If I had only 3 words to sum up what makes a successful dieting strategy, it’d be this: fix your environment.

Keep the tools around that minimize friction towards attaining the objective & increase any friction that veer you from that path.

To help you build the ideal dieting framework, here’s the set of tool I cycle through myself.

No aspartame. No seed oils. No fake ingredients that worsen gut function. Build the kitchen so that eating correctly eliminates willpower and the cut runs as a default system.

A couple notes before we begin:

→ If you’d like the 9-page PDF guide sent to you, just comment “Summer Shred Toolkit” and I’ll send it your way.

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→ For the complete fat loss strategy, visit here:

I. Volume Carb Swaps

Easy swaps of calorically dense versions for fiber-rich analogs that give you the same eating experience at a fraction of the caloric intake.

Retrograded Gluten-Free Overnight Oats — Easy hack to make your oats more filling: Microwave your oats the day before. Refrigerate for 12 hrs to retrograde the starch. Add your whey + fruit + cinnamon. More fiber. More volume. More satiating.

52USA Konjac Pasta — 12 calories per serving, clean ingredients (organic konjac, water, tapioca, citric acid), and the best texture of any shirataki on the market.

Miracle Noodle Konjac Rice — 5 calories per serving rice base for stir-fries & burrito bowls.

Miracle Noodle Egg White Pasta — 50 calories per serving. Satiating, protein-dense pasta alternative.

Palmini Hearts of Palm Pasta — Plant-based, potassium-dense noodle with an al dente texture. Holds sauce better than zoodles. Doesn’t get watery like shirataki.

Palmini Hearts of Palm Rice — Holds up in stir-fries where cauliflower rice disintegrates.

Spaghetti Squash — Roast once on Sunday, shred into noodles that last 2—3 days. A whole squash runs ~130 calories & yields ~6–8 cups of finished volume.

Butternut Squash — Naturally sweet, fiber-dense & high volume per calorie. Cube, toss with salt, roast at 425°F for 30 min.

Zucchini Noodles (Zoodles) — Spiralize fresh or buy pre-spiralized. Pasta swap. 2-minute sauté for hot dishes. Nearly zero caloric cost.

Cauliflower Rice — Sub for rice bases/bowls. ~25 cal per cup. Trader Joe’s Organic = my weekly staple.

Bibb Lettuce Wraps — Default tortilla swap option when you want a wrap.

Egg White Wraps — When you actually need a tortilla. 30—50 cal/wrap. Original, Southwest, Everything Bagel Wraps. Clean ingredients. No seed oils/modified starch.

Lundberg Organic Whole Grain Rice Cakes Cinnamon Toast — 70 cal each. Satisfies the crunch. Pre-training vehicle for peanut butter powder or salsa.

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II. Zero / Low-Cal Beverages & Hydration

A dual win: 1) eliminate the calories & 2) use the drinks themselves as friction- reducers for mid-afternoon cravings.

Zevia — Stevia-sweetened soda. You don’t even have to worry about the artificial sweeteners anymore.

Seltzer (LaCroix / Spindrift / Bubly / Kirkland) — Any seltzer brand. Spindrift is king. Kirkland (Costco) a good budget pick.

Kettle & Fire Bone Broth — 35–45 cal per cup. 10g protein. Glycine-dense. No better tool to satisfy the warm & savory craving.

Herbal Teas — Teas (especially hot) are great for appetite suppression & satiety boost.

Electrolytes — Tons of great brands out there. Highly specific to bioindividualized requirements. Match Na/K/Mg/Ca/Cl to your sweat rate, training load & baseline dietary micronutrient intake.

Matcha — Smoother energy curve than coffee for afternoons from the L-theanine content. Opt for ceremonial grade & USDA organic. Verify the “Sold By” isn’t an Alibaba-coded dropshipper.

Recipe: Nighttime Inositol-Glycine Sweet Tea

Functional benefits & sweetness without stevia’s bitterness. Inositol supports insulin sensitivity. Glycine supports sleep.

• 12 oz boiling water

• 1—2 Honey Vanilla Herbal tea bags

• 3—5g glycine powder

• 2—3g myo-inositol powder

• Squeeze of lemon

Stir until dissolved. Drink hot or pour over ice.

III. High-Volume Low-Cal Produce

If there’s one variable to rule them all, it’s volume. These are the highest-ROI produce choices for exactly that. Each category is ranked by a composite score based on pure calorie density, satiety index, & volume-to-calorie ratio.

Fruit (Ranked)

1. Watermelon — 30 kcal/100g · 0.4g fiber · 91% water. The king of volume-per-calorie. Two full cups runs ~90 cal. Peak summer seasonal pick.

2. Strawberries — 32 kcal/100g · 2.0g fiber. Highest fiber-to-sugar ratio of any berry. 500g lands at ~160 cal with 10g fiber.

3. Cantaloupe — 34 kcal/100g · 0.9g fiber · 90% water. Summer peak. Dense beta-carotene. Slower eating than watermelon because of density.

4. Honeydew — 36 kcal/100g · 0.8g fiber. Near-identical to cantaloupe with a cleaner sweetness.

5. Raspberries — 52 kcal/100g · 6.5g fiber. The highest fiber content of any fruit on this list.

6. Blackberries — 43 kcal/100g · 5.3g fiber. Lower-sugar berry with the same polyphenol profile as blueberries.

7. Peaches & nectarines — 39 kcal/100g · 1.5g fiber. Summer peak.

8. Blueberries — 57 kcal/100g · 2.4g fiber. Slightly higher cal than the other berries but anthocyanin density is unmatched.

9. Navel/blood oranges — 47 kcal/100g · 2.4g fiber. Ranked highest on the Holt satiety index among fruits. Peel format slows eating and pith fiber extends fullness.

10. Apples — 52 kcal/100g · 2.4g fiber. Pectin soluble fiber forms a satiety gel in the gut.

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Raw Crunch Vegetables (Ranked)

1. Cucumber — 15 kcal/100g · 0.5g fiber · 95% water. Pound-for-pound the lowest calorie density on this list. Eat by the whole cucumber w/ sauce of choice.

2. Celery — 16 kcal/100g · 1.6g fiber · 95% water. They’re not “negative-calorie” but it’s closer with celery than almost anything else. 6 cal per stalk.

3. Iceberg lettuce — 14 kcal/100g · 1.2g fiber · 96% water. Not nutrient-dense, but for pure volume crunch it’s excellent. Great taco shell.

4. Radishes — 16 kcal/100g · 1.6g fiber. Peppery bite. Near-zero cal. Pairs with almost anything.

5. White button / crimini mushrooms — 22 kcal/100g · 1.0g fiber. Meaty texture. Excellent bulk-up for ground beef or eggs. Much better when cooked.

6. Cherry tomatoes — 18 kcal/100g · 1.2g fiber · 95% water. Technically a fruit, but you get the point.

7. Bell peppers (all colors) — 31 kcal/100g · 2.1g fiber. Red has 3x the vitamin C of orange juice per serving. Sweet crunch vehicle.

8. Sugar snap peas — 42 kcal/100g · 2.6g fiber. Higher cal than the others here but higher fiber & a satisfying whole-pod chew.

9. Jicama — 38 kcal/100g · 4.9g fiber. Way underused. Chopped into fries or sticks & seasoned well.

10. Kohlrabi — 27 kcal/100g · 3.6g fiber. Dense fiber, potassium, Vit C content. Peels like a radish. Best roasted.

Cruciferous (Ranked)

1. Cauliflower — 25 kcal/100g · 2.0g fiber. Riced, roasted, mashed, or eaten raw. Most versatile crucifer.

2. Green cabbage — 25 kcal/100g · 2.5g fiber. Shredded raw in slaws, fermented as kraut, sautéed in butter. One head is ~6 cups of finished volume.

3. Napa cabbage — 16 kcal/100g · 1.0g fiber. Softer than green cabbage. Works raw in salads where regular cabbage is too dense.

4. Broccoli — 34 kcal/100g · 2.6g fiber. Roasted & seasoned at 425°F.

5. Red cabbage — 31 kcal/100g · 2.1g fiber. 10x the anthocyanins of green cabbage. Shred for tacos, slaws, or stir-fries.

6. Broccoli rabe (rapini) — 22 kcal/100g · 2.7g fiber. Grandma Phys classic. Sautéed with garlic & chili flakes.

7. Broccolini — 35 kcal/100g · 2.5g fiber. Milder & sweeter than broccoli. Longer tender stems. Faster to cook.

8. Brussels sprouts — 43 kcal/100g · 3.8g fiber. Highest-cal cruciferous here, but also highest fiber. Halve, drizzle balsamic glaze, & roast cut-side down for caramelized flavor.

9. Romanesco — 28 kcal/100g · 3.2g fiber. Broccoli-cauliflower hybrid. Same profile as cauliflower with a nuttier, more complex flavor when roasted.

10. Collard greens (sautéed) — 32 kcal/100g · 4.0g fiber. Technically cruciferous. Avoid raw. Ideal braised or as a wrap replacement for heavy flour tortillas.

Pantry & Frozen Volume

Frozen cherries — ~90 cal per cup. Let the cold slow eating pace & the tartness satisfy without triggering more.

Frozen dragonfruit — ~80 cal per cup. Potassium & magnesium-dense. Ideal for tropical smoothies.

Frozen mango chunks — ~100 cal per cup. Partially thawed. Eats like sorbet.

Frozen pineapple chunks — ~80 cal per cup. Bromelain is elite for digestion. Blends into protein smoothies for volume at low caloric cost.

Canned pumpkin purée (100% pumpkin) — 40 cal per half cup. Stir a spoonful into Greek yogurt, oats, or a shake for hidden volume & 3g fiber.

Grillo’s dill pickles — Light pre-training fuel. Great pre-HIIT. Live fermented, crunch and salt in one bite. Also one of the most underrated craving killers.

Raw kimchi & sauerkraut — Fermented vegetables to support gut microbiome diversity = enhanced ghrelin (hunger-hormone) signaling. Near-zero cal. Serve cold as a side to any protein.

Air-popped popcorn — ~30 cal per cup. Season with Tajin, Old Bay, or nutritional yeast. The volume-to-calorie ratio tough to beat.

Frozen spinach (chopped, whole-leaf) — Denser nutrition/$ than fresh. Thaw → squeeze dry → stir into eggs or shakes for more volume.

IV. Fiber & Satiety Stack

If your gut is in a healthy condition, fiber is the most underused satiety lever available. Soluble fiber absorbs 10–40x its weight in water → forms a viscous gel → stomach stretches → receptors in the gut lining fire signals up the vagus nerve to the brain → brain reads as fullness.

Psyllium Husk Powder — Viva Naturals mixes best. 5g in 12 oz of water 15–20 minutes before your biggest meal. Start low & work up to 5—10g.

Organic Chia Seeds — Soak in overnight oats or kefir for more filling breakfast. Expand 10—15x in liquid. Cheap alternative to psyllium.

Organic Inulin Powder — Prebiotic soluble fiber with mild sweetness. Ideal for overnight oats & yogurt bowls.

V. Bored Mouth Cures

Japanese culture understands the idea of “you’re not hungry, you’re just bored” best with the term kuchisabishii (口寂しい), which translates to “lonely mouth”. Some of my favorite tools for curing bored mouth.

Zellie’s 100% Xylitol Gum — My top gum pick. Xylitol has the oral health upside and the chew itself mitigates any snack impulse.

Pur 100% Xylitol Gum — Another clean gum. Cheaper alternative with a little less flavor.

Spry Xylitol Mints — Berry > Cinnamon > Peppermint > Lemon

Brushing your teeth after the last meal — Free one, yet under-discussed. Toothpaste makes food unappealing for an hour. A Pavlovian signal that the eating window has closed.

VIII. Sweetener Toolkit

Not all zero-calorie sweeteners are equal. Some of the ones we’re mitigating: aspartame, sucralose, acesulfame potassium, & saccharin.

Allulose — ~70—90% as sweet as sugar. Behaves exactly like sugar in heat → caramelizes, browns, dissolves. The only sweetener to use in baking or anything reduced on a stove.

Myo-inositol — Mild sweetness plus functional benefits (leptin/insulin sensitivity + anxiety reduction). 2—3g stirs into a hot drink well.

Glycine — ~70% as sweet as sugar. Clean, sweet taste Pairs synergistically with inositol. Also S-tier for dropping body temperature & reducing time to fall asleep at ~3—5g before bed.

Lakanto Monk Fruit Drops — Cleaner aftertaste than stevia if you dislike bitterness.

VI. Flavor Weapons

The path to upgrading every bowl.

Sauces & Dressings

Primal Kitchen BBQ, Ketchup, Steak Sauce, Mayo — Avocado oil base without seed oils, sugar, or corn syrup. One of only a few “mainstream” clean-sauce brand that actually delivers on flavor.

Noble Made Buffalo — Personal favorite buffalo sauce made with extra virgin olive oil.

True Made Foods No Sugar Added Ketchup — Sweetened with butternut squash, carrots, & apple instead of HFCS or sucralose. The cleanest no-sugar ketchup made.

G Hughes Sugar-Free BBQ or Asian Marinades — Ideal when you need a Asian-style or sweet-glaze flavor profile for bowls/stir-fry.

Fresh Salsa or Pico — 15–20 cal per 1/4 cup. Staple for any TexMex/Southwestern bowls. Make your own or buy refrigerated. Trader Joe’s selection also strong.

Huy Fong OG Sriracha — Still the best sriracha. Small amount of sugar but the flavor cannot be topped.

Coconut Aminos — Deep umami. 65% less sodium than soy sauce. Slightly sweet naturally.

White Miso — ~25 cal per tbsp. Savory flavor. Great for broths, marinades, & dressings with small quantities. Fermented so also great for digestion.

VII. Spreads & Nut Butter Hacks

Organic Peanut Butter Powder — Defatted peanut powder. 1/3 the calories of peanut butter. Mix with water for spread → add cocoa for chocolate peanut butter mousse.

Powdered Almond Butter Powder — The defatted almond butter powder alternative.

Organic Cacao Powder — ~3g carbs per tablespoon. Clean, intense chocolate. Foundation of any high-protein chocolate dessert hack.

VI. Flavor Enhancers

Bragg Nutritional Yeast — 45 cal per 2 tbsp. Cheesy-nutty umami. High B1 (thiamine). On popcorn, eggs, & roasted veggies.

Everything Bagel Seasoning (Trader Joe’s / Costco) — Zero-cal flavor for eggs, Greek yogurt based dips, & cottage cheese.

Old Bay — How to take baked sweet potatoes to the next level.

Mina Harissa — Newest addition to my lineup. North African pepper paste. ~15 cal per tbsp. Elevates marinades, bowls, & roasted veggies with minimal calorie cost.

IX. High-Protein Desserts & Frozen Snacks

The Base Ingredients

Ninja Creami — Remains my favorite health investment over the last couple years. Once you acquire, you’ll wonder how you ever operated in your B.C. era (Before Creami). It pays for itself in saved calories within a month.

Nonfat Plain Greek Yogurt — 17g protein, 90 cal per 6 oz. The foundation of half the recipes here.

2% Good Culture Low-Fat Cottage Cheese — 14g protein per 4 oz. Clean ingredients (milk, live cultures, salt). No gums or thickeners.

Siggi’s Nonfat Plain Skyr — Highest protein density of the three (17g per 5.3 oz), Icelandic-style. Thicker than Greek yogurt. Amazon

Transparent Labs Grass-Fed Whey Isolate — Minimal ingredient. No artificial flavors or sweeteners. Chocolate and vanilla are the workhorses. Amazon

Equip Grass-Fed Collagen Peptides — 14g hydrolyzed collagen peptides per scoops. Dissolves well into any hot drink.

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The Recipes

Recipe: Collagen Hot Cocoa

Evening wind-down, sleep support (glycine), & dessert in one mug.

• 12 oz hot water or unsweetened almond milk

• 2 scoops grass-fed collagen peptides powder

• 1 tbsp raw cacao powder

• 3—5g glycine

• 2—3g myo-inositol

• Pinch of sea salt

• Allulose or monk fruit (if you’d like more sweetness)

Blend for ~20—30 seconds until frothy. ~120 cal.

Recipe: Ninja Creami Chocolate Peanut Butter Ice Cream

More Ninja Creami recipes to come this summer. But for now, here’s a basic one to make a full pint at 450 cal & 50g protein total.

• 1 cup Good Culture 2% cottage cheese

• ½ cup unsweetened almond milk (or Fairlife skim)

• 1 scoop chocolate whey isolate

• 2 tbsp powdered peanut butter

• 1 tbsp raw cacao powder

• 2 tbsp allulose (what prevents the rock-solid freeze)

• ¼ tsp sea salt

• ½ tsp vanilla extract

Blend smooth, pour into Creami pint, freeze 24 hours, spin on “lite ice cream” setting, add another splash of milk, re-spin.

Recipe: Protein Fluff

High-speed blender or stand mixer, 5 minutes, massive bowl of mousse.

• 1 scoop whey isolate

• ½ cup frozen berries

• 2–3 tbsp unsweetened almond milk

• Sweetener to taste

Blend on high, adding almond milk tablespoon by tablespoon until the mixture quadruples in volume. Eat immediately. ~180 cal & 25g protein.

Recipe: Whey Protein Mousse (no blender)

• 1 scoop whey isolate

• 2 tbsp cold water ( too much ruins it)

• Pinch of salt

Shake hard in a closed container for 30 seconds. The texture transforms into a dense mousse. Top with cinnamon & fresh berries.

Recipe: Greek Yogurt + Sugar-Free Pudding Hack

• 1 cup nonfat plain Greek yogurt

• 1 tbsp dry Simply Desserts sugar-free pudding mix (chocolate, vanilla, or banana)

Mix for 60 seconds. The texture transforms into dense pudding instantly. ~130 cal, 20g protein. Simply Desserts is stevia-and-erythritol sweetened.

Recipe: Frozen Banana Nice Cream

• 1 frozen banana, sliced

• 1 tbsp raw cacao

• Splash of unsweetened almond milk

Blend until smooth. ~110 cal. Real ice cream texture.

Recipe: Cottage Cheese Chocolate Freeze

• ¾ cup Good Culture cottage cheese

• 1 tbsp raw cacao

• Sweetener to taste

• Small handful of frozen berries

Blend smooth, transfer to bowl, freeze 45 minutes (not fully frozen, just firm). Dense chocolate mousse texture.

Ready-to-Grab

GoodPop No Added Sugar Popsicles — Real fruit. Organic. No artificial sweeteners. ~25–50 cal per pop.

Final Word

It’s 2026. We no longer need to make dieting down painful. The tools are everywhere to make your life easier in getting there.

This year is the year you’ll stack the environment in your favor & build your dream physeek. Simple.

Until next week.

