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Comparative Table – Training Design Drivers by Metabolic Archetype™
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✅ When we honor our biological design—by giving the body what it truly needs and avoiding the things that degrade it—health is not just a possibility; it becomes the natural expectation.
Why are 91% of the population metabolically unhealthy?
It is really quite simple. A given geography has a certain climate, seasonality, terrain and more which determines the type and availability of food as well as physical demands associated with it. When there is "Systemic Coherence" with these things, Biological Fitness occurs.
Systemic Coherence:
Systemic coherence occurs when the interrelated parts of a biological system are aligned with one another and with their environmental context, creating functional harmony. In this state, nutrition, physiology, training, and recovery strategies are congruent with the individual’s evolutionary and metabolic design, leading to resilience, adaptability, and optimal performance.
✅ Central point: Metabolic archetypes are still very real, because the overwhelming majority of our genetic history was shaped before agriculture. Most humans are mismatched with modern industrial diets. (see related post for evolutionary history)
Exercise: for the Archetype columns - 1) review the Primary Fuel Bias row (#1), perhaps note the Core Genetic Traits row (#2) just for context. Then review the Strength Work row (#5), Cardio Focus row (#6), HIIT/Explosive row (#7) and Fasted Training row (#8) for their differences in needs. See what you conclude.
Even though physical activity intensity, duration and frequency necessitate certain fuel to support it (glucose, fats, etc), it is metabolically incorrect to require the same physical activity for all archetypes and then have that necessitate the food choice - that creates metabolic dysfunction as you probable conclude from the exercise.
Your genes determine the food and physical activity that will have "Systemic Coherence" developed over millions of years - adhering to the Archetype needs yields Biological Fitness.
Work with your genes - not against them.
✅ These are the "proper" ranges/levels where we should be for markers.
(see table further down for references)
🧪 Shared Core Markers (Baseline – Both Seasons)
Marker | Description | Proper Range |
TyG Index (Triglyceride:Glucose) | Early marker of insulin resistance, lipid-glucose mismatch | < 4.0 |
Fasting Glucose | Glucose regulation; elevated levels signal poor metabolic control | 75–85 mg/dL |
Fasting Insulin | Indicates baseline insulin burden and metabolic inflexibility | < 5 μIU/mL |
Adiponectin | Anti-inflammatory adipokine; low levels correlate with insulin resistance | > 8 μg/mL (men) / > 10 μg/mL (women) |
HDL Cholesterol | Reverse cholesterol transport; antioxidant and anti-inflammatory roles | > 60 mg/dL |
Triglycerides | Indicates lipid clearance; high levels impair insulin signaling | < 70 mg/dL |
Atherogenic Index of Plasma (AIP) | Log(TG/HDL); cardiovascular and metabolic risk indicator | < 0.11 |
CRP-hs (High-sensitivity CRP) | Low-grade inflammation marker; predicts chronic disease risk | < 0.5 mg/L |
Homocysteine | Methylation and cardiovascular risk marker | 6–8 µmol/L |
GGT (Gamma-Glutamyl Transferase) | Proxy for oxidative stress and liver detox capacity | < 25 U/L (ideal) |
Uric Acid | Elevated in overreaching, inflammation, and mitochondrial dysfunction | < 5.0 mg/dL |
8-OHdG or Equivalent Oxidative Marker | Oxidative DNA damage; elevated in high mitochondrial turnover | Low (qualitative/lab-specific) |
IL-6 / TNF-alpha (if available) | Cytokine markers of immune stress and catabolic signaling | Low / Undetectable |
BHB (Fasted Ketones) (Winter only) | Represents mild ketogenesis or metabolic flexibility in low feeding states | 0.3–0.6 mmol/L |
CK (Creatine Kinase) (Optional) | Recovery and muscle damage marker for high-output individuals | < 200 U/L post-training |
🧪 Shared Core Markers (Baseline – Both Seasons) with References
Marker | Proper Range | Evidence / References |
TyG Index (Triglyceride:Glucose) | < 4.0 | Guerrero-Romero et al., 2016 (Endocrine); demonstrated TyG > 4.5 strongly predicts insulin resistance |
Fasting Glucose | 75–85 mg/dL | Kraft, 2008 (Diabetes Epidemic & You); Chen et al., 2010 (Diabetes Care) – showed mortality risk rises above ~90 mg/dL; low–80s align with hunter-gatherer fasting glucose values |
Fasting Insulin | < 5 μIU/mL | Reaven, 1988 (Syndrome X); Kraft, 2008 – most metabolically healthy populations fall around 2–5 μIU/mL |
Adiponectin | > 8 μg/mL (men), > 10 μg/mL (women) | Arita et al., 1999 (Biochem Biophys Res Comm); Yamamoto et al., 2004 (Circulation) – higher adiponectin is protective, inversely related to IR |
HDL Cholesterol | > 60 mg/dL | Gordon et al., 1989 (NEJM); Miller et al., 2008 (Circulation) – each 1 mg/dL HDL increase lowers CVD risk 2–3% |
Triglycerides | < 70 mg/dL | Nordestgaard et al., 2007 (JAMA); Okinawa/Japanese rural cohort studies show TGs ~50–70 in longevity populations |
Atherogenic Index of Plasma (AIP) | < 0.11 | Dobiasova & Frohlich, 2001 (Clin Chem) – <0.11 = low risk; >0.21 = high risk |
CRP-hs | < 0.5 mg/L | Ridker et al., 1997 & 2002 (NEJM, Circulation) – lowest-risk quartile is <0.5 |
Homocysteine | 6–8 µmol/L | Homocysteine Studies Collaboration, 2002 (JAMA) – risk rises steeply above 9–10 |
GGT | < 25 U/L | Lee et al., 2003 (Hepatology); Fraser et al., 2007 – lowest mortality quartile is consistently <25 |
Uric Acid | < 5.0 mg/dL | Fang & Alderman, 2000 (Arch Intern Med); Okinawan cohort average: 3.5–4.5 mg/dL |
8-OHdG or Oxidative Stress Marker | Low (lab-specific) | Collins, 2004 (Free Radic Biol Med) – elevated levels predict CVD and cancer risk |
IL-6 / TNF-α | Low/Undetectable | Ridker et al., 2000 (Circulation); Calder et al., 2017 (Nat Rev Immunol) – elevated baseline cytokines predict frailty & mortality |
BHB (Fasted Ketones, Winter only) | 0.3–0.6 mmol/L | Cahill, 2006 (Annu Rev Nutr); Phinney & Volek, 2012 – physiologic ketones in low feeding states hover 0.3–0.6 |
CK (post-training) | < 200 U/L | Brancaccio et al., 2007 (Clin Lab); upper reference for healthy athletes is ~200–300 U/L |
⚖️ Why These Differ from “Normal” Ranges
Population vs. Proper: Clinical labs often set “normal” based on the central 95% of the tested population. But modern populations are metabolically unfit compared to evolutionary or longevity populations.
Mortality Curves: Many of the ranges above (e.g., fasting glucose, CRP, uric acid, GGT) are justified by lowest all-cause mortality quartiles — not the average.
Evolutionary / Longevity Cohorts: Data from hunter-gatherers, centenarian Okinawans, and rural subsistence groups consistently support lower insulin, triglycerides, and inflammatory markers than Western averages.
