One study is interesting but not definitive. I notice the same group
found something similar--but in Wyoming. I wonder why they moved from
Wyoming to Spokane?

        George M. Carter

**
Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human
oxaluria and kidney stone risk. J Nutr. 2005 Jul;135(7):1673-7.

Department of Food Science and Human Nutrition, Washington State
University, Spokane, WA and.

Currently, the recommended upper limit for ascorbic acid (AA) intake
is 2000 mg/d. However, because AA is endogenously converted to oxalate
and appears to increase the absorption of dietary oxalate,
supplementation may increase the risk of kidney stones. The effect of
AA supplementation on urinary oxalate was studied in a randomized,
crossover, controlled design in which subjects consumed a controlled
diet in a university metabolic unit. Stoneformers (n = 29; SF) and
age- and gender-matched non-stoneformers (n = 19; NSF) consumed 1000
mg AA twice each day with each morning and evening meal for 6 d
(treatment A), and no AA for 6 d (treatment N) in random order. After
5 d of adaptation to a low-oxalate diet, participants lived for 24 h
in a metabolic unit, during which they were given 136 mg oxalate,
including 18 mg (13)C(2) oxalic acid, 2 h before breakfast; they then
consumed a controlled very low-oxalate diet for 24 h. Of the 48
participants, 19 (12 stoneformers, 7 non-stoneformers) were identified
as responders, defined by an increase in 24-h total oxalate excretion

Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66
treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31% increase
in the percentage of oxalate absorption (10.5 +/- 3.2% treatment A vs.
8.0 +/- 2.4% treatment N) and a 39% increase in endogenous oxalate
synthesis with treatment A than during treatment N (544 +/- 131 A vs.
391 +/- 71 mumol/d N). The 1000 mg AA twice each day increased urinary
oxalate and TRI for calcium oxalate kidney stones in 40% of
participants, both stoneformers and non-stoneformers.

PMID: 15987848 [PubMed - in process]

***
Chai W, Liebman M, Kynast-Gales S, Massey L. Oxalate absorption and
endogenous oxalate synthesis from ascorbate in calcium oxalate stone
formers and non-stone formers. Am J Kidney Dis. 2004 Dec;44(6):1060-9.

Department of Family and Consumer Sciences (Nutrition), University of
Wyoming, Laramie, WY 82071, USA.

BACKGROUND: Increased rates of either oxalate absorption or endogenous
oxalate synthesis can contribute to hyperoxaluria, a primary risk
factor for the formation of calcium oxalate-containing kidney stones.
This study involves a comparative assessment of oxalate absorption and
endogenous oxalate synthesis in subpopulations of stone formers (SFs)
and non-stone formers (NSFs) and an assessment of the effect of
ascorbate supplementation on oxalate absorption and endogenous oxalate
synthesis. METHODS: Twenty-nine individuals with a history of calcium
oxalate kidney stones (19 men, 10 women) and 19 age-matched NSFs (8
men, 11 women) participated in two 6-day controlled feeding
experimental periods: ascorbate-supplement (2 g/d) and no-supplement
treatments. An oxalate load consisting of 118 mg of unlabeled oxalate
and 18 mg of 13C2 -oxalic acid was administered the morning of day 6
of each experimental period. RESULTS: Mean 13C2 -oxalic acid
absorption averaged across the ascorbate and no-supplement treatments
was significantly greater in SFs (9.9%) than NSFs (8.0%). SFs also had
significantly greater 24-hour post-oxalate load urinary total oxalate
and endogenous oxalate levels with both treatments. Twenty-four-hour
urinary total oxalate level correlated strongly with both 13C2 -oxalic
acid absorption (SFs, r = 0.76; P < 0.01; NSFs, r = 0.62; P < 0.01)
and endogenous oxalate synthesis (SFs, r = 0.95; P < 0.01; NSFs, r =
0.92; P < 0.01). CONCLUSION: SFs are characterized by greater rates of
both oxalate absorption and endogenous oxalate synthesis, and both
these factors contribute to the hyperoxaluric state. The finding that
ascorbate supplementation increased urinary total and endogenous
oxalate levels suggested that this practice is a risk factor for
individuals predisposed to kidney stones.