Your friend,
Phys

Ask someone about the origins of AI as we know it today and they’ll probably trace it back to 2022 when ChatGPT launched and became the fastest consumer app to hit 100M users in just 2 months. But few know the story actually started in 1956 at Dartmouth. It felt like it blossomed out of thin air, but it was really just building for more than seven decades.

Peptides follow the same arc – Amara’s Law:

“We tend to overestimate the effect of a technology in the short run & underestimate the effect in the long run.”

This idea is best modeled by the Gartner Hype cycle.

After a few mainstream podcasts and wave of viral X posts in 2025, “peptides” became the buzzword that means everything and nothing at the same time. To most, it all became relevant overnight.

But this short amino acid chain science has been building for over a century. Albeit quietly. In Soviet military labs, University of Arizona basements, Gila monster saliva, & Croatian gastroenterology departments.

As we write this in April 2026, we’re sitting near the peak of inflated expectations. And a sharp bifurcation is forming. The hype riders vs. the elite practitioners. The former as tactic hunters. The latter as strategic health infrastructure builders. If you’re reading this — congrats on finding your way into the latter.

Downloadable PDF plot below for detailed viewing (abridged version):

Peptide Hype Cycle

525KB ∙ PDF file

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1902–1953: The birth of peptides

The first peptide ever identified came in 1902 when William Bayliss & Ernest Starling discovered secretin, a chemical messenger released from the gut lining signaling the pancreas to secrete digestive enzymes.

Two decades later in 1921, Frederick Banting & Charles Best isolated insulin from canine pancreases. By 1922, a dying 14-year-old diabetic named Leonard Thompson received the first human injection.

This marked the first exogenous peptide therapy ever used in humans. Insulin proved the model that every peptide discussed here follows: isolate or synthesize a signaling molecule → deliver it exogenously → restore or redirect a biological process.

In 1954, chemist Vincent du Vigneaud rang in the era of synthetic peptide design as we know it today. He completed the first total synthesis of oxytocin & vasopressin assembling peptides amino acid by amino acid proving they can be built from scratch. He won the Nobel Prize the following year.

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1963–1979: The infrastructure gets built

Prior to 1963, making peptides in a lab was an arduous process. Every amino acid had to be coupled individually in solution, purified, & verified. Bruce Merrifield came along and invented solid-phase peptide synthesis (SPPS) that won him the Nobel Prize in Chemistry in 1984. SPPS automated the process by anchoring the growing chain to an insoluble resin bead making peptide production scalable.

Without SPPS, no peptide sold today would exist. Meanwhile, behind closed doors in the USSR, a mastermind was developing a parallel peptide vector.

Bioregulators: The classified Soviet program

In 1971, a military physician named Vladimir Khavinson started extracting peptide complexes from animal organs at the Kirov Military Medical Academy in Leningrad. The classified program objective was to protect soldiers, cosmonauts, & athletes from radiation exposure, extreme cold, & operational stress.

Khavinson’s team isolated short-chain peptides (2 to 4 amino acids long) from the thymus, pineal gland, brain cortex, prostate, & retina of calves. These became the first peptide bioregulators:

• Thymalin (from the thymus) regulated cellular immunity.

• Epithalamin (from the pineal gland) restored melatonin production and endocrine function.

Khavinson eventually proposed these ultra-short peptides could bind directly to DNA promoter regions and modulate gene expression. These were epigenetic switches that told aging cells to behave younger.

By 1982, Thymalin received formal registration for medical use in the USSR. Six peptide pharmaceuticals would eventually be approved for clinical use.

It wouldn’t be for another decade until the rest of the world heard of bioregulators.

Growth hormone secretagogues: An accidental discovery

In 1977, endocrinologist Cyril Bowers at Tulane University was studying small opioid-like peptides (enkephalin analogs) when he noticed certain chemical modifications that caused pituitary cells to release growth hormone.

This was the birth of the growth hormone secretagogue field.

1980–1989: Three parallel threads

The 1980s saw three separate research programs develop in parallel.

Thread 1: GH secretagogues mature

By 1984, Bowers synthesized GHRP-6 making it the first synthetic hexapeptide to dose-dependently release growth hormone. He was building the key before anyone knew the lock existed, which became known as “reversed pharmacology”. GHRP-6 worked through a receptor nobody had identified yet.

The endogenous hypothalamic hormone GHRH was discovered shortly after. Interest in GHRPs faded as most assumed GHRH was the primary GH regulator. That assumption turned out to be wrong. GHRP-6 & GHRH operated through completely distinct receptors and had synergistic effects on GH release.

Sermorelin, the synthetic form of GHRH, entered development during this period and would eventually receive FDA approval in 1997 as a diagnostic agent for GH deficiency.

Thread 2: Melanocortins emerge in the desert

At the University of Arizona, biologist Mac Hadley & chemist Victor Hruby were modifying alpha-melanocyte-stimulating hormone (α-MSH) — a naturally occurring peptide involved in skin pigmentation. Their goal was to create a stable synthetic analog that could induce tanning without UV exposure helping to reduce skin cancer risk.

Melanotan I came first: a linear 13-amino-acid peptide that closely resembled natural α-MSH but lasted longer in the body.

Then came Melanotan II: a cyclic heptapeptide that was much more potent and metabolically stable. Most peptides are straight chains where enzymes can attack the exposed ends and break them down fast. MTII had no free ends for enzymes to grab onto giving it longer lasting effects.

MT-II also bound to more than just MC1R (pigmentation) but also MC3R, MC4R, and MC5R. All of which were receptors involved in sexual function, appetite, & energy balance.

Thread 3: Soviet bioregulators go clinical

By the mid-1980s, Khavinson extracted over 20 peptide complexes from animal organs and synthesized 15 additional short peptides. Thymalin and Epithalamin had been in clinical use within the Soviet military medical service. Others followed: Cortexin (brain cortex, for cerebral function), Prostatilen (prostate), Retinalamin (retina).

Bioregulator treatment slowed age-related biomarker decline and suppressed tumor development in animal models showing lifespan increases of 20-40%.

But the work was still classified & published in Russian journals leaving it entirely invisible to Western science until the Soviet Union collapsed.

1990–1999: The discovery decade

Nearly every major category of peptide discussed online today has its roots in the 1990s.

BPC-157: Gastric juice yields a healing compound

In the early 1990s, Croatian pharmacologist Predrag Sikirić based at the University of Zagreb isolated a stable pentadecapeptide (15 amino acids) from human gastric juice. They named it Body Protection Compound-157 (BPC-157).

Sikirić sought to understand why the stomach heals its own lining despite constant exposure to hydrochloric acid. His team found a peptide fragment from a larger protective protein having cytoprotective effects across many tissue types including the gut, tendons, ligaments, muscle, bone, & vasculature.

Over the next three decades, Sikirić’s lab would produce the vast majority of published BPC-157 research: acceleration of wound healing, reductions in inflammation, & protection of GI lining from previous damage.

Exendin-4: The Gila monster connection

The Ozempic story is most unique in its origins. In 1991, endocrinologist John Eng was studying the venom of the Gila monster, a venomous lizard native to the American Southwest, when he identified a 39-amino-acid peptide called Exendin-4. It had extensive structural homology to human GLP-1, the incretin hormone that stimulates insulin secretion after meals.

The big difference between endogenous GLP-1 & Exendin-4: the former has a plasma half-life of ~2 min & Exendin-4 has a natural mutation extending its half-life to 2.5 hours.

After struggling to find institutional support, Eng patented Exendin-4 personally. He partnered with Amylin Pharmaceuticals years later to develop what became the first GLP-1 receptor agonist: exenatide.

Retrospectively, this was the start of a metabolic revolution. In 1991, the response was silence.

The Soviet collapse and bioregulator declassification

When the Soviet Union collapsed in 1991, Khavinson’s classified research became accessible. The St. Petersburg Institute of Bioregulation and Gerontology was established. The peptide bioregulator program transitioned from military secrecy to an open scientific publication.

Khavinson refined his approach as he shifted from crude organ extracts (Cytomaxes) to chemically synthesized short peptides (Cytogens). Epitalon became the most internationally recognized molecule from this program and one becoming increasingly popular today. In 2025, a UK-based group published the first independent replication confirming dose-dependent telomere extension in normal human cells

The synthetic bioregulator Thymogen (a dipeptide for immune correction) also emerged from this era. By the 2000s, Khavinson amassed over 105 patents and 775 published papers spanning four decades of research.

GH secretagogues: 2nd generation

The GHRP family expanded rapidly through the 1990s.

GHRP-2 (pralmorelin) was synthesized as a more potent second-generation analog having a stronger GH release than GHRP-6 with better sustained elevation over time. Hexarelin followed with similar potency.

In 1998, Novo Nordisk characterized ipamorelin as the first selective growth hormone secretagogue. Unlike GHRP-6 and GHRP-2, ipamorelin released GH without spiking cortisol, ACTH, or prolactin.

Melanotan II: Too hard to ignore (*winks*)

In 1996, the Arizona team ran a Phase I clinical trial of Melanotan II to evaluate its tanning efficacy. Five low-dose subcutaneous injections produced visible skin darkening. The tanning worked.

But MT-II’s broader receptor binding demonstrated unforeseen outcomes…inducing erections in each male subject. MC4R activation in the central nervous system was triggering penile erection through hypothalamic / spinal pathways independent of sexual arousal.

Many of the forums & Reddit threads have been detailing these very cases over the last decade.

Despite this not being the intended objective, it redirected the entire melanocortin research program. Sexual dysfunction became the new target. PT-141 (bremelanotide) was synthesized by Palatin Technologies as a derivative of the MT-II scaffold, which optimized for central melanocortin activity with reduced melanogenic effects.

Thymosin Beta-4 & TB-500

Allan Goldstein first described Thymosin Beta-4 (TB4) in the 1960s, but it didn’t gain traction until the 1990s. TB4 functions by maintaining a ready-to-deploy reservoir that cells can rapidly assemble into structural filaments when tissue is damaged. This is what allows reparative cells like fibroblasts, stem cells, & endothelial cells to physically migrate into a wound site and start rebuilding.

The synthetic fragment TB-500 was a TB4 fork, which distilled it into a shorter, more accessible molecule. It’s now become one of the most widely used recovery peptides in sports performance & recovery alongside BPC-157.

2000–2009: From labs to prescription pads

GLP-1 goes pharmaceutical

After a 14-yr period, the FDA approved the Gila monster peptide (exenatide (Byetta)) as the first GLP-1 receptor agonist for type 2 diabetes in 2005.

Novo Nordisk watched closely and began developing its own GLP-1 analog. Liraglutide used a different strategy. They attached a fatty acid chain (C16) to the GLP-1 peptide, allowing it to bind reversibly to albumin in the bloodstream. This slowed renal clearance and extended the half-life enough for a single daily dosing. It received EU approval in 2009 and went on the market as Victoza.

CJC-1295: Long-acting GHRH

ConjuChem Biotechnologies developed CJC-1295, a modified version of GHRH(1-29) with a Drug Affinity Complex (DAC) that bound to serum albumin extending its half-life to 6-8 days. The “no-DAC” version (Mod GRF 1-29) used the same GHRH analog without the albumin-binding complex. It was shorter acting requiring more frequent dosing, but it preserved pulsatile GH release that mirrors natural endocrine rhythms. Phase II trials showed dose-dependent GH increases of 2-10x sustained for 6+ days after a single injection.

Khavinson publishes landmark human data

In 2003, Khavinson & Morozov published the results of a 6-8 year clinical assessment of Thymalin & Epithalamin in 266 elderly subjects. The bioregulators normalized immune function, endocrine markers, & cardiovascular indices.

Mortality in the treatment groups was 28% lower than controls.

Though the story was compelling, the data came from Russian institutions and was published in Russian journals, which was met with Western skepticism.

Thymosin Alpha-1: Approved everywhere but the US

Thymosin Alpha-1 (Ta1) is a 28-amino-acid peptide derived from thymus tissue. It was approved under the brand name Zadaxin in 36 countries for hepatitis B, hepatitis C, & as an immunotherapy adjunct, though it’s never been submitted for FDA approval in the US.

Nootropic peptides: Selank and Semax

Two synthetic peptides with nootropic & anxiolytic properties emerged from Russian pharmaceutical development.

Semax: a synthetic analog of ACTH(4-10) with a Pro-Gly-Pro tripeptide extension known for its neuroprotection and was approved in Russia for anti-stress, cognitive enhancement, stroke recovery, & ADHD.

Selank: a synthetic analog of the immunomodulatory peptide tuftsin, also with a Pro-Gly-Pro extension showing anxiolytic effects (comparable to benzodiazepines without side effects/dependency risk) and was approved in Russia for generalized anxiety.

GHK-Cu: A copper tripeptide

In 1973, biochemist Loren Pickart discovered GHK-Cu (glycyl-L-histidyl-L-lysine complexed with copper) as a naturally occurring human tripeptide first identified in human plasma.

Endogenous concentrations decline significantly with age → plasma levels at age 60 (~80 ng/mL) are less than half at age 20 (~200 ng/mL).

GHK has now become a staple in the cosmetic & regenerative health space either applied topically or applied subcutaneously.

Through the 2000s, its research profile widened considerably given it modulates expression of hundreds of genes tied to:

• wound healing

• collagen synthesis

• antioxidant defense

• extracellular matrix remodeling

Mechanistically, GHK-Cu is unique in that it acts like a bioregulator but drives direct tissue repair like a healing peptide. And that’s why we’re seeing it show up in so many different protocols.

2010–2019: The pharmaceutical explosion

GLP-1 becomes a metabolic optimization story

The 2010s marked the shift of GLP agonists from a niche T2 diabetes treatment to one of the most powerful metabolic optimization tools in existence.

After liraglutide’s (Victoza) 2010 FDA approval in 2010 for type 2 diabetes, Saxenda (liraglutide at higher doses) became the first GLP-1 approved specifically for weight loss.

Shortly after, dulaglutide (Trulicity) arrived with once-weekly dosing. Then in 2017, semaglutide (Ozempic) shifted the entire metabolic landscape.

By 2019, oral semaglutide (Rybelsus) proved that a peptide could survive stomach acid and reach therapeutic levels orally. This was done via a co-formulated absorption enhancer called SNAC that raised local stomach pH and improved absorption.

Melanocortins reach the market

In 2014, the EU approved Melanotan I (Scenesse) for a rare condition causing extreme photosensitivity. This marked the first regulatory validation of melanocortin-based pigmentation therapy. The US followed with FDA approval in 2019.

That same year, bremelanotide (PT-141) sold under the brand name Vyleesi received FDA approval for hypoactive sexual desire disorder in premenopausal women.

Melanotan II has never received regulatory approval though. Its non-selective receptor binding (what made it versatile) also caused some regulatory complications.

The underground peptide economy gains momentum

By the late 2010s, a grey market peptide economy matured. Compounding pharmacies were focused on formulating BPC-157, TB-500, ipamorelin, & CJC-1295 for clinical use under physician prescription. The “Wolverine Stack” (BPC-157 + TB-500 for accelerated tissue repair) entered the world of sports medicine & decentralized biohacking communities.

Mitochondrial peptides are born

A newer class of peptides derived from mitochondrial DNA began attracting research attention.

MOTS-c: a mitochondria-derived peptide known for its effects on metabolic regulation & insulin sensitivity.

Humanin: another mitochondria-derived peptide known for its neuroprotective properties in Alzheimer’s disease models & anti-apoptotic effects.

AOD-9604: a modified fragment of HGH developed specifically for its fat-reducing properties without the diabetogenic effects of full-length HGH. It received Generally Recognized as Safe (GRAS) status from the FDA as a food ingredient.

2020–2026: Peak hype + peak friction

The GLP era

In 2021, Wegovy (semaglutide) received FDA approval for chronic weight management.

Average weight loss in clinical trials = ~15% of body weight. The GLP-1 era officially arrived.

In 2022, tirzepatide (Mounjaro) received FDA approval as the first dual GLP-1/GIP agonist for T2 diabetes.

Clinical trials showed ~21% average weight loss.

In 2023, tirzepatide (Zepbound) received obesity approval. By 2024, GLP-1 drug sales neared $14 billion.

By the end of 2024, soaring demand brought on new shortages. Compounding pharmacies began producing semaglutide copies under shortage exemptions. Chinese peptide imports to the US doubled to $328 million. Online peptide advertising increased 678% from 2022.

Meanwhile, the research pipeline continued moving. Retatrutide, a triple agonist targeting GLP-1, GIP, & glucagon receptors, entered late-stage clinical trials.

Orforglipron, an oral, non-peptide GLP-1 receptor agonist from Eli Lilly, advanced toward potential FDA approval. Though it remains much less effective than its injectable predecessors.

WADA says enough

In January 2022, the World Anti-Doping Agency added BPC-157 to its Prohibited List under category S0 (Non-Approved Substances). GHRPs (GHRP-2, GHRP-6, hexarelin, ipamorelin) were already banned under S2 (Peptide Hormones and Growth Factors).

FDA crackdown

In September 2023, the FDA placed 19 peptides in Category 2 meaning compounding pharmacies could no longer legally produce them. The stated rationale across these compounds included immunogenicity risk, peptide-related impurities, & insufficient human safety data.

Demand didn’t disappear. If anything, the restrictions amplified interest. Many turned to research chemical vendors and unregulated online suppliers. And so the peptide wild west was born.

Not without growing pains though. Enforcement escalated in June 2025 when the FDA raided Amino Asylum. More than 50 warning letters went to GLP-1 compounders a few months later and state-level enforcement followed. By March 2026, one of the biggest hubs, Peptide Sciences, voluntarily closed its doors.

The reclass

On February 27, 2026, HHS Secretary RFK, Jr. appeared on Joe Rogan hinting that he expects ~14 of the 19 previously restricted peptides to return to Category 1 status restoring the ability of licensed compounding pharmacies to produce them.

6 weeks later on April 15, 2026, the FDA made it official with a formal meeting scheduled for July 2026 where panelists will consider whether 12 peptides should be permitted for routine compounding.

2026 & beyond: Where we go from here

As of mid-2026, we’re sitting at the Peak of Inflated Expectations marked by the Hollywood GLP mismanagement look & the predatory TikTok affiliate culture.

Collectively, all of it has pushed expectations beyond what the evidence currently supports. And to be clear – the evidence is substantial by iteself.

So where do we go from here?

Like most technology curves, the correction is acute followed by a long-term stabilization.

The timeline forward is characterized by a few principles:

1. Real-world friction corrects the overshoot: Results are going to be bioindividualized & health context-dependent. Many will begin to discover that peptides amplify most lifestyle inputs rather than replace them. In other words, you can properly dose the MOTS-c all you want, but if diet isn’t dialed in, training is inconsistent, & sleep quality/circadian regulation is subpar, outcomes will fall short of expectations.

