Last night, world-famous magician and endurance artist David Blaine taught me how to hold my breath.

For four months, David held the Guinness world record for oxygen-assisted static apnea (holding your breath after breathing pure oxygen): 17 minutes and 4.4 seconds. His record was then surpassed by Tom Sietas on September 19, 2008. David’s record for doing what I’ll describe is between 7 and 8 minutes.

I was born premature and, unlike David, I couldn’t then remember the last time I held my breath for more than one minute. It has always been my physiological Achilles heel.

What were the results of his training?

My first baseline test: 40 seconds.
15 minutes later: 3 minutes and 33 seconds (!!!).

Out of roughly 12 TEDMED attendees he also taught, all but one beat Harry Houdini’s lifelong record of 3 minutes and 30 seconds. One woman held her breath for more than 5 minutes. Here is a photograph of the session. I’m sitting in the vest, four people to the right of Roni Zeiger, MD, Google Health product manager.

Here’s how we did it…

The David Blaine Method

DISCLAIMER: THIS IS FOR INFORMATIONAL PURPOSES ONLY. DO NOT ATTEMPT IN WATER OR WITHOUT PROPER SUPERVISION.

First and foremost, this is not a joke. David himself has almost died on several occasions. See 2:15 forward for a warning:

Moving onward to the method, which we did seated.

These notes were taken on a scrap of paper while performing the exercises. Much of it was written after I lost almost all sensation in my hands following the purging exercises, and after colors began to morph. After 3:20–I really, really wanted to beat Houdini’s record–I was shaking. Needless to say, this means these cliff notes are a bit shaky and may not be 100% accurate.

FYI, the above side-effects are common.

Definitions:

Deep breathing: “Deep breathing” involves taking a big breath in through the mouth, holding for one second, and then exhaling for 10 seconds through your mouth through your almost-closed mouth with tongue pressed against your lower teeth. It should be a hissing exhalation and make a “tsssssss…” sound. All breathing and exercises are performed though the mouth.

Purging: “Purging” involves a strong exhalation as if you were trying to blow a toy sailboat across a pool, followed by a big but faster inhalation. David’s cheeks were puffed out as he demonstrated the exhalation (imagine the big bad wolf blowing the pigs’ homes down). Be careful not to heave or rock back and forth, which wastes oxygen. Keep as still as possible.

Semi-purging: Breathing between the above two. More forceful than deep breathing but less forceful than full purging. Used for recovering after each time trial.

The Steps:

1:30 deep breathing
1:15 purging (if you feel like you’re going to pass out, do it less intensely)

Hold breath for target 1:30, no more
After 1:30:
Take 3 semi-purge breaths

1:30 deep breathing
1:30 purging

Hold breath for target 2:30, no more
After 2:30
Take 3 semi-purge breaths

2:00 deep breathing
1:45 purging

Hold breath for as long as possible
After exhalation:
Take 3-10 hard semi-purge breaths until your recover

Other Observations

David’s record using the above method: 7:47. His heart rate dropped below 20 beats per minute

He had us move our right index finger slightly every 30 seconds or so while holding our breath to indicate we were alright. More motion would waste O2.

He also suggested, and this was incredibly useful, going from A to Z in your head during time trials, visualizing a friend for each letter whose name starts with that letter. Use celebrities or historical figures when needed. This serves to distract you from the fact that you’re holding your breath.

If you continually check your time, it seems you hold your breath for less time. It is the opposite of the above. Too much focus on the time creates tension. All of the test subjects, myself included, had a harder time holding their breath when David announced the time every 5 seconds vs. 30 seconds. If I do this a second time, I will have someone else watch the time for me.

Do not let any air out whatsoever after taking your big inhalations for the time trials. This is important protective training for water-based breath holding. Why? If you pass out in the water (not good), you want the uncontrolled release of bubbles to indicate to those supervising that you’ve passed out.

It is easier to hold your breath if you haven’t eaten for 4-6 hours. It is also easier to hold your breath if you have less body mass to support. David will purposefully lose 30+ pounds during serious training to improve his lung-to-body volume ratio.

