Gout: The Missing Chapter from Good Calories, Bad Calories

234 Comments

Total read time (bolded sections): 2-3 minutes
Total read time (complete): 12 minutes

Last week, I had a wonderful conversation with Gary Taubes, my favorite science journalist and author of the incredible (and I consider definitive), Good Calories, Bad Calories. His ability to synthesize and recall research, both in writing and in speaking, is one of the most amazing feats I’ve ever witnessed.

It is with great pleasure, therefore, that I offer you the director’s-cut chapter that didn’t make it into the book.

The chapter addresses important misconceptions about diet, fructose, blood pressure, and diabetes through the lens of gout.

If you don’t know someone with gout, you probably will. It is common and becoming more so. The misguided prescriptions from misinformed doctors, which Taubes addresses, have affected my family, and I’d rather save you the trouble if I can.

But what the hell is “gout” anyway?

Like many, I’d heard it a million times but never knew. Here it is…

British physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent; the idea being that uric acid accumulates in the circulation [and] crystallizes into needle-sharp urate crystals. These crystals then lodge in the soft tissues and in the joints of the extremities –- classically, the big toe — and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one’s eyeballs.

Sound like something to avoid?

Disclaimer as requested by Gary: This chapter is in draft form and has not gone through the same fact-checking as the rest of Taubes’ published work, even though there are 32 citations (some incomplete). I wanted to show the writing process at its mid-point. The only deletions I’ve make are “TK”, which–for unknown reasons–is traditional shorthand in publishing for indicating that something is “to come”.

I have bolded several sections for those who would like a 2-3-minute skim of content highlights before digesting the entire piece, which is 7 pages long.

Enter Gary Taubes:

—-

Gout and the condition known technically as hyperuricemia, or elevated levels of uric acid, are the most recent examples of this kind of institutional neglect of the potential health effects of fructose, and how pervasive it can be.

Gout itself is an interesting example because it is a disease that has gone out of fashion in the last century and yet the latest reports suggest it is not only as prevalent as ever, but becoming more so. Recent surveys suggest that nearly 6 percent of all American men in their fifties suffer from gout, and over ten percent in their seventies. The proportion of women afflicted is considerably less at younger ages but still rises over 3 percent by age 60.(1) Moreover, the prevalence of gout seems to have doubled over the last quarter century, coincident (perhaps not coincidentally) with the reported increase in obesity, and it may have increased five- or even six-fold since the 1950s, although a large portion of that increase may be due to the aging of the population.(2)

Until the late 17th century, when the spread of gout reached almost epidemic proportions in Britain, the disease afflicted almost exclusively the nobility, the rich and the educated, and so those who could afford to indulge an excessive appetite for food and alcohol. This made gout the original example of a disease linked to diet and over-consumption, and so, in effect, the original disease of civilization.

But once gout became easily treatable, in the early 1960s, with the discovery of the drug allopuranol, clinical investigators and researchers began to lose interest. And the pathology of gout has been understood since the British physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent; the idea being that uric acid accumulates in the circulation to the point that it falls out of solution, as a chemist would put it, and so crystallizes into needle-sharp urate crystals. These crystals then lodge in the soft tissues and in the joints of the extremities – classically, the big toe — and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one’s eyeballs.(3) Because uric acid itself is a breakdown product of protein compounds known as purines – the building blocks of amino acids – and because purines are at their highest concentration in meat, it has been assumed for the past 130-odd years that the primary dietary means of elevating uric acid levels in the blood, and so causing first hyperuricemia and then gout, is an excess of meat consumption.

The actual evidence, however, has always been less-than-compelling: Just as low cholesterol diets have only a trivial effect on serum cholesterol levels, for instance, and low-salt diets have a clinically insignificant effect on blood pressure, low-purine diets have a negligible effect on uric acid levels. A nearly vegetarian diet, for instance, is likely to drop serum uric acid levels by 10 to 15% percent compared to a typical American diet, but that’s rarely sufficient to return high uric acid levels to normality, and there is little evidence that such diets reliably reduce the incidence of gouty attacks in those afflicted.(4) Thus, purine-free diets are no longer prescribed for the treatment of gout, as the gout specialist Irving Fox noted in 1984, “because of their ineffectiveness” and their “minor influence” on uric acid levels.(5) Moreover, the incident of gout in vegetarians, or mostly vegetarians, has always been significant and “much higher than is generally assumed.” (One mid-century estimate, for instance, put the incidence of gout in India among “largely vegetarians and teetotalers” at 7%.)(6) Finally, there’s the repeated observation that eating more protein increases the excretion of uric acid from the kidney and, by doing so, decreases the level of uric acid in the blood.(7) This implies that the meat-gout hypothesis is at best debatable; the high protein content of meats should be beneficial, even if the purines are not.