2. Maturing human data replaces hype with bioindividual precision: Expect to see much of Khavinson’s work replicated and even more mechanistic studies. Do not expect the RCTs to originate from the NIH, but instead from decentralized institutions/clinics running their own. Even the language shifts from generalized “peptides” to highly individualized, objective-driven interventions.

3. Oral / nasal delivery & commoditization strip away the mystique: The one thing standing in the way more than any other component for most is the fear of needles. A 2022 survey put that number at ~63% having at least some fear. Orforglipron-style molecules (oral + mass-manufacturable) transform GLP-1 therapy from an exclusive injectable to a widely accessible oral drug. This drives the most adoption and where we cross the chasm from early adopted crowd to gen pop adoption.

4. Regulatory stabilization prevents a deep trough: The RFK-led HHS reclassification (now formalized with a July 2026 FDA review) restores compounding access and pulls volume out of the gray market.

Beyond 2027, here’s what the Slope of Enlightenment & eventual Plateau of Productivity look like for each peptide category:

• GLPs: On the Slope, more large-scale outcome trials and decentralized data gathering clarify metabolic effects while microdosing/adjacent protocols mitigate side effects & muscle loss. By the Plateau, they sit as routine staples integrated into primary care and boringly effective lifestyle adjuncts.

• Healing peptides (BPC-157, TB-500/thymosins): The Slope brings targeted human RCTs and imaging data from decentralized, broscience style sources. This proves localized repair without systemic risks. On the Plateau, they become standard adjuncts in gut healing, sports medicine & post-surgical protocols.

• GH secretagogues: Maturing pharmacokinetic and safety studies on the Slope refine dosing windows & cortisol mitigation. At the Plateau, they stabilize as niche tools for GH deficiency cases, muscle loss in older adults, & GLP adjacent protocols.

• Bioregulators (Khavinson short peptides like Pinealon & Epitalon + GHK-Cu): Western replication trials on the Slope finally validate epigenetic gene regulation & oral bioavailability. By the Plateau, they emerge as foundational healthspan optimization tools for circadian rhythm regulation, skin, hair, thymus, & stress resilience.

• Nootropic peptides (Selank, Semax): The Slope brings clean cognitive and anti-anxiety trials detailing blood-brain-barrier penetration and neurotransmitter modulation. On the Plateau, they settle as targeted adjuncts for focus, recovery from stress, or mild neuroinflammation especially in older adults with early onset neurodegeneration.

• Melanocortins: Dose-response & long-term safety data on the Slope define targeted therapeutic windows for tanning, libido, & appetite with less of the old nausea worries. At the Plateau, they become staples at specialized med spas & peptide clinics. More accessibility, female adoption, & mobility enabled by nasal spray applications.

• Antimicrobial peptides (LL-37): The Slope sees microbiome and infection outcome studies proving selective pathogen control without dysbiosis. The Plateau integrates these as next-generation adjuncts for gut, skin, and chronic low-grade infections.

• Mitochondrial peptides (MOTS-c, SS-31): Early human energetics & fatigue trials on the Slope map vitality gains. By the Plateau, they anchor regenerative protocols for mitochondrial decline targeted for insulin/leptin sensitivity, chronic fatigue, or age-related vitality loss.

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Final word

Before we depart, here’s one practical takeaway to remember: peptides amplify inputs & will never replace the lifestyle boulders.

If the first century of our peptide timeline built the molecules, the next decade will build the infrastructure of sovereign decentralized testing, cleaner clinical evidence, & delivery innovation.

We’re cautiously optimistic as we continue our own research & spread the lessons learned from the research of other elite practitioners in the community.

In the meantime, steer clear of Peptide TikTok, study what’s presented here (much more to come), & stay elite. We’ll see you guys next week.

Your friend,
Phys

A younger dude recently came to me. Trouble falling asleep. Trouble staying asleep. Waking up around 2–3 AM every morning. After walking through his foundations: diet, bloods, gut function, daily routine including light environment, digital diet, movement, social habits and any acute/chronic stressors. Everything dialed in.

Having dealt with the same issue myself, I asked: “Do you wear a sleep tracker?”

“Yep.”

I told him to take it off for a month.

Three weeks later: “I’ve felt more refreshed this past week than I have in over 2 years.”

Turns out the research community already had a formal term for it: orthosomnia, where sleep tracker obsession itself disrupts sleep architecture increasing pre-sleep anxiety.

He’s not alone. People buy the Whoop or OURA to sleep better only to sleep worse because the device said so. The cycle repeats.

“So be ignorant…?”

Nope — it’s about learning to read the biologically built-in signals your body already provides.

Here are 12 proxies that replace performative tech with something more reliable: your own awareness.

I. The Morning Read (what your body tells you before you do anything)

#1: Sleep Quality → Morning Focus + Tolerance

Replaces: Oura/WHOOP/Apple Watch sleep scores

Can you sustain focus without a headache/brain fog for 30+ minutes upon waking? Does the guy chomping on his bagel with cream cheese in your ear not bother you (as much)? If yes to both, your glymphatic system cleared metabolic waste (beta-amyloid, tau proteins) overnight, cortisol awakening response rose on schedule, and excitatory glutamate isn’t lingering from incomplete NREM cycling. Some of the markers of restorative sleep.

#2: Caffeine Tolerance → Coffee Response Gauge

Replaces: Cortisol timing apps, adenosine receptor speculation

Do 2–3 cups of coffee feel like jet fuel? If they barely register or make you anxious, you’ve either: 1) saturated adenosine receptor tolerance or 2) your autonomic nervous system scale is habitually tipped towards the sympathetic side without enough parasympathetic tone.

#3: HRV / Autonomic Balance → Morning Wood / Bean

Replaces: HRV wearables

The single best free proxy for vascular and nervous system health that exists. We speak about this one at length here:

II: The Calibration Check (are your neurochemical signals functioning correctly?)

#4: Dopamine Sensitivity → Music Response

Replaces: Dopamine detox protocols

When you turn on a banger, does it hit like a mild drug?

Let this serve as an honest marker of intact mesolimbic reward signaling. If music feels flat, your D2 (dopamine) receptor density is downregulated & prolactin likely elevated from chronic overstimulation/digital anhedonic state of excess social media, stims, & gooning. The fix lies in deleting the low-cost dopamine vectors & activating the dopaminergic system via valuable accomplishment.

#5: Hormone Balance → Reply Guy Test

Replaces: Frequent testosterone/estrogen panels

If a reply guy on social media sends you into a tailspin, he’s entered into your OODA loop successfully (only you have the keys). There’s a good chance your androgen levels are outpacing estradiol’s modulatory role (generally a T/E2 or DHT/T imbalance). Or your inhibitory GABA tone is paired with an excess glutamate buildup. The combination of hormones and neurochemistry represents a nice proxy for fuse length.

Note: Biannual bloodwork remains a non-negotiable.

#6: Stress Resilience → Breath & RHR Awareness

Replaces: HRV-guided breathwork apps, stress scores

Can you bring a racing heart & spiraling thoughts under control with 5 slow, deep breaths? A direct test of vagal efferent tone and your capacity to upregulate parasympathetic output via the baroreflex.

III: The Functional Layer (what your body reveals through function)

#7: Body Composition → Mirror

Replaces: InBody, DEXA scans

Use a mirror & pair it with:

1. Visual references

   

2. Body fat estimation descriptions

I still recommend getting a baseline DEXA scan as early as possible, then every few years afterwards to monitor bone mineral density & visceral adipose tissue as you age. An example of what a typical read out provides below.

#8: Gut Health → Daily Poops

Replaces: GI-MAP, Viome, microbiome sequencing kits

Do you have a daily, well-formed bowel movement? Bonus points if around the same time of day. Daily poops are an easy proxy for a favorable gut microbial profile & fortified gut barrier integrity.

Added bonus: can you trust a fart?

#9: Energy / Metabolic Health → Post-Meal Vitality Check

Replaces: Continuous glucose monitors

Sustained energy post-meal reflects efficient glucose uptake & an adequate insulin/leptin response. Conversely, postprandial crashes point to insulin resistance, poor metabolic flexibility, or mitochondrial inefficiency.

#10: Immune Function → Acute Stress Recovery

Replaces: Inflammatory marker panels (i.e. CRP), immune “scores”

How fast do you bounce back from a hard training session, a bad restaurant meal, or a stressful stretch? If a minor stressor knocks you out for 2–3 days, you may have an elevated low-grade inflammation baseline, slow resolution of acute inflammation, or nutrient insufficiency limiting immune cell turnover. Resilience is the metric.

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IV: The Cognitive Output Layer (what your biology produced in terms of cognition & action)

#11: Screen Time → Daily Value Audit

Replaces: Screen time reports

Screen time has evolved into a virtually useless metric. We all live in the digital world and will continue to. At the end of the day, one thing matters: “What of value did I accomplish today?” You can create any daily value audit that works best for you, but one I like is conducting an analog (pen + notebook) version of the Daily Examen. This forces you to confront what you delivered to your future self, your family, & society.

Simple: Be still → Be grateful → Be reflective of what you got done today → Be authentic of what you fell short on → Be deliberate in what lies ahead tomorrow

#12: Cognitive Health → Memory Recall Speed

Replaces: Brain training apps, cognitive assessment tools

The inability to recall specific details from yesterday’s conversations suggests impaired hippocampal consolidation, which is often downstream of disrupted deep sleep, neuroinflammation, or inadequate acetylcholine precursor availability (choline + tyrosine + taurine + B-vitamins + DHA).

Final Word: Don’t Be Neurotic

The health space is dominated by a principle of being overquantified by the underqualified. Because of the over-quantification trend, we’ve quietly become addicted to the data and it’s come at a steep cost/

What were once useful tools are now symbols of performative self-improvement. The stress of optimization ironically created the very dysfunction most are trying to prevent. And often too afraid to openly admit.

The irony would be turning these proxies into a rigid checklist you obsess over.

The real goal here is building bioindividual interoception: the ability to perceive and accurately interpret your body’s internal signals. Higher interoceptive awareness consistently correlates with better emotional regulation, improved decision-making, & stronger health outcomes across time & space.

Your body gives off useful data and the best health tool you own is the skill of being able to listen to it. (free by the way)

Your friend,
Phys

Refer a friend

It’s neither your imagination nor another Reddit-induced symptom. The same molecule that sedates most is exciting your neurons through a receptor system few know of.

Here’s why that’s happening & a ranked protocol to fix it.

Contents:

• How Glycine Promotes Sleep

• Why Glycine Wires Some People Up

• The Four Factors Behind the Paradox

• The Protocol: Ranked by Priority & ROI

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How Glycine Promotes Sleep (When It Works)

Glycine is one of two inhibitory neurotransmitters in the central nervous system — GABA being the other. Its functions range from glutathione synthesis to bile acid conjugation to neurotransmission and is a big reason why you hear so much chatter on eating nose-to-tail in the social media space.

Glycine activates NMDA receptors triggering the thermoregulatory cascade that initiates natural sleep: peripheral vasodilation → drops core body temperature → shortens sleep onset latency.

In Yamadera et al. (2007), 3 g of glycine taken one hour before bedtime:

• Improved subjective sleep quality

  

• Shortened sleep onset

  

• Improved next-day cognitive performance

  

But unfortunately, there’s biochemical variation (many such cases).

The Paradox: Why Glycine Wires Some People

Glycine acts as an inhibitory neurotransmitter, but it also functions as a co-agonist with glutamate at the NMDA receptor’s glycine binding site.

By taking exogenous glycine, you saturate both the inhibitory glycine receptors & the NMDA co-agonist site. And the latter mechanism is how you start to activate glutamatergic excitation across the brain.

Zhang et al. (2014) showed this switch is dose-dependent & bidirectional:

• Low extracellular glycine → favors long-term NMDA depression → net inhibition + calmer brain

• Higher glycine → flips to long-term NMDA potentiation → strengthened excitatory synapses + heightened arousal

The same molecule that zonks one person out in 30 min leaves another staring at the ceiling at 2 AM with monkey brain, night sweats, & a heart rate that won’t drop below 75 bpm.

That’s the glycine paradox summed up. And where you fall on that spectrum comes down to four predisposing factors.

The Four Factors Behind the Paradox

1. Impaired Cellular Energy Metabolism (The Master Variable)

GABA & glycine normally inhibit neurons by opening chloride channels allowing chloride ions to flow in and create a calming negative charge. But this requires low intracellular chloride levels maintained by the KCC2 transporter.

KCC2 relies on a potassium gradient generated by the Na⁺/K⁺-ATPase pump, which consumes ATP to function properly. When ATP levels drop due to factors like B-vitamin deficiencies, thyroid/mitochondrial issues, or insulin resistance, the pump fails leading to chloride buildup inside neurons.

Opening the channels causes chloride to flow outward depolarizing the cell and flipping glycine (and potentially GABA) from inhibitory to excitatory.

This is why both creatine (increased phosphocreatine stores) & niacinamide (a direct NAD+ booster) can rescue glycine intolerance: it restores ATP → rebuilds the chloride gradient → flips the switch back to calm.

2. Elevated Glutamate Tone / GABA-Glutamate Imbalance

NMDA receptors need both glutamate and glycine to fire. If your glutamate tone is already elevated (anxiety, MSG in hyperpalatable foods, glutamine supps, neuroinflammation), glycine simply completes the circuit unbalancing your inhibitory-to-excitatory signaling.

Glutamine converts to glutamate in the brain via glutaminase. It’s a great tool for fortifying the gut barrier (especially for the elite athletes here), but it can easily be a hidden trigger. More on that later.

3. Genetic & Epigenetic Vulnerabilities

For those who’ve done genetic testing, certain variants tilt the scales toward excitation:

• GLRA1/GLRB: Weaker inhibitory glycine receptors.

• GlyT1/GlyT2: Slower glycine clearance, prolonging NMDA exposure.

• MTHFR: Impaired methylation and ATP production; glycine itself feeds into this loop.

• GAD1/GAD2: Poor glutamate-to-GABA conversion, especially with low B6.

4. Environmental & Lifestyle Factors

If your system is already wired for excitation (poor daylight exposure + bright evenings via blue heavy LEDs/screens + excessive nnEMF), bringing glycine into the picture floods NMDA sites & furthers excitatory signaling.

The Protocol: Ranked by Priority & ROI

The interventions below are ordered by mechanistic importance and expected return on investment. Start at the top and work down. Most will resolve the issue within the first three tiers.

Tier 1 — Immediate

1a. Reduce Dose & Adjust Timing

Drop from 3 g → 500 mg & titrate up by 500 mg increments every 3–5 days. Take glycine after dinner (2–3 hours before bed) rather than at bedtime giving time for the initial NMDA-mediated cortical arousal to subside.

Dose: Start at 500 mg, 2–3 hrs before bed. Titrate to tolerance. If 1 g still produces insomnia, move to intervention 1b.

1b. Switch Magnesium Form Away from Glycinate

Replace magnesium glycinate with a non-glycine form for your nighttime dose. Reserve glycinate for daytime if desired.

Forms (ranked):
➜ Magnesium acetyl-taurinate (200–400 mg Mg; taurine adds GABAergic support)
➜ Magnesium L-threonate (200 mg Mg; crosses BBB, supports synaptic Mg²⁺)
➜ Magnesium chloride (200–400 mg Mg; well-absorbed, no excitatory amino acids).

1c. Swap Isolated Glycine for Collagen Peptides

Thomas et al. (2023) showed that 15 g collagen peptides (providing ~3.5 g glycine) reduced nighttime awakenings by 27% without the core temperature changes seen with pure glycine.

Dose: 10–15 g collagen peptides (hydrolyzed, grass-fed bovine or wild-caught marine), 1 hr before bed, dissolved in liquid without food.

Tier 2 — Foundational (Weeks 1-4)

2a. Restore Cellular Energy Metabolism via B Vitamins + Creatine

Han et al. (2025) noted that subclinical deficiencies in B1, B2, B3, B6, folate, & B12 compromise neuronal energy metabolism and neurotransmitter synthesis sufficiently to produce insomnia, anxiety, and cognitive dysfunction.

Priority B vitamins:
➜ B3 (Niacinamide): 500 mg at bedtime.
➜ B1 (Thiamine): 100–300 mg benfotiamine or thiamine HCl. Rate-limiting for Krebs cycle.
➜ B2 (Riboflavin): 25–50 mg riboflavin-5'-phosphate. Supports electron transport chain.
➜ B6 (P5P): 25–50 mg. Cofactor for GAD enzyme (glutamate → GABA).
➜ B12: 500—750 mcg methylcobalamin or hydroxocobalamin. Check serum B12 on next bloods.
➜ B9 (5-MTHF): 400–800 mcg. Supports methylation.
➜ B7 (Biotin): 150 µg for first 100 g protein + every additional 50 g protein requires an extra 35 µg biotin.
Track intake via Cronometer, Microgram or any micronutrient tracking app.

2b. Optimize Electrolytes (Sodium, Potassium, Magnesium, Calcium)

Target a sodium-to-potassium ratio of ~1:2–3 by intake. The sad story of SAD (Standard American Diets) is inverted (high sodium + low potassium = cardiovascular issues).

Targets:
➜ Potassium: 3,500–6,000 mg/day (primarily from food)
➜ Sodium: 1,500–2,500 mg/day
➜ Magnesium: 800–1,200 mg/day (food + supplement, non-glycinate form at night)
➜ Calcium: 1,000—1,200 mg/day (food preferred)

2c. Eliminate Glutamine Supplementation & Reduce Dietary Glutamate

If you are supplementing L-glutamine for gut related use cases, trial a 2–4 week washout & assess sleep quality changes. Eliminate all hyperpalatable foods high in added glutamate.

Action: Discontinue L-glutamine. Or at least, prioritize around breakfast. Minimize MSG & hydrolyzed protein sources. Reassess after 2–4 weeks.

Tier 3 — Diagnostic + Environmental

3a. Order Targeted Bloodwork

Test. Don’t guess.

Priority labs on next bloodwork:
➜ Serum B12 + methylmalonic acid (functional B12 status)
➜ Full thyroid panel: TSH, free T3, free T4, reverse T3, TPO antibodies (thyroid dysfunction = impaired ATP)
➜ Fasting insulin + glucose (poor insulin sensitivity = impaired neuronal energy)
➜ Homocysteine (elevated = impaired methylation, B12/folate/B6 functional status)
➜ RBC magnesium (serum Mg is unreliable; RBC reflects intracellular stores)
➜ Serum ferritin (iron is cofactor for SHMT enzyme interconverting glycine)

Optional (if above is unrevealing):
➜ Organic acids test (OAT): screens for B vitamin functional deficiencies, mitochondrial dysfunction
➜ MTHFR / COMT / GAD1 genotyping: leverage if there's a pattern of paradoxical supplement responses

3b. Light & EMF Hygiene

Blue-light blockers post-sunset, dimming lights to <50 lux in the evening (incandescents), and minimizing social media time/digital exposure 45—60 min before bed can significantly reduce the excitatory load that glycine is being added on top of.

