1c is a rearview mirror, and the decisions that flatten the curve: food order, a walk, seated calf raises, and nothing within two hours of bed.

What you will learn

After you eat, glucose rises and insulin tells cells to take it in; a healthy curve is back to baseline in about 90 minutes.
A sharp spike brings a sharp insulin response, a crash, hunger within the hour, and over years, insulin resistance and stored fat.
A1c is a three-month average, a rearview mirror. A glucose monitor is the windshield.
Same food, different order: vegetables and protein first, starches last, cut the 60-minute glucose rise by about 37% and insulin by about half.
Walk after eating: even 2 to 5 minutes helps. Laird's rule from six months on a monitor: 15 minutes light or 5 harder, or he cannot avoid a spike.
Seated calf raises (the soleus pushup) cut the post-meal glucose rise by 52% in one study. Small movement all day beats one big workout.
Nothing within two hours of bed: you are more insulin resistant at night and about to lie still for eight hours.

Sources

Shukla AP, et al. Food order has a significant impact on postprandial glucose and insulin levels. Diabetes Care. 2015;38(7):e98-e99.
Buffey AJ, et al. The acute effects of interrupting prolonged sitting time in adults with standing and light-intensity walking on biomarkers of cardiometabolic health. Sports Medicine. 2022;52:1765-1787.
Hamilton MT, Hamilton DG, Zderic TW. A potent physiological method to magnify and sustain soleus oxidative metabolism improves glucose and lipid regulation. iScience. 2022;25:104869.
Morris CJ, et al. Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans. PNAS. 2015;112:E2225-E2234.
The two-curve chart is an illustrative pattern based on typical CGM responses; your numbers will vary. Laird's six months on a CGM is his own experience, not a promise of results.

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Sleep, stress and weight

The glucose spike that looked like pizza. I had not eaten a thing.

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On stressful afternoons Laird's glucose monitor drew a curve that looked like pizza with nothing eaten. Stress and short sleep put you in the same fat-storing hormonal state as a big meal, and the fixes are unglamorous: earlier bedtime, morning light, walks instead of scrolling.

What you will learn

Stress raises cortisol, cortisol tells the liver to release stored sugar, insulin rises to deal with it: the same fat-storing state as after a big meal, without the food.
One short night of sleep cut insulin sensitivity by about 20 to 25% in healthy adults, so every meal the next day hits harder.
Six nights of four-hour sleep left young men clearing sugar more slowly; a tired brain wants high-calorie food more. The cycle compounds.
Your body is protecting you from a famine that is not coming. Biology, not laziness.
The fixes: earlier bedtime, 7+ hours, morning sunlight, walks instead of doomscrolling, breathwork, saying no more often.
When Laird dialed in sleep and stress, weight moved in ways diet alone never produced. You cannot out-diet a broken nervous system. Pick one fix tonight.

Sources

Kuo T, McQueen A, Chen TC, Wang JC. Regulation of glucose homeostasis by glucocorticoids. Advances in Experimental Medicine and Biology. 2015;872:99-126.
Donga E, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. Journal of Clinical Endocrinology and Metabolism. 2010;95:2963-2968.
Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354:1435-1439.
Greer SM, Goldstein AN, Walker MP. The impact of sleep deprivation on food desire in the human brain. Nature Communications. 2013;4:2259.
Laird Doman, Why You Can't Exercise Your Way to Weight Loss, domanhealth.com: his own experience, not a promise of results.

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Metabolism and blood sugar

What your body does with food, and the small decisions around a meal that decide fuel or storage.

Metabolic health, explained

Only 1 in 8 American adults is metabolically healthy. Are you the one?

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What metabolic health is, the five markers with their optimal cutoffs, the 12.2% figure, why it matters, and one step to take: know your five numbers.

What you will learn

Metabolic health is how well your body turns food into energy. You cannot feel it, but you can measure it.
The five markers: waist, blood pressure, fasting glucose, triglycerides, HDL cholesterol, with the optimal cutoffs.
Only 12.2% of US adults hit all five without medication.
Markers out of range raise the risk of type 2 diabetes, heart disease and stroke, usually with no symptoms.
One step: know your five numbers. Ask for them at your next checkup.