The alternative hypothesis is suggested by the association between gout and the entire spectrum of diseases of civilization, and between hyperuricemia and the metabolic abnormalities of Syndrome X. In the past century, gout has manifested all of the now-familiar patterns, chronologically and geographically, of diseases of civilization, and so those diseases associated with western diets. European physicians in World War I, for instance, reported a reduced incidence of gout in countries undergoing food shortages.(8) In primitive populations eating traditional diets, gout was virtually unknown or at least went virtually unreported (with the conspicuous exception of Albert Schweitzer who says he saw it with surprising frequency.) The earliest documented cases reported in Asia and Africa were in the late 1940s.(9) And even in the 1960s, hospital records from Kenya and Uganda suggested an incidence of gout lower than one in a thousand among the native Africans. Nonetheless, by the late 1970s, uric acid levels in Africa were increasing with westernization and urbanization,(10) while the incidence of both hyperuricemia and gout among South Pacific islanders was reportedly sky-rocketing. By 1975, the New Zealand rheumatologist B.S. Rose, a colleague of Ian Prior’s, was describing the native populations of the South Pacific as “one large gouty family.”(11)

Gout has also been linked to obesity since the Hippocratic era, and this association is the origin of the assumption that high-living and excessive appetites are the cause. Gouty men have long been reported to suffer higher rates of atherosclerosis and hypertension, while stroke and coronary heart disease are common causes of death.(12) Diabetes is also commonly associated with gout. In 1951, Menard Gertler, working with Paul Dudley White’s Coronary Research Project at Harvard, reported that serum uric acid levels rose with weight, and that men who suffered heart attacks were four times as likely to be hyperuricemic as healthy controls.(13) This led to a series of studies in the 1960s, as clinical investigators first linked hyperuricemia to glucose intolerance and high triglycerides, and then later to high insulin levels and insulin resistance.(14) By the 1990s, Gerald Reaven, among others, was reporting that insulin resistance and hyperinsulinemia raised uric acid levels, apparently by decreasing uric acid excretion by the kidney, just as they raised blood pressure by decreasing sodium excretion. “It appears that modulation of serum uric concentration by insulin resistance is exerted at the level of the kidney,” Reaven wrote, “the more insulin-resistant an individual, the higher the serum uric acid concentration.” (15)

These observations would suggest that anything that raised insulin levels would in turn raise uric acid levels and might cause gout, which would implicate any high carbohydrate diet with sufficient calories. But this neglects the unique contribution of fructose. The evidence arguing for sugar or fructose as the primary cause of gout is two-fold. First, the distribution of gout in western populations has paralleled the availability of sugar for centuries, and not all refined carbohydrates in this case. It was in the mid-17th century, that gout went from being exclusively a disease of the rich and the nobility to spread downward and outward through British society, reaching near epidemic proportions by the 18th century. Historians refer to this as the “gout wave,”(16) and it coincides precisely with the birth and explosive growth of the British sugar industry(17) and the transformation of sugar, in the words of the anthropologist Sydney Mintz, from “a luxury of kings into the kingly luxury of commoners.”(18) British per capita sugar consumption in the 17th century was remarkably low by modern standards, a few pounds per capita per year at the turn of the century, but the change in consumption over the next century and a half was unprecedented: between 1650 and 1800, following the British acquisition of Barbados, Jamaica and other “sugar islands”, total sugar consumption in England and Wales increased 20- to 25-fold.(19)

The second piece of evidence is much less circumstantial: simply put, fructose increases serum levels of uric acid. The “striking increase” in uric acid levels with an infusion of fructose was first reported in the Lancet in the late 1960s by clinicians from Helsinki, Finland, who referred to it as fructose-induced hyperuricemia.(20) This was followed by a series of studies through the late 1980s confirming the existence of the effect and reporting on the variety of mechanisms by which it came about. Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid. Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it.(21) Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism.(22)

These mechanistic explanations of how fructose raises uric acid levels were then supported by a genetic connection between fructose metabolism and gout itself. Gout often runs in families, so much so that those clinicians studying gout have always assumed the disease has a strong hereditary component. In 1990, Edwin Seegmiller, one of the few veteran gout researchers in the U.S., and the British geneticist George Radda, who would go onto become director of the Medical Research Counsel, reported that the explanation for this familial association seemed to be a very specific defect in the genes that regulate fructose metabolism. Thus, individuals who inherit this defect will have trouble metabolizing fructose and so will be born with a predisposition to gout. This suggested the possibility, Seegmiller and Radda concluded, that this defect in fructose metabolism was “a fairly common cause of gout.”(23)

As these observations appeared in the literature, the relevant investigators were reasonably clear about the implications: “since serum-uric-acid levels are critical in individuals with gout, fructose might deserve consideration in their diet,” noted the Helsinki clinicians in The Lancet in 1967, and so the chronic consequences of high-fructose diets on healthy individuals required further evaluation.(24) Gouty patients should avoid high-fructose or high-sucrose diets, explained Irving Fox in 1984, because “fructose can accelerate rates of uric acid synthesis as well as lead to increased triglyceride production.”(25) Although none of these investigators seemed willing to define what precisely constituted a high-fructose or a high-sucrose diet. Was it 50 pounds of sugar a year? 100 pounds? 150 pounds? 300 pounds? And would high-fructose diets induce gout in healthy individuals or would they only exacerbate the problem in those already afflicted? In 1993, the British biochemist Peter Mayes published an article on fructose metabolism in the American Journal of Clinical Nutrition that is now considered the seminal article in the field. (This was in the special issue of the AJCN dedicated to the health effects of fructose.) Mayes reviewed the literature and concluded that high-fructose diets in healthy individuals were indeed likely to cause hyperuricemia, and he implied that gout could be a result, as well, but the studies to address that possibility had simply never been done. “It is clear,” Mayes concluded, “that systematic investigations in humans are needed to ascertain the precise amounts, both of fructose consumption and of its concentration in the blood, at which deleterious effects such as hyperlipidemia and hyperuricemia occur.”(26) Add to this Reaven’s research reporting that high insulin levels and insulin resistance will increase uric acid levels, and it suggests, as Mayes had remarked about triglycerides, that sugar (sucrose) and high fructose corn syrup would constitute the worst of all carbohydrates when it comes to uric acid and gout. The fructose would increase uric acid production and decrease uric acid excretion, while the glucose, though its effect on insulin, would also decrease uric acid excretion. Thus, it would be reasonable to assume or at least to speculate that sugar is a likely cause of gout, and that the patterns of sugar consumption explain the appearance and distribution of the disease.

Maybe so, but this hypothesis has never been seriously considered. Those investigators interested in gout have focused almost exclusively on alcohol and meat consumption, in part because these have historical precedents and because the implication that gouty individuals and particularly obese gouty individuals shy away from meat and alcohol fit in well with the dietary prescriptions of the 1970s onward.

More than anything, however, this sugar/fructose hypothesis was ignored, once again, because of bad timing. With the discovery and clinical application of allopurinol in the 1960s, those clinical investigators whose laboratories were devoted to studying the mechanisms of gout and purine metabolism – James Wyngaarden’s, for instance, at Duke and Edwin Seegmiller’s at NIH – began focusing their efforts either on working out the nuances of allopurinol therapy, or to applying the new techniques of molecular biology to the genetics of gout and rare disorders of hyperuricemia or purine metabolism. Nutritional studies were simply not considered worthy of their time, if for no other reason than that allopuranol allowed gout suffers to eat or drink whatever they wanted. “We didn’t care so much whether some particular food might do something,” says William Kelley, who is a co-author with Wyngaarden of the 1976 textbook, Gout and Hyperuricemia and who started his career in Seegmiller’s lab at NIH. “We could take care of the disease.”(27)

This exodus, however, coincided with the emergence of research on fructose-induced hyperuricemia. By the 1980s, when the ability of fructose and sucrose consumption to raise uric acid levels in human subjects was demonstrated repeatedly, the era of basic research on gout had come to an end. The major players had left the field and NIH funding on the subject had dwindled to a trickle. Wyngaarden published his last research paper in 1977 and spent the years 1982 to 1989 as director of the National Institutes of Health. Kelley published his last papers on the genetics of gout in 1989, when he became dean of medicine at the University of Pennsylvania. Irving Fox, who did much of the basic research on fructose- and alcohol-induced hyperuricemia in Kelley’s lab, went to work in the biotechnology industry in the early 1990s. Only Edwin Seegmiller remained interested in the etiology of gout, and Seegmiller says that when he applied to the NIH for funding to study the relationship between fructose and gout, after elucidating the genetic connection with Radda in 1990, his grant proposals were rejected on the basis that he was too old and, as an emeritus professor, technically retired.(28) “In the 1950s and 1960s, we had the greatest clinical scientists in the world working on this disease,” says Kelley. “By the 1980s and 1990s, there was no one left.”

Meanwhile, the medical journals would occasionally run articles on the clinical management of the gout, but these would concentrate almost exclusively on drug therapy. Discussions of diet would be short, perhaps a few sentences, and confused about the science. On those occasions when the authors would suggest that gouty individuals might benefit from low-purine diets, they would invariably include “sugars” and “sweets” as among the recommended foods with low-purine contents.(29) In a few cases – a 1996 article in the New England Journal of Medicine, for instance (30)– the articles would also note that fructose consumption would raise uric acid levels, suggesting only that the authors had been unaware of the role of fructose in “sugars” and “sweets.” Even when the New England Journal published a report from Walter Willett and his Harvard colleagues in March 2004, this same kind of nutritional illiteracy manifested itself. Willett’s article had reported that men with gout seemed to eat more meat than healthy men. But Willett, who by this time was arguably the nation’s most influential nutritional epidemiologist, later explained that they had never considered sugar consumption in their analysis because neither he nor his collaborators had been aware of the hyperuricemic effect of fructose. Willett’s co-author, Gary Curhan, a nephrologist and gout specialist with a doctorate in epidemiology, said he might have once known that fructose raised uric acid levels, but it had slipped his mind. “My memory is not what it used to be,” he said. He also acknowledged, in any case, that he never knew sucrose was half fructose.

The addenda to this fructose-induced hyperuricemia story may be even more important. When the New England Journal of Medicine published Willett’s gout study, it ran an editorial to accompany it written by the University of Florida nephrologist Richard Johnson. Over the past decade, Johnson’s research has supported the hypothesis that elevating the uric acid concentration in the circulation also damages the blood vessels leading into the kidneys in such a way as to raise blood pressure directly, and so suggests that fructose consumption will raise blood pressure.

This is another potentially harmful effect of fructose that post-dates the official reports exonerating sugar in the diet. And it is yet another mechanism by which sugar and high fructose corn syrup could be a particularly unhealthy combination. The glucose in these sugars would raise insulin levels, which in turn would raise blood pressure by inhibiting the kidney’s secretion of sodium and by stimulating the sympathetic nervous system, as we discussed in an earlier chapter, and the fructose would do it independently by raising uric acid levels and so damaging the kidney directly. If this were the case, which has never been tested, it would potentially explain the common association of gout and hypertension and even of diabetes and hypertension.(31) Johnson is only now looking into this possibility, however. Unlike Willett and his colleagues, Johnson had long been aware of the ability of fructose to raise uric acid levels, and so was studying that phenomenon in his laboratory. But it was only in the summer of 2004, he explained, three months after his NEJM editorial was published, that he realized that sucrose was half fructose and that his research of the past years was even relevant to sugar.(32)

A decade later, Thomas Benedek described the epidemiology of gout in The Cambridge World History of Human Disease this way: “Worldwide the severity and prevalence of gout have changed paradoxically since the 1940s. In the highly developed countries, as a result of the advent of effective prophylactic drug therapy, the disease is now rarely disabling. Elsewhere, however, it has become more prevalent, predominantly as a result of `improved diets.’”

###

Footnotes and endnotes:

The economist and historian Ralph Davis estimates that the supply of sugar from the Caribbean into Britain rose from three or four thousand tons a year in the late fifteenth century to over two hundred thousand tons by the 1770s, or an increase of over fifty-fold. (davis r, the rise of the atlantic economies, cornell university press, 1973, p. 251, 255)

1 Kramer hm, curhan g, the association between gotu and nephrolithiasis: the national health and nutrition examination survey III. 1988-1994. Am J Kidney Dis 2002;40:37-42

2 Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE. Epidemiology of gout: is the incidence rising? J Rheumatol. 2002 Nov;29(11):2403-6.

2Interview with choi, sept 16, 2004

2Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, Heyse SP, Hirsch R, Hochberg MC, Hunder GG, Liang MH, Pillemer SR, Steen VD, Wolfe F. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States.

2Arthritis Rheum. 1998 May;41(5):778-99.

3 gout, the patrician disease, p. 3

4

5 hydrick and fox, p. 748-749.

