Homo sapiens ascorbicus, a biochemically corrected robust human mutant

Area of Science:

• Biochemistry
• Genetics
• Human Physiology

Background:

• Homo sapiens possess a defective gene for L-gulonolactone oxidase (GLO), preventing endogenous synthesis of ascorbate (vitamin C).
• This genetic defect results in an "inborn error of carbohydrate metabolism" known as hypoascorbemia, historically recognized as scurvy.
• Unlike most mammals, humans require exogenous sources of ascorbate to maintain normal physiological functions.

Purpose of the Study:

• To investigate the implications of the defective GLO gene in humans.
• To evaluate the adequacy of current recommended dietary allowances for ascorbate.
• To explore the potential health benefits of correcting the human ascorbate synthesis defect.

Main Methods:

• Comparative analysis of ascorbate synthesis in humans versus other mammals.
• Assessment of the human GLO gene's functional status.
• Evaluation of health outcomes in humans with corrected ascorbate levels.

Main Results:

• Humans lack the functional GLO gene, necessitating dietary ascorbate intake.
• Current recommended daily allowances of ascorbate are insufficient for optimal human health.
• Elevated ascorbate intake, mimicking mammalian synthesis, demonstrated significant health benefits.

Conclusions:

• The human inability to synthesize ascorbate is a significant genetic defect with widespread health consequences.
• Restoring physiological ascorbate levels through supplementation offers substantial benefits for health maintenance, disease treatment, and anti-aging.
• Biochemical reversal of this ancient mutation could lead to a more robust human subspecies, Homo sapiens ascorbicus.