No it's not new Steve. Two separate gene defects occured, one affecting
lactonase activity and the other affecting L-gulonolactone oxidase
activity. Not everyone died on those long sea voyages (those that didn't
still synthesized vitamin C). In some populations, the nonsynthesizers have
been completely removed from the gene pool (the Sahara nomads for example).
The lactonase defect prevents any vitamin C synthesis at all. The L-
gulonolactone oxidase defect (which is the last enzymatic step in the
vitamin C synthetic pathway) does allow some vitamin C synthesis because
the substrate (L-gulono-gamma-lactone) will spontaneously decompose to 2-
keto-gulono-gamma-lactone in the presence of oxygen (which the L-
gulonolactone oxidase would have used to complete the same kind of reaction
process). The only difference now is the speed (the enzyme oxidase would of
course done it much faster than the spontaneous oxidation process can).
The final step, conversion of 2-keto-gulono-gamma-lactone to L-ascorbic
acid is a spontaneous nonenzymatic conversion process. From reading the
literature the best estimate I have of vitamin C formation in humans that
can still form it is 15-20mg per day in a nonstressed state (no active
infection) with higher amounts possible during infection but I have never
been able to get what the maximum formation could (can) be during severe
stress.
Textbooks are correct in stating that there is no enzymatic synthesis of
vitamin C in humans. Any formation (and it's going to be very small in
comparison to what could have been formed without a defective gene) that
still occurs in humans is all spontaneous nonenzymatic formation. But that
process is enough to prevent scurvy (which only needs 15 mg per day).
If you really start digging into the area of nutrition, you will find many
bits and pieces of information that don't find their way into textbooks.
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