Sources

Araújo J, Cai J, Stevens J. Prevalence of optimal metabolic health in American adults: NHANES 2009 to 2016. Metabolic Syndrome and Related Disorders. 2019;17(1):46-52.
National Heart, Lung, and Blood Institute (NIH). Metabolic syndrome.

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Glucose and insulin resistance

Your blood sugar can look normal for years while insulin quietly climbs.

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One metaphor all the way through: glucose is fuel, insulin is the key that unlocks the cell. Sticky locks mean more keys, which is why fasting glucose can look normal for years while insulin climbs. Three levers, then the takeaway.

What you will learn

Glucose is fuel; after a meal it rises in your blood and your cells need to let it in.
Insulin is the key that unlocks cells. Insulin resistance is sticky locks: the body makes more insulin to force them open.
That is why glucose looks normal for years: extra insulin keeps it steady, until it cannot keep up.
Three levers: protein and fiber first, a walk after meals, strength training.
Ask your doctor about fasting insulin, and start with your next meal.

Sources

Tabák AG, et al. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes (Whitehall II). The Lancet. 2009;373(9682):2215-2221.
Shukla AP, et al. Food order has a significant impact on postprandial glucose and insulin levels. Diabetes Care. 2015;38(7):e98-e99.
Buffey AJ, et al. The acute effects of interrupting prolonged sitting time in adults with standing and light-intensity walking. Sports Medicine. 2022;52(8):1765-1787.
American Diabetes Association. Standards of Care in Diabetes: physical activity and resistance training.

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Zone 2 and fat burning

The pace where your body burns fat. It is slower than you think.

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Your muscles burn two fuels. At easy effort fat leads; as you push harder the mix crosses over to sugar. Zone 2 is the talking pace where fat burning sits near its peak and your mitochondria keep up, and it is a fitness you can build.

What you will learn

Muscles run on fat and sugar. At easy effort fat is the main fuel; as intensity climbs the mix crosses over to sugar.
In trained cyclists, fat burning per minute peaked around 64% of maximum oxygen uptake and fell sharply above it.
Zone 2 is roughly 60 to 70% of max heart rate: full sentences, but you would rather not. Zones are approximate; the talk test is the practical guide.
Lactate stays low because your mitochondria keep up, and this pace trains them to use fat (see the mitochondria video).
Pro cyclists, moderately active people and men with metabolic syndrome burn very different amounts of fat at the same effort: fitness you can build.
Sprinting burns more per minute, mostly sugar, and you cannot keep it up. Plan: 3 to 4 sessions of 30 to 45 minutes at talking pace, plus short walks after meals.

Sources

Brooks GA, Mercier J. Balance of carbohydrate and lipid utilization during exercise: the crossover concept. Journal of Applied Physiology. 1994;76:2253-2261.
Achten J, Gleeson M, Jeukendrup AE. Determination of the exercise intensity that elicits maximal fat oxidation. Medicine and Science in Sports and Exercise. 2002;34:92-97.
San-Millán I, Brooks GA. Assessment of metabolic flexibility by means of measuring blood lactate, fat, and carbohydrate oxidation responses to exercise in professional endurance athletes and less-fit individuals. Sports Medicine. 2018;48:467-479.
US HHS. Physical Activity Guidelines for Americans, 2nd edition. 2018.

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Mitochondrial biogenesis

Exercise builds you more power plants. Here is how.

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Mitochondria are the power plants inside your muscle cells. Inactivity and age leave you with fewer, leakier ones; exercise flips a master switch (PGC-1 alpha) that builds new ones, clears the worn-out ones, and does so at every age.

