Amylase Enzyme - Preferential or Compensatory Adaptation?

I have seen it argued that human adaptation for the increased production of the digestive enzyme ‘amylase’ (the enzyme responsible for starch digestion) seen since the advent of agriculture is evidence that humans have become adapted for Preferential reliance upon starches and therefore can be said to no longer be Hypercarnivores by physiology and digestive function. However, this is a mistake and upon reviewing the evidence it is clear that we are still very much Hypercarnivores.

Human evolution, especially dietary evolution, has largely revolved around adaptive shifts to survive in varied environments. The ability to digest starch, via the evolution of increased salivary and pancreatic amylase, is a notable adaptation. However, this capacity does not necessarily indicate an evolution "away" from an animal-based diet towards one reliant on starches. Instead, evidence from biochemistry, cellular biology, and gastroenterology suggests that amylase adaptation is a compensatory response to mitigate potential detriments from increased starch consumption in situations where traditional, hypercarnivorous diets were unavailable.

Amylase Production and Its Evolutionary Context

Increased amylase production in humans is well-documented, particularly in populations historically exposed to high-starch diets (Perry et al., 2007). Gene copy number variations (CNVs) of the salivary amylase gene ‘AMY1’ correlate with starch intake; more copies of ‘AMY1’ equate to higher amylase levels, facilitating more efficient starch digestion (Inoue & Inoue-Murayama, 2021). This adaptation allowed certain populations to harness energy from starches more effectively. However, biochemically, the increased production of amylase doesn’t equate to a dietary shift optimal for starch but rather reflects a compensatory adaptation - an evolved trait designed to minimize adverse effects when starch becomes a dietary necessity.

Biochemistry of Amylase and Starch Breakdown

Amylase catalyzes the hydrolysis of starch into maltose and glucose, aiding in energy acquisition. However, unlike cellulose, which humans cannot digest, starch can be metabolized when amylase is present. This enzymatic process primarily occurs in the oral cavity and small intestine. Crucially, the presence of increased amylase in some human populations doesn’t necessarily denote an evolutionary advantage of starch as a primary food source but rather provides a biochemical workaround to process these foods in emergencies or periods of scarcity of animal protein.

Biochemically, glucose generated from starch digestion rapidly raises blood glucose levels, potentially inciting chronic hyperglycemia and insulin resistance (Ludwig, 2002). This phenomenon could signify that although we can digest starch, our metabolic response is not optimally adapted to it, suggesting that hypercarnivorous biochemistry remains predominant.

Further evidence that the adaption of increased amylase is a compensatory mechanism and not the evidence of a shift towards carbohydrates becoming our “preferred” food is the fact that our cellular level energy production processes are still preferentially geared towards animal fats and proteins.

Mitochondrial Adaptation to Protein and Fat Metabolism

Human mitochondria are particularly efficient at metabolizing lipids and proteins, as demonstrated by the abundance of enzymes in human muscle tissue optimized for fat oxidation (Phinney, 2004). Unlike herbivores, humans lack the extensive enzymatic machinery to handle sustained high-glycemic loads, as seen in starch-heavy diets. Our cellular machinery has adapted to thrive on high-fat, high-protein intakes characteristic of a hypercarnivorous diet.

At a cellular level, fatty acids are oxidized to produce energy in the form of ATP via beta-oxidation, a process essential for hypercarnivorous species. Increased reliance on starch requires humans to rely more on glycolysis and glycogenesis, pathways that can cause oxidative stress and increase the production of reactive oxygen species (ROS) in tissues not evolutionarily adapted to handle high glucose loads (Volek & Phinney, 2012). This cellular stress indicates a maladaptive reaction to starch, further supporting the notion that starch digestion capacity is more of a compensatory adaptation than a sign of dietary optimization.

Genetic Adaptations Associated with Carnivory

The evolution of genes associated with starch digestion, such as ‘AMY1’, contrasts with genetic signatures tied to fat and protein metabolism. For instance, the FADS gene cluster, which regulates fatty acid desaturation, shows adaptations supporting the efficient conversion of dietary fat to essential fatty acids, an evolutionary advantage for a diet rich in animal sources (Ameur et al., 2012). These genetic traits align more closely with hypercarnivory and high-fat intake, signifying that while starch adaptation exists, it is likely a secondary or compensatory feature.

Gastroenterology and Digestive System Limitations

Human digestive morphology provides further evidence of hypercarnivorous ancestry. The relatively small size of the human large intestine and absence of a cecum (common in herbivores for cellulose fermentation) indicates that humans evolved to digest high-protein, low-fiber foods rather than starch-rich plants (Milton, 2003). The reliance on amylase and other compensatory enzymes, rather than a more specialized fermentative capability for starch digestion, underscores that humans are not primarily starch-adapted.

Amylase and the Mitigation of Digestive Damage

Gastrointestinal issues such as bloating, inflammation, and dysbiosis are frequently observed in populations consuming high-starch diets (Simopoulos, 2002). Increased amylase production may mitigate some of the acute digestive distress associated with high starch intake but does not entirely prevent these adverse effects. Chronic intake of starch-heavy diets has been linked to increased gastrointestinal cancers, especially in individuals lacking high ‘AMY1’ copy numbers (Carrera-Bastos et al., 2011). These gastrointestinal responses further reinforce that our digestive system evolved for meat digestion and that starch adaptation is merely a secondary, mitigating measure.

Conclusion

The evolution of amylase production in humans reflects a fascinating example of dietary plasticity. However, the increase in ‘AMY1’ gene copy numbers and the resultant amylase production should not be interpreted as a sign that humans are physiologically optimized for starch-based diets. Rather, it suggests a compensatory adaptation to handle suboptimal food sources in environments where animal protein may be limited. Biochemical, cellular, and gastroenterological evidence supports the hypothesis that human physiology remains best suited to a hypercarnivorous diet, with starch-digesting adaptations serving primarily to mitigate potential digestive and metabolic harm when animal-based foods are scarce.

References:

• Ameur, A., Enroth, S., Johansson, A., Zaboli, G., Igl, W., Johansson, A. C. V., Rivas, M. A., Daly, M. J., Schmitz, G., Hicks, A. A., & Feuk, L. (2012). Genetic adaptation of fatty-acid metabolism: an Ethiopian perspective. *Nature Genetics*, 44(9), 972–976.

• Carrera-Bastos, P., Fontes-Villalba, M., O'Keefe, J. H., Lindeberg, S., & Cordain, L. (2011). The western diet and lifestyle and diseases of civilization. *Research Reports in Clinical Cardiology*, 2, 15–35.

• Inoue, T., & Inoue-Murayama, M. (2021). Evolution of copy number variation of the amylase gene in various mammals. *Scientific Reports*, 11, 22468.

• Ludwig, D. S. (2002). The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. *JAMA*, 287(18), 2414-2423.

• Milton, K. (2003). The critical role played by animal source foods in human (Homo) evolution. *Journal of Nutrition*, 133(11), 3886S–3892S.

• Perry, G. H., Dominy, N. J., Claw, K. G., Lee, A. S., Fiegler, H., Redon, R., Werner, J., Villanea, F. A., Mountain, J. L., Misra, R., Carter, N. P., Lee, C., & Stone, A. C. (2007). Diet and the evolution of human amylase gene copy number variation. *Nature Genetics*, 39(10), 1256–1260.

• Phinney, S. D. (2004). Ketogenic diets and physical performance. *Nutrition & Metabolism*, 1(1), 2.

• Simopoulos, A. P. (2002). The importance of the ratio of omega-6/omega-3 essential fatty acids. *Biomedicine & Pharmacotherapy*, 56(8), 365-379.

• Volek, J. S., & Phinney, S. D. (2012). *The Art and Science of Low Carbohydrate Performance.* Beyond Obesity LLC.