Actions:
➜ Blue-light blockers (red ones) after sunset
➜ Dim ambient light to <50 lux after 8 PM
➜ Device-free wind-down period 45—60 min before bed
➜ Kill nnEMF sources (phone/router)

Tier 4 — GABAergic Support (Add as Needed)

4a. Add GABAergic Compounds to Counterbalance NMDA Activity

Evidence-based GABAergic agents (ranked by strength of evidence):

Amino acids & related compounds:
➜ Taurine (3–5 g): Activates GABA-A & glycine receptors. Calms neural excitability without binding NMDA.
➜ L-Theanine (400–800 mg): Upregulates brain GABA. Structurally similar to glutamate so competitively inhibits glutamate binding at AMPA receptors.
➜ Myo-inositol (2–4 g): Involved in GABA-A receptor function via phosphoinositide signaling. Evidence for anxiolytic & sleep-promoting effects at higher doses.

Herbal GABAergics:
➜ Lemon balm (300–600 mg extract): Inhibits GABA-transaminase (the enzyme that degrades GABA) raising synaptic GABA levels. Reduced insomnia by 42% as standalone in one trial.
➜ Passionflower (250–500 mg extract): GABA-A positive allosteric modulator via chrysin and other flavonoids. Comparable to oxazepam (30 mg) for generalized anxiety in one RCT.
➜ Valerian root (300–600 mg extract): Contains valerenic acid, a GABA-A positive modulator.
➜ Chamomile (200–400 mg extract): Apigenin binds GABA-A benzodiazepine site with moderate affinity.
➜ Magnolia bark (200–400 mg): Contains honokiol & magnolol, potent GABA-A positive allosteric modulators with anxiolytic & sedative properties.
➜ Lavender/Bergamot (aromatherapy): Modulates voltage-dependent calcium channels and GABA-A receptors.
➜ Baikal Skullcap (250–500 mg): Baicalein & baicalin compounds modify the GABA-A receptors

Glycine Insomnia: Step-Through Protocol

SUMMARIZED

Alright that’s a wrap for this week. Sleep deeply.

Your friend,
Phys

Brooke opens up the presentation with a quote from a name that may look familiar.

Five years prior in 2013, Brooke co-founded Intervene Immune alongside Greg Fahy, a cryobiologist and the leading researcher of what’s become the now popular TRIIM Trial (Thymus Regeneration, Immunorestoration, and Insulin Mitigation).

As we await the results of this trial, the strongest evidence we’ve seen yet supporting the thymic-longevity thesis just landed in Nature.

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What We Used to Believe

The way the medical textbooks are written makes it appear pretty straightforward. The thymus was a childhood organ. It matured T cells. It built the immune arsenal. Then it shrank into an inconsequential lump of fat by midlife.

It was the accepted view for decades. Until 2023, when researchers at Massachusetts General Hospital published a huge finding: adults who had their thymus surgically removed had significantly higher rates of death, cancer, & autoimmune disease.

The Study

Researchers from Harvard, Maastricht University, & Aarhus University analyzed over 27k adults across two major prospective cohorts: the National Lung Screening Trial (NLST, n = 25,031) & the Framingham Heart Study (FHS, n = 2,581).

They built a deep learning system trained on thousands of CT scans to score “thymic health” quantifying how much functional thymic tissue remained versus fatty degeneration. Then they tracked outcomes over 12 years.

The Findings

1. High thymic health = dramatically lower mortality.

In the NLST, those with the highest thymic health scores had an ~50% reduction in risk of death from any cause compared to those with the lowest scores.

In the FHS, we get an even stronger effect. High thymic health was associated with a 76% lower risk of all-cause death.

Each step up in thymic health also corresponded to progressively lower mortality.

2. Lower cancer incidence and cancer-specific mortality.

Individuals with high thymic health were 36% less likely to develop lung cancer.

The high thymic health subjects also had ~50% less likely to die from it.

As the thymus involutes, two things happen simultaneously:

1. Naïve T cell output drops constricting the T cell receptor (TCR) arsenal. Fewer unique T cells = less defense to recognize novel tumor antigens. As we get older, age-related mutations produce tumor-specific neo-antigens and the naïve T cell pool fails to recognize them (Wang et al., 2020).

2. The involuted thymus shifts its output ratio toward regulatory T cells over effector T cells. More regulatory ones suppress anti-tumor immune responses. Senescent T cells upregulate PD-1 (programmed death 1) expression further enhancing the PD-1/PD-L1 axis that lets cancer cells evade destruction.

Palmer et al. (2018) predicted similarly: declining T cell output from thymic involution meant an age-related rise in cancer incidence. Across 25k+ people, they saw all forms of cancer mortality were significantly lower in the high thymic health group.

3. Cardiovascular disease risk dropped dramatically.

In the NLST, cardiovascular mortality was 63% lower in the high thymic health group.

In the FHS, it was 92% lower.

Subjects with high thymic health also had a 74% lower cumulative incidence of cardiovascular events like myocardial infarction, heart failure, & cerebral embolism.

Atherosclerosis is an immune-inflammatory disease so T cells are key to its progression:

Thymic output declines → the body compensates by cloning existing T cells rather than producing new ones → drives the accumulation of senescent T cells (shortened telomeres, restricted receptor diversity, & pro-inflammatory) → more pro-inflammatory cytokines → more destabilization of arterial plaques.

Thymic dysfunction also shifts the balance of T cell subsets meaning fewer defensive regulatory T cells & more pro-inflammatory Th1/Th17 cells.

4. The effect extended across most disease categories.

Beyond cancer & CVD, those with higher thymic health were less likely to die from:

• Pulmonary disease mortality: 61% lower for high thymic health

• Endocrine, metabolic, & nutritional disease mortality: 68% lower

• Digestive disease mortality (liver, gallbladder, pancreas): 54% lower

Thomas et al. (2020) showed that thymic involution has a dual-pathway model driving both immunosenescence (reduced immune competence) & inflammaging (chronic sterile inflammation).

T cells do more than fight infections. They recognize & eliminate senescent cells. So when thymic output drops, this clearance function fails, & the aging cell burden grows across every tissue.

5. Chronic inflammation and metabolic dysfunction tracked with thymic decay.

When researchers analyzed blood inflammatory proteins in the FHS, 16 of 68 tested proteins were negatively correlated with thymic health. The list included IL-6, IL-18, VEGFA, HGF, and several CXCL chemokines, which are all major drivers of systemic inflammation, atherosclerosis, & cancer progression.

The same trends held true for cardiometabolic markers. Higher HDL cholesterol was positively correlated with better thymic health. Triglycerides, fasting glucose, & blood pressure were all negatively associated.

Another reason to keep a close eye on the trig/HDL ratio over time.

It shouldn’t come as a surprise, but obesity accelerates thymic involution (especially visceral fat tissue):

More visceral fat (inflammatory “organ”) → increased chronic inflammation accelerates thymic decay → thymic decay reduces immune competence → allows aging cell accumulation → senescent cells produce more inflammation → cycle compounds with age.

Promising Thymus Regeneration Paths

In September 2023, ARPA-H announced funding for a dedicated Thymus Rejuvenation program.

But the private sector is moving faster as multiple startups are now directly targeting thymus regeneration:

Intervene Immune → Brooke & Fahy’s company is furthest along clinically. Their TRIIM-X trial uses personalized combos of growth hormone, DHEA, & metformin to regrow thymic tissue in adults using already-approved drugs. So far interim results look promising.

Thymmune → Engineering functional thymus tissue from stem cells building replacements rather than regenerating what’s left.

TECregen → Emerged with $12.6M in seed funding to selectively regenerate thymic tissue using ligand engineering without the systemic toxicity that’s plagued growth factor approaches.

Tolerance Bio → $20.2M funded. Targeting immune tolerance through the thymus. Focused on autoimmune disease rather than pure regeneration.

Repair Biotechnologies → Developing gene & protein therapies to reverse thymic atrophy directly.

Where We Go From Here

An obvious question remains: “What can we do about it now?”

First, bioindividuality will remain key in the advancement of the therapeutic efforts moving forward. One of the best voices in our space summarized this:

And Dr. Bakri isn’t the only one paying attention:

We’ve had decades of asking why cancer patients fail immunotherapy, while the better question may have been whether their immune system was ever equipped for the fight to begin with.

Expect at least 1-2 regeneration protocols developed in 2026. As always, we’ll stay tuned & continue our research efforts on what promising regeneration protocols might look like in the future. More to come.

See you guys next week,
Phys

The one you’ll find in 90%+ of supplements on the shelf/Amazon is ubiquinone (marketed as CoQ10).

Ubiquinol is the reduced form. The type your cells use to scavenge free radicals, stabilize membranes, & protect LDL particles from the oxidation.

Now we have finally have a pair of studies released this month showing the efficacy (& superiority) of ubiquinol like we’ve never seen before.

Contents:

• The Study

• Findings

• The Bioavailability Gap

• How Ubiquinol Works

• Ubiquinol’s Cardiometabolic Benefits

• Practical Takeaways

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The Study

Researchers in Bangkok published a pilot RCT looking at what happens when you give adults 100 mg/day of ubiquinol for 12 weeks and studied the shifts in oxLDL as the primary outcome.

Study Snapshot

Who were the subjects?

• 20 Thai adults with prediabetes (fasting blood glucose = 100–125 mg/dL) → chosen for a distressed CoQ10 system & upstream mitochondrial dysfunction

• Ages 18–60

What did researchers study?

Using a randomized, double-blind, placebo-controlled design:

• Ubiquinol group (n = 10): 100 mg/day ubiquinol (≥ 96%) in MCT oil

• Placebo group (n = 10): Identical capsule with MCT oil only

• Duration: 12 weeks

• One capsule daily after first meal

What was measured?

• Plasma oxLDL at baseline & week 12

• Fasting glucose, liver enzymes, kidney function, CBC

Findings

Ubiquinol significantly reduced oxLDL within the treatment group.

The ubiquinol group saw oxLDL drop from 53.16 to 50.16 U/L over 12 weeks (p = 0.049). The placebo group showed no significant change (51.65 → 49.28, p = 0.237).

Why oxLDL?

LDL-C alone isn’t an efficient screening test for heart disease.

Oxidized LDL (oxLDL) is what happens when a normal LDL particle undergoes harm by reactive oxygen species.

The mechanism: LDL gets oxidized → becomes pro-inflammatory & pro-atherogenic → penetrates the arterial wall → gets engulfed by macrophages → forms foam cells → initiates plaque buildup

LDL-C tells you how much cholesterol is circulating. oxLDL tells you how much of it has already been damaged and is actively contributing to arterial injury.

The Bioavailability Gap

In the same week, we got pharmacokinetic proof ubiquinol is superior to ubiquinone.

A randomized, double-blind crossover study (Mei et al., 2026) published in March 2026 compared the two forms head-to-head in 12 healthy adults aged 45–65.

Each subject got a single equivalent dose of both formulations (240 mg), separated by a 14-day washout. Plasma CoQ10 was tracked for 48 hours.

The results:

• Peak plasma concentration (Cmax): ubiquinol was 2.2x higher than ubiquinone

• Total plasma exposure over time (AUC₀₋ₜ): ubiquinol was 2.0x higher

• Total systemic exposure extrapolated to infinity (AUC₀₋∞): ubiquinol was 3.4x higher

That final number matters most for long-term supplementation. It represents total bioavailability or what reaches systemic circulation.

How Ubiquinol Works

Ubiquinol provides LDL protection via three pathways:

1. Direct radical scavenging: Donates hydrogen atoms to neutralize lipid peroxyl & alkoxyl radicals. This interrupts the chain reaction of lipid peroxidation — the process converting normal LDL into oxLDL.

2. Antioxidant recycling: Regenerates other lipid-soluble antioxidants like vitamin E. This amplifies the total antioxidant capacity beyond what ubiquinol alone provides.

3. Mitochondrial stabilization: Ubiquinol is embedded in the electron transport chain. When mitochondrial function is preserved, less reactive oxygen species leak out. Less ROS = less LDL oxidation upstream.

Ubiquinol’s Broader Cardiometabolic Benefits

Some more of what the data supports:

Endothelial Function

A randomized, double-blind trial (Sabbatinelli et al., 2020) gave dyslipidemic adults 100 & 200 mg/day of ubiquinol for 8 weeks. Both doses significantly improved flow-mediated dilation, a direct measure of how well your blood vessels dilate & constrict.

Blood Pressure

A meta-analysis of 45 RCTs (Karimi et al., 2025) found that CoQ10 significantly reduced systolic blood pressure –3.5 mmHg on average.

Glycemic Control

A newly released double-blind, placebo-controlled trial (Palakornkitti et al., 2026) showed 20 adults given 100 mg/day ubiquinol for 12 weeks significantly improved insulin sensitivity.

Cardiovascular Mortality

The KiSel-10 trial (Alehagen et al., 2013), a five-year placebo-controlled study of 440 elderly adults, combined 200 mg CoQ10 with 200 µg selenium daily. The treatment group had a ~50% relative reduction in cardiovascular mortality vs. placebo (5.9% vs. 12.6%).

Heart Failure

The Q-SYMBIO trial (Mortensen et al. 2014) demonstrated that 420 patients in a 2-year trial given 300 mg CoQ10 daily reduced cardiac and all-cause mortality by 44% & 42%, respectively.

Antioxidant Capacity

A randomized, double-blinded, placebo-controlled trial (Ho et al., 2020) gave 31 healthy college athletes 300 mg of ubiquinone/day for 12 weeks. The treatment group had improved insulin sensitivity and increased total antioxidant capacity.

Statin-Induced CoQ10 Depletion

***CoQ10 is especially important if you’re running a statin*** (topic for another time)

Statins inhibit HMG-CoA reductase — the same pathway that produces CoQ10. Inhibit this enzyme and you start to deplete CoQ10 levels and impair mitochondrial energy production in muscles and the heart.

We have a few clear cases where CoQ10 taken adjacent to statins showed strong benefits:

1. Caso et al. (2007): 100 mg/day of CoQ10 across 32 hyperlipidemic patients for 30 days significantly reduced muscle pain by 40%, compared to Vit E alone, in patients treated with statins.

   

2. Fedacko et al. (2013): 60 patients supplementing with CoQ10 at 200 mg/day for three months significantly improved muscle pain & weakness in patients with statin-associated myopathy.

3. Skarlovnik et al. (2014): CoQ10 at 100 mg/day for 30 days significantly reduced statin-related muscle symptoms in ~75% of patients.

Practical Takeaways

1. If you’re taking CoQ10, check the form.

Ubiquinone/CoQ10 (the oxidized form) is cheaper & more common, but ubiquinol (the reduced form) has superior bioavailability & higher plasma concentrations after ingesting. If you’re over 40 or if you have any degree of metabolic dysfunction, your ability to convert ubiquinone → ubiquinol declines. Opt for ubiquinol.

2. Start at 100 mg/day.

Depending on cardiometabolic condition & antioxidant status, most will find 100–300 mg/day sufficient. If taking 200+ mg/day, split into two doses (morning + afternoon).

3. Always take it with fat. Morning or lunch is ideal.

Highest ROI lever. CoQ10 is fat-soluble and requires dietary fats for absorption. Without fat, bioavailability drops by ~75%. Take it with eggs, avocado, Brazil nuts, EVOO, or fatty fish (i.e. wild salmon, sardines). Morning or early afternoon is preferred because CoQ10 supports ATP production and some people have mild energizing effects that can interfere with sleep if taken late. Peak plasma concentration hits 6–8 hours post-dose, so morning intake aligns peak levels with daytime energy demand.

4. If you’re on a statin, ubiquinol is essential.

100–200 mg/day of ubiquinol taken at the opposite end of the day from your statin (morning vs. evening or vice versa) helps restore what the drug strips out. The objective is to mitigate its collateral damage on the mitochondria.

5. oxLDL deserves a spot on your biomarker radar.

oxLDL provides a better indicator on CV risk than LDL-C alone. Well worth the addition especially if older or you have some level of mitochondrial dysfunction you want to investigate.

6. Amplify ubiquinol’s effects.

Two synergistic micronutrients to pair with:

➜ Selenium (200 µg/day) is the cofactor for thioredoxin reductase, which is the enzyme that recycles oxidized CoQ10 back into active ubiquinol. Without adequate selenium, your body can’t efficiently reactivate the CoQ10 you’re supplementing.

➜ Vitamin E (200–400 IU mixed) forms a synergistic antioxidant loop with ubiquinol in the lipid membrane. Vitamin E handles initial chain-breaking during lipid peroxidation. Ubiquinol regenerates it back to its active form.

Aim to fulfill these needs through a food first approach (i.e. sardines, wild salmon, pasture-raised eggs, mackerel).

Ubiquinol sits at the intersection of three crucial cardiometabolic areas:

1. the oxidative state of lipoproteins,

2. the efficiency of mitochondrial antioxidant systems,

3. the ATP generation of high-energy tissues like cardiac/skeletal muscles.

If elite cardiometabolic health is in your set of long-term health objectives, ubiquinol may be worth a look.

Stay after it,
Phys

Cook your carbs, chill them overnight, and a sizeable fraction of their starch recrystallizes into a structure your digestive enzymes can’t break down. Instead, it travels to your gut feeding beneficial bacteria with metabolic benefits: enhanced insulin response, reduced visceral fat, & better liver markers.

It’s a simple combo: A fridge and a little bit of patience.

Contents:

• What Happens When Starch Retrogrades

• The Birth of Resistant Starch Type 3 (RS3)

• The Metabolic Outcomes

• Retrogradation Protocol

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What Happens When Starch Retrogrades

Raw starch is made of two polymers: amylose (linear chains) and amylopectin (branched chains). Cooking breaks apart these crystalline structures through gelatinization: granules swell → organization collapses → the starch becomes accessible to digestive enzymes. This is why freshly cooked carbs produce steeper glucose spikes.

When gelatinized starch cools, the disaggregated polymers reassemble into new, partially ordered crystalline structures. They wrap into tight double helices, which are denser, more compact, and resistant to the enzymes that normally break starch into glucose. This reassembly is called retrogradation.

Two details that matter for application:

1. 24 hours at 40°F = minimum threshold. Amylose retrogrades rapidly within the first 12 hours. Amylopectin retrogrades more gradually over days. The full 24-hour chill maximizes resistant starch (RS3) yield across rice, spuds, & pasta.

2. Gentle reheating doesn’t undo it. Retrograded structures hold below ~265°F covering microwaving, stovetop warming, and standard oven/air fryer reheating. You can chill your rice overnight, warm it the next morning, & still retain the full metabolic advantage.

The Birth of Resistant Starch Type 3 (RS3)

Resistant starch exists in five forms. RS3 (retrograded starch) is the only type you can produce in your own kitchen from foods you already eat.