What you will learn

Mitochondria turn food and oxygen into ATP, the energy your cells run on. A muscle cell holds hundreds to thousands.
With inactivity and age they get fewer and sloppier: more leak, less power.
Hard muscle work trips two sensors (AMPK for low fuel, calcium for each squeeze) that flip a master switch called PGC-1 alpha: build more.
In the founding 1967 study, 12 weeks of running doubled mitochondrial enzyme capacity in rats; in people, one bout raises the switch within hours and a few weeks of training measurably adds mitochondria.
Steady moderate work and short hard intervals both do it, and exercise also recycles damaged mitochondria (mitophagy).
Similar gains at every age from 21 to 87 after 16 weeks of training. Aim for 150 minutes a week you can talk through, plus a couple of harder efforts.

Sources

Holloszy JO. Biochemical adaptations in muscle: effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. Journal of Biological Chemistry. 1967;242(9):2278-2282.
Pilegaard H, Saltin B, Neufer PD. Exercise induces transient transcriptional activation of the PGC-1alpha gene in human skeletal muscle. Journal of Physiology. 2003;546:851-858.
Little JP, et al. A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle. Journal of Physiology. 2010;588:1011-1022.
MacInnis MJ, Gibala MJ. Physiological adaptations to interval training and the role of exercise intensity. Journal of Physiology. 2017;595:2915-2930.
Drake JC, Wilson RJ, Yan Z. Molecular mechanisms for mitochondrial adaptation to exercise training in skeletal muscle. FASEB Journal. 2016;30:13-22.
Short KR, et al. Decline in skeletal muscle mitochondrial function with aging in humans. PNAS. 2005;102:5618-5623.
Short KR, et al. Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity. Diabetes. 2003;52:1888-1896.
US HHS. Physical Activity Guidelines for Americans, 2nd edition. 2018.

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Autophagy

Your cells have a recycling crew. It mostly clocks in when you stop eating.

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Autophagy means self-eating: the cell wraps its worn-out parts in a membrane, dissolves them in a lysosome, and reuses the pieces. Fed turns it down (mTOR), fasting and exercise turn it up (AMPK), and in people the timing is still an estimate.

What you will learn

Autophagy is the cell breaking down its own damaged proteins and worn-out parts and reusing the building blocks (Nobel Prize 2016, worked out in baker's yeast).
The crew wraps the junk in a double membrane (the autophagosome), which fuses with a lysosome, the cell's acid bath.
When you eat, a sensor called mTOR says build and the crew stands down. When you fast, AMPK rises, mTOR quiets, and the crew clocks in.
In mice, 24 and 48 hours without food raised autophagy in brain cells; exercise turns it on too.
In people it may ramp up after about 18 to 24 or more hours without food. That is an estimate: nobody can measure it directly in living people yet.
A longer fast now and then can turn it on; an overnight fast alone probably does not. Talk with your doctor first, especially with diabetes medication, pregnancy, or a history of disordered eating.

Sources

Nobel Assembly at Karolinska Institutet, 2016 (Yoshinori Ohsumi, mechanisms of autophagy).
Mizushima N, Komatsu M. Autophagy: renovation of cells and tissues. Cell. 2011;147:728-741.
Kim J, et al. AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1. Nature Cell Biology. 2011;13:132-141.
Alirezaei M, et al. Short-term fasting induces profound neuronal autophagy. Autophagy. 2010;6:702-710.
He C, et al. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis. Nature. 2012;481:511-515.
Human timing: no direct measurement in living human tissue; estimates come from animal and limited human data.

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Sleep, light and the brain

The night shift: what sleep does for your brain, and how light sets the clock that runs it.

The glymphatic system

Your brain has a washing machine. It only runs while you sleep.

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Your brain has no ordinary lymph vessels, so it uses a plumbing system of its own: cerebrospinal fluid washes in along arteries, between the cells and out along veins, carrying waste like beta-amyloid. The taps open in deep sleep. Mostly shown in mice so far; human research is catching up.