Want More?

I’ve finally met someone who screws with their body as much as I screw with mine. There are some incredible possibilities.

Would you like to see more on this blog with David Blaine? If so, follow him here on Twitter to let us know. He has a hell of lot to teach, and I’d enjoy more body hacking and mischief.

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Odds and Ends:
Tim Ferriss – Most Popular Blog Posts
Tim Ferriss on TED – Swimming Hacks, Dancing, and More

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.’”

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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

But who keeps a food journal? Exactly.

Unless you have extreme note-taking OCD like me, it’s too much of a pain in the ass to write down what you eat and track it all. I use the online food database here to keep my facts straight, but data entry sucks no matter how you slice it.

Here are first-look highlights of the FoodScanner, which launched a few hours ago and is now available…

1. DailyBurn’s FoodScanner is the first and only application that uses the iPhone’s camera to scan the UPC codes of foods and link them with full nutritional information (calories, macronutrients, etc.).

2. With a built-in database of more than 200,000 foods, it is the easiest way to accurately log what you eat during the day and keep an up-to-date calorie and nutrient count. All information is automatically synced with DailyBurn’s sophisticated workout and nutrition-tracking web application.

3. You don’t have to use the new 3GS with auto-focus. It works accurately on all iPhones using the most accurate scanning technology for iPhone – Occipital’s Red Laser.

4. You can also track natural foods (not processed) by searching by name or brand.

Full disclosure: I am an advisor to DailyBurn, but I chose to work with them specifically because I selfishly wanted to have the tools I need to geek out in less time. Here is another favorite new feature: breakdown of meals by protein/carbohydrate/fat composition (http://dailyburn.com/foods once logged in).

Keep in mind that FoodScanner is not a tool for teaching people to eat bar-coded foods. In fact, it can be quite the opposite: an awareness-building tool that makes you less likely to eat crap. Though the manual natural food tracking still requires some automating in the future, the technology is moving in the right direction.

iPhone screenshots can be seen in Gizmodo’s review.

I’ve invited Dr. Michael Eades and Dr. Mary Dan Eades, two of my favorite bariatric (obesity treatment) doctors in the US and the first to introduce insulin resistance to the mainstream, to explain the facts and benefits of increased saturated fat intake…

The sub-headings are mine, and a few edits have been made for space and context. Please see Dr. Michael Eades’ references and responses to questions in the comments.

Mid-Section Fat Loss: Problem Solved?

A couple of generations ago two physicians—one on the East Coast, one on the West—while working long hours with many patients, serendipitously stumbled onto a method to rapidly decrease fat around the mid-section. We’re sure that other doctors figured out the same thing, but these two were locally famous and published their methods. Interestingly, neither was looking to help patients lose weight.

Blake Donaldson, M.D., who practiced in Manhattan, was looking for a treatment for allergies; Walter Voegtlin, M.D., a Seattle gastroenterologist, was trying to figure out a better method for treating his patients with Crohn’s disease and ulcerative colitis. Dr. Donaldson got his inspiration from a meeting he had with the aforementioned Vilhalmur Stefansson; Dr. Voegtlin came up with the same idea based on his knowledge of comparative anatomy. Though they came at two different questions from very different angles, they arrived at the same dietary answer. Both solved the problems they were seeking to solve and, coincidentally, noticed that their overweight patients lost a tremendous amount of fat from their abdominal areas while undergoing the treatment. As happened later with us and with Dr. Atkins, word of their success in combating obesity spread rapidly, and before long both physicians were deluged with overweight patients seeking treatment, completely changing the character of their medical practices. In retirement, both wrote books about their methods. Donaldson’s was published in 1961; Voegtlin’s in 1972. And as far as we can tell, although their years of practice overlapped, they never knew one another.

What was their secret? What did these two men independently discover? What kind of nutritional regimen did they use to bring about such great results in their patients?

Both had their patients follow an all-meat diet.

An all-meat diet?

Yes, an all-meat diet. Remember that when these physicians were in practice, there hadn’t been all the negative publicity about saturated fat and red meat that there has been in recent years. At that time, most people considered meat as simply another food, just like potatoes, bread, or anything else. No one worried about eating it. The (misguided) hypothesis that fat in the diet causes heart disease hadn’t reared its ugly head, so telling people at that time to go on an all-meat diet didn’t provoke the same sort of knee-jerk emotions that it does—at least in some quarters—now.

The patients who followed these all-meat diets rapidly lost weight from their midsections and improved their blood sugar and blood pressure problems if they had them. Calculations of cholesterol in all its various permutations was still decades away, but both doctors even used the all-meat diet for their patients with heart disease without problem. The all-meat diet proved to be a safe, filling, rapid way to help patients lose abdominal fat while improving their health. And remember, one of these diets was developed to treat GI problems, the other to treat allergies. The rapid weight loss that followed was a surprising, but welcome side effect.

7 Reasons to Eat More Saturated Fat

In the not-so-distant past, the medical establishment considered all fats equally loathsome: all fats were created equal and they’re all bad for you. Things have changed in that quarter, if only slightly. You have no doubt heard the drumbeat of current medical thinking on fats: some fats are now good for you—olive oil and canola oil*—but others are bad for you—trans fats and all saturated fats. That’s an improvement from the old cry, but far from the truth.

It seems that no matter how the story spins from the denizens of the anti-fat camp, one piece of their advice remains staunchly constant: “You should sharply limit your intake of saturated fats.” The next admonition will invariably be, “which have been proven to raise cholesterol and cause heart disease.” Their over-arching belief is that saturated fat is bad, bad, bad.

You see with just a glance at [our suggested meal plans] that we’ve included fatty cuts of meat, chicken with the skin, bacon, eggs, butter, coconut oil, organic lard, and heavy cream in the plan. Aren’t we worried that these foods will increase your risk of heart disease and raise your cholesterol? In a word, nope. In fact, we encourage you to make these important fats a regular part of your healthy diet. Why? Because humans need them and here are just a few reasons why.

1) Improved cardiovascular risk factors

Though you may not have heard of it on the front pages of your local newspaper, online news source, or local television or radio news program, saturated fat plays a couple of key roles in cardiovascular health. The addition of saturated fat to the diet reduces the levels of a substance called lipoprotein (a)—pronounced “lipoprotein little a” and abbreviated Lp(a)—that correlates strongly with risk for heart disease. Currently there are no medications to lower this substance and the only dietary means of lowering Lp(a) is eating saturated fat. Bet you didn’t hear that on the nightly news. Moreover, eating saturated (and other) fats also raises the level of HDL, the so-called good cholesterol. Lastly, research has shown that when women diet, those eating the greatest percentage of the total fat in their diets as saturated fat lose the most weight.

2) Stronger bones

In middle age, as bone mass begins to decline, an important goal (particularly for women) is to build strong bones. You can’t turn on the television without being told you need calcium for your bones, but do you recall ever hearing that saturated fat is required for calcium to be effectively incorporated into bone? According to one of the foremost research experts in dietary fats and human health, Mary Enig, Ph.D., there’s a case to be made for having as much as 50 percent of the fats in your diet as saturated fats for this reason. That’s a far cry from the 7 to 10 percent suggested by mainstream institutions. If her reasoning is sound—and we believe it is— is it any wonder that the vast majority of women told to avoid saturated fat and to selectively use vegetable oils instead would begin to lose bone mass, develop osteoporosis, and get put on expensive prescription medications plus calcium to try to recover the loss in middle age?

3) Improved liver health

Adding saturated fat to the diet has been shown in medical research to encourage the liver cells to dump their fat content. Clearing fat from the liver is the critical first step to calling a halt to middle-body fat storage. Additionally, saturated fat has been shown to protect the liver from the toxic insults of alcohol and medications, including acetaminophen and other drugs commonly used for pain and arthritis, such as nonsteroidal anti-inflammatory drugs or NSAIDs, and even to reverse the damage once it has occurred. Since the liver is the lynchpin of a healthy metabolism, anything that is good for the liver is good for getting rid of fat in the middle. Polyunsaturated vegetable fats do not offer this protection.