6 Duncan’s diseases of metabolism, p. 632.

7 Hydrick cr and fox ih, nutrition and gout, in present knowledge in nutrition, fifth edition, the nutrition foundation, Washington dc, 1984, p. 743

8 duncans diseases of metabolism, p. 638

9 Traut ef, rheumatic diseases, diagnosis and treatment, the C.V. Mosby Company, St. Louis, 1952 p. 303.

9benedek, in Cambridge history of diseases

9Trowel hc, a case of gout in a ruanda African, the east African medical journal, oct. 1947, p. 346-348

10 Beighton p et al, 1977, rheumatic disorders in th south African negro, part IV. Gout and hyperuricemia. South Af Med J. 51(26):969-72

11 Gout in the Maoris, B.S. Rose, Seminars in Arthritis and Rheumatism. Vol. 5, no. 2, (November) 1975, pg. 121-145.

12 duncan’s diseases of metabolism, 1947, p. 631

13 gertler mm, et al, erum uric acid in relation to age and physique in health andin coronary ehart disease, Ann Intern Med. 1951 Jun;34(6):1421-31. Reiser S, Uric Acid and Lactic Acid, in REISER S AND HALLFRISCH J, METABOLIC EFFECTS OF FRUCTOSE, crc press, boca raton fl, 1987 p. 113-134

13

14 duncan’s diseases of metabolism, p. 631

14 reaven gm, The Kidney: An Unwilling Accomplice in Syndrome X, Am J Kid Dis, Vol. 30, n0 6, December, 1997: pp. 928-931.

15 Facchini F et al, Relationship Between Resistance to Insulin-Mediated Glucose Uptake, Urinary Uric Acid Clearance, and Plasma Uric Acid Concentration, JAMA, December 4, 1991, vol. 266, no. 21, 3008-3011

16 Wyngaarden and Kelley p. ix

17 mintz

18 Sydney Mintz, Sweetness and Power, The Place of Sugar in Modern History, penguin books, ny 1985 p. 96.

19 mintz p. 64, 66

20 perheentupa j raivio k, fructose-induced hyperuricaemia, lancet, September 9, 1967, p.528531

21 emmerson bt, getting rid of gout

22 mayes pa, metabolism of fructose, ajcn, 1993

22hydrick c fox i, nutrition and gout, in modern reviews of nutrition

23 Seegmiller JE, Dixon RM, Kemp GJ, Angus PW, McAlindon TE, Dieppe P, Rajagopalan B, Radda GK. Fructose-induced aberration of metabolism in familial gout identified by 31P magnetic resonance spectroscopy.

23Proc Natl Acad Sci U S A. 1990 Nov;87(21):8326-30

24 peerheentupa ibid

25 hydrick and fox, p. 748-749.

26 Mayes pa, metabolism of fructose, ajcn 1993

27 Kelley interview

28 seegmiller interview

29 See for instance, fam ag, gout, diet and the insulin resistance syndrome, j. rheum. 2002;29, 1350-55

30 Emmerson BT. The management of gout.

30N Engl J Med. 1996 Feb 15;334(7):445-51

31 get citation from Richard Johnson articles on uric acid and hypertension.

32 Johnson interview, june 3, 2004

Posted on: October 5, 2009.

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234 comments on “Gout: The Missing Chapter from Good Calories, Bad Calories

  1. I had a gout attack about 2 weeks ago, I’m 52 and it was my first. My father has had gout attacks in the past so heredity probably played a factor though I don’t think his attack was as bad as mine.

    I’ve been on a ketogenic diet for the past four months so I’m sure sugar or high carbs did not play a factor in my attack.

    From what I’ve seen online there doesn’t appear to be any good agreement on the lifestyle cause. What I mean by that is there’s no agreement on what to eat or what to avoid. Purines are cited by some but are ruled out by others with some saying purines from vegetables are okay (like mushrooms) but not from meats. Some sites (like Kaiser Permanente) say drinking coffee and carbonated beverages are good for gout prevention.

    From what I can deduce from my gout attack: I’ve lost about 35 pounds in a little over 4 months so the stress of that on my system may have played a factor, though I have lost that much weight in the past in a similar or shorter period of time with no gout. I added protein drinks to my diet to so I wouldn’t just have to add more meats, maybe the added protein was a factor? I was snacking on beef sticks which I’m guessing were made of all kinds of organ meats and such. My bloodwork also showed my electrolytes were off.

    I was put on Allopurinol and Prednisone for the gout and prescription of Potassium Chloride for the electrolyte imbalance. I couldn’t take pain killers like Ibuprofen due to the electrolyte imbalance so I had to tough out the excruciating pain for a few days before the other meds reduced inflammation and uric acid levels. I’ll probably supplement with lite salt later for the electrolytes.

    I never really stopped my keto diet but I’ve eaten less red meat the past two weeks and backed-off on losing weight quickly. I think the stress on the body probably wasn’t good. My big toe joint, where the attack occured, is about 90% recovered. I’ve had one beer in the past four months, the only alcohol, so that’s not a factor.

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    • @BAS I would consider a possible link between too much protein at that time being converted via gluconeogenesis into increase blood glucose. Postprandial glucose testing after eating different amounts and types of protein could help you tweak your ketogenic diet according to your physiology.

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  2. I believe I have had mild attacks on and off for the past 6 years. Until recently, the attacks were really mild and to be honest, I believed I had pulled a muscle somehow. I am mid 30′s and drink (only at weekends) and eat fairly well and excercise on a regular basis.

    Following a rather unhealthy Christmas (stoppped excercising and drank heavily and ate rubbish foods including large amounts of sugar) in January this year, I had my first full blown attack which my Dr confirmed as suspected gout. Have to admit, he was fairly unhelpful and gave me base details of how to reduce the risk. The usual, lose weight, cut down on drinking, eat better blah. blah, blah. . .

    I did my own research and believed to have made a fairly good self diagnosis which attributed to a combination of factors which had occured over Christmas. One of these extra factors was getting sinusitis and having to take anti-biotics which in turn killed the naturally occuring bacteria. I had read that your gut is one of your main defenses against uric acid and figured this must have been the catalyst for the attack.

    However, I experienced a new attack this week. This time, the factors are different. I assisted another Dept at work 3 weeks ago and ended up being over tired and didn’t get to the gym. As I didn’t attend the gym, I found myself eating more biscuits/ chocolate etc while sitting on the sofa. My intake of sugary drinks increased also. After 3 weeks, I felt a twinge in my foot (my usual gouty location) and stopped instantly. I then had a can of Pepsi on Monday and bang, next day gout came on in full swing.

    This artiicale confirms what I have believed for a long time, my gout is caused by excess sugar consumption and lack of excercise. Big thanks to Tim Ferris for this article / blog as it near enough confirms my own theories. I think research should be started again to find a better long term solution to this horrific affliction as we need to FULLY determine what is the cause and best way to deal at first instance instead of self diagnosis.

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  3. Your gout article rightfully refers to the work of Dr. Richard Johnson, who has moved from U. Fla to U. Col in Denver. His work clearly shows that dietary fructose is processed in the body to produce uric acid, and hence raises the level of uric acid in the blood.

    But there is more to the question of why the high concentration of serum uric acid precipitates as the crystals of monosodium urate (MSU) which cause gout. Consider that most gout attacks originate while the individual is sleeping. Why? The answer is sleep apnea, which is the frequent cessation of breathing for many seconds at a time during sleep. The resulting reduction of oxygen in the blood has three effects, each of which can make MSU precipitation more likely. The first is cell catabolism, in which ATP undergoes a chain of chemical transitions which culminates in the cellular generation of excess uric acid fed into the blood. The second is that the reduced oxygen in the blood makes the blood more acidic (lower pH) so it can hold less uric acid in solution. These two effects are transient, so blood tests taken after awakening misses their peaks. The third effect is long term. Over time the chronic intermittent reduction in oxygen causes gradual reduction of kidney function, so uric acid is removed from the blood more slowly.

    So fructose ingestion raises the uric acid baseline, but sleep apnea causes it to reach an abrupt tipping point which leads to gout. I’ve told hundreds of gout experts about this physiology, and the only one who already knew about it was Dr. Johnson. Unfortunately, he thought it was common knowledge.

    Dr. Johnson’s recent book The Fat Switch is written for general readership. It describes how fructose activates a biological switch in the body to cause it to store fat rather than burn fat. It is an excellent companion to The Four Hour Body.

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    • @Burton Abrams Very interesting. My mother suffers from gout and also sleep apnea. What effect would a CPAP machine have on all this? In my mothers case would her gout be far worse if you she was not receiving positive airway pressure and thus more air being delivered to her lungs and more oxygen being delivered to the bloodstream?

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      • Sky – My experience was that when I completely overcame my sleep apnea, my gout attacks ceased immediately and completely. If your Mom’s CPAP machine is properly adjusted for her, and if she always uses it whenever she sleeps, I expect that her gout attacks would be greatly mitigated. Unfortunately, many sleep physicians don’t recommend total adherence to CPAP usage. I think that is a big disservice to the patient.
        MSU crystals form quickly (minutes), but then dissolve very slowly (months). Most gout attacks last for about a week because the immune system places a protein sheath around the crystals so that they are no longer sensed by other immune system cells which activate the gout pain and inflammation. (A gout attack is initiated by the immune system chemically sensing the presence of these crystals, not by the physical fact that these crystals are needle shaped.) So a gout attack can be initiated if the sheath is ruptured, either chemically by an uricosic drug such as allopurinol or physically by undue stress on the affected joint. Sleep apnea may be the reason why the crystals are formed in the first place, but once formed they may initiate multiple gout attacks by these other means.

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      • Hi Burton,
        Your comment is well informative. I really enjoyed a lot. I got the full of knowledge about immune system. It’s amazing tips about health related well I want to know about how acne will be cured and give some knowledge about that for better natural health.

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  4. Talk about timing. Today I was diagnosed with high uric acid and swelling in my ankle probably developing into gout. I have been prescribed allopurinol and colchicine. Yesterday fruit was a daily staple. Tomorrow it will not be.thanks so much!

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    • Ew, Colchicine…. Pretty toxic stuff. Gave me severe, explosive diarhea and nausea. My condition improved on a microdosage of Lithium Orotate (like 25 mg. Available online) combined with a macro dose of Vitamin C (1,000 mg+).

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  5. Potassium deficiency is deeply involved in gout and high uric acid as an accentuating factor because uric acid is less soluble in acidic urine. Potassium bicarbonate supplements will reverse this. In view of the fact that this is not considered by current rheumatologists, it would be very valuable for you to bring it into your future writing. It is not only that potassium is not considered by physicians in regard to gout, many of them do not even believe that a potassium deficiency is likely. This even though many of them prescribe what are actually supplements, but prescribed under euphemistic terms such as salt substitutes, sodium free baking powder, ORT salts (oral rehydration therapy for diarrhea), polarizing solutions, GIK (glucose, insulin, potassium) salts, vegetables, or glucosamine. A deficiency is further defined out of existence by defining the blood serum content normal as 4.2 when the actual figure is 4.8. For gout, though, the chloride is not acceptable. But potassium bicarbonate powder dissolved in fruit juice or half teaspoon sprinkled on cereal will work very well. It may be obtained from businesses which add it to wine. If you supplement potassium, be very certain that vitamin B-1 is adequate, because otherwise heart disease can be triggered.

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    • Very interesting….given how crucial potassium is in general, and the new
      emphasis on low sodium, which knocks potassium out of balance and has its own issues.

      Wouldn’t just adding the juice of a couple of fresh lemons per day solve the acidity problem?

      Readers of this blog probably aren’t having fruit juice or cereal, by the way.

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  6. Potassium deficiency is deeply involved in gout and high uric acid as an accentuating factor because uric acid is less soluble in acidic urine. Potassium bicarbonate supplements will reverse this. In view of the fact that this is not considered by current rheumatologists, it would be very valuable for you to bring it into your future writing. It is not only that potassium is not considered by physicians in regard to gout, many of them do not even believe that a potassium deficiency is likely. This even though many of them prescribe what are actually supplements, but prescribed under euphemistic terms such as salt substitutes, sodium free baking powder, ORT salts (oral rehydration therapy for diarrhea), polarizing solutions, GIK (glucose, insulin, potassium) salts, vegetables, or glucosamine. A deficiency is further defined out of existence by defining the blood serum content normal as 4.2 when the actual figure is 4.8. For gout, though, the chloride is not acceptable. But potassium bicarbonate powder dissolved in fruit juice or half teaspoon sprinkled on cereal will work very well. It may be obtained from businesses which add it to wine. You may see an article on this concept in http://www.webmedcentral.com/article_view/4217 . If you supplement potassium, be very certain that vitamin B-1 is adequate, because otherwise heart disease can be triggered (see http://charles_w.tripod.com/kandthiamin.html ).
    Sincerely, Charles Weber

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  7. “everything today in a box or can or bottle has soy added.”

    Not sure about soy, but I have seen that gliadin (from wheat) is added to damned near everything in a box, can, or bag — even to potato chips and fish! That’s because it’s an appetite stimulant, which makes you want to eat (and buy) more. The food researchers discovered that in the mid-1970′s, when modern Frankenwheat started to become the dominant form of industrial food-like substance. (See Dr. Wm. Davis’ excellent book on that subject).

    Not coincidentally, gliadin is hidden behind several other names, and is not required to be on the nutrition label at all, thanks to the political power of the Monsanto company, who spends enormous amount of money “influencing” (corrupting) politicians.

    I used to have gout. My last attack was in 1999, the year I cut out all wheat from my diet, along with other grains, trans-fats, and sugar. Another side-effect from that change of diet in addition to freedom from gout was the loss of 100 lbs.

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  8. Has anyone interested in this comment thread read Beating Gout: A Sufferer’s Guide to Living Pain Free? Was it helpful or would you deem it another run of the mill generic info product?

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  9. beer used to give me gout bad.i stopped 12 yrs ago and attacks subsided.recently i went on bromeleian,cherry extract(tart),quercetin with c,celery seed extract,potassium citrate and in the beginning i wasgetting small attacks all over as the uric crystals were being dissolved.now after10 months or so,i am feeling better.i eat red meat at least 2-3 times week,pork,chicken.no probs.i really do think sweets,cakes and such give me attacks and make my arhtritis worse.its a horrible thing gout.but beer definitely is bad.