What you will learn

The brain makes waste all day, including beta-amyloid, the protein linked to Alzheimer's disease.
Inside the brain there are no ordinary lymph vessels. The glymphatic system does the job: fluid in along arteries, through the tissue, out along veins.
Awake, the taps are nearly closed. In sleeping mice the space between cells opened about 60% and beta-amyloid clearance roughly doubled.
In people, slow waves in deep sleep are followed by pulses of fluid washing through the brain (fMRI). One night without sleep raised beta-amyloid about 5% on PET scans.
Side sleeping moved fluid best in anesthetized rodents: a cheap bonus.
Protect deep sleep: same wake time, a dark cool room, no food or alcohol within 2 to 3 hours of bed. Let the wash run all night.

Sources

Iliff JJ, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid beta. Science Translational Medicine. 2012;4:147ra111.
Xie L, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342:373-377.
Fultz NE, et al. Coupled electrophysiological, hemodynamic, and cerebrospinal fluid oscillations in human sleep. Science. 2019;366:628-631.
Shokri-Kojori E, et al. Beta-amyloid accumulation in the human brain after one night of sleep deprivation. PNAS. 2018;115:4483-4488.
Lee H, et al. The effect of body posture on brain glymphatic transport. Journal of Neuroscience. 2015;35:11034-11044.

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Light and your body clock

Your body has a clock. Light is how you set it.

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A master clock in your brain takes its time from light through special cells in the retina. Morning light anchors it; evening light, blue most of all, pushes melatonin later and shorter. Ten minutes outside in the morning and dim, warm light at night set the clock for you.

What you will learn

The master clock (the SCN) is set by light through melanopsin cells in the retina, not by the clock on the wall.
Morning bright light anchors the clock and sets tonight's melatonin timing. Outdoors is far brighter than indoors: a cloudy day is still over 1,000 lux; a lit room is 100 to 500 (approximate).
Evening light suppresses melatonin, blue light most of all. Ordinary room light before bed cut melatonin about in half and shortened its window by about 90 minutes.
Reading on a lit screen before bed delayed the melatonin rise by about 1.5 hours, cost REM sleep and next-morning alertness. Light while you sleep is linked to worse blood sugar handling the next morning.
A week of camping with only natural light shifted people's clocks about two hours earlier.
Ten minutes outside within an hour of waking, dim and warm light after sunset, screens down an hour or two before bed, same wake time daily.

Sources

Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion cells that set the circadian clock. Science. 2002;295:1070-1073.
Hattar S, et al. Melanopsin-containing retinal ganglion cells. Science. 2002;295:1065-1070.
Khalsa SB, et al. A phase response curve to single bright light pulses in human subjects. Journal of Physiology. 2003;549:945-952.
Brainard GC, et al. Action spectrum for melatonin regulation in humans. Journal of Neuroscience. 2001;21:6405-6412.
Gooley JJ, et al. Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans. Journal of Clinical Endocrinology and Metabolism. 2011;96:E463-E472.
Chang AM, et al. Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness. PNAS. 2015;112:1232-1237.
Mason IC, et al. Light exposure during sleep impairs cardiometabolic function. PNAS. 2022;119:e2113290119.
Wright KP, et al. Entrainment of the human circadian clock to the natural light-dark cycle. Current Biology. 2013;23:1554-1558.

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Muscle, aging and resilience

How the body rebuilds itself, what wears it down, and the kind of stress that makes it stronger.

Muscle protein synthesis vs breakdown

Your muscle is rebuilt every day. Here is who wins the tug of war.

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Muscle is never finished: old protein is torn down and new protein built, all day. Two levers tip the tug of war toward building, protein (leucine is the trigger) and lifting, and both matter more with age, when breakdown slowly starts to win.

What you will learn

Over 24 hours muscle is a tug of war between breakdown and building; the side that wins the day decides gain, hold or loss. Each meal tips it toward building; between meals and overnight, breakdown pulls back.
Lever one: eat protein. About 2.5 to 3 g of leucine flips the build switch, roughly 25 to 30 g of good protein in one meal.
Lever two: lift something heavy. It pushes building up and keeps muscle more responsive to protein for up to 24 hours.
In young lifters, building topped out near 20 g of protein after a workout; doubling it to 40 g added little. Older muscle listens less: about 0.40 g per kg per meal versus 0.24 for the young.
After 30, breakdown slowly wins: about 3 to 8% of muscle lost each decade, faster after 60. That loss is called sarcopenia: weaker, slower, more likely to fall.
Tomorrow: about 30 g of protein a meal (roughly 0.4 g per kg a meal, about 1.6 g per kg a day if building) and lift something heavy twice a week.