4) Healthy lungs

For proper function, the airspaces of the lungs have to be coated with a thin layer of what’s called lung surfactant. The fat content of lung surfactant is 100 percent saturated fatty acids. Replacement of these critical fats by other types of fat makes faulty surfactant and potentially causes breathing difficulties. Absence of the correct amount and composition of this material leads to collapse of the airspaces and respiratory distress. It’s what’s missing in the lungs of premature infants who develop the breathing disorder called infant respiratory distress syndrome. Some researchers feel that the wholesale substitution of partially hydrogenated (trans) fats for naturally saturated fats in commercially prepared foods may be playing a role in the rise of asthma among children. Fortunately, the heyday of trans fats is ending and their use is on the decline. Unfortunately, however, the unreasoning fear of saturated fat leads many people to replace trans fats with an overabundance of polyunsaturated vegetable oils, which may prove just as unhealthful.

5) Healthy brain

You will likely be astounded to learn that your brain is mainly made of fat and cholesterol. Though many people are now familiar with the importance of the highly unsaturated essential fatty acids found in cold-water fish (EPA and DHA) for normal brain and nerve function, the lion’s share of the fatty acids in the brain are actually saturated. A diet that skimps on healthy saturated fats robs your brain of the raw materials it needs to function optimally.

6) Proper nerve signaling

Certain saturated fats, particularly those found in butter, lard, coconut oil, and palm oil, function directly as signaling messengers that influence the metabolism, including such critical jobs as the appropriate release of insulin. And just any old fat won’t do. Without the correct signals to tell the organs and glands what to do, the job doesn’t get done or gets done improperly.

7) Strong immune system

Saturated fats found in butter and coconut oil (myristic acid and lauric acid) play key roles in immune health. Loss of sufficient saturated fatty acids in the white blood cells hampers their ability to recognize and destroy foreign invaders, such as viruses, bacteria, and fungi. Human breast milk is quite rich in myristic and lauric acid, which have potent germ-killing ability. But the importance of the fats lives on beyond infancy; we need dietary replenishment of them throughout adulthood, middle age, and into seniority to keep the immune system vigilant against the development of cancerous cells as well as infectious invaders.

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Footnotes:

*We advocate the use of olive oil, but recommend against the use of canola oil, despite its widely perceived healthful reputation. In order to be fit for human consumption, rapeseed oil (which is canola oil) requires significant processing to remove its objectionable taste and smell. Processing damages the oil, creating trans fats. Also, the oil is sensitive to heat, so if used at all, it should never be used to fry foods.

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The above post is an exclusive excerpt from Dr. Eades’ newest book, which is directed at people who want to reduce abdominal fat. Despite the title, the principles it details are ideal for anyone who wants to decrease both visceral (internal) and subcutaneous (under the skin) fat in the abdomen.

Tim Ferriss on Vibram Shoes from Kevin Rose on Vimeo.

“The human foot is a work of art and a masterpiece of engineering.”
—Leonardo Da Vinci

“OK, dude, what’s up with the goofy shoes?”

It was the second day of Pavel’s RKC kettlebell course, and I’d seen more than a few people wearing what appeared to be gecko feet. The sheer goofiness compelled me to ask Rudy Tapalla, a CrossFit instructor from Chicago, why on earth he would put these ridiculous gloves on his toes. He seemed to have good mojo — he was shorter than me but had a vertical jump to match Michael Jordan — so I figured he might have good reasons.

He did, though I didn’t realize it at the time.

I remained a skeptic but tested them a month later. Now, I have three pairs and find it hard to wear other shoes. Vibram Five Fingers shoes (”VFFs” to the die-hard fans) are worth a closer look.

After two weeks of wearing them, the lower-back pain I’d had for more than 10 years disappeared and hasn’t returned since I started experimentation about 8 weeks ago.

Sound ridiculously implausible?

