8: How the Sugar Industry Was Able to Supress Information on the Dangers of Sugar

Posted on March 8, 2013 by Stanley Roth

Mother Jones Magazine published this investigative journalism report on October 31, 2012. Every statement made in the article is supported, documented, and footnoted with links to original documents and materials, many from government records and the sugar industry’s own files. It is an amazing piece of journalism (gaps in footnote numbers represent links to documents deleted by the sugar industry after publication).

Big Sugar’s Sweet Little Lies

How the industry kept scientists from asking: Does sugar kill?

By Gary Taubes and Cristin Kearns Couzens | Wed Oct. 31, 2012 2:03 AM PDT

On a brisk spring Tuesday in 1976, a pair of executives from the Sugar Association stepped up to the podium of a Chicago ballroom to accept [1] the Oscar of the public relations world, the Silver Anvil [2] award for excellence in “the forging of public opinion. [3]” The trade group had recently pulled off one of the greatest turnarounds in PR history. For nearly a decade, the sugar industry had been buffeted by crisis after crisis as the media and the public soured on sugar and scientists began to view it as a likely cause of obesity, diabetes, and heart disease. Industry ads claiming that eating sugar helped you lose weight had been called out [4] by the Federal Trade Commission, and the Food and Drug Administration had launched a review [5] of whether sugar was even safe to eat. Consumption had declined 12 percent in just two years, and producers could see where that trend might lead. As John “JW” Tatem Jr. and Jack O’Connell Jr., the Sugar Association’s president and director of public relations, posed that day with their trophies, their smiles only hinted at the coup they’d just pulled off.

Their winning campaign, crafted with the help of the prestigious public relations firm Carl Byoir & Associates, had been prompted by a poll showing that consumers had come to see sugar as fattening, and that most doctors suspected it might exacerbate, if not cause, heart disease and diabetes. With an initial annual budget of nearly $800,000 ($3.4 million today) collected from the makers of Dixie Crystals, Domino, C&H, Great Western, and other sugar brands, the association recruited a stable of medical and nutritional professionals to allay the public’s fears, brought snack and beverage companies into the fold, and bankrolled scientific papers that contributed to a “highly supportive” FDA ruling, which, the Silver Anvil application boasted, made it “unlikely that sugar will be subject to legislative restriction in coming years.”

The story of sugar, as Tatem told it, was one of a harmless product under attack by “opportunists dedicated to exploiting the consuming public.” Over the subsequent decades, it would be transformed from what the New York Times in 1977 had deemed “a villain in disguise [6]” into a nutrient so seemingly innocuous that even the American Heart Association and the American Diabetes Association approved it as part of a healthy diet. Research on the suspected links between sugar and chronic disease largely ground to a halt by the late 1980s, and scientists came to view such pursuits as a career dead end. So effective were the Sugar Association’s efforts that, to this day, no consensus exists about sugar’s potential dangers. The industry’s PR campaign corresponded roughly with a significant rise in Americans’ consumption of “caloric sweeteners,” including table sugar (sucrose) and high-fructose corn syrup (HFCS). This increase was accompanied, in turn, by a surge in the chronic diseases increasingly linked to sugar. Since 1970, obesity rates in the United States have more than doubled, while the incidence of diabetes has more than tripled. (The chart below uses sugar “availability” numbers rather than the USDA’s speculative new consumption figures [7].)

Sugar/Diabetes Chart

Precisely how did the sugar industry engineer its turnaround? The answer is found in more than 1,500 pages of internal memos, letters, and company board reports we discovered buried in the archives [13] of now-defunct sugar companies as well as in the recently released papers of deceased researchers and consultants who played key roles in the industry’s strategy. They show how Big Sugar used Big Tobacco-style tactics to ensure that government agencies would dismiss troubling health claims against their products. Compared to the tobacco companies, which knew for a fact that their wares were deadly and spent billions of dollars trying to cover up that reality, the sugar industry had a relatively easy task. With the jury still out on sugar’s health effects, producers simply needed to make sure that the uncertainty lingered. But the goal was the same: to safeguard sales by creating a body of evidence companies could deploy to counter any unfavorable research.

For 40 years, the sugar industry’s priority has been to shed doubt on studies suggesting that its product makes people sick.

This decades-long effort to stack the scientific deck is why, today, the USDA’s dietary guidelines [14] only speak of sugar in vague generalities. (“Reduce the intake of calories from solid fats and added sugars.”) It’s why the FDA insists that sugar is “generally recognized as safe” despite considerable evidence suggesting otherwise. It’s why some scientists’ urgent calls for regulation of sugary products have been dead on arrival, and it’s why—absent any federal leadership—New York City Mayor Michael Bloomberg felt compelled to propose a ban on oversized sugary drinks [15] that passed in September.