Once formed, RS3 behaves like dietary fiber. It passes through your stomach and small intestine intact arriving in your colon where trillions of bacteria ferment it into beneficial metabolites.

Sonia et al. (2015) showed that cooked white rice cooled at 4°C for 24 hours then reheated had a 158% increase in RS containing 1.65 g RS per 100 g vs. just 0.64 g without cooling.

One more lever worth knowing: multiple heat-cool cycles increase RS3 content further. Each round of retrogradation adds another layer of enzyme-resistant crystalline structure. Batch-cook Sunday → refrigerate → reheat portions through the week = the carbs get more metabolically favorable with each cycle.

The Metabolic Outcomes

Weight Loss & Visceral Fat Reduction

Li et al. (2024) gave 37 overweight participants received 40 g/day of resistant starch (or a placebo) alongside isoenergetic balanced diets for 8 weeks.

The RS group lost an average of 6.2 lb and had significant reductions in visceral fat levels, total fat mass.

Pro-inflammatory markers (TNF-α & IL-1β) & liver enzymes (ALT/AST) also improved significantly.

How it works: RS intake → ↑ beneficial gut bacteria → altered bile acid profiles + reduced intestinal inflammation + inhibited lipid absorption → weight loss/metabolic optimization

Blood Sugar Control Across Populations

Strozyk et al. (2022) tested cooled rice (39°F for 24 hours, then reheated) against freshly cooked rice in 32 patients with type 1 diabetes. The area under the glycemic curve dropped by 60% with the cooled rice meal and peak glucose increase fell from 70 → 49 mg/dL.

Gut Health & the Butyrate Connection

When RS3 reaches the colon, resident bacteria ferment it into short-chain fatty acids (SCFAs) → primarily butyrate, along with acetate & propionate. Each plays a distinct role:

1. Butyrate = the preferred energy substrate for colonocytes (the cells lining your colon) maintaining gut barrier integrity & reducing intestinal permeability.

2. Propionate = regulates lipid metabolism in the liver.

3. Acetate = enters systemic circulation and influences appetite signaling & fat oxidation.

Resistant starch also stimulates the release of GLP-1 & PYY by SCFA binding to fatty-acid receptors on colonocytes. GLP-1 enhances insulin sensitivity and slows gastric emptying. PYY suppresses appetite.

Retrogradation Protocol

The 3 Rules

Rule 1: Cook fully, then cool for a minimum of 24 hours at 39°F (standard refrigerator temperature). Amylose retrogrades rapidly in the first 12 hours, but 24 hours at 39°F produces the highest RS3 yields across rice, potato, & pasta.

Rule 2: You can reheat gently, but stay below 130°C. Standard microwave reheating, stovetop warming, & oven temperatures up to about 130°C preserve retrograded RS3 structures.

Rule 3: Batch-cook & cycle. If you’re ambitious, multiple cook-cool cycles increase RS3 content with each round. So if you cook a large batch on Sunday, refrigerate, & reheat portions through the week, each cooling cycle reforms additional crystalline structures that resist digestion.

A Simple Meal-Prep System

Sunday Meal Prep Day: Cook a large batch of sweet/white potatoes (boiled/baked), rice, or pasta with your protein & seasonal vegetable source. Let your carb sources cool to room temp (~30 minutes), then transfer to glass containers & refrigerate (38-40°F).

What Covers My Monday–Thursday Meals:

• Breakfast: Overnight oats (naturally retrograded) with whey, fruit (berries, apple, banana), peanut butter powder, Ceylon cinnamon

• Lunch: Salad/slop bowl of your choice with protein source (90/10 grass-fed beef, chicken thighs/breasts, albacore tuna), cooked & cooled potatoes, veggie sources, EVOO + apple cider vinegar dressing

• Dinner: Protein source (wild-caught salmon/cod/shrimp, 90/10 grass-fed beef, chicken thighs/breasts), cooked & cooled rice (can reheat for 2 minutes) with cooked seasonal vegetables (brussels sprouts, broccoli, squash), splash of apple cider vinegar

Two Multipliers Worth Adding

Two simple additions to multiply the retrograded starch effect.

Vinegar

Leeman et al. (2005) tested four potato meal combinations in 13 healthy subjects. Cold-stored potatoes alone reduced the glycemic index by 26% vs. freshly boiled. When served with olive oil & white vinegar, they reduced glycemic index (GI) by 43%.

Östman et al. (2005) showed vinegar added to a bread meal reduced the GI by 36% and increased subjective satiety scores.

This works through acetic acid delaying gastric emptying → slowing the rate of food leaving your stomach → flattening the glucose curve further.

Practical dose: 1–2 tablespoons of vinegar (apple cider or white wine) per carb-dense meal. As a dressing or mixed into the dish.

Fiber

Soluble & insoluble fiber alongside retrograded starch further slows digestion. When a preceding meal is rich in dietary fiber, the glycemic response to the next starchy meal is also lower.

Practical dose: Pair retrograded starches with non-starchy vegetables. An additional lever = adding 1—2 tbsp psyllium husk fiber before meals.

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The food you eat and the structure it arrives in are two different variables. Retrogradation lets you optimize the second without changing the first.

Same rice. Same oats. Same potato. Same pasta. Much different metabolic outcome.

About as high efficiency as a metabolic “hack” gets. Use wisely, friends.

We’ll see you guys next week,
Phys

When a cell becomes senescent, it stops dividing. Normal. But the issue arises when they start to release excess pro-inflammatory molecules damaging surrounding & otherwise well-functioning cells. This is the senescence-associated secretory phenotype: SASP.

Last week, a team of researchers at the University of Alberta released the most-comprehensive systematic review & meta-analysis connecting the dots between this process and a molecule many still overlook (and what we called the new creatine in 2025).

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The Study

Wang et al. (2026) at the Mazankowski Alberta Heart Institute ran two parallel analyses.

First: 27 clinical trials across 1,030 participants measured how taurine impacted metabolic, inflammatory, cardiovascular, & cognitive markers. All mapped onto pathological features of accelerated aging.

Second: 6 studies tracking plasma taurine levels in people recovering from COVID-19 compared full recoveries to those who developed long COVID (PASC). Since the SARS-CoV-2 infection triggers accelerated cellular senescence, this enables the long COVID population as one of the best models of inflammaging we have.

Study Snapshot

Who was included?

• 27 clinical trials, 1,030 participants

• Populations: T2 diabetes, obesity, heart failure, hypertension, liver disease, dementia, psychosis

• Median taurine dose: 3,000 mg/day (range: 1,000 – 6,000 mg/day)

• Median treatment duration: 8 weeks (range: 1 – 16 weeks)

What outcomes were measured?

1. Glycemic control (HbA1c, fasting glucose, insulin, HOMA-IR)

2. Lipid panel (triglycerides, LDL, HDL, total cholesterol)

3. Inflammatory markers (CRP, TNF-α, IL-6, IL-10)

4. Oxidative stress (malondialdehyde)

5. Cardiovascular metrics (blood pressure, heart rate, aerobic capacity)

6. Cognition

The Findings

1. Taurine improved nearly every metabolic marker

Across pooled analyses, taurine significantly improved glycemic control & lipid profiles. Here’s what the data showed:

• HbA1c: reduced by ~0.2–0.3% (10 studies)

• Fasting blood glucose: reduced by ~8–15 mg/dL (8 studies)

• Fasting insulin: reduced by ~1.5–2.5 μIU/mL (7 studies)

• HOMA-IR: reduced by ~0.5–1.0 points (7 studies)

• Total cholesterol: reduced by ~10–20 mg/dL (12 studies)

• Triglycerides: reduced by ~15–30 mg/dL (12 studies)

• LDL-C: reduced by ~5–12 mg/dL (8 studies)

2. Taurine crushed inflammatory markers dose-dependently

• CRP dropped significantly across 7 studies — estimated reduction of ~1–2 mg/L

• TNF-α dropped significantly across 6 studies

• IL-6 trended down across 6 studies

• Malondialdehyde (oxidative damage biomarker) also dropped significantly across 6 studies

A dose-response relationship with TNF-α and IL-6 was also present. More taurine → greater reduction in inflammatory cytokines.

For inflammation specifically, 3,000 mg/day appeared to be the sweet spot balancing clinical efficacy with gut tolerability.

3. Blood pressure dropped. Exercise capacity went up.

Taurine lowered both systolic blood pressure by ~5–7 mmHg & diastolic by ~3–5 mmHg across 9 studies. And across the 3 studies measuring aerobic capacity, there was a clinically meaningful improvement.

4. Long COVID patients had significantly lower taurine

People with persistent long COVID had lower plasma taurine levels compared to those who recovered fully.

Lower taurine = less capacity to manage the inflammatory and oxidative burden driving the condition.

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Why This Extends Beyond Long COVID

The implications of this go far beyond long COVID or even infections generally. The pathways taurine targets (NF-κB suppression, NLRP3 inflammasome deactivation, mitochondrial stabilization, p53-p21 senescence signaling) drive mitochondrial dysfunction, cardiovascular decline, & neurodegeneration.

Here’s the mechanistic loop:

Taurine ↓ → Reduced anti-inflammatory & antioxidant capacity → Chronic NF-κB activation → SASP amplification → More taurine consumed at inflammation sites → Greater depletion → Accelerated aging

Singh et al. (2023) already established taurine deficiency as a driver of aging across species.

Now, this recent meta-analysis shows that replenishing taurine reverses the downstream markers of that deficiency in humans.

Practical Takeaways

1. Dose by objective

The meta-regression data and individual trial designs allow us to be more specific than a simple “take 3 grams.” Here’s how the dosing breaks down by goal:

Metabolic Optimization

3,000 mg/day for 8–16 weeks. This was the dose used in the majority of the diabetes and obesity trials (Moludi 2022, Maleki 2020, Esmaeili 2020, Haidari 2020). All of which showed significant improvements in glycemic & lipid markers.

Chronic Inflammation & Elevated Oxidative Stress

3,000–6,000 mg/day. The meta-regression showed a dose-response curve for TNF-α and IL-6 meaning benefits increased with dose.

Blood Pressure

1,500–2,000 mg/day is sufficient. The Sun et al. (2016) prehypertension trial used 1,600 mg/day for 12 weeks and showed significant reductions in both the systolic (—7.2 mmHg) & diastolic (—4.7 mmHg) blood pressures.

Cardiovascular / Aerobic Capacity

1,500 mg/day for a minimum of 2 weeks. The heart failure trials (Ahmadian 2017 & Beyranvand 2011) used this dose and showed improvements in functional capacity and cardiac output.

Start at 1,000 mg/day & titrate up over 1–2 weeks.

Nootropics Depot Taurine Powder is my go-to. A third-party tested, pure powder form. At 3,000 mg/day, it works out to 165 days of supply for ~$23 ($0.14/day). What ends up being the best cost-per-outcome ratios in the supplement space.

2. Food first

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3. Split doses on empty stomach

Best taken on an empty stomach, split across 2 dosages with the final dose 30–60 minutes before sleep. The short half-life and renal saturation kinetics make split dosing quantitatively superior to a bolus.

4. Who benefits most

• Chronic low-grade inflammation (metabolic disease, high visceral obesity, type 2 diabetes)

• Post-infectious states

• Aging adults with declining cardiovascular and/or metabolic markers

• Diets low in wild-caught seafood/dark meat

The conventional view of aging is dominated by genes, telomeres, & time. But we’re getting more evidence pointing to the need for certain molecules to manage inflammatory states, protect mitochondria/ATP production, & suppress the senescent cascade.

Taurine is certainly becoming one of them.

This isn’t the first time we spoke of it and we doubt it’ll be the last.

Your friend,
Phys

You think face-down is enough.
You think off your desk is enough.
You think do not disturb is enough.

Nope.

Here’s why you’re not all you could be with your phone in the room.

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The Brain Drain Effect

Researchers at the University of California had people complete tasks measuring working memory & fluid intelligence (solving novel problems). They randomly assigned them to keep their phones in one of three locations: on the desk, in their pocket/bag, or in another room entirely.

Those with phones on their desks performed significantly worse than those whose phones were in another room. But the most interesting part…the phones weren’t even powered on.

Yet cognitive capacity still dropped.

The effects showed up on both memory test & reaction time measures. These were significant impairments in critical cognitive functions.

Why “Face-Down” Is A Myth

Your brain operates like computer RAM with limited cognitive resources. When your phone is close by, a portion of that RAM gets allocated to not thinking about it. This is the idea of attentional resource allocation.

It’s not conscious. You’re not sitting there actively resisting the urge to check 𝕏 or Instagram. But your brain’s executive control system is working in the background spinning to suppress the automatic attention response to a salient object in your environment.

The same suppression happening runs on cognitive horsepower. Resources that would otherwise be allocated for the actual task you’re working at.

Skowronek et al. (2023) confirmed this: people processed information 9% slower when phones were present versus absent.

It’s an invisible cognitive tax. Every moment your phone is within spitting distance, you accept operating at a diminished cognitive potential.

The Addiction Multiplier

This same effect even scales with phone dependency.

Those with higher levels of dependence had a much larger cognitive impairment from phone presence. If you’re someone who checks your phone more than 186 times per day (yep…that was the new average in 2025), the attention tax is even greater.

People in the top third of dependency scores showed significant performance hits even when their phones were in their pockets. Low-dependency users needed to keep the phone out of sight and that was enough. But high-dependency users needed complete spatial separation for restoring full cognitive capacity.

The digital cycle looks something like this: more phone dependence → higher likelihood your phone is present → greater cognitive degradation → more likely to use your phone as a cognitive crutch → more phone dependence.

Rinse & repeat.

Your phone has trained your brain to allocate cognitive fuel to monitor its status. Even unconsciously when it’s “off”.

Beyond Productivity: The Human Cost

Cognitive tests are one thing, but the effect extends beyond that to human connection.

Przybylski & Weinstein (2012) studied face-to-face conversations with smartphones present vs. absent again. When a phone was visible on the table, strangers who were asked to have meaningful conversations reported significantly lower relationship quality, less closeness, & less trust.

While the effect was present for casual conversations, it was even more pronounced when the topics were deemed meaningful.

The Simple Solution

In keeping with our theme, we’ll opt for the intelligently-designed system over any sheer willpower method. Each & every time.

A vote to abstain from the cheap dopaminergic source is a vote for a more focused you. A more powerful cognition built to last decades.

The solution is simple, but not easy (at least at first to break the dependency): reduce the friction to focus & increase the friction to distraction.

If you can sit with momentary boredom or uncertainty without reaching for stimulation (a subtle sign of elite health), you've built the cognitive capacity modernity systematically erodes.

Defeat the distraction epidemic one microhabit (microvictory) at a time.

You don’t “lock in”.
You don’t magically become focused.

You train to become focused like you would for building aerobic capacity or strength. Through progressive adaptive overload & environmental design.

For more on developing the top 1% focus, check out the below where we built a system that’s working for many:

Train your focus like your future depends upon on it. Because it does.

Dial in,
Phys

But most don’t know the story of Dr. Brown-Séquard. It turns out exploring health through self-experimentation is nothing new. Just forgotten about.

Here’s the story of the “ballsy” scientist who had thousands of physicians worldwide injecting the "Elixir of Life."

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The Legend of Brown-Séquard

Dr. Charles-Édouard Brown-Séquard wasn’t exactly a fringe biohacker with nothing to lose. Distinguished physiologist. Fellow of the Royal Society. Harvard Medical School professor. Like many in their old age, he watched his strength gradually diminish in his later years of life.

Throughout his life, Brown-Séquard hypothesized that testicles produce a sort of “dynamogenic power” that declines with age causing an old age weakness. In his 1869 lectures, he proposed injecting semen into the blood of elderly patients to restore vitality.

Then in May 1889 at age of 721, Brown-Séquard's own strength had deteriorated to the point he couldn't stand for more than 30 minutes without exhaustion. So he decided to test his theory. On himself.

Taking freshly removed testicles from dogs and guinea-pigs, he crushed them immediately after extraction and mixed the juice with blood from the testicular veins and semen.

On May 15th, he started self-administering subcutaneous injections of his solution. After the third one, Brown-Séquard experienced what he called a "radical change." Just one week prior, he was unable to stand for more than 30 minutes. Now, he was working on his feet for several hours at a time.

But it wasn’t just his energy he saw improve. Brown-Séquard reported an increase of 16 lb in forearm strength tested with a dynamometer matching his strength to that of 26 yrs prior. He even reported improvement in bowel movements & cognition.

Validation of His Findings

On June 1st, he presented his findings to the Société de Biologie in Paris, somewhat expecting to be dismissed as delusional.

Dr. Variot sat in the audience that day.

Acting independently, Variot administered similar injections to three elderly men himself using testicles from rabbits and guinea-pigs. He told his patients only that they were receiving “fortifying injections,” with no mention of the source or expected effects.

All three experienced nearly identical improvements to those Brown-Séquard observed in himself.

Then Variot conducted the control part of the experiment. He injected two other patients with pure water, however no strengthening effects occurred. When he subsequently gave these same patients the actual testicular extract, they experienced the same improvements.

The “Counterproof”

Five and a half weeks after his final injection, Brown-Séquard stopped treatment to observe how long effects would persist. For four weeks, he maintained his improved condition. Then, by July 3rd, he noticed a rapid return to his previous state of weakness.

This reversal, he noted, served as “excellent counterproof” of the treatment’s genuine effects.

Word Spreads

Three months post-experiment, press coverage spread to the US in the August edition of Scientific American Supplement2.

Frank Leslie’s Illustrated Newspaper3 published similar experiments conducted by former U.S. Army Surgeon-General William A. Hammond using testicular extracts :

“the result of the application to several old gentlemen has been to renew their vital energies to a noticeable extent, and to give them an invigoration that was sensibly felt.”

By the end of 1890, more than 12k physicians across the globe were injecting what came to be known as the “Elixir of Life”.

I don’t tell this story as a matter of convincing you animal nuts are just the revival we need in the longevity movement.

I say this as a reminder to balance two thoughts simultaneously in today’s health landscape:

1. Proceed with caution in what is the wild wild west of the peptide/research compound space today. (COAs & 99%+ purity always)

2. But if you’re waiting for an RCT on every potential intervention — expect to be late.

Stay wise. Stay dialed in. Stay after it.

Your friend,
Phys

Progressive overload.
Intelligent exercise selection.
Enough frequency to drive growth.

Today we cover exactly how to do that.

Contents:

• Anatomy of the Core

• 7 Core Training Principles

• Exercise Arsenal (Video Demonstrations)

• 3 Example Programs

Anatomy of the Core

First let’s get some definitions down to help us later on:

1. Rectus abdominis (the six-pack) runs vertically from sternum to pelvis and its primary action is spinal flexion.

2. Transverse abdominis (TVA) wraps around your torso like a natural weight belt and is responsible for the tight, drawn-in waistline look.

3. Obliques run diagonally along the sides handling rotation, lateral flexion, & bracing.

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The 7 Core Training Principles

1. Kitchen Reveals. Training Builds.

Two distinctly different functions. You can get lean enough to see your abs through diet alone, but if you haven’t built them with progressive resistance, you’ll end up having a pretty underwhelming core. The guys with abs that pop at 12% body fat are the ones hitting them hard in a hypercaloric/gaining state.

2. Thickness Is What Separates Good From Great

The difference between just visible abs and the 3D look is thickness. And thickness comes from the same place it comes from everywhere else on your body: adaptation via progressive overload. BW crunches and air bikes won’t build muscle any more than an air squat will build your quads or a band curl your bis.

3. Close the Gap: Spinal Flexion Over Hip Flexion

The most important mechanical principle about ab training. The true function of the abs is to shorten the distance between the pelvic basin and the sternum.

Full sit-ups & full leg raises aren’t primary ab movements since they shift the majority of the load to the hip flexors and psoas. It’s why we’ll prioritize exercises that isolate spinal flexion (curling the rib cage toward the pelvis) & pelvic tilting (curling the pelvis toward the rib cage).

Key point to remember: If you’re not “closing the gap” on each rep, you’re training your hip flexors, not your abs.

3. You Need Progressive Overload, They Need Weight to Grow

Weighted exercises like an ab machine or cable crunch with resistance produce significantly greater rectus abdominis activation compared to bodyweight-only movements.

To increase the size of the muscle, you need to progressively increase the stimulus. Add reps first. Once you hit the top of the rep range across all sets, add weight. Simple.

4. Train Them More Often Than You Think

The abdominals have a higher proportion of slow-twitch (Type I) muscle fibers —(~60%) and receive among the best blood supply of any muscle group in the body.

More slow-twitch fibers means less exercise-induced damage per session. Better blood supply means faster nutrient delivery, faster waste removal, & quicker recovery. They’re also relatively small muscles that function constantly as postural stabilizers.

All of this means the abs recover quickly and respond well to higher frequency training at 3—4x/week.

5. Genetics Determine Shape — Not Your Potential

Your ab shape (symmetrical, staggered, a six-pack or a four-pack) is genetically determined by the tendinous inscriptions of the rectus abdominis.

While most have three paired intersections, there’s bioindividual variation in thickness & depth through the muscle. Haque et al. (2015) found that 96% had three tendinous intersections (yielding a six-pack appearance), while a small minority had four or five.

Though you can’t control the offset & shape, you can control how thick, dense, & developed they become.

6. Abs Respond Fast (When Trained Properly)

Because of their fiber composition and blood supply, abs develop relatively quickly when you finally give them the right stimulus.

In The Wild Physique, Vince Gironda talks about the best abdominals he’d ever seen belonging to French-Canadian gym owner Leo Robert:

“he had chunky abdominal muscles from the bottom of his rib cage to well below the navel…perfectly aligned in three straight rows. He was the envy of every bodybuilder in his day.”

When Gironda himself finally committed to building his own core after neglecting it for years, he achieved “world-class abs in just six weeks.”

He swore by short, intense sessions with minimal rest. The abs don’t need much, but when you hit them with the right resistance & intensity, they’ll respond faster than almost any muscle on your body.

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The Exercise Arsenal

Here are the 6 best movements for building a 3D core:

1. Ab Crunch Machine (Top Pick)

Machines lock you into a fixed path, making it nearly impossible to cheat with momentum or hip flexors. If your gym has a front-pad loaded machine (pad against your chest), even better since it forces pure spinal flexion.

Execution:

• If chest padded — adjust the pad to chest height. Feet flat, grab handles lightly. Do NOT death-grip it and pull with your arms.

• Initiate by exhaling hard and curling your rib cage down toward your pelvis. Embrace “close the gap” between sternum & belly button.

• Squeeze hard at the bottom for 1–2 seconds. Return on a controlled eccentric.

Common Mistakes: Pulling with the arms, hinging at the hips instead of flexing the spine, going too heavy and losing the contraction.

Alternative: Cable crunch is the next best option (below).

2. Cable Crunch

Constant tension throughout the range of motion. Easy to progressively overload with small weight jumps.

Execution:

• Kneel in front of a high pulley with a rope attachment. Hold the rope at the sides of your head (not behind your neck).

• Keep your chest up. Flex your spine, curling rib cage toward pelvis. Hips stay stationary.

• Squeeze at the bottom, exhale fully, return under control.

Common Mistakes: Sitting back into the hips (turns it into hip flexion), pulling with arms, rounding at the neck instead of thoracic spine.

3. Hanging Leg Raise

Excellent for the lower portion of the rectus abdominis. The hanging position also decompresses the spine.

Execution:

• Hang from a pull-up bar, shoulder-width grip. Legs straight (or slightly bent for progression).

• Allow your lower back to round — you want posterior pelvic tilt.

• Drive knees up toward your chest, exhaling fully and forcefully as you curl up. Think about bringing your pelvis toward your rib cage.

• Control the descent. Don’t swing. Pause & hold the stretch feel at the bottom to kill momentum before the next rep.

Common Mistakes: Swinging wildly, keeping the lower back arched (shifts load to hip flexors), stopping at 90° (leaves most of the ab work on the table).

Progression: Straight legs → weighted (dumbbell between feet) → toes to bar.

4. Ab Wheel Rollout

Anti-extension movement that hammers the entire rectus abdominis and TVA under serious eccentric loading. One of the best versatile movements you can do at home. You don’t need anything fancy — $14 on Amazon.

Execution:

• Kneel on a pad, grip the ab wheel directly under your shoulders.

• Brace hard. Tuck pelvis slightly (posterior pelvic tilt).

• Roll forward slowly, extend arms overhead while keeping your core tight.

• Go as far as you can control without hips sagging, then pull back by flexing your abs (not yanking with arms).

Common Mistakes: Letting the lower back hyperextend, using hip flexion to pull back, going too far too soon.

Progression: Half rollouts → full from knees → standing rollouts (advanced).

5. Decline Reverse Crunch

Targets the lower abs with greater range of motion than a flat reverse crunch. Decline angle adds resistance via gravity.

Execution:

• Lie on a decline bench, head at top, hands gripping behind your head.

• Bring knees toward chest by curling your pelvis up off the bench — not just the legs.

• Squeeze at top, exhale fully, slowly lower. Keep constant tension — don’t let your lower back fully settle between reps.

• Add a dumbbell between feet to progress.

Common Mistakes: Using momentum to swing legs, only moving legs without lifting pelvis, going too fast.

6. Stomach Vacuum

Targets the transverse abdominis — the deep stabilizer that cinches your waist tight. Golden-era bodybuilders swore by this for a narrow, controlled midsection.

Execution:

• Stand upright, exhale all air from your lungs.

• Draw your belly button in toward your spine as hard as possible — imagine trying to touch your belly button to your backbone.

• Hold 15–30 seconds. Breathe shallowly through your chest if needed. Release and repeat.

• 2 different methods highlighted in the video below.

Three Protocols

In a gain phase, train abs 3–4x per week. In a cut phase, you can hit them 2—3x per week. Each session should take 10–15 minutes.

Progression strategy: Add reps first. Once you hit the top of the rep range (with elite form) across all sets, bump up the weight. It’s no different than progressing on other movements.

Time saving hacks: Get an ab wheel for at home use & conduct the stomach vacuums while working at a standing desk.

If there’s anything to take away here:

1. Stop treating your abs like they exist in a different physiological universe than the rest of your training. They need resistance. They need progressive overload. They need to be trained during a surplus when your body is best suited to build muscle.

2. Diet leans you out & reveals. Training properly builds. Do both & you’ll have an S-tier core.

Your friend,
Phys

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The age anxiety epidemic is real.

These kinds of posts now circulate on every social platform.

The reality here is simple: fixating on a problem on what you can’t control is a far worse psychological toxin than biological aging itself.

It’s dysregulation of your autonomic nervous system.
It’s disruption of your flow state.
It’s theft of your finite resources.

We need to go upstream to solve age neuroticism.

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Where Age Neuroticism Originates From

We’ve never lived in a safer, more abundant society in recorded human history. Crime is down. Opportunity has never been greater. Any knowledge that cost thousands in consulting fees even 5 years ago is now virtually free.

So it’s safe to conclude the anxiety is less about scarcity and more attributable to other factors.

Driver #1: Comparison-induced inadequacy

For hundreds of thousands of years, the social world was roughly 150 people. You knew where you stood.

Then 2004 happened.

The aperture opened from hundreds to millions overnight. And it got filled with people who look exactly like you. Someone your age, in your field, with similar starting conditions, with the same targets in life. But seemingly miles ahead.

Their highlight reel became your measuring stick.

Now your social media feed is an algorithmically optimized threat-generator designed to continuously capture your attention through fear. And it’s damn good at its job.

Driver #2: Time speeds up as you age

It’s true. Kind of.

Time perception accelerates with age but it’s environmental & behavioral. Good news is these patterns are malleable.

The brain encodes time through novelty. New experiences create dense memory traces. Familiar experiences create thin ones. When you look back on a period of rich novelty (like childhood), it feels long because it was full of new encoding.

Think about why ages 8–18 feel subjectively longer than 20–30 or 30–40. You were encountering everything for the first time. First time you learned to tie your shoes. First baseball tournament. First date. First time you got dumped. First job. First real failure. First real success. The decade felt like two.

Now consider your routine today.

Same working environment.
Same meals.
Same commute.
Same two hobbies.
Same people.
Same genre of books.

Every day rhymes with the last. The routine is the single greatest accelerator of perceived time there is.

If you accept “time goes faster as you get older” as an inert fact, your brain will stop looking for novelty. It’ll settle into the rhythm and the rhythm will rip decades away from you.

Driver #3: Once you have kids, life’s over

One worth naming outright because it operates quietly but it’s driving fertility rates in ways no one wants to discuss openly.

The fear is real. I know it because I’ve watched it in my own age group. It’s this private terror that parenthood represents the closing of a door. The end of freedom. The death of the self that existed before.

But I’ve never met a single person worth listening to with children who has expressed that sentiment after the fact. Not one. What I hear instead, almost universally, is some version of what I heard recently from a mentor: “What parenthood ends is the chapter, not the story. The fear of losing a version of yourself that hasn’t been fully realized exists. But the version that emerges on the other side tends to be more realized, not less.”

A Few Solutions

Solution #1: Frame shifts yield vibe shifts

My solution offered to the above post this past week.

Solution #2: Your story is your competitive advantage

Every moment in your life up to this point has molded you into who you are today. No time is “wasted.”

To figure out what you are, you have to figure out what you’re not. And figuring out what you’re not requires crossing bridges to places you never intended to go.

Years spent as a degenerate? Perfect. Write about them. Send the ladder down. People desperately want to know how someone dug themselves out of the same hole they’re currently in. Your failure synthesized into intelligence has an audience of thousands.

Punted a few biz opportunities? If you are a sentient human, you took something away from it. Now continue creating & redefining. Hold all else equal. Test again. Keep iterating. Life is a pattern recognition game. And it’s best played as a closed loop control system.

Invested years in the wrong relationship? You got more from that than a four-year degree in human psychology ever could have given you.

Come to view your past in peace. Recognize that without these experiences, the path forward doesn’t exist in the ideal form.

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Solution #3: Log off & go upstream before you react

Social media has made 30 feel like a deadline. Hustle culture made 40 the new 30, and then AI anxiety made 12 months feel like a window that’s already closing.

*points to Charlie Munger’s most useful heuristic* → “Show me the incentive, I’ll show you the outcome”

Apply this to every piece of age-anxiety content you encounter. Before you internalize it, ask:

• Would this source have anything to gain by proposing the opposite narrative? (“Invert. Always invert.”)

• What does this person benefit from by pushing this particular fear?

The answer is always the same. Manufactured urgency is a business model. Fear of falling behind is infinitely monetizable. The algorithm serves you the content that keeps you most agitated: agitation drives engagement & engagement drives revenue. Simple.

Log off with intent. The digital world has real value, but there is real skill for knowing when you’ve flown too close to the sun.

Solution #4: Slow time down by building new side quests

To subjectively slow time & make your 20s/30s feel as long as your teens, you need to maintain the neurological conditions of a beginner.

Build adjacent territories: Pick up BJJ. Study a second language. Take on a new writing project. Build the ecomm biz. The goal is deliberately inducing the state that produces dense memory encoding and the subjective experience of time expanding.

Neuroplasticity declines with routine but you reserve the right to deny the time accelerator that is monotony at any point.

Solution #5: Engage with a wide range of ages

The echo chamber of same-age peers reinforces the illusion that everyone is on the same timeline and that the milestones are universal. Far from the truth.

Spend meaningful time with people in their 50s and 60s who are doing interesting things. Spend time with people in their 20s who are just starting out. The former dissolves the urgency of the arbitrary milestones. The latter shows you what raw beginnings actually look like from the outside.

Both will give you perspective that your peer group structurally can’t.

Solution #6: One barometer to rule them all

Here’s the simplest mental model I can give you for navigating the digital world without burning neurons in the comparison game: it’s last week you vs. this week you.

An annualized version I find effective: is my life better this year than last year? Not in every dimension because that’s not how life works. But in the trajectory. In the vector sum.

If yes: you’re winning. You’re getting what you want out of life, which is the only honest definition of happiness.

If no: get precise by going deeper. “I’m behind” is too vague to act on. Get specific about what you actually want. You’ll be surprised how little you’ve actually considered this until you whip out the ol’ pen & paper. Get specific about what it costs. Then pay that price.

Solution #7: Narrow your scope

All anxiety is predicated on living in the future & evading what is now.

Goals are the mountain that appear unattainable to scale. Systems are the steps that look laughably simple.

The mountain is just many of those tiny steps.

This is why goals underperform, resolutions rarely stick, and systems remain king.

Focus: narrow your scope → more proximity to the task → greater presence → more control → clearer thinking → greater fulfillment → incrementally closer to self-actualization. (You’ll sleep better too.)

The Fear Of Getting Older

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There’s a single thread running through all seven solutions: perspective.

The physical reality remains unchanged in the near term, but you can bend the reality of what lies ahead to your own will by crafting the very lens you wish to view it through.

The age anxiety epidemic is real. The psychological suffering it produces is real. But the cure exists and all it starts with is an improved mindset & a frame shift.

Accept that you have time, but move with calm urgency. And remember: you are never too late.

Head down, friends. The best is yet to come.

- Phys

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And yet you still wake up drenched at 2 AM in the damp sheet swamp.

Good news is we may be on the verge of validating on the best thermoregulatory tools to prevent this. A new study out of Waseda University’s Sleep Research Institute just dropped the most rigorous physiological evaluation of far-infrared (FIR) emitting sleepwear ever conducted. And the findings are worth paying attention to.

The Nishida Study

Published last month (January 2026) in Sensors, Nishida et al. did something no previous FIR sleep study had done: it measured core body temperature, sweating rate, skin temperature, humidity, EEG-based sleep staging, & heart rate variability. All in a controlled lab environment for the duration of the entire night.

15 healthy young men completed two overnight sleep sessions: one wearing FIR-emitting garments (polyester fibers embedded w/ ceramic nanoparticles emitting in the 5–20 µm wavelength band), one wearing visually identical control garments. Neither the participants nor the researchers knew which was which.

The results were promising.

Result 1: Core temperature dropped

FIR garments produced consistently lower tympanic membrane temperature across the entire night. The decline in core body temperature is one of the most critical physiological prerequisites for both sleep onset & deep sleep maintenance. FIR garments appeared to passively facilitate this process via enhanced radiative heat dissipation on the skin.

Result 2: Mid-sleep sweating decreased

A condition-by-time interaction showed reduced sweating during the middle portion of the night precisely when thermoregulatory disruptions tend to fragment sleep.

Result 3: REM sleep increased

The proportion of REM sleep was significantly higher in the FIR condition (22.2% vs. 18.6% at p = 0.027), without any change in total sleep time or NREM architecture. Though total sleep duration was steady, they subjects had better-distributed sleep favoring REM expression.

Result 4: Modest HRV improvement

A transient increase in low-frequency HRV power during early sleep reflected baroreflex-mediated cardiovascular adjustments consistent with enhanced heat dissipation, while parasympathetic tone remained stable.

No changes were observed in sleep efficiency, total sleep time, or subjective sleep quality ratings.

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How FIR Garments Work

FIR-emitting textiles/garments have ceramic nanoparticles that enhance emissivity in the 5–20 μm wavelength band, which is the same range that aligns with the human body’s peak thermal radiation output. When you wear them, the fabric absorbs your body’s radiant heat and re-emits it, promoting peripheral vasodilation and more efficient radiative heat exchange at the skin surface.

Now you might think — the cooler, the better…but there’s a Goldilocks zone to the thermoregulation game that FIR supports.

When falling asleep, your body wants to shed core heat through the skin (especially at the hands & feet). Raymann et al. (2008) demonstrated that even subtle manipulations of skin temperature (as little as 0.4°C) can increase sleep depth and reduce the probability of early-morning awakening.

Unlike active cooling systems, mattress pads, or just general climate control, FIR sleepwear operates at the skin-textile boundary itself.

Further Supporting Evidence

The Nishida study didn’t emerge out of nowhere. Several prior investigations laid groundwork, but each had significant limitations relative to what the Waseda team explicitly addressed.

Lee et al. (2024) evaluated a FIR-emitting blanket over 14 days in middle-aged men. The FIR group showed a significant 28% increase in combined deep sleep plus REM time compared to placebo with a large effect size.

Even more notably, blood serotonin, melatonin, BDNF, & nitric oxide concentrations all significantly increased in the FIR group.

Bontemps et al. (2021) also published a systematic review examining FIR-emitting garments specific to sport performance and recovery. It highlighted that FIR garments’ greatest potential was through their effects on thermoregulation and hemodynamic function.

Our Interpretation

The Nishida study is the best representation of the FIR impact on sleep. They explicitly framed their results as demonstrating “physiological feasibility, rather than clinical efficacy.”

FIR garments subtly improve the thermal microclimate during sleep through passive radiative mechanisms, but they don’t overhaul your sleep. It’s a fine-tune of the thermal environment.

Our hypothesis runs like this: if you’re thermoregulatory-challenged at night, FIR blankets/garments can be especially promising. If not, the impact will be marginal.

A reminder: no single tool will ever be a replacement for the fundamentals (circadian signaling + light environment + nervous system regulation), but improved development of FIR as a thermoregulatory tool shows promise in enhancing how well you sleep.

As always — we’ll keep an eye on developments in the future & stay up-to-date on the latest here.

Your friend,
Phys

More than a third of adults over 301 wake up to urinate at night. The condition is so common we've normalized it, but it’s still far from even normal function.