It doesn’t once we look at how feet and posture adapt…

Nasty Pictures and Maladapted Feet

Each human foot has 26 bones, 33 joints, and more than 100 muscles and tendons. It’s a surprisingly malleable structure.

From the cached version of the most excellent Nature’s Magic Bullet, referred to me by Joseph Mascaro:

Most people, including doctors, have never seen a natural foot, unaltered by footwear. The following images of habitually bare feet are taken from a study performed almost 100 years ago, published 1905 in the American Journal of Orthopedic Surgery, which examined the feet of native barefoot populations in the Philippines and Central Africa. A line can be drawn that runs through the heel, ball, and big toe of a habitually bare foot. The little toes spread naturally and fan out to provide a wide, stable base for walking or standing.

How do our shod feet compare? The following more common image, also taken from the 1905 study, demonstrates feet that are shaped like the owner’s shoes. No such line can be drawn, and the little toes crowd to a point—a comparatively unstable, narrow base for walking or standing.

The Simple Biomechanics of Bad Posture

Postural compensation is unavoidable while wearing shoes that elevate the heels. It’s necessary to maintain balance.

Chronic use of heels can result — and usually does — in some degree of kyphosis-lordosis and related pains in the lower back and mid-upper back.

Reversing Degeneration – Embracing the Barefoot Alternative

Vibram Five Finger models: KSO (blue), Classic (brown), Sprint (gray)

Laboratory studies show that the plantar arch alone returns at least 17 percent of the energy of impact. Running shoes have largely replaced our arches, but they are neither as effective nor as durable. Barefoot runners can clearly do as well as shoed runners, but it takes time to develop the strength in the foot to use our natural arch fully.

(Source: The Barefoot Route)

Ethiopian Abebe Bikila ran a world-record 2:15:17 marathon at the 1960 Olympics in Rome.

Barefoot.

The unadorned human foot is built for running. In fact, some researchers have proposed that bipedalism is an evolved trait related to “persistence hunting”, which is common among predators like wolves. Don’t think a human can run an antelope to death? Think again.

So how do we reclaim our rightful arch strength, our stability, and undo the damage of years of unnatural posture? Not to mention rediscover the joy of feeling the terrain under our feet?

Going barefoot is one option, and one that I enjoy, but there are limits. In the concrete jungle, glass and other dangers make going Bushman a roll of the dice at best. Tetanus or a trip to the ER? I’ll pass.

The Vibram Five Fingers shoes, to differing degrees, allow you to both walk without a heel (as would wrestling shoes, the Nike Free, Vivo Barefoot shoes, or thin flip-flops) and condition toe-spread, especially the big toe, for lateral stability.

I first tested the KSO (”keep stuff out”) model, which fits most like an aqua sock and has more padding than other models I tested.

I then tested the Classic model, the least complicated of all, and the Sprint model, which is almost a hybrid of the KSO and Classic.

I wear a size 9.5 men’s shoe in the US and tested EU 42 for the KSO and Classic, and an EU 43 for the Sprint.

The results, in brief:

My favorite model is, by far, the Classic. It’s easiest to get on, even with my worthless nub of a little toe, and it most closely mimics the true barefoot feel. The only downside is that, to get a snug fit and not have the heel come off the foot, you must slide the top slip-tie until it is quite tight. This will feel unusual for the first 24 hours or so. I have used the Classic to go trail running in SF and it is euphoric.

I love the KSO, but it is more of a process to get on, and far more conspicuous. At first, it’s fun to get a lot of attention with the shoes (gentlemen, you will not believe the “peacocking” effect of these puppies), but giving each person you meet a 5-minute explanation gets old fast. The Classic blends in more than the KSO or any model with straps. Black will help all models fade into the ground, but I prefer colors.

The Sprint model was so uncomfortable at first that I shelved them, never intending to test them again. It was the only model, and not due to size differences, that oddly pulled my little toe out, causing minor pain but great discomfort after even 10 minutes. I sent an e-mail to their US CEO, who responded back with a suggestion to “seat the heel”, particularly with the Sprint model. This means:

Slide your foot back to nestle your heel into the heel pocket. It’s important to get your heel deeply seated. Secure the instep strap BEFORE latching the heel straps. This will ensure the foot is positioned properly.

