As to ascorbic acid,
right from the beginning I felt that the medical
profession misled the public.
If you don't take ascorbic acid with your
food you get scurvy, so the medical profession said that if you don't
get scurvy you are all right.
I think that this is a very grave error.
Scurvy is not the first sign of the deficiency but a premortal
syndrome, and for full health you need much more, very much more.
I am
taking, myself, about 1 g/day.
This does not mean that this is really
the optimum dose because we do not know what full health really means
and how much ascorbic acid you need for it.
What I can tell you is that
one can take any amount of ascorbic acid without the least
danger.
Albert Szent-Györgyi
(cited by Pauling 1976a, 1986a)
Scurvy is a definite clinical end point, and preventing scurvy was the
basis of the US RDA nutritional recommendations for vitamin C from the
1940s until the 10th edition (FNB 1989a,
1994a).
Approximately 10
mg/day of vitamin C prevents overt symptoms of scurvy, and the RDA of
the 10th edition was arbitrarily set at 60 mg/day to ‘provide
an adequate margin of safety’ against scurvy (FNB 1989a p
118). "This level of intake will prevent signs of scurvy for
at least 4
weeks" in the fictional condition that a person completely stopped
getting vitamin C.
Scurvy is an acute severe disease resulting from
particularly low vitamin C intake but the lack of a frank deficiency
per se does not necessarily reflect optimal metabolism. Thus, while the
goal of the early RDA was to protect against overt scurvy, the goal
could be to obtain optimal amounts of nutrients (Sigal & King
1937; Bourne 1949;
Pauling
1968,
1970b,
1974;
Hughes 1981;
Hemilä 1984,
1985,
1986, 1991;
Levine
1986;
Levine
et al. 1995;
Ginter
1989; Eaton
et al. 1996).
There
were no studies described in the RDA
recommendations which would suggest that 60 mg/day is any better than
10 mg/day as regards any health status outcome in the long term (FNB
1989a pp
115-24).
In the 10th edition of the RDA, this lack of concern
with optimal intakes was explicitly recognized: "RDAs are not
necessarily optimal levels
of intake" (FNB 1989a p
8). In the 10th edition (FNB 1989a p
1) the
"RDAs are defined as the levels of intake of essential nutrients that
… are … adequate to meet the nutrient needs of
practically all healthy persons." However, ‘nutrient
need’ is a vague concept and was not defined in any more
detail in the RDA recommendations. The concept of ‘nutrient
need’ gives the false impression that exact amounts of
vitamins are required daily, so that larger amounts could not have any
active physiological effects, simply providing passive reserves, such
that 60 mg/day of vitamin C would only cause
‘reserves’ large enough to prevent signs of scurvy
for 4 weeks. Such reasoning clearly demonstrates the lack of
consideration of the principles of biochemical reaction kinetics, as
the rates of biochemical reactions change smoothly with increasing
concentrations. The physiological purpose of vitamin C is not to be
‘in reserve against scurvy’ but to participate in
chemical reactions in the body, and the rates of these reactions depend
on concentrations, which depend on the levels of intake. Consequently,
an exact level of ‘nutrient need’ sharply
distinguishing a frank deficiency from ‘normal
health’ is not a sound concept (Hemilä 1984,
1985,
1991).
Furthermore, mathematical modeling of nutrient doseresponse
relationships in animals does not identify any parameter with
‘nutrient need’, the dose-response relations
following the saturation type of functions (Morgan et al. 1975;
Schulz
1987,
1991),
as
expected on biochemical grounds (Pauling 1968).
In
contrast to the ‘nutrient need,’ the concept of
‘optimal intake’ seems to be consistent with
biochemical knowledge (Pauling 1968;
Hemilä 1984,
1985,
1986, 1991).