Sources

Phillips SM. Protein requirements and supplementation in strength sports. Nutrition and Metabolism. 2004;1:9 (protein turnover and net balance).
Moore DR, et al. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. American Journal of Clinical Nutrition. 2009;89:161-168.
Moore DR, et al. Protein ingestion to stimulate myofibrillar protein synthesis requires greater relative protein intakes in healthy older versus younger men. Journals of Gerontology Series A. 2015;70:57-62.
Churchward-Venne TA, et al. Supplementation of a suboptimal protein dose with leucine or essential amino acids. Journal of Physiology. 2012;590:2751-2765.
Burd NA, et al. Enhanced amino acid sensitivity of myofibrillar protein synthesis persists for up to 24 h after resistance exercise in young men. Journal of Nutrition. 2011;141:568-573.
Volpi E, Nazemi R, Fujita S. Muscle tissue changes with aging. Current Opinion in Clinical Nutrition and Metabolic Care. 2004;7:405-410.
Schoenfeld BJ, Aragon AA. How much protein can the body use in a single meal for muscle-building? Journal of the International Society of Sports Nutrition. 2018;15:10.
US HHS. Physical Activity Guidelines for Americans, 2nd edition. 2018 (muscle-strengthening on 2 or more days a week).

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Protein on a GLP-1

Losing weight on a GLP-1? 38% of the weight lost in one big trial was lean mass.

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For people on GLP-1 medications: why muscle matters, how a smaller appetite squeezes protein off the plate, protein first at every meal, a simple 30 g a meal target, strength training, water and fiber, and a nudge to talk with your prescriber. No medication names, no dosing, no products.

What you will learn

In one big trial, 38% of the weight lost was lean mass, which includes muscle.
Why muscle matters: metabolism, strength for daily life, fewer falls and fractures with age.
Smaller appetite, smaller meals: it is easy to fall short on protein. Eat protein first.
A simple target: about 30 g a meal, about 90 g a day. Your needs may differ.
Lift something 2 to 3 times a week, drink water, eat fiber, and talk with your prescriber.

Sources

Wilding JPH, et al. Once-weekly semaglutide in adults with overweight or obesity (STEP 1). NEJM. 2021;384(11):989-1002. DXA substudy.
Mozaffarian D, et al. Nutritional priorities to support GLP-1 therapy for obesity: a joint advisory. American Journal of Clinical Nutrition. 2025;122:344-367.
Paddon-Jones D, Rasmussen BB. Dietary protein recommendations and the prevention of sarcopenia. Current Opinion in Clinical Nutrition and Metabolic Care. 2009;12(1):86-90.
US HHS. Physical Activity Guidelines for Americans, 2nd edition. 2018.

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Telomeres

Every cell carries a fuse. Here is what burns it faster.

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Chromosomes end in protective caps called telomeres that shorten a little with each cell division. Chronic stress, smoking, obesity and short sleep are linked to faster wear; vigorous exercise and Mediterranean-style eating are linked to better-kept caps. Telomere length is a marker, not a verdict.

What you will learn

Telomeres are the caps on the ends of chromosomes, like the tips on shoelaces, and every division burns off a little.
Too short and the cell stops dividing or dies: in a dish, that is about 50 divisions, the Hayflick limit. An enzyme, telomerase, can rebuild the caps in some cells.
The most stressed of 58 mothers had telomeres about a decade older than the least stressed.
Smoking, obesity and short sleep are linked to shorter caps; a pack a day for 40 years was about 7 extra years of telomere aging.
In active women, high stress was not linked to shorter telomeres; Mediterranean-style eating was linked to longer ones in about 4,700 nurses.
These are links, not proof, and home tests are noisy. The same unglamorous basics may help protect the fuse: sleep, movement, real food, less stress.