The standard advice is something like: Stop drinking water after 6 PM. Cut sodium. Front-load hydration.

You try them. They help marginally. But you're still waking up.

Because surface-level interventions never address upstream causes.

Nighttime peeing signals deeper issues.

If you’re waking even 1x to pee, there’s a high chance at least one factor outlined here is driving it.

Here’s the guide to help you stop peeing tonight.

Cause #1: Circadian Dysregulation

Your brain-kidney-bladder axis operates on a 24-hour clock. At night, circadian signals should increase arousal thresholds, melatonin, & vasopressin reducing urine production and maintaining bladder capacity. However, blunted rhythms result in higher nighttime urine production.2

Duffy et al. (2016)3 tracked urine production over 40 hours in young versus older adults. Total 24-hour output was identical, but older adults produced significantly more urine during nighttime hours.

They explained:

“…this reduction in amplitude of the circadian rhythm of urine output with aging contributes to nocturia in otherwise healthy older adults by causing more urine to be produced during the nighttime hours than in young adults.”

Solutions

• Minimize blue/white light post-sunset: red/amber bulbs, f.lux/Night Mode, blue blockers

• Suppress nnEMF before bed (WiFi off, airplane mode)

• Maximize natural light exposure at sunrise, midday, & sunset

• Complete darkness: blackout curtains & eye mask

• Consistent meal timing to synchronize gut microbiota circadian cycles

• Epitalon (3-6mg before bed) → circadian amino acid complex to reset pineal gland function

Cause #2: Nervous System Dysregulation

Sympathetic hyperactivity and poor vagal tone create an overactive bladder. The imbalance increases bladder sensitivity and triggers urgency signals even when bladder volume is low.

Solutions

• Track HRV, resting heart rate, & blood pressure (relative metrics…it’s today you v. last week you)

• Analog brain dump before bed

• Cut social media 2 hours pre-sleep

• 4-7-8 breathing to activate parasympathetic response

• Magnesium (Tauromag or glycinate) + L-theanine + glycine

  • Combine all three with the PreSleep formula (Save 10% w/ PHYS10)

• Herbal teas: chamomile, mulungu, magnolia bark

• Sauna + cardio 2-3x weekly

Cause #3: Cold Temperatures

Every 1°C drop in bedroom temperature raises nighttime peeing odds by 7-10%.4

Temperatures below 60°F activate TRPM8 cold-sensing channels, heightening bladder excitability. Winter exacerbates this through greater indoor-outdoor temperature differentials.

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Our mission is simple: develop a first principles-based, bioindividualized health system that encourages consistent growth & resilience over time.

One focused on rational approaches, denial of neuroticism, & treatment of health as infrastructure, not the mission.

Here’s how to forge your own indomitable health system from first principles that will last you decades.

Why To Shape Your Health With Mental Models

Mental models are simplified frameworks for understanding how the world works. They’re tools rooted in objective truths and natural laws that help us dial in our signal-to-noise ratio, recognize patterns, & make better decisions.

In health, they shift us from pathogenic fixes to salutogenic design shifting wellness into an antifragile structure rather than a fragile pursuit.

They're timeless principles you could apply 500 years ago or 500 years from now to human nature, and they’d remain equally true.

The template looks like this: Make microdecisions based on the models → execute microactions consistently → develop habits → iteratively build default systems running in the background → stack microvictories

Those who truly embrace bioindividuality build their health systems from the ground up. They begin with first principles, extract truth from reality, & iterate until they receive the positive feedback they’re after.

The models and traps laid out here accelerate that process helping you discover what is true for you, not what healthfluencers performatively display as their front-stage self.

The Models

Model #1: Via Negativa

Principle: Improve by removing what’s harmful rather than adding more.

Application: Before asking what needs to be added to solve a problem, run through: 1) what can be subtracted & 2) if it can’t be subtracted, is there a more efficient substitution?

Four practical moves you can act on immediately:

• Eliminate what’s likely to derail your nutritional system from your kitchen

• Declutter unused materialistic items

• Stop digitally hoarding browser tabs

• Delete toxic relationships

Model #2: Vector Sum Thinking

Principle: Net direction and magnitude of all forces in a situation.

Application: No digitally-based algorithm rewards vector-style thinking (though you will be rewarded personally). In fact, it penalizes this harshly. No single intervention is exclusively positive. Even the best levers carry some risk (i.e. resistance training, cardio, sunlight exposure). We do them because on net they’re beneficial.

Model #3: Strategic Alignment

Principle: In military doctrine — objectives define strategies, strategies determine operations, & operations dictate tactics.

Application: Most health confusion stems from adopting performative tactics that serve someone else’s strategy entirely. When someone advocates a tactic (dogmatic diet, certain style of training/protocol, supplement), ask: "What objective does this serve, and is that my objective?"

Model #4: Law of Diminishing Returns

Principle: Past a certain threshold, each additional unit of input yields progressively less output.

Application: Optimize hard enough and you begin to create solutions to problems that don’t exist. Often for the sake of fulfillment you’re failing to obtain in other areas of life. Build infrastructure around high ROI fundamentals first. And don’t be the dude obsessing over exogenous compounds when you’re hitting Zone 5 carrying groceries up a flight of stairs & failing to squat your own bodyweight.

Model #5: Closed-Loop Control System

Principle: Uses feedback loops to regulate homeostasis.

Application: There are two things you can control in any system: your inputs & how you treat those inputs. Most fixate on the former while neglecting the latter. How you treat your inputs is as important as the inputs themselves. Failure to treat inputs properly creates an open-loop control system destined to repeat the same mistakes. Closed-loop control systems provide the fuel for pattern recognition letting you update & improve your inputs.

Model #6: Activation Energy

Principle: The initial push needed to start a process.

Application: Lowering activation energy is the first step to effortless system adoption. It builds health infrastructure by embedding intentional habits into your daily flow rather than relying on sporadic willpower. The truly elite fight activation through intelligent environmental design a single time, not repeatedly before execution.

Model #7: Momentum

Principle: Objects in motion stay in motion.

Application: Days I start with a microvictory (i.e. training, 60-minute deep work session) are significantly more productive than days I don’t. The first hour of the day is your most neuroplastic and therefore your highest ROI period to create. Using it well transforms an isolated effort into the fuel that makes the rest of the day feel naturally effortless.

Model #8: Antifragility

Principle: Fragile systems break under stress. Robust systems resist stress. Antifragile systems grow stronger from stress.

Application: Real longevity selects for resilience. Browse the longevity space today and experts are either being wrecked by a snack bar or put in shambles from a single seed oil-cooked dinner. The priority is to build your health infrastructure to evade the arc of an effeminate neurotic.

Model #9: Relativity

Principle: Perceptions depend on context. Everything is relative to a frame of reference.

Application: In The Stress of Life, stress researcher Hans Selye explained:

“Most people do not fully realize to what extent the spirit of scientific research and the lessons learned from it depend upon the personal viewpoints of the discoverers.”

Especially when perusing social media, always remember: context is king.

Model #10: Trade-Offs

Principle: “There are no solutions, only tradeoffs” (Thomas Sowell)

Application: If it wasn’t obvious — Sowell wasn’t talking about health or fitness, but he might as well have been. The spirit of this sentiment holds true as ever in our space. Health (& life) is a game of opportunity costs. Every choice involves surrendering something to gain something else.

Model #11: Signal-to-Noise Ratio

Principle: The ratio of meaningful information (implementable) to irrelevant interference.

Application: Nothing will spin your wheels faster than losing sense of what hinders progress. The most likely culprits are cheap dopamine and the chase of novelty. The next protocol. The next peptide. The next shiny object. Recall we’re after timeless truths. Never miss the forest for the trees.

Model #12: Inversion

Principle: Instead of asking “how do I succeed?” ask “how would I guarantee failure?” Then avoid those things. “Invert, always invert.” (Carl Gustav Jacob Jacobi)

Application: Synergistic with the via negativa principle. When you begin developing your own personalized health framework, think less about what you need to be healthy and more about what it takes to be unhealthy.

Model #13: Parkinson’s Law

Principle: Work expands to fill the time available.

Application: Timebox and batch your system. Start with the end, then work backwards. When you don’t do the work, the work you should have done becomes the anxiety you now have. It’s how you solve for the spiritual-biological misalignment that is anxiety.

More on leveraging Parkinson’s:

Model #14: Hanlon’s Razor

Principle: “Never attribute to malevolence that which can be adequately explained by stupidity.”

Application: This ties directly into one of the most overlooked components of health: nervous system regulation. Despite what you might see online, we live in the safest time in human history.

Reprogram yourself with the idea that no one is out to get you. There is no villain orchestrating your demise. Very few actually care enough about you (and what you’re doing) to allocate more than three seconds of thought toward you. Accept this as a beautiful feature of life.

Model #15: Roseto Effect

Principle: From a 1960s study of a Pennsylvania town showing low heart disease rates (despite poor diets and habits) attributed to strong community bonds that reduced stress. As social ties eroded, rates normalized.

Application: The relational infrastructure of health is just as important (if not more) as the metabolic one. Don’t deny the opportunity to break bread with friends & family even if that means ingesting a seed oil-cooked dinner. (see: vector sum thinking).

Model #16: Friction

Principle: Increase the friction to the bad. Decrease the friction to the good.

Application: Elite performers all have something in common. It’s not superhuman discipline. It’s not lofty goals. It’s ruthless adherence to their system. At the bedrock of those systems are vices that are difficult to execute and virtuous habits that are seamless day to day.

Model #17: Environmental Determinism

Principle: On a long enough time horizon — you become your environment.

Application: Who you populate your social circle with. What fills your pantry. Where you spend your time. These are primary variables determining your outcomes, not mere background variables. Highly synergistic with the friction principle. Surround yourself with the things and people that multiply happiness and value to the world, while dividing the pain.

The Traps

Trap #1: Tactic Hunting

Principle: Chasing isolated tactics without strategic integration.

Application: Once you spend enough time in this space, you’ll notice a sharp dichotomy in types of practitioners.

On one pole, you have the tactic hunter who asks:

• What diet?

• What training split?

• What supplement protocol?

On the opposite, you have the strategy builder who asks:

• Does this tactic align with my objective?

• Have I tried any variation of this in the past?

• What lifestyle changes would make the integration of this tactic feasible?

The tactic hunter chooses in isolation of other variables. The strategy builder constructs cohesive systems aligned with personal objectives, lifestyle frameworks, and past experiences.

Trap #2: Front Stage Self

Principle: What you see is not all there is.

Application: This applies to both how you treat information in the health space and how you build a strong foundation for yourself from that same information. Superficial wellness is the prioritization of performative health displays over authentic, backstage systems. The former scores transient engagement points, while the latter leads to robust health infrastructure.

Trap #3: Overgeneralization

Principle: Drawing broad conclusions from limited evidence.

Application: What’s yours is yours. What’s mine is mine. Results of the most well-designed RCTs don’t necessarily translate to you as a salutogenic practitioner. In fact, it’s more likely they do NOT. We speak about this one at length in the Case for Broscience.

True learning is a shift in behavior. Without the application of these models to your own bioindividualized system — they became useless mental masturbation tools.

Implement.
Set up technical feedback tools.
Assess efficacy.
Iterate.

Only then can you become the master of your own health.

Your friend,
Phys

PS: We’ll be releasing some new paid sub features (protocols + peptides/bioregulator deep dives + community chat) in the next couple months. So for the OGs here, we’re dropping a limited time offer to hop in while it’s as low as we can go.

Get 20% off for 1 year

Morning wood is one of the most reliable gauges of integrative health function across five systems: vascular, metabolic, hormonal, circadian, & nervous.

Yet one component that gets left out of most PCP conversations is this: the loss of these events over time often precedes diagnosable cardiovascular disease cases 5-10 years in advance.

We’re trained to believe it’s purely about libido, but there’s way more to it. The complexity behind morning wood is exactly what makes it such an elite leading indicator for future health outcomes.

Here’s what your morning wood (or lack thereof) is telling you.

The Biological Drivers

Search for “morning wood” in academic research and you’ll come up empty. The formal term is nocturnal penile tumescence (NPT) — defined as spontaneous erections occurring during REM sleep.

Unlike erotically induced erections that are psychogenic, morning wood is purely physiological. It’s driven by the parasympathetic nervous system and the release of nitric oxide from the endothelium and nitrergic nerves.

During REM sleep, your brain downregulates sympathetic tone & upregulates parasympathetic activity1. This shift triggers a series of events across multiple systems in the body enabling increased blood flow to the penis.

When this highly integrated system fails, it reveals a dysfunction somewhere in the chain.

The Five Systems Test

Morning wood’s clinical power lies in its dependence on multiple systems working in cooperation. Its presence confirms functional integrity. Its absence signals compromise across one or more pathways.

System 1 → Endocrine System: Androgens

Testosterone is the main hormonal regulator of morning wood and the relationship is dose-dependent. Granata et al. (1997)2 studied 201 men and found that below 200 ng/dL serum testosterone, morning wood becomes suboptimal or disappears entirely.

But testosterone doesnt working alone. Dihydrotestosterone (DHT), the 5α-reduced metabolite of testosterone, plays an equally critical role. When 150 men aged 50–70 years3 received transdermal DHT treatment, early-morning erections improved significantly after three months.

Gooren at. (1985)4 showed DHT therapy not only improved morning wood but increased nocturnal sexual dreams.

Foresta et al. (2003)5 similarly demonstrated that transdermal DHT therapy significantly improved morning wood in hypogonadal men and that DHT acts as the active androgen in maintaining nitric oxide-mediated erectile activity.

System 2 → Neurohormonal System: Dopaminergic Pathways

Initiating and maintaining morning wood depends on central dopaminergic signaling.

Testosterone increases nitric oxide synthase (NOS) activity in the medial preoptic area of the brain — a region critical for sexual behavior. The flow works like this: testosterone pulse → activation of central NOS → increased peripheral NO → dopamine release → morning wood.

Interestingly, dopamine’s role here differs from its role in waking erections. Dopamine uptake inhibitors improve stimulus-bound erections during wakefulness6 but paradoxically reduce morning wood & REM sleep.

System 3 → Circadian & Sleep Architecture

Morning wood is coupled with REM sleep architecture. The sleep-related rise in serum testosterone7 is linked to the appearance of the first REM episode establishing a bidirectional relationship: sleep architecture influences testosterone secretion AND testosterone modulates sleep quality.

Schiavi et al. (1992)8 also found age-independent positive associations between sleep efficiency, decreased REM latency, number of REM episodes, and circulating testosterone levels.

System 4 → Nervous System Regulation: Parasympathetic Tone

Morning wood generation is a parasympathetic event. The penile erection reflex9 operates through sacral parasympathetic nerve fibers (S2-S4), which release acetylcholine and activate nitrergic nerve endings in the penis.

Without taking your foot off the sympathetic gas, the parasympathetic brake will never be engaged (morning wood becomes implausible).

System 5 → Endothelial Function: Blood Flow & NO Bioavailability

The most consequential system interrogated by morning wood.

Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) acts as the molecular signal for systemic vascular vasodilation. When NO bioavailability is compromised, the morning erection potential suffers.

Because penile arteries are smaller in diameter10 (1–2 mm) than coronary arteries (3–4 mm), the same degree of endothelial dysfunction produces disproportionately greater reduction in penile blood flow.

The penis is a more sensitive barometer of systemic endothelial health than the heart itself. This is precisely what makes it predictive for cardiovascular disease.

The Cardiovascular Connection

So how is not having morning wood the canary in the CVD coal mine?

The relationship between morning wood & CVD is more than correlational given its mechanistic roots in shared vascular biology. And the epidemiological evidence grows stronger every few years.

Here are some of the data:

• ED is present in > 50% of men with a history of CVD11.

• 1 in 8 men with ED12 reports a prior cardiovascular event.

• A meta-analysis across 154k men with ED13 showed relative risk increases of 59% & 34% for ischemic heart disease & stroke, respectively.

• The greater the ED severity = the greater the CVD risk.

The ED signal becomes even more powerful in younger men. Among men aged 40–49 years, the incidence of heart disease in those with ED was nearly 50 TIMES higher14 than in men without it.

In 1991, Gossetti et al.15 evaluated sexual function in men with advanced atherosclerosis. Of 386 patients, 148 (38%) reported prior erectile dysfunction. When 44 underwent preoperative testing, all 44 showed impaired morning wood: 77% had complete absence, 23% had mild absence.

Penile blood flow studies conducted by Karacan et al. (1989)16 demonstrated a stepwise reduction in penile blood flow amplitude across three groups. Morning wood degradation represents a continuum of vascular compromise that tracks with systemic arterial disease.

Not Just for Men

Women experience the same phenomenon — nocturnal clitoral tumescence, or what we’ll call “morning bean.”

During REM, parasympathetic-mediated increases in pelvic blood flow produce clitoral engorgement and vaginal lubrication in women17. The same endothelial dysfunction, parasympathetic neuropathy, & NO signaling deficits that degrade morning wood in men also impair sleep-related blood flow in women.

Female sexual dysfunction shares overlapping vascular/neurological risk factors with male ED: hypertension, diabetes, & metabolic disease. Therefore, the biological rationale for treating a lack of morning wood/bean as a systemic health indicator is equally sound for both sexes.

The Functional & Integrative Solution Stack

Now that you understand why morning wood is one of the most critical measures of vitality, here’s how to improve your own Morning Wood System.

Circadian Biology & Sleep Architecture

1. Daily sunlight → Minimum effective dose = 10 min ~sunrise + 10 min ~sunset + 30 min around peak UV hours. Red/NIR exposure on thyroid/pelvic areas for fertility & parasympathetic support.

2. Consistent wake/bed times → Embrace 24-hr rhythmicity. Test Epitalon to regulate the clock.

3. Light environment at home → Minimal overhead lights at night. Replace LEDs with incandescents. Blue light blockers/Night Shift Mode. Add vitamin D lamp if seasonal affective disorder is present.

4. Optimize sleep conditions → Total blackout in bedroom. 60–64 °F. Hot shower before bed. Nasal breathe w/ mouth tape (SomniFix or 3M micropore).

5. Kill nnEMF sources at night → WiFi routers. Bluetooth. Phones.

6. Supplement strategically before bed → 400—600 mg magnesium + 3—5g glycine + 400—600 mg L-theanine + 1—2g myo-inositol.

Nervous System Regulation

1. Analog brain dumps before bed → An effective anti-anxiety tool.

2. 24-hour social media fast → 1x weekly. Regular digital detachment preserves attention span & mental clarity.

3. Curate your digital signal-to-noise ratio → Mute words aggressively. Delete sources of chronic doomerism. Ignore > negatively engaging.