Some early authors on vitamin C and infectious diseases
commented on the question of optimal intake. King (1936)
commented
that
"The fact that there is a wide zone of vitamin deficiency between
scurvy and optimum health is of more interest in relation to human
health than the problem of clinical scurvy," and from his own study on
the effects of vitamin C on diphtheria toxin on guinea pigs he
concluded that "It is evident from the data presented that the level of
vitamin C intake for optimum in vivo detoxification of diphtheria toxin
is considerably greater than that necessary to protect from scurvy or
to show a favorable growth rate" (Sigal & King 1937
p 8).
Perla (1937)
and
Perla and Marmorston (1937
p
686) asked: "Is one
certain of the optimal vitamin requirements? Can the criteria of
growth, progressive increase in weight and absence of clinical
evidences of deficiency be accepted as adequate? Is it not possible
that all these may be present and still, under a given stress, such as
invasion with micro-organisms or injections of poisons, the apparent
optimal amounts do not prove to be so?"
With the disappearance of
deficiency diseases as a serious problem in the Western countries, and
the increasing interest in the role of nutrition in affecting chronic
diseases (FNB 1994a,
1994b;
Lachance
& Langseth 1994),
"A
new
paradigm for determining RDAs was indicated" (King 1996).
After the
10th edition of the RDA, the approach of the nutritional
recommendations was extensively revised. In the most recent US
recommendations (FNB 2000)
the possibility of affecting chronic
diseases with vitamin C was extensively discussed. In these latest
recommendations, the length of the vitamin C chapter is 91 pages (FNB 2000
pp
95-185), in contrast to the 10 pages of the 10th edition of
RDA
(FNB 1989a pp
115-24). Although the latest recommendations thoroughly
discuss the epidemiological literature relating vitamin C intake with
chronic diseases, the authors conclude that there are no appropriate
studies that would yield data about what might be proper doses for
preventing the chronic diseases. Instead, the latest vitamin C
recommendations consider that "In the absence of other data, maximal
neutrophil concentration with minimal urinary loss appears to be the
best biomarker at the present time" (FNB 2000 p
140). This end point
is, however, a surrogate and there is no evidence cited that vitamin C
level in neutrophils has any relation to some clinical disease end
point, so that the maximal level in these cells would correspond to
optimal intake level in the long term (FNB 2000 pp
95-185). However,
there are quite a few examples in which the effect on a surrogate
marker diverged from the effect on a clinical outcome (Fleming
& DeMets 1996; DeGruttola et al. 1997).
A further important restriction of both the early and the current RDAs
is that they apply specifically to ‘healthy
persons’ (FNB 1989a
p
1) and ‘apparently healthy
individuals’ (FNB 2000 p
23). Consequently, the RDA levels
are not intended to provide reference levels of intake for people who
are sick, for example, with the common cold or more severe infections.
While the nutritional recommendations have great importance in
nutrition politics, they cannot be used as a basis for claiming that
amounts in excess of RDA levels are known to be useless. The early RDA
recommendations used an acute clinical outcome that is irrelevant when
considering the possible long-term effects of vitamin C intake, and the
new recommendations use a surrogate that has no known validity as
regards its long-term health effects.
Kunkel (1996;
Kunkel
& Thompson 1988) criticized the lack of
appropriate philosophical considerations behind the nutritional
recommendations: "The reasoning, however, can become circular and
unsound when the considered moral judgments, moral principles and
relevant background are not independent sources of information. If they
are mixed or, for example, an intuition is mistaken for a scientific
conclusion, the reasoning can be flawed."
References
NOTE: All the links in the
main text should be freely accessible at least as an abstract, but some
links
below require a permission from publisher for any access.
Ginter E (1989) Ascorbic acid in cholesterol metabolism and in
detoxification of xenobiotic substances: problem of optimum vitamin C
intake. Nutrition 5:369-74
Perla D (1937) The effect of an excess of vitamin C on the natural
resistance of mice and guinea pigs to Trypanosome infections.
Am J Hyg 26:374-81
p
379
Perla D, Marmorston J (1937) Role of vitamin C in resistance.
Part I Arch Pathol 23:543-75 Part II
23:683-712
p
686