Sources

Harley CB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature. 1990;345:458-460.
Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains. Experimental Cell Research. 1961;25:585-621.
Greider CW, Blackburn EH. Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell. 1985;43:405-413. Nobel Prize 2009 (Blackburn, Greider, Szostak).
Epel ES, et al. Accelerated telomere shortening in response to life stress. PNAS. 2004;101:17312-17315.
Valdes AM, et al. Obesity, cigarette smoking, and telomere length in women. Lancet. 2005;366:662-664.
Jackowska M, et al. Short sleep duration is associated with shorter telomere length in healthy men. PLoS ONE. 2012;7:e47292.
Puterman E, et al. The power of exercise: buffering the effect of chronic stress on telomere length. PLoS ONE. 2010;5:e10837.
Crous-Bou M, et al. Mediterranean diet and telomere length in Nurses' Health Study. BMJ. 2014;349:g6674.

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Inflammaging

A slow fire you cannot feel. It is burning right now.

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Inflammation is the body's fire alarm: fast, useful, then off. Inflammaging is a low, constant background level that rises with age, never switches off, and cannot be felt. It wears on vessels, joints, brain and metabolism, and the boring basics lower it. You can measure it with an hs-CRP test.

What you will learn

Acute inflammation flares for a cut or a cold and then switches off. Inflammaging is the low, constant kind that never does.
No pain, no fever: you cannot feel it, which is why it is easy to miss for decades.
It is linked to heart disease, type 2 diabetes, frailty and dementia, through blood vessels, joints, brain and metabolism.
What feeds the fire: deep belly fat, senescent zombie cells, short or poor sleep, smoking, a leaky gut, high blood sugar.
What calms it: regular exercise lowers CRP over time, weight loss lowers CRP (about 0.13 mg/L per kilogram lost), Mediterranean-style eating lowered CRP and IL-6 in a trial, sleep, not smoking.
Ask your doctor for an hs-CRP test: under 1 mg/L low heart risk, 1 to 3 average, over 3 higher. Then move, sleep, eat well, and measure again.

Sources

Franceschi C, et al. Inflamm-aging: an evolutionary perspective on immunosenescence. Annals of the New York Academy of Sciences. 2000;908:244-254.
Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nature Reviews Cardiology. 2018;15:505-522.
Trayhurn P, Wood IS. Adipokines: inflammation and the pleiotropic role of white adipose tissue. British Journal of Nutrition. 2004;92:347-355.
Coppé JP, et al. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual Review of Pathology. 2010;5:99-118.
Irwin MR, et al. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis. Biological Psychiatry. 2016;80:40-52.
Kasapis C, Thompson PD. The effects of physical activity on serum C-reactive protein and inflammatory markers. Journal of the American College of Cardiology. 2005;45:1563-1569.
Selvin E, et al. The effect of weight loss on C-reactive protein: a systematic review. Archives of Internal Medicine. 2007;167:31-39.
Estruch R, et al. Effects of a Mediterranean-style diet on cardiovascular risk factors: a randomized trial. Annals of Internal Medicine. 2006;145:1-11.
Pearson TA, et al. Markers of inflammation and cardiovascular disease: AHA/CDC scientific statement. Circulation. 2003;107:499-511.

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Hormesis: cold and heat

A little stress makes you stronger. Here is the mechanism.

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Hormesis: a small, short stress triggers a protective response that leaves you stronger, while too much tips into harm. Cold water sends norepinephrine surging and wakes up brown fat; heat switches on repair proteins, and frequent sauna use is linked to lower mortality in a 20-year Finnish study.

What you will learn

A little stress on the rising side of the dose curve makes you stronger; too much tips over the top into harm.
In one small study, an hour in 57°F (14°C) water raised norepinephrine by about 530% and dopamine by about 250%: the alert, lifted feeling.
Ten days of mild cold increased brown fat activity in adults. Brown fat burns fuel to make heat.
Heat raises heart rate and blood flow and switches on heat shock proteins, repair helpers that refold damaged proteins.
In 2,315 Finnish men over about 20 years, 4 to 7 sauna sessions a week versus one was linked to about 40% lower all-cause mortality and about half the fatal heart disease. A link, not proof.
Start mild and short (cool showers, 10 to 15 minutes of sauna), build slowly, never plunge alone, and ask a doctor first with heart or blood pressure conditions.

