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Rapid Responses: Rapid Responses published:
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Did we notice the 'oliphant'?
- Ivan Y Toshin (4 February 2008)
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Me , My Gout and Fruits
- Amarasinghe A.W. Amarasinghe (12 February 2008)
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Re: Me , My Gout and Fruits
- GEORGE Y CALDWELL (13 February 2008)
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Sugar sweetened soft drinks and fructose are not unique or significant risk factors for gout
- John S White (10 June 2008)
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Reflections on Omission of Dietary Salt in Recent Gout-Fructose Study
- Hendrickus A Brokking (13 June 2008)
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Ivan Y Toshin, Moscow State University 119899
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SIR, with great interest I read the report of Drs. Choi and Curhan "Soft drinks, fructose consumption...". It's a nice study that presents a reasonably well justified epidemiological evidence. However, attributing the risk specifically to sugar content of the soft drinks does appear too preliminary. First of all, what we know as 'soft drinks' contain much more than just sugar. They, invariably, contain a large amount of the E-labeled food additives such as preservatives, coloring agents, flavors said to be 'nature identical' etc (see, for instance, the impressive Wikipedia list of them [1]). The list of papers in MEDLINE dealing with safety concerns over food additives is not less impressive, let's just mention here the most recent title [2]. Given the insidious chemical nature of most of these additives, I would not be surprised, as a biochemist, if they would induce considerable inflammation, among other effects. This conclusion can be inferred by simply looking at the frightening chemical formulae of these additives that remind rather of oil chemistry and oil procesing and not so much of food. Now, the matter of oliphant: it's rather the elephant was meant, but in a hostile sense. The elephant as in 'the elephant in the room' which has to be noticed, somehow... As suggested by the original [3], the 'oliphant' is not something very evil in itself but becomes so in the hands of some people. REFERENCES [1] http://en.wikipedia.org/wiki/Food_additive, http://en.wikipedia.org/wiki/List_of_food_additives [2]. Joint FAO/WHO Expert Committee on Food Additives.Evaluation of certain food additives and contaminants.World Health Organ Tech Rep Ser. 2007;(940):1-92, 1 p following 94. PMID: 17687927 [3] J. R. R. Tolkien (1987), The Two Towers, vol. 2, The Lord of the Rings, Boston ISBN 0-395-08254-4 Competing interests: None declared |
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Amarasinghe A.W. Amarasinghe, Consultant Psychiatrist 102 Bayberry Hills, McDonough,Georgia 30253-4005 USA
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Gurus of yester frowned on steak and wine
Competing interests: None declared |
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GEORGE Y CALDWELL, GENERAL PRACTITONER 31 BALMORAL PARK, #18-33, SINGAPORE 259858
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It is true that certain fruit will cause Gout. Of course Alcohol inhibits the excretion of both Uric and Oxalic Acids, those that cause Gout, and makes the attack more lasting. There is NO "Normal" Serum Uric Acid level. This "threshold level" can vary from person to person and depends on family genes and background. The fruit involved is usually high in Oxalic Acid which will play a "Cox and Box" game with Uric Acid. The one will replace the other in causing pain. To wit: Summer berry fruit, strawberries, raspberries, gooseberries, rhubarb, pineapple, figs, Apricot, nutmeg, persimmon, dates, mango, mangosteen, durian, Citrus peel (orange, lemon or lime) i.e. marmalade, and add on chocolate, coffee and strong (uric acid) tea. Apart from Mango and Durian these are all Oxalic Acid containing fruits. These other two are full of nucleo-protein hence the breakdown through Xanthine to Uric Acid. "Diet DOES play a part (the main part) in the causation of Gout", and much ordinary "common" Arthritis too, also Carpal Tunnel Syndrome, Achilles tendonitis, Tennis and golfer's elbow, or forearm, backache, etc. Which is the reverse of the sales-talk when Allopurinol was first came on sale. The Uric Acid comes from the breakdown, via Alanine and Guanine, of the Nucleo-protein DNA in the high quality fish and meat protein, such that has a highly nucleated content and histology. Remember the cross-section of tongue? The treatment still remains old fashioned and cheap: Meadow Saffron (Colchicine) plus the German Benzbromarone ("Narcaricin") ? not yet available in England. Lots of water, maybe with some Effervescent Potassium Citrate and abstaining from those luxury foods and alcohol, until better. To prevent and get rid of most kidney stones then consume three times a day a portion, cooked or un-cooked, of the large "White Radish" called Moolie in the Super-markets (maybe Indian shops) or "Daikon" in Japanese shops. Japanese must have few if any kidney stones or crystals in their urine. This is as old-fashioned as the Great Fire of London and was recommended by Nicholas Culpeper in his Herbal ? 1662. It works every time. Look it up. Anecdote: Two mangoes a day bring on stiffness of my fingers in four days. One mango a day will take 21 days to do the same. Competing interests: None declared |
