Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study

Choi and Curhan have presented compelling prospective data which
suggests a strong association between fructose consumption and the risk of
gout in North American men [1]. Whatever the validity of their
conclusions, the team deserves our unanimous respect and gratitude for
attempting to identify a dietary cause of a chronic inflammatory
condition: after all, scores of us who do - or will - suffer from one or
more inflammatory diseases know it is all too common for our physicians to
routinely and with surprising promptness ascribe our ailments not to
dietary indiscretion, not to environmental factors, but to either medical
ignorance, genetics, or, what is most disturbing and really quite
insulting, our psychological state. For our part, we demand a rather more
scientific answer to our inquiry, and Choi and Curhan have nobly attempted
to meet this reasonable demand.

That being said, we must expose a rather unfortunate oversight made
by our etiologists. Inasmuch as ordinary salt commonly, but not always
[2], causes an increase in the renal excretion of water [3, 4] and a
corresponding increase in fluid intake [3, 4], one can justifiably wonder
if in neglecting the potential impact of salted foods and beverages on
fructose consumption, Choi and Curhan have overlooked an important
variable. I am not at all suggesting that salt per se is a cause of
inflammation, whether it be the inflammation of arthtritis, colitis,
psoriasis, ad infinitum. Sodium chloride is rapidly excreted by healthy
kidneys, and the association between salt consumption and hypertension, a
condition often encountered in the arthritic [5], remains controversial,
some studies showing a weak association, others an apparently strong
association.

I submit that the very reason a clear association between
hypertension and salt consumption has not yet been made may well be the
reason which goes far to explain why Choi and Curhan's fructose may be
nothing more than a helpless scapegoat [6] in a search for a cause of
gout. The reason is, that our reviewers, researchers and etiolgists have,
with a few exceptions [2], habitually neglected in their work on salt and
human health to carefully dissociate NaCl from those many foods and
beverages which are ordinarily salted [3, 7]; they have also occasionally
committed the grave error of validating the findings of these specious
studies in subsequent work in which salt was administered in a
standardized fashion - but on hypertensive, rather than healthy subjects
[4]. If it can be established that salt itself is innocuous [2, 8], we
must explore the possible role those foods and drinks ordinarily salted,
the concentrated starches, the processed animal products, the packaged
convenience foods, might themselves have in the etiology of inflammation,
apart from their sodium chloride component. It would seem reasonable to
begin such investigations with special reference to food and drinks
sharing common properties: for instance, by exploring the possible role
additives and chemicals [9] or techniques used in preparing these foods
and drinks for the diner (e.g., sustained application of high heat,
resulting in oxidation of unstable fats and distortion of sensitive
proteins), might have.

I find it rather striking, incidentally, that Choi and Curhan found
those subjects with the highest sugar sweetened soft drink consumption
consumed more meat, high-fat dairy, and caffeine, and less low-fat dairy
[1, Table 1]. This suggests that soda drinkers are less apt to act on
current health recommendations, and summons the thought whether one or
more of these transgressions might be of greater significance than the
consumption of our beleaguered monosaccharide: perhaps a violation of one
of the above, or one not identified by Choi and Curhan (e.g., recreational
drug use), or perhaps a cause not yet found by modern science.

There is no doubt that in studies which fail to dissociate salt from
the foods and drinks in which it is commonly found, fluid intake
increases; and, further, that many of us opt not for ordinary water but
for soda or fruit juice to allay the resultant thirst. But this hardly
proves that fructose or salt consumption causes obesity [3] or gout,
however tempting it might thus be to implicate one or the other.

To close, the BMJ is to be commended for furnishing the general
public this platform for discussion and debate on subjects which should
intimately concern each member of the human race, namely, disease,
nutrition, and the pursuit of health and graceful aging. I personally
thank them for affording me this opportunity to contribute to this forum
in a small but meaningful way.

REFERENCES

1. Choi HK, Curhan G. Soft drinks, fructose consumption, and the
risk of gout in men: prospective cohort study. BMJ. 2008; 336: 309-312.

2. Luft FC, Fineberg NS, Sloan RS, Hunt JN. The effect of dietary
sodium and protein on urine volume and water intake. J Lab Clin Med. 1983
Apr; 101(4): 605-10.

3. He FJ, Marrero NM, MacGregor GA. Salt intake is related to soft
drink consumption in children and adolescents: a link to obesity?
Hypertension. 2008 Mar; 51(3): 629-34.

4. He FJ, Markandu ND, Sagnella GA, MacGregor GA. Effect of salt
intake on renal excretion of water in humans. Hypertension. 2001; 38:
317–320.

5. Panoulas VF, Metsios GS, Pace AV, John H, Treharne GJ, Banks MJ,
Kitas GD. Hypertension in rheumatoid arthritis. Rheumatology (Oxford).
2008 May 29. [Epub ahead of print].

6. In this connection, see John White's earlier reply to this
article in which he ably identifies some disturbing anomalies in the
research lending itself to the arthritis-fructose theory.

7. Cutler JA, Follmann D, Allender PS. Randomized trials of sodium
reduction: an overview. Am J Clin Nutr. 1997 Feb; 65(2 Suppl): 643S-651S.

8. Beevers DG, Hawthorne VM, Padfield PL. Salt and blood pressure
in Scotland. Br Med J. 1980 Sep 6; 281(6241): 641-2.

9. See Ivan Toshin's foregoing Rapid Response of February 4, 2008,
entitled, "Did we notice the 'oliphant'?"

Competing interests:
None declared