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GLP-1 Genes & Metabolic Archetypes™
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GLP-1 Variants Are Evolutionarily Linked to Archetypes
•The geographic and ancestral patterns of GLP-1 variants are not random but correlate with historical dietary patterns.
•The same civilizations and geographies that shaped the Metabolic Archetypes™ likely influenced GLP-1 receptor variations.
•This means that someone’s Metabolic Archetype™ assignment already has a high probability of aligning with their GLP-1 receptor function.
•Some metabolic archetypes may naturally have lower GLP-1 production, making them more prone to weight gain if not eating according to their archetype.
•Genetic predisposition could mean lower GLP-1, but obesity itself can further impair GLP-1 secretion.
•Eating outside their archetype (e.g., high-carb diet in a low-GLP-1 producer) could exacerbate metabolic dysfunction.
•This suggests that interventions should be tailored based on an individual’s Metabolic Archetype™, rather than assuming a universal response to diet.
The GLP-1 receptor (GLP1R) variants are not randomly distributed across populations but are likely to follow evolutionary selection patterns similar to the Metabolic Archetypes™.
There’s a strong case that GLP-1 receptor function, like other metabolic traits, has been shaped by environmental pressures, dietary availability, and regional selection over time.
GLP-1 Variants and Evolutionary Selection
•GLP-1 plays a critical role in insulin secretion, satiety, and energy homeostasis. Different populations, based on their historical diets and metabolic demands, likely experienced different selective pressures on GLP-1 function.
•Populations historically dependent on carbohydrate-rich diets (agrarian societies) may have favored GLP-1 receptor variants that enhance insulin secretion to manage higher glycemic loads.
•Populations that relied on high-protein, high-fat, or low-carb diets (hunter-gatherers, pastoralists, or Arctic populations) might have evolved GLP-1 receptor variants that prioritize satiety and fat oxidation over insulinogenic response.
Do GLP-1 Variants Align with Metabolic Archetypes?
Yes, and they likely correlate with the same civilizations and geographies that align with the Metabolic Archetypes™:
1. Carb-Efficient Metabolizers™ (Agrarian Lineages)
•Geographic correlation: South Asia, East Asia, Central America, and parts of the Middle East.
•Evidence: Some East Asian and South Asian populations have higher basal GLP-1 levels, supporting their historically high-carb diets.
•Likely GLP-1 pattern: Increased GLP-1 receptor sensitivity for stronger insulin response to efficiently handle carbohydrate-heavy diets.
• Higher GLP-1 levels historically matched high-carb diets.
• If they develop a GLP-1 deficiency, their nutritional strategy would not compensate as well since they rely on carbohydrates for energy and incretin-driven insulin secretion for regulation.
2. Fat-Adapted Metabolizers™ (Hunter-Gatherer, Pastoralist, Arctic, or Steppe Nomads)
•Geographic correlation: Indigenous Arctic populations, certain African tribes, Mongolian steppe populations, and some Northern European groups.
•Evidence: Some Inuit and Maasai populations show lower postprandial GLP-1 responses, which aligns with their traditional reliance on protein and fat over carbs.
•Likely GLP-1 pattern: Weaker GLP-1 receptor function, favoring fat oxidation and ketone utilization over carbohydrate-dependent energy metabolism.
• Naturally have low GLP-1 but do not need it.
• Their high-fat, low-carb metabolism stabilizes hunger and energy, reducing reliance on GLP-1-driven glucose control or satiety.
• Nomadic, Arctic, and Desert civilizations evolved in environments where carbohydrate intake was scarce, and these groups naturally became efficient at fat metabolism, requiring less incretin signaling.
3. Dual-Fuel Metabolizers™ (Hybrid Diet Adaptations)
•Geographic correlation: Mediterranean, Andean, and regions with a mixed hunter-gatherer/agricultural background.
•Evidence: Mediterranean populations with a balance of carbs and fats (olive oil, seafood, grains) show a moderate GLP-1 response, optimizing both insulin release and fat oxidation.
•Likely GLP-1 pattern: Moderate GLP-1 response, allowing metabolic flexibility between carbs and fats.
• Their mixed diet matches their ancestral background, allowing them to switch fuels more easily than purely carb-efficient groups.
• Some carb intake may be needed for optimal satiety regulation.
4. Carb-Sensitive Fat Storers™ (Ancestral Post-Agricultural Groups)
•Geographic correlation: Some Indigenous American, Pacific Islander, and Australian Aboriginal populations.
•Evidence: Indigenous populations with historically low-carb diets (e.g., Pacific Islanders pre-Western diet exposure) have higher rates of type 2 diabetes when exposed to refined carbohydrates, suggesting a mismatch in GLP-1-mediated insulin response.
•Likely GLP-1 pattern: Reduced or inefficient GLP-1 signaling, leading to a weaker incretin effect and a higher risk of metabolic dysfunction when exposed to modern high-carb diets.
• Naturally has low GLP-1 but struggles with satiety and insulin regulation in high-carb environments.
• Their ancestral background includes populations that transitioned from hunter-gatherer or pastoralist diets to agrarian grain-based diets, but not all adapted well to high-carb intake.
• Once adapted, keto effectively replaces the need for GLP-1-driven hunger control, allowing them to function well despite low GLP-1.
5. Hyper-Metabolic Outliers™ (Warrior & High-Exertion Populations)
•Geographic correlation: Various regions where extreme survival pressures existed.
•Evidence: Certain high-altitude populations (e.g., Tibetans, Andeans) show enhanced GLP-1 signaling, possibly as an adaptation to energy-dense but inconsistent food availability.