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John S White, President, White Technical Research Argenta, IL 62501 USA
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Authors Choi and Curhan pose a provocative hypothesis: that consumption of sugar sweetened soft drinks—and especially the fructose component—is strongly associated with an increased risk of gout. However, the evidence presented fails to convince that 1) the risks for gout posed by soft drink consumption are uniquely due to the fructose component; and 2) these beverages are significant risk factors for gout. Sugar sweetened soft drinks are sweetened either with sucrose (world- wide, except for USA) or high fructose corn syrup (HFCS, predominantly USA). Sucrose is a disaccharide of glucose and fructose covalently bonded together; HFCS is a blend of monosaccharide (free) glucose and fructose. In both sweeteners, the glucose:fructose ratio is close to 1. To attribute to fructose the increased risk of incident gout with increased soft drink consumption seems unreasonable, when each serving of soft drink contains an equivalent amount of glucose. The authors note that intake of caffeine, fructose, meats and high fat dairy foods tended to increase with increasing consumption of sugar sweetened soft drinks (Table 1). However, they make no attempt to explain the contradictory observation that BMI and intake of caffeine, meats and high fat dairy foods decrease with increasing consumption of free fructose. This contradiction necessarily casts doubt on the quality of the data and/or method of analysis, since nutritive sweeteners in soft drinks are half fructose and glucose. It is simply not possible for sugar sweetened soft drinks and a principal caloric constituent (fructose) to have divergent associations with intakes of caffeine, meats and high fat dairy foods. Finally, it must be observed that the incidences of gout linked to sugar sweetened soft drinks reported in this paper do not appear unreasonable when viewed against one of the author’s own published data. 755 cases of gout were reported during 12 years of the study in 46,393 male subjects—an incidence of 1.6%. This is consistent with the incidence of gout in the general population reported by Lawrence et al (1.3%), but is significantly lower than that reported previously by author Curhan et al (2.7%) (1,2). Choi and Curhan reported that increasing intake of sugar sweetened soft drinks was associated with increased risk of gout (Table 2). However, the effect was significant only at soft drink serving frequencies of 5-6/week and greater, which accounted for 143 of the 755 reported gout cases (19%). But it must be noted that the 0.3% incidence of gout represented by this serving frequency (143 cases ÷ 46,393 subjects) represents a very small fraction of the 2.7% incidence reported by author Curhan for the general population (2). Furthermore, the significant fructose effect for “sweetened cola” and “other sweetened soft drinks” appeared only at serving frequencies of 1/day and greater (Table 2). These serving frequencies represented even fewer (7%) of the 755 reported gout cases. And it must be further noted that the 0.1% incidence of gout represented by this serving frequency represents an even smaller fraction of Curhan’s 2.7% estimate for the general population (2). Thus, incident gout attributed to elevated sugar sweetened soft drink consumption of all types in this study is very low, indeed, and is of questionable significance. The hypotheses that fructose and caloric beverages play a unique role in obesity, diabetes and now gout have stirred great interest among scientists and the press, but to date no compelling evidence has appeared. Choi and Curhan offer nothing new in support of these hypotheses. REFERENCES 1. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, Gabriel S, Hirsch R, Hochberg MC, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States: Part II. Arthritis Rheum. 2008 Jan;58:26-35. 2. Kramer HM, Curhan G. The association between gout and nephrolithiasis: the National Health and Nutrition Examination Survey III, 1988-1994. Am J Kidney Dis. 2002 Jul;40:37-42. Competing interests: The author is a consultant to the food and beverage industry in the area of nutritive sweeteners. His clients include research institutes, food industry councils, trade organizations and individual companies. |
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Hendrickus A Brokking, Student Sobey's, L9T 5G5
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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 |
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