Sources

Mattson MP. Hormesis defined. Ageing Research Reviews. 2008;7:1-7.
Šrámek P, et al. Human physiological responses to immersion into water of different temperatures. European Journal of Applied Physiology. 2000;81:436-442.
van der Lans AA, et al. Cold acclimation recruits human brown fat and increases nonshivering thermogenesis. Journal of Clinical Investigation. 2013;123:3395-3403.
Cypess AM, et al. Identification and importance of brown adipose tissue in adult humans. New England Journal of Medicine. 2009;360:1509-1517.
Kregel KC. Heat shock proteins: modifying factors in physiological stress responses and acquired thermotolerance. Journal of Applied Physiology. 2002;92:2177-2186.
Laukkanen T, et al. Association between sauna bathing and fatal cardiovascular and all-cause mortality events. JAMA Internal Medicine. 2015;175:542-548.

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Everyday exposures

The chemicals in ordinary products, what they do to hormones, and the easy swaps.

Endocrine disruptors, explained

More than 90% of Americans have BPA in their bodies.

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Hormones are keys and cells have locks. Endocrine disruptors mess with the keys in three ways: the fake key, the stuck key, the lost key. Then the good news (BPA fell 66% in three days of fresh food) and three easy swaps.

What you will learn

Hormones are messengers: each one is a key that fits a lock on your cells.
The fake key turns the lock when it should not (BPA can act like estrogen).
The stuck key fits but will not turn, so the real hormone cannot get in (some phthalates).
The lost key never reaches the lock (some PFAS may affect thyroid hormone).
Three swaps: no plastic in the microwave, skip "fragrance", filter your water (certified for PFAS).

Sources

Calafat AM, et al. Exposure of the US population to bisphenol A. Environmental Health Perspectives. 2008 (NHANES 2003 to 2004: BPA in 93% of urine samples).
Rudel RA, et al. Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention. Environmental Health Perspectives. 2011.
National Institute of Environmental Health Sciences. Endocrine Disruptors.
NSF International. NSF/ANSI 53 and 58 certification for PFAS reduction.

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Peptides, honestly

What the research says and where it stops. Experience and context, not prescriptions.

BPC-157

A peptide that grows new blood vessels. In rats. Here is what we actually know.

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A 15-amino-acid peptide based on a protein in human gastric juice. In rats and cell studies it grew new blood vessels (angiogenesis, through VEGFR2 and nitric oxide) and sped tendon-to-bone healing. In people: no published trials showing it is safe or that it works, and it is not FDA approved.

What you will learn

A peptide is a short chain of amino acids. BPC-157 is 15 of them, first studied in rats for gut injuries.
In rats and cells it grew new blood vessels toward damage, through the VEGFR2 receptor and nitric oxide signaling.
In rats it sped Achilles tendon-to-bone healing; in a dish, tendon cells spread and moved faster.
Why people care: tendons have almost no blood supply and heal slowly, so a vessel-growing signal is an appealing theory.
What we know is rats and cells. What we do not know: whether it works in people, whether it is safe, and what it does long term.
Not FDA approved for any use; barred from pharmacy compounding in 2023 and back under FDA review in 2026; banned in sport. A conversation for your physician, not a forum.