•Likely GLP-1 pattern: Variable—some with enhanced incretin response (fast metabolism, insulin-sensitive) and others with a blunted response (metabolically conservative, efficient fat storage).
• Unclear GLP-1 levels but may have a unique satiety regulation mechanism.
• High caloric demand could override low GLP-1 hunger regulation, leading to extreme caloric intake needs.
How Well Each Archetype’s Nutrition Approach Mitigates Low GLP-1 Effects
The following table considers:
• Which archetypes are most likely to have low GLP-1 genetically?
• How well does their natural diet minimize GLP-1’s role in metabolism?
• Are there any transitional challenges?
• What ancestral geographic/civilizational group best represents the archetype?
The Role of GLP-1 Deficiency in Modern Metabolism
GLP-1 deficiency is only a “problem” in mismatched diets.
•For Fat-Adapted Metabolizers™ & Carb-Sensitive Fat Storers™: GLP-1 naturally runs low, but this isn’t a problem on the right diet (ancestral low-carb, high-fat).
•For Carb-Efficient Metabolizers™ & Hyper-Metabolic Outliers™: If GLP-1 is low, they suffer from poor satiety and glucose regulation because their metabolism was designed for high-carb, whole-food diets.
Modern food environments push nearly all archetypes into metabolic dysfunction by:
•Increasing reliance on frequent eating & processed carbs, which disrupt natural fuel use.
•Blunting satiety signals with artificial flavors & hyperpalatable ingredients.
•Disrupting hunger regulation, making lower GLP-1 states worse.
When Would Lower GLP-1 Be More Problematic?
Lower GLP-1 becomes an issue when other systems are impaired, which might push someone toward a Carb-Sensitive Fat Storer™ profile. This could happen if:
•They have weaker β-cell insulin secretion capacity.
•They have reduced muscle insulin sensitivity (e.g., IRS1 SNPs impacting insulin signaling).
•They experience poor appetite control due to weaker leptin or PYY signaling.
If a person with a naturally lower GLP-1 response (e.g., a carb-sensitive fat storer) is eating a high-carb, frequent-meal diet, they would struggle with satiety and likely overconsume. If they were following a diet more suited to their metabolic archetype—e.g., a higher-protein, higher-fat, or lower-frequency meal pattern—they might maintain a healthier weight.
The Effect of Modern Food Environments on Each Metabolic Archetype
1.Fat-Adapted Metabolizers™ & Carb-Sensitive Fat Storers™ are the most disrupted by modern diets.
•They are least suited to high-carb processed foods.
•GLP-1 deficiency is naturally handled in ancestral nutrition but made worse in modern environments due to artificial food exposure.
•Western diets lead to insulin resistance, inflammation, and metabolic dysfunction.
2.Dual-Fuel Metabolizers™ have some protection, but still face issues with modern food.
•Excess refined carbs make them lose metabolic flexibility.
•They handle low GLP-1 better than carb-efficient types but still rely on some incretin signaling.
3.Carb-Efficient Metabolizers™ are most adapted to high-carb diets but struggle with processed food & meal frequency.
•If GLP-1 is low, satiety and glucose regulation become problematic.
•They must rely on ancestral, whole-food carb sources instead of modern refined foods.4.Hyper-Metabolic Outliers struggle when GLP-1 is low because they require high-caloric intake.
•Modern hyperpalatable food may encourage overconsumption.
•Their natural caloric needs are high, so they need clean fuel sources.⸻
This table examines modern diet, Metabolic Archetypes™ and GLP-1:
• How the modern diet interacts with the archetype’s natural metabolism.
• How modern food disrupts or aligns with their historical adaptations.
• How GLP-1 deficiency is amplified or mitigated by the modern environment.
It is possible for someone to have genetic variants that result in lower GLP-1 production and still function metabolically well enough to fit into the Carb-Efficient, Dual-Fuel, or even Hyper-Metabolic Outlier archetypes. Here’s why:
1. Alternative Satiety & Insulin Regulation Pathways. Even if someone has lower GLP-1 production, other systems can compensate:
•GIP (Gastric Inhibitory Polypeptide): Some individuals may have stronger GIP signaling, which can partially compensate for lower GLP-1, helping maintain insulin secretion and glucose control.
•Pancreatic β-cell function: Even with low GLP-1, if someone has highly responsive β-cells (e.g., strong insulin secretion from other signals like amino acids or neural input), they may still regulate glucose well.
•Insulin Sensitivity: If muscle and liver insulin sensitivity is high (e.g., good mitochondrial function, low inflammation), they can handle carbs well despite lower incretin support.
2. Mitochondrial Efficiency & Metabolic Rate
•If a person has high mitochondrial efficiency (e.g., variants in PPARGC1A, UCP1, UCP2), they may still be a Hyper-Metabolic Outlier even with lower GLP-1.
•High energy expenditure (e.g., increased brown fat activity, elevated thyroid hormone signaling) can allow someone to process carbs effectively despite weaker GLP-1-driven satiety.
3. Carb Handling Without High GLP-1
•Some Carb-Efficient Metabolizers might have a strong first-phase insulin response, meaning they don’t need high GLP-1 for post-meal glucose control.
•Dual-Fuel Metabolizers can adapt by efficiently using fatty acids when glucose isn’t available, relying less on incretin-driven insulin regulation.
4. Other Satiety & Appetite Regulation Mechanisms. If someone has:
•Higher leptin sensitivity (better fat-derived satiety signaling)
•Stronger PYY (Peptide YY) response (gut-derived satiety)
•More dopamine-driven reward signaling from protein & fat,they may regulate appetite well despite lower GLP-1.