For Immediate Release:

VITAMIN C DOES NOT CAUSE KIDNEY STONES

(Orthomolecular Medicine News Service, July 5 2005)

By Steve Hickey, PhD and Hilary Roberts, PhD.

(OMNS) It is strange how some medical authors seem desperate to show
that vitamin C causes harm. One recurrent scare story is that vitamin C
might cause kidney stones. However, although such warnings pop up
regularly, these reports do not demonstrate an increase in the number
or size of stones; instead, they rely on vague indicators of improbable
risk.

The authors of such uncritical papers have probably not read the
literature, for this is an old story. Decades ago, the idea that
vitamin C causes kidney stones formed part of the medical attack on
Linus Pauling. While it was initially a reasonable hypothesis,
unexpected kidney stones are not found in people taking large amounts
of vitamin C. (1,2)

There is no evidence that vitamin C causes kidney stones. Indeed, in
some cases, high doses may be curative. (3) A recent, large-scale,
prospective study followed 85,557 women for 14 years and found no
evidence that vitamin C causes kidney stones. (4) There was no
difference in the occurrence of stones between people taking less than
250 milligrams per day and those taking 1.5 grams or more. This study
was a follow up of an earlier study on 45,251 men. This earlier study
indicated that doses of vitamin C above 1.5 grams reduce the risk of
kidney stones. (5) The authors of these large studies stated that
restriction of higher doses of vitamin C because of the possibility of
kidney stones is unwarranted.

People with recurrent stone formation may have an unusual biochemistry,
leading to increased production of oxalate from vitamin C. (6) Oxalate
and urate can accumulate in kidney stones. In practice, there is an
increased excretion of both oxalate and urate with gram level doses of
vitamin C (ascorbate). Various authors over the years have used this
increase to predict that vitamin C will cause kidney stones; however,
these predictions have never been confirmed.

Around three quarters of all kidney stones are composed of calcium
oxalate; unlike some other stone types, these can form in acidic urine.
Although vitamin C does increase the production of oxalate in the body,
there is no evidence that it increases stone formation. It could even
have the reverse effect, for several reasons. Firstly, vitamin C tends
to bind calcium, which could decrease its availability for formation of
calcium oxalate. Secondly, vitamin C has a diuretic action: it
increases urine flow, providing an environment that is less suitable
for formation of kidney stones. Finally, stone formation appears to
occur around a nucleus of infection. High concentrations of vitamin C
are bactericidal and might prevent stone formation by removing the
bacteria around which stones form.

Vitamin C could also prevent other types of kidney stones. Less common
forms of stone include uric acid stones (8%), that form in gout, and
cystine stones (1%), which can occasionally be formed in children with
a hereditary condition; these stones are not side effects of vitamin C.
Other stones include those made from calcium phosphate (5%), which
dissolve in a vitamin C solution. Acid urine, produced by ascorbate,
will also dissolve the struvite stones (magnesium ammonium phosphate)
that often occur in infected urine.

Recently, Linda Massey and colleagues from Washington State University
have claimed that vitamin C increases the risk of kidney stones. (7)
Their paper illustrates how the claims of risk have little basis in
fact. Massey claims that vitamin C supplementation can increase the
amount of oxalate. Vitamin C can increase oxalate absorption and, if
degraded in the body, ascorbate can be converted into oxalate. However,
while oxalate is a constituent of some types of kidney stone, an
increase in its concentration does not mean that more or larger kidney
stones will be formed. The formation of kidney stones is influenced by
many factors and, as we have seen, vitamin C might be predicted to
inhibit several aspects of stone generation. Massey suggests that this
increase in oxalate may increase the risk of stones. This is a weak
suggestion, which is contradicted by substantial evidence, quoted
above.