I have since been able to wear the Sprint model for 1-2 days at a time, no more than 1 hour of walking at a stretch, but the velcro strap can still bite into the skin without the KSO-like mesh below it. I find it the least comfortable of the three models.

But what about flat feet?

I had clinically-diagnosed arch problems as a child — flat feet supreme — and was prescribed not only custom orthopedic insoles but also exercises for the feet themselves, rolling up towels with the toes, etc.. For those who like random anecdotes, my mom e-mailed me this addition after I published this post:

You didn’t mention that you leapt at the orthopedist examining your feet, like Spidey to a wall.

Sounds like me. I was a little hellion. But we digress…

Needless to say, the exercises fell by the wayside, and I took to increasing levels of support through the shoes themselves. VFFs have been nothing short of spectacular for me, despite my history of flat feet.

Barefoot runners are often asked “but what do you use for arch support?”, to which they respond: “your arches”. I’ve found that my arches, and foot as a whole, feels better with less support rather than more.

Cautions and Cons

-Do not overdo it at first. Chances are that the ligaments and musculature of your feet is underdeveloped. Use them for no more than 1/2 – 1 mile in the first 24 hours, then take a day off. I suggest alternating VFFs with “normal” shoes or flat-soled shoes like Chuck Taylors for the first week. I now use VFFs for no more than three days in a row, as I’ve had some bruising on the heel with more, and such bruising is slow to heal and massively inconvenient. Asphalt is somewhat forgiving, concrete much less so (The Embarcadero in SF, for example), and marble or stone is brutal (casino floors in Las Vegas, etc.).

-Beware the sizing. There are complaints online of the VFF website sizing suggestions being inaccurate for some people. Get sized at a retail location that carries VFFs if possible. If you can’t, check the VFF return policy on their site or order through Amazon to ensure swaps are simple.

-Be prepared to wash them. VFFs are machine washable and should be air dried. There are five-toed socks like the Injinji brand, but I have found all of them to be incredibly painful between the toes, no matter which model of shoe is worn. I now only wear VFFs barefoot. One nice side-effect of the toe separation? No more athlete’s foot or foot skin issues.

In Closing

To embrace barefoot living or the barefoot alternative, you will have to change how you walk and run, avoiding the heel strike we’ve all used since putting thick Nike padding under our soles. No need to obsess, though, as your gait will adapt naturally — reverting to a natural state, as it were — as you avoid the discomfort of doing otherwise.

The fastest runners have a style quite similar to that of a person running without shoes. They absorb shock by landing lightly on their forefeet rather than on their heels, and their landing leg is beneath the torso, with the leg slightly bent to absorb impact.

…

According to exercise physiologist and Olympic marathoner Pete Pfitzinger, the key to starting out is to go slowly. He advises walking barefoot for a few weeks to toughen up the skin on the bottom of the foot as well as the muscles in the ankles and feet. Once you are ready to run, start with a mere five minutes, increasing slowly and running barefoot every couple of days. From there, build to up to 20 minutes over a month. After a few weeks of this, the feet and ankles will be stronger, thus reducing the risk of injury. Possible places to train include sandy beaches and golf courses.

The barefoot running technique has been described as falling forward. It has also been described as gently kissing the ground with the balls of your feet.

(Source: The Barefoot Route)

For those interested in developing the most efficient and low-impact running gait, I suggest starting with the Chi Running DVD (skip the book, which gets into too much pseudo-Asian chi mumbo jumbo) and moving to the Pose Method of Running book if interested in more specific details.

Experiment with rediscovering your feet and proper biomechanics.

If a few weeks can eradicate 10+ years of lower-back pain for me, it might just do something for you.

At the very least, you get to wear some goofy shoes that encourage you to wiggle your toes.

Other things you might not have seen:
Tim Ferriss in NY Times Styles: Too Much Information? Ignore It.
Tim Ferriss on Twitter – what I am doing right now?
Tim Ferriss Investments – what have I invested in recently?