4. Embrace life as a two-player game → It’s today you versus last week you. It doesn’t get easier, but it gets simpler.

Metabolic Health

1. Resistance training → 3—4x/week

2. Fasted low-intensity cardio → 30—45 min sessions 3-4x/week (avoid excessive Z3+ training > 250 min/week)

3. HIIT → 1—2 sessions/week (HR should be above 90% max)

4. Post-prandial walks → Walk post meals 10—15 min. Stand for 45 min if unable to walk.

5. Keep body fat < 18% → Ideally 12—15% as a male.

6. Use daylight diet/time-restricted feeding → Big breakfast. Medium lunch. Small dinner > 2 hrs before bed.

7. Test metabolic biomarkers → Guide provided below with functional ranges.

Oral Microbiome

1. Switch to nano-hydroxyapatite toothpaste → Remineralizes enamel without the negative impacts of fluoride-based products.

2. Scrape your tongue daily → Removes bacteria that brushing misses & improves oral microbiome health.

3. Avoid alcohol-based mouthwash → Destroys beneficial oral bacteria, dries protective mucosa, & negatively impacts vascular function.

Functional Nutrition

1. Embrace functional foods & herbs → Pasture-raised eggs. Raw local honey. Watermelon. Pomegranate. Oysters. Cacao. Wild-caught salmon. Ginger. Saffron.

2. Critical micronutrients → Balance Zn:Cu ratio (~10:1). All B vitamins. Vitamins A, C, E, K2 (via whole foods). Magnesium (1g elemental/day). Selenium (2—3 Brazil nuts/day). Vitamin D (via sunlight). Iodine. Molybdenum.

3. Take care of the gut → Consume fermented foods (kimchi, kefir, sauerkraut, yogurt), bone broth/collagen, & prebiotics (green bananas, gluten-free oats, garlic, apples, onions). Cycle glutamine or BPC-157 if needed.

4. Supplementation → Nattokinase. Taurine. Ginkgo biloba. Alpha-GPC. Ubiquinol. L-citrulline. PT-141 (nuclear option once foundations locked in).

As with every bioindividualized protocol you develop — apply tactics that only fit the strategy & prioritize subtractions/substitutions before additions.

That’s all for this week. DMs & comments are open for any questions/more specifics.

See you guys next week.

Your friend,
Phys

We predict it will be the pillar of most cardiometabolic optimization stacks over the next decade. As more & more move away from the Big Pharma-sponsored solutions, they're choosing health sovereignty through powerful, naturally-occurring compounds.

My top pick to represent that future?

Toku Flow.

Last summer, I had the opportunity to speak with Justin (the founder) — this team is serious about developing products made for the elite practitioners in our health space. Their first product is a clear proof of that — combining two supplements already in my personal cardiometabolic lineup (nattokinase + MK-7) & should be in most individual’s cardioprotective stack, especially those with familial cardiac history.

Here’s how Toku separates itself from the supplement pack.

The Formula

Toku Flow combines three clinically-dosed compounds for cardiovascular support: nattokinase, vitamin K2 MK-7, & organic oat beta-glucan. Our priority in the supplement space has always been simple (but quite rare): transparency with clinically significant dosages.

Nattokinase (10,800 FU)

The 10,800 FU dosage in Toku Flow isn’t arbitrary. It’s directly informed by a large-scale clinical study involving 1,062 participants1, where this exact dose led to exceptional cardiometabolic outcomes:

• 39% reduction in arterial plaque size

• 25% improvement in carotid artery flexibility

• 18% reduction in total cholesterol

• 17% reduction in triglycerides

If you want the full breakdown on nattokinase (every RCT/clinical trial summarized), we wrote about it at length here.

Vitamin K2 MK-7 (180 µg)

K2 is most bioavailable in the MK-7 form.

A three-year trial2 involving more than 240 healthy postmenopausal women showed MK-7 at 180 µg/day improved arterial stiffness.

A one-year clinical trial3 also demonstrated that MK-7 improved overall vascular health slowing the progression of arterial calcification.

Organic Oat Beta Glucan (3g)

Beta-glucan is a soluble fiber extracted from oats best known for its lipid optimizing effects.

A 2022 systematic review & meta-analysis of 14 trials4 found that oat beta-glucan (doses 1.5-6 g/day) lowered total cholesterol by 11.6 mg/dL & LDL by 9.7 mg/dL.

What Sets Toku Apart

In a growing nattokinase supplement market (*avoid much of Amazon*), Toku Flow distinguishes itself with efficacious dosing, transparency, & quality. Here’s how it stands out:

1. Dosing transparency: Most nattokinase caps fall into a couple categories: 1) underdosed significantly or 2) they’re hiding behind proprietary blends. Toku doses their nattokinase at more than 175% of the label claim. Any nattokinase brand that is serious about their customers’ health understands the importance of the overage concept when it comes to dosing proteolytic enzymes (see article above on why dosing nattokinase much higher is needed).

2. Soy-free nattokinase: Toku is atypical in that it’s fermented from chickpeas, not soybeans. Without soy, yet still maintains it’s full fibrinolytic activity.

3. No filler junk: Freeze-drying isolates the enzyme cleanly. No magnesium stearate. No silicon dioxide. No other flow agents.

How I Use It

Since I started supplementing with Toku in late summer 2025, it’s become a staple for my nighttime system as an easy (& delicious) bedtime hot chocolate.

Mixes well. Tastes great. And has proven effective at keeping blood pressure & LDL-C numbers low.

SHOP TOKU FLOW @ 20% OFF

The current hype of the health space is peptides & exogenous hormone replacement therapy. We see it everywhere. These absolutely have their place in many protocols, however what we’re seeing a lot of in this space is a sudden neglect of the basics of cardiometabolic health.

So a reminder is in store: Test your metabolic biomarkers (don’t guess). Build your aerobic engine. Focus on the metabolic & cardioprotective components — much else comes down stream of these.

Until next time,
Phys

Onto Instagram for “just for 5 minutes”. 30 minutes later.

Time stolen.
Brain rotted.
Attention ripped away.

Only to be left feeling spiritually drained from corrosive inaction.

A few of these experiences were enough to have spent the last 14 months documenting the art of learning focus. Tinkering with different systems, states of mind, & tactics. Determining what’s needed to stiff-arm algorithmic control & ruthlessly direct attention for maximizing agency.

Here’s exactly how to unlock a top 1% focus.

Understanding Your Attentional Architecture

You can’t optimize what you don’t understand so let’s start here. Your brain operates on three integrated systems:

1. The Radar Station

Sweeps continuously across your external world & inner territory generating a menu of potential targets competing for recognition.

2. The Gatekeeper

Evaluates that menu & determines which target gets granted entry to your conscious awareness.

3. The Spotlight

The actual concentrated beam of mental energy you aim at the selected subject.

Why Most Focus Protocols Fail

• Too extreme: “Delete all social media forever” (impractical when your job requires it)

• Too neurotic: 27 different apps, browser extensions, & tracking systems (Tools are components to a system, but not the system. We use some but not to the point of tool fatigue.)

• Zero progression: All-or-nothing approaches with no gradual building

• Ignores root causes: Treats symptoms rather than rewiring the underlying patterns & biological systems

• Lacks synergy: Arbitrary set of tactics that share no cohesiveness

We’re running this differently based on three core themes:

1. Progressive overload → Treating focus like a muscle by gradually increasing the challenge (discomfort).

2. Environmental control → Making the right behaviors automatic through intentional design by increasing the friction to the bad & decreasing the friction to the good.

3. Sustainable integration → Building a system you can maintain long-term, not a temporary (ineffective) “detox”.

Read more

Separated by 3,000 miles, I hadn’t seen Patrick or his family in over a year. Patrick is the youngest of three sons. His parents just celebrated their 30th anniversary. His dad, Hal, owns a fourth-generation beer distribution business.

At Friday night’s rehearsal dinner, something felt off.

After an hour of catching up with Patrick’s family, I pulled him aside: “Is everything alright with Hal? He seems…off.”

I’ve known Hal for over a decade. A burly Irish Catholic. Never missed Sunday Mass. Loved his family like he loved the Lord. The rare man whose wife still adored him and whose kids didn’t hate him— the true longevity specimen of our day. At his worst, he was still the most charismatic man in the room.

Patrick sighed, looked down, started to tear up: “He’s struggling. Overeating. Not moving. Doesn’t get out of bed until 1 PM. He’s depressed.”

Two weeks after the wedding, I got a text: “Heading home. Dad has pneumonia. I quit my job to take over the business and be with him through treatment.”

Two days later: “Things took a turn. He’s in rough shape. ECMO next.”

This past Monday, I got the text I felt was coming: “My dad passed this morning.”

62 years old.

Hal saw his youngest child get married. He convinced himself his mission was complete on this Earth.

Here’s the harsh reality: if you stop giving the Universe a reason to keep you here, it will violently rip that opportunity from your hands and give it to someone else.

“What does this have to do with the state of our health…”

There’s a deeper point that awoke the sleeping giant this past week as it relates to our side of the health space: we lost the plot when we started replacing vitality with fragility. And vitality is at least half of the longevity equation. Its inverse is doubt. It’s the idea that those who lack the conviction to exist forecast their own mortal demise.

I don’t just say this as a matter of emotional response to a tragic situation. Perhaps partially so. After all, I’ve known Hal for quite a long time. But there’s more to it.

Vitality is rooted in biological truth, though immeasurable. And that’s why we avoid it — because we hate what we cannot measure. It doesn’t fit into our tidy models. It doesn’t match the cleanliness of our spreadsheet health’ing. We can’t quantify elite vitality like we can an inflammatory marker.

We find comfort in “everything will be alright, here’s exactly what to do.” The alternative is complexity and uncertainty without guardrails that we fear will send us spiraling. That’s why we tell ourselves stories. To at least provide ourselves the illusion of understanding the world we reside in.

It’s Nothing New

This idea of vitality has long been established, yet we’re quick to either forget or fail to integrate the core truths of humanity in search for the extension of its own existence.

Schweitzer wrote in Out of My Life and Thought:

The most immediate fact of man’s consciousness is the assertion “I am life that wills to live in the midst of life that wills to live”

Frankl argued humans thrived on what he called the “will to meaning” and suggested without conviction, men succumb to the “existential vacuum".

Nietzsche’s Will to Power hinted similarly at the importance of embracing life’s vitality as a path to fulfillment so as to fuel life’s fire and stave off the fragile self. The unwavering Übermensch was defined by his ability to accept challenges despite adversity and to never be perturbed by the suffering of life.

Even the “Research” Declares It to Be So

I don’t suggest academic research as the final blessing. The unwavering spirit towards life is unquantifiable in every rational sense. Though, consilience — obtaining a similar conclusion via unique vectors — is all the more reason we find this principle to hold true.

One of the landmark studies in this area titled “Purpose in Life as a Predictor of Mortality across Adulthood”1 from Hill & Turiano (2015) suggested those with a higher purpose in life predicted a 15% lower mortality risk.

In 2002, Levy et al.2 found those with more positive self-perceptions of aging demonstrated a survival advantage of 7.5 years & every one-point increase in positive perception reduced mortality risk by 13.5%.

The Nurses’ Health Study3 of nearly 70k women in 2019 again showed those in the highest optimism quartile lived 14.9% longer than the lowest.

When we invert this idea instead focusing on the impacts of pessimism on health, we see the detriment of our denial for the will to live. In 2015, Pänkäläinen et al.4 wrote:

“among men in the highest quartile of pessimism, the risk for coronary heart disease (CHD) was approximately four-fold”

How to Build Vitality

N=1 isn’t simply a health meme. All of a life is an n=1 game. You’ll never be able to copy-paste a path or protocol in this life. You might not like it, but there’s a divine reason for it.

The most resilient lives are governed by those who navigate the valley of despair with calm urgency, reach peaks of accomplishment, only to find the valley yet again. They overcome each challenge with a steadfast persistence as a function of their own moral duty, not frivolous obligation. But this divine calling wasn’t a spontaneous moment of enlightenment, it was built through proper positioning.

Here’s a starting point. First, embrace the words of the late Scott Adams in one of his final interviews before he was faced with death. When asked what the meaning of life was, he answered: “to be useful to humanity.”

Dig a layer deeper and we can apply one of the better mental models for building this highly individualized sense of self-positioning: ikigai.

Ikigai translates to “live” (iki) “with value” (gai). Rooted in Japanese philosophy, it’s about building purpose through discovering the big 4:

• What energizes you

• What skills you’re praised for

• What society needs from you

• What sustains you

You blaze the trail to discover what it is you set foot on this Earth to do. You will never find yourself. You will never escape yourself. You will only set out on the path your true purpose. And that true purpose is the lifeblood for vitality — the real longevity pill.

At the root of every man’s purpose sits two things: to love & to build. That’s it — but how to love & how to build is entirely up to you. That’s the beauty of the journey. And what a sin it is to not enjoy the journey.

Now, it’s only fair to remind you of the words of St. Ignatius Loyola: “Ite inflammate omnia" (“Go forth, and Set the World on Fire”).

Your friend,
Phys

Now we finally have what is one of the more well-designed compound studies we’ve seen in a while. Across any intervention.

Some claim overhyped. Others say pre-workout, stress response elixir.

Here’s the latest data & practical takeaways on Rhodiola rosea.

The Study

Last month, researchers at Jacksonville State University published the first dose-response, crossover trial1 examining Rhodiola’s effects on both resistance performance & cognitive function in the same trained population.

The 3 big areas targeted:

1. Does Rhodiola improve strength, power, & muscular endurance in resistance-trained athletes?

2. Does it enhance cognitive performance at rest?

3. What’s the optimal dose?

Previous research hinted Rhodiola increased bar velocity but reduced repetitions to failure2. Others showed improved power across repeated efforts but no single-bout benefits3. The results were contradictory and unclear.

This study aimed to resolve those very contradictions.

Study Snapshot

Who were the subjects?

• 27 resistance-trained adults (13 male + 14 female) ages 18 - 40 yrs

• Minimum 2 years consistent resistance training experience

What did researchers study?

Using a randomized, double-blind, crossover design, participants completed four separate 7-day periods:

1. CON: control = no supplement

2. PL: placebo = maltodextrin

3. LDRR: low-dose Rhodiola = 200 mg/day

4. HDRR: high-dose Rhodiola = 1,500 mg/day

Each period was separated by a 7-day washout. On day 7, the subjects took their final dose 60 minutes before testing. The Rhodiola extract was also standardized to 3% salidroside & 1% rosavin (active compounds driving adaptogenic impacts).

What outcomes were measured?

1. Bench Press & Leg Press 1RM

2. 3rd set reps to failure at 60% 1RM

3. 3rd set reps lifting volume (load × reps)

4. Tendo mean & peak power (barbell velocity)

5. 30-second Wingate test (anaerobic capacity)

6. Stroop Color-Word Test (executive function)

7. RPE, heart rate, blood pressure

The Findings

1. Low-dose Rhodiola was superior for muscular endurance

Bench Press Set-3 Performance:

• LDRR increased repetitions to failure by +4.3 reps (+40% vs. control)

• LDRR increased third set volume by +372.6 lb (+32% vs. control)

• Placebo showed no significant change

Leg Press Set-3 Performance:

• LDRR increased repetitions to failure by +14.2 reps (+59% vs. control)

• LDRR increased Set-3 volume by +5,888 lb (+62% vs. control)

2. Rhodiola increased maximal strength without sacrificing endurance

Bench Press 1RM:

• LDRR increased 1RM by +12.3 lb (+8% vs. control)

Leg Press 1RM:

• LDRR increased 1RM by +78.7 lb (+11% vs. control)

• HDRR increased 1RM by +105.2 lb (+15% vs. control)

Prior research suggested Rhodiola created a trade-off → more speed, fewer reps. But this study shows both low and high doses improved strength & endurance simultaneously.

3. Power output increased across the board

Tendo Mean Power (Bench Press):

• LDRR increased mean power by +29.7 W (+15% vs. control)

  

Tendo Peak Power (Bench Press):

• HDRR increased peak power by +34.2 W (+11% vs. control)

Low-dose optimized mean power across reps.

High-dose optimized peak power output.

4. Cognitive performance improved significantly & dose-dependently

The Stroop test measures your brain’s ability to process conflicting information quickly under time pressure.

Total Stroop Score:

• LDRR: +37.7 items (+13% vs. control)

• HDRR: +48.4 items (+17% vs. control)

This further proved the dose-dependent cognitive benefits of Rhodiola. More Rhodiola = better cognitive performance.

5. No changes in perceived effort or cardiometabolic conditions

Despite massive improvements in performance:

• RPE remained unchanged across all conditions

• Heart rate & blood pressure showed no consistent changes

The benefits were predominantly neuromuscular & cognitive.

How Rhodiola Works

Rhodiola’s active compounds (salidroside & rosavins) work through a few rapid-onset central nervous system (CNS) pathways:

1. Monoamine oxidase (MAO) inhibition: Prevents breakdown of dopamine, serotonin, norepinephrine → Enhances motivation, focus, & motor drive

2. β-endorphin modulation: Improves stress resilience & effort tolerance

3. Catecholamine pathway support: Optimizes neurotransmitter signaling for power output & cognitive control

So the mechanism looks something like this:

Rhodiola supplementation → MAO inhibition → Enhanced motor drive + cognitive control → More reps, more power, improved neuronal function → Greater training stimulus

Practical Takeaways

1. Rhodiola functionality is use case-specific

Good for: Multi-set resistance work, late-set endurance, power maintenance, cognitive performance
Not so good for: Single-bout explosive efforts (sprints, isolated 1RM)

If your training emphasizes high volume hypertrophy or strength-endurance, Rhodiola is valuable. For pure powerlifting with full rest, you’re not getting nearly as significant of a benefit.

2. Dose matters

Low-dose (200 mg/day):

• Optimizes late-set repetitions

• Maximizes mean power output

• Best for hypertrophy and strength-endurance phases

High-dose (1,500 mg/day):

• Optimizes peak power output

• Enhances cognitive performance most strongly

Both doses improved cognitive function significantly. If you’re prioritizing mental performance alongside training, aim for 1,500 - 1,800 mg. As always — titrate up starting with the minimum viable dose.

3. The 7-day loading protocol

Rhodiola begins to show real impacts within a week.

Recommended protocol:

• Load for 7 consecutive days at your chosen dose

• For best results (physical & cognitive performance wise) → administer 60 minutes before training/deep work session

• Use a standardized extract: 3% salidroside + 1% rosavin

Reputable Source

Nootropics Depot Rhodiola is my go-to choice.

✅ Third-party tested for purity, potency, & heavy metals (COA available on every batch)

✅ Pharmaceutical-grade manufacturing

✅ $0.33/Serving

Get Nootropics Depot Rhodiola Here

As always — take what fits & leave what doesn’t.

Stay after it & we’ll see you guys next week with one of my favorite topics. A skill for you to own the next decade. And it’s deserving of a comprehensive protocol.

Your friend,
Phys