This evidence suggests that a high vitamin C intake has no effect on
the number of kidney stones, or may even be protective.

Massey links oxalate to risk by use of a measure called the Tiselius
Risk Index or TRI. (8) However, this measure is applied incorrectly.
Indeed, in the presence of high doses of vitamin C, this index should
be modified to accommodate the formation of calcium ascorbate in urine.
The TRI measure was developed for subjects that had not been
supplemented with vitamin C and, on the basis of simple chemistry,
requires modification for use with ascorbate supplementation. Since
vitamin C might affect many stages of stone formation and growth,
application of the TRI measure to supplemented individuals is suspect.
The TRI is applied in this case as a predictive measure, for which it
has not been validated. Furthermore, the TRI is derived from the
concentration of calcium oxalate, making the argument for increased
risk rather circular. Even more importantly, Massey uses the TRI to
predict an increased theoretical risk, which substantial evidence
indicates is absent.

In Massey's study, 29 stoneformers and 19 non-stoneformers were
supplemented with one gram of vitamin C, twice each day. After five
days on a low-oxalate diet, the subjects were challenged before
breakfast with 136 mg oxalate, including 18 mg oxalic acid. They
remained on the low oxalate diet for the remainder of the day. Of the
48 people, 12 stoneformers and 7 non-stoneformers had an increased
total oxalate excretion of greater than 10% after supplementation.

However, the number or size of kidney stones did not increase.

Also, we can note that seven of the subjects who showed an increased
level of oxalate were not stoneformers. The important question of why
some people form kidney stones, and others do not, was neatly
sidestepped.

Massey's argument boils down to the vague idea that there could
possibly be an increase in kidney stone formation in some rare people.
This might be the case if vitamin C increased oxalate without affecting
any other part of the process; this is known to be false. If this is
the sort of evidence presented as acceptable, we can be comfortable
with the claim that the areas of the moon not yet visited by man may be
made of green cheese.

References:

1) Hickey S. Roberts H. (2004) Ascorbate: the Science of Vitamin C,
Lulu press.

2) Hickey S. Roberts H. (2004) Ridiculous Dietary Allowance, Lulu
press.

3) McCormick W.J. (1946) Lithogenesis and hypovitaminosis, Medical
Record, 159, 410-413.

4) Curhan, G. C., Willett, W. C., Speizer, F. E., Stampfer, M. J.
(1999) Megadose Vitamin C consumption does not cause kidney stones.
Intake of vitamins B6 and C and the risk of kidney stones in women, J
Am Soc Nephrol., Apr, 10, 4, 840-845.

5) Curhan G.C. Willett W.C. Rimm E.B. Stampfer M.J. (1996) A
prospective study of the intake of vitamins C and B6, and the risk of
kidney stones in men, J Urol, 155(6), 1847-1851.

6) Chalmers A.H, Cowley DM, Brown J.M. (1986) A possible etiological
role for ascorbate in calculi formation, Clin Chem, 32(2), 333-336.

7) Massey L.K. Liebman M. Kynast-Gales S.A. (2005) Ascorbate increases
human oxaluria and kidney stone risk, J Nutr, 135(7), 1673-1677.

8) Tiselius H.G. (2000) Stone incidence and formation, Clinical Urology
26(5), 452-462.

What is Orthomolecular Medicine?

Linus Pauling defined orthomolecular medicine as "the treatment of
disease by the provision of the optimum molecular environment,
especially the optimum concentrations of substances normally present in
the human body." Orthomolecular medicine uses safe, effective
nutritional therapy to fight illness. For more information:
http://www.orthomolecular.org

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Date: 05-Jul-05

Mark, some people have no business posting comments about scientific
studies.  You summarized by saying that 1000mg of vit. C daily raises
the risk of kidney stones, whereas the study doesn't say either.  Can
anyone besides me point out the mistake this Pharma Blogger made on
both his assertions?