Sources

Seiwerth S, et al. BPC 157 and standard angiogenic growth factors: gastrointestinal tract healing, lessons from tendon, ligament, muscle and bone healing. Current Pharmaceutical Design. 2018;24:1972-1989.
Hsieh MJ, et al. Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation. Journal of Molecular Medicine. 2017;95:323-333.
Brcic L, et al. Modulatory effect of gastric pentadecapeptide BPC 157 on angiogenesis in muscle and tendon healing. Journal of Physiology and Pharmacology. 2009;60 Suppl 7:191-196.
Krivic A, et al. Achilles detachment in rat and stable gastric pentadecapeptide BPC 157. Journal of Orthopaedic Research. 2006;24:982-989.
Chang CH, et al. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. Journal of Applied Physiology. 2011;110:774-780.
US FDA, bulk drug substances for compounding: BPC-157 placed in Category 2 in 2023; status under review in 2026 (check the FDA compounding page before relying on it).
World Anti-Doping Agency Prohibited List, S0 (non-approved substances).
Laird Doman, domanhealth.com: decisions about peptides belong with you and your physician.

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The Wolverine stack

BPC-157 and TB-500: what the theory says, and where the evidence stops.

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BPC-157 and TB-500 are often combined online. TB-500 is a fragment of thymosin beta-4, a protein that binds the cell's scaffolding and helps cells move. In theory one grows the roads and the other sends the workers. There are no published human studies of the combination.

What you will learn

TB-500 is a synthetic fragment of thymosin beta-4, a 43-amino-acid protein in most human cells that binds actin and helps cells crawl.
In animals, thymosin beta-4 sped skin wound repair in rats and helped heart repair in mice. Small human trials were for a blistering skin disease and dry eye, not sports injuries, and none tested TB-500 itself.
The theory of the stack: BPC-157 works locally (new vessels, tendon cells) and TB-500 more systemically (cell migration, less inflammation): roads and workers.
Published human studies of the combination: zero.
Neither is FDA approved; both are banned in sport; BPC-157 was barred from compounding in 2023 and both were under FDA review in 2026; unregulated sellers mean unknown quality.
A clean theory is not a result. Promising in animals, unproven in people. Talk to a physician who knows the space, and be wary of anyone selling certainty.

Sources

Goldstein AL, Hannappel E, Sosne G, Kleinman HK. Thymosin beta4: a multi-functional regenerative peptide. Expert Opinion on Biological Therapy. 2012;12:37-51.
Malinda KM, et al. Thymosin beta4 accelerates wound healing. Journal of Investigative Dermatology. 1999;113:364-368.
Bock-Marquette I, et al. Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature. 2004;432:466-472.
RegeneRx clinical trials of thymosin beta-4 (RGN-137, epidermolysis bullosa; RGN-259, dry eye): small phase 2 studies.
Seiwerth S, et al. Current Pharmaceutical Design. 2018;24:1972-1989. Hsieh MJ, et al. Journal of Molecular Medicine. 2017;95:323-333.
US FDA bulk drug substances list (2023 Category 2 for BPC-157; 2026 review of both). World Anti-Doping Agency Prohibited List (BPC-157 S0; thymosin beta-4 and TB-500 S2).
Laird Doman, domanhealth.com: decisions about peptides belong with you and your physician.

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Working with Laird

What a functional health coach does, and how a consult works.

What a functional health coach does

Most health plans are built for an average person. You are not average.

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A hook on the average-person plan and the short doctor visit, then what a functional health coach actually does, the six things we work on, consult then plan then coaching with the real prices, Laird's own 280 to 180, and the ask.

What you will learn

A doctor visit is short. Your habits are where the work is.
A functional health coach looks at the patterns behind how you feel, and works on them in order.
What we work on: sleep and stress, metabolic health, weight loss that holds, protein and strength, nutrition on a GLP-1, your labs in plain English.
Consult ($149, one hour), then a plan, then coaching ($199 a month, month to month).
Before I coached it, I lived it: 280 to 180 pounds.

Sources

Prices and format as listed on domanhealth.com at the time of rendering.
Laird's own experience, not a promise of results.

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Want help applying this to you?

One hour, one on one, with Laird. Your whole picture, your numbers, and your first steps in order. $149, in person in Northern Utah or by phone or Zoom. Coaching after that is month to month.

Request the consult

Educational only, not medical advice. Claims are kept to mainstream, conservative findings and each one is cited on screen. Results Laird describes are his own experience, not a promise. Talk with your physician before changing medication, fasting, or starting a new protocol.

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