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    • Hi Mike,

      I am interested in what you said about bromeleain and cherry extract etc. In what manner do you include these into your daily life? Tablets/powders? And how do you know the crystals are dissolving?
      My diet is changing as we speak and steering clear of fructose is the new challenge.

      Any help would be awesome.

      Cheers,
      Ryan

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  10. also people SOY is a no no.everytime i eat anything with soy(boxed or frozen foods)i get gout and my jpoints ache for days.cereals,cookies,ice cream etc all made with soy.you cant eat anything in a box.
    i see websites that say soy is good for gout as well as fish oil(also made with soy) and i cant beleive it.vitamins also are made with soy,use only non soy.
    good luck

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  11. 10 years suffered with G attacks now becoming more frequent. Last month had one in my ankle….I have very high levels of uric acid I maintain 600-625 without symptoms. What I noticed triggers it is not necessarily increasing the levels but rather any change either down or up. Now this article is interesting as I love my sweets from time to time but hours before my last attack which was my first ankle attack I ate 10-15 large marshmallows. My attack makes sense now as fructose intake was way up. I am quiet excited about this article as often I get dumfounded by the trigger as my diet is often very low in purine foods and yet the attacks come. Now I have a yet another possible piece of the puzzle to monitor. With hopes that I can pinpoint a dietary direction that can lead to life with less Gout.

    As a chronic sufferer what really helps is 1.5 liter of water every hour for 4 hours, seem to flush out the system. It seems to help as much as taking the medication. I have tested this quite often and alkali (7-9ph) water lowers the attacks symptoms as fast as medication Which is in line with reducing fructose levels and helping the elimination system. This make sense. I look forward to the results of monitoring my fructose levels.

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  12. Potassium deficiency is deeply involved in gout and high uric acid as an accentuating factor because uric acid is less soluble in acidic urine. Potassium bicarbonate supplements will reverse this. In view of the fact that this is not considered by current rheumatologists, it would be very valuable for you to bring it into your future writing. It is not only that potassium is not considered by physicians in regard to gout, many of them do not even believe that a potassium deficiency is likely. This even though many of them prescribe what are actually supplements, but prescribed under euphemistic terms such as salt substitutes, sodium free baking powder, ORT salts (oral rehydration therapy for diarrhea), polarizing solutions, GIK (glucose, insulin, potassium) salts, vegetables, or glucosamine. A deficiency is further defined out of existence by defining the blood serum content normal as 4.2 when the actual figure is 4.8. For gout, though, the chloride is not acceptable. But potassium bicarbonate powder dissolved in fruit juice or half teaspoon sprinkled on cereal will work very well. It may be obtained from businesses which add it to wine. If you supplement potassium, be very certain that vitamin B-1 is adequate, because otherwise heart disease can be triggered (see
    Sincerely, Charles Weber

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  13. The 4hour body diet requires the daily consumption of legumes. How does this influence people who get gout? Can they consume legumes daily or should it be replaced by something else? If so, could you please recommend alternatives?

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  14. Its just TOO SIMPLE!!
    Modern crappy artificial diet is to blame.
    Eat more natural unprocessed foods, less repacked garbage and fast food and say good bye gout

    well Tim this is a great article by the way
    thanks for sharing this fact

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    • Not quite so simple, Ironthumb. In my case I’ve always been a fairly heavy drinker of beer and whisky until 5 years ago when I gave up alcohol completely. I also used to consume a lot of sucrose in my hot drinks, as well as sprinkling it on my cereals and putting it in my cooking. On top of all that I ate plenty of wheat in the form of bread.
      Since going LCHF 20 months ago, my intake of sugars has been cut right back to only the occasional piece of fruit or perhaps some berries mixed with cream. While I’ve always eaten copious amounts of red meat and fat, I would say that this has dropped slightly as a consequence of my LCHF lowered appetite. All of our food these days comes from the outer aisles of the supermarket – fresh vegetables, nuts, cream, cheese, eggs, beef, lamb, pork, chicken and fish. Now and then I eat chocolate which I’ve mixed myself from equal portions of dark 72% or greater chocolate and coconut oil.
      I’m 60 now and I’ve only ever had gout in the last 8 months – at least a year into my LCHF journey. One would think that I would have lessened my odds of getting it. I’ll perhaps do some research on the potassium angle that Charles Weber mentioned above and see if I can find an answer there. Unless you or anybody else has other ideas, of course.

      Cheers
      Gregg

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