The truth about kidney stone formation...

There are five types of kidney stones

1. Calcium phosphate stones are common and easily dissolve in urine
acidified by Vitamin C.

2. Calcium oxalate stones are also common but they do not dissolve in
acid urine.

3. Magnesium ammonium phosphate (struvite stones) are much less common,
often appearing after an infection. They dissolve in vitamin C
acidified urine.

4. Uric acid stones result from a problem metabolizing purines (the
chemical base of adenine, xanthine, theobromine [in chocolate] and uric
acid). They may form in a condition such as gout.

5. Cystine stones result from a hereditary inability to reabsorb
cystine. Most children's stones are this type, and these are rare.

Vitamin C actually plays a role in preventing and dissolving most
kidney stones, as the very common calcium phosphate variety exist only
in a non-acidic urinary tract.  So feel free to take your vit. C in
dosages equivalent to what is common throughout the animal kindgom
(ie., 1000mg and up), or eat lots of kiwi and oranges.

What about magnesium ammonium phosphate stones, the same struvite
stones associated with urinary tract infections that require surgical
removal?  Both the infection and the stone are easily eradicated (and
preventable) with large doses of vitamin C.

Interestingly, common calcium oxalate stones can form in an acidic
urine whether one takes vitamin C or not. However, if a person gets
adequate quantities of B-complex vitamins and magnesium, this type of
stone will not form. Any common B-complex supplement twice daily, plus
about 400 milligrams of magnesium, is usually adequate.  Does ascorbate
(the active ion in vitamin C) increase the body's production of
oxalate?  Yes, and this is the "marker" referred to in the study
Thorson posted.  In practice, however, an increase in oxalate stone
formation does not follow consumption of vitamin C in fruits or
supplements.  In The Vitamin C Connection (publ. 1983), Drs. Emanuel
Cheraskin, Marshall Ringsdorf, Jr. and Emily Sisley explain that acidic
urine, or slightly acidic urine, reduces the UNION of calcium and
oxalate and thus reduces the possibility of kidney stones. "Vitamin C
in the urine tends to bind calcium and decrease its free form. This
means less chance of calcium's separating out as calcium oxalate
(stones)."  page 213.

The diuretic effect of vitamin C also reduces the static conditions
generally necessary for stone formation. One can always avoid excessive
oxalates in the diet, rather than reducing a crucial nutrient such as
vitamin C.  And if a doctor thinks a person is especially prone to
forming oxalate stones, the patient can simply change his regular
vitamin C to a buffered (non-acidic) form.  Problem solved.

As for vitamin C utilization in the animal kingdom, it's all but
universal.  A gorilla gets about 4,000 mg of vitamin C in its natural
diet on a daily basis. The US RDA for humans is only 60 mg. Who do you
suspect has it right, the National Academy of Sciences, or the
gorillas?  Do you think thousands of gorillas are out in the wild
cramped up every day, wailing from the jungle floor, suffering an
epidemic of kidney stones?  Is vitamin C a naturally-occuring nutrient
in the food chain?  Do you think the drug companies might be trying to
prepare the public for an assault on the freedom of access to high-dose
vitamin C in the market place?  If you aren't familiar with the Codex
Alimentarius steamrolling across Europe, and next the USA, you need to
do so.  Visit the Alliance for Natural Health and find out what's
really going on.

There are likely to be a number of factors predisposing to kidney
stones, and certainly genetics play a role, however the need for
balance in our nutrient status is crucial for overall quality of
health, not just prevention of kidney stones.  The point is that
imbalance in an individual's nutrient state can be a factor in kidney
stone formation whether ascorbic acid is supplemented, or not.  Did the
study analyse or evaluate these other confounding factors?  No.  Did
the study actually observe the formation of a kidney stone as a result
of supplementing vitamin C?  No.

PeterB

<Pharma Blogging snipped>