In fact, a growing body of research suggests that sugar and its nearly chemically identical cousin, HFCS, may very well cause diseases that kill hundreds of thousands of Americans every year, and that these chronic conditions would be far less prevalent if we significantly dialed back our consumption of added sugars. Robert Lustig, a leading authority on pediatric obesity at the University of California-San Francisco (whose arguments Gary explored in a 2011 New York Times Magazine cover story [17]), made this case last February in the prestigious journal Nature. In an article titled “The Toxic Truth About Sugar, [18]” Lustig and two colleagues observed that sucrose and HFCS are addictive in much the same way as cigarettes and alcohol, and that overconsumption of them is driving worldwide epidemics of obesity and type 2 diabetes (the type associated with obesity). Sugar-related diseases are costing America around $150 billion a year, the authors estimated, so federal health officials need to step up and consider regulating the stuff.

“The fact that no confirmed scientific evidence links sugar to the death-dealing diseases…is the lifeblood” of the Sugar Association.

The Sugar Association dusted off [19] what has become its stock response: The Lustig paper, it said, “lacks the scientific evidence or consensus” to support its claims, and its authors were irresponsible not to point out that the full body of science “is inconclusive at best.” This inconclusiveness, of course, is precisely what the Sugar Association has worked so assiduously to maintain. “In confronting our critics,” Tatem explained [20] to his board of directors back in 1976, “we try never to lose sight of the fact that no confirmed scientific evidence links sugar to the death-dealing diseases. This crucial point is the lifeblood of the association.”

The Sugar Association’s earliest incarnation [21] dates back to 1943, when growers and refiners created the Sugar Research Foundation to counter World War II sugar-rationing propaganda [22]—”How Much Sugar Do You Need? None!” declared one government pamphlet. In 1947, producers rechristened their group the Sugar Association and launched a new PR division, Sugar Information Inc., which before long was touting sugar [23] as a “sensible new approach to weight control.” In 1968, in the hope of enlisting foreign sugar companies to help defray costs, the Sugar Association spun off its research division as the International Sugar Research Foundation. “Misconceptions concerning the causes of tooth decay, diabetes, and heart problems exist on a worldwide basis,” explained a 1969 ISRF recruiting brochure [24].

As early as 1962, internal Sugar Association memos had acknowledged the potential links between sugar and chronic diseases, but at the time sugar executives had a more pressing problem: Weight-conscious Americans were switching in droves to diet sodas—particularly Diet Rite and Tab—sweetened with cyclamate and saccharin. From 1963 through 1968, diet soda’s share of the soft-drink market shot from 4 percent to 15 percent. “A dollar’s worth of sugar,” ISRF vice president and research director John Hickson warned in an internal review, “could be replaced with a dime’s worth” of sugar alternatives. “If anyone can undersell you nine cents out of 10,” Hickson told the New York Times [25] in 1969, “you’d better find some brickbat you can throw at him.”

By then, the sugar industry had doled out more than $600,000 (about $4 million today) to study every conceivable harmful effect of cyclamate sweeteners, which are still sold around the world under names like Sugar Twin and Sucaryl. In 1969, the FDA banned cyclamates in the United States based on a study suggesting they could cause bladder cancer in rats. Not long after, Hickson left the ISRF to work for the Cigar Research Council. He was described in a confidential tobacco industry memo [26] as a “supreme scientific politician who had been successful in condemning cyclamates, on behalf of the [sugar industry], on somewhat shaky evidence.” It later emerged that the evidence suggesting that cyclamates caused cancer in rodents was not relevant to humans [27], but by then the case was officially closed. In 1977, saccharin, too, was nearly banned on the basis of animal results that would turn out to be meaningless in people.

Meanwhile, researchers had been reporting that blood lipids—cholesterol and triglycerides in particular—were a risk factor in heart disease. Some people had high cholesterol but normal triglycerides, prompting health experts to recommend that they avoid animal fats. Other people were deemed “carbohydrate sensitive,” with normal cholesterol but markedly increased triglyceride levels. In these individuals, even moderate sugar consumption could cause a spike in triglycerides. John Yudkin, the United Kingdom’s leading nutritionist, was making headlines [28] with claims that sugar, not fat, was the primary cause of heart disease.

In 1967, the Sugar Association’s research division began considering “the rising tide of implications of sucrose in atherosclerosis.” Before long, according to a confidential 1970 review of industry-funded studies, the newly formed ISRF was spending 10 percent of its research budget on the link between diet and heart disease. Hickson, the ISRF’s vice president, urged his member corporations to keep the results of the review under wraps. Of particular concern was the work of a University of Pennsylvania researcher on “sucrose sensitivity,” which sugar executives feared was “likely to reveal evidence of harmful effects. [29]” One ISRF consultant recommended [30] that sugar companies get to the truth of the matter by sponsoring a full-on study. In what would become a pattern, the ISRF opted not to follow his advice. Another ISRF-sponsored study, by biochemist Walter Pover of the University of Birmingham, in England, had uncovered a possible mechanism to explain how sugar raises triglyceride levels. Pover believed he was on the verge of demonstrating this mechanism “conclusively” and that 18 more weeks of work would nail it down. But instead of providing the funds, the ISRF nixed the project, assessing its value as “nil.”

One diabetes expert testified that anything more than 70 pounds per person per year—about half of what is sold in America today—might spark epidemics.

The industry followed a similar strategy when it came to diabetes. By 1973, links between sugar, diabetes, and heart disease were sufficiently troubling that Sen. George McGovern of South Dakota convened a hearing of his Select Committee on Nutrition and Human Needs to address the issue. An international panel of experts—including Yudkin and Walter Mertz, head of the Human Nutrition Institute at the Department of Agriculture—testified that variations in sugar consumption were the best explanation for the differences in diabetes rates between populations, and that research by the USDA and others supported the notion that eating too much sugar promotes dramatic population-wide increases in the disease. One panelist, South African diabetes specialist George Campbell, suggested that anything more than 70 pounds per person per year—about half of what is sold in America today—would spark epidemics.

In the face of such hostile news from independent scientists, the ISRF hosted its own conference the following March, focusing exclusively on the work of researchers who were skeptical of a sugar/diabetes connection. “All those present agreed that a large amount of research is still necessary before a firm conclusion can be arrived at,” according to a conference review [31] published in a prominent diabetes journal. In 1975, the foundation reconvened in Montreal to discuss research priorities with its consulting scientists. Sales were sinking, Tatem reminded the gathered sugar execs, and a major factor was “the impact of consumer advocates who link sugar consumption with certain diseases.”

Following the Montreal conference, the ISRF disseminated a memo [32] quoting Errol Marliss, a University of Toronto diabetes specialist, recommending that the industry pursue “well-designed research programs” to establish sugar’s role in the course of diabetes and other diseases. “Such research programs might produce an answer that sucrose is bad in certain individuals,” he warned. But the studies “should be undertaken in a sufficiently comprehensive way as to produce results. A gesture rather than full support is unlikely to produce the sought-after answers.”

Industry-funded science projects were vetted by a panel with reps from Hershey’s, Coca-Cola, General Mills, and Nabisco.

A gesture, however, is what the industry would offer. Rather than approve a serious investigation of the purported links between sucrose and disease, American sugar companies quit supporting [33] the ISRF’s research projects. Instead, via the Sugar Association proper, they would spend roughly $655,000 between 1975 and 1980 on 17 studies [34] designed, as internal documents put it, “to maintain research as a main prop of the industry’s defense. [35]” Each proposal was vetted by a panel [36] of industry-friendly scientists and a second committee [37] staffed by representatives from sugar companies and “contributing research members [38]” such as Coca-Cola, Hershey’s, General Mills, and Nabisco. Most of the cash was awarded to researchers whose studies seemed explicitly designed to exonerate sugar. One even proposed to explore whether sugar could be shown to boost serotonin levels in rats’ brains, and thus “prove of therapeutic value, as in the relief of depression,” an internal document noted [39].

At best, the studies seemed a token effort. Harvard Medical School professor Ron Arky, for example, received money from the Sugar Association to determine whether sucrose has a different effect on blood sugar and other diabetes indicators if eaten alongside complex carbohydrates like pectin and psyllium. The project went nowhere, Arky told us recently. But the Sugar Association “didn’t care.”

In short, rather than do definitive research to learn the truth about its product, good or bad, the association stuck to a PR scheme designed to “establish with the broadest possible audience—virtually everyone is a consumer—the safety of sugar as a food.” One of its first acts was to establish a Food & Nutrition Advisory Council [40] consisting of a half-dozen physicians and two dentists willing to defend sugar’s place in a healthy diet, and set aside roughly $60,000 per year (more than $220,000 today) to cover its cost [41].

Working to the industry’s recruiting advantage was the rising notion that cholesterol and dietary fat—especially saturated fat—were the likely causes of heart disease. (Tatem even suggested, in a letