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Homo sapiens ascorbicus, a biochemically corrected robust human mutant.

I Stone

    Medical Hypotheses
    |June 1, 1979
    PubMed
    Summary
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    Humans cannot synthesize vitamin C due to a defective GLO gene, leading to hypoascorbemia (scurvy). Supplementing vitamin C to levels produced by other mammals can reverse this genetic defect, improving health and longevity.

    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.

    Related Experiment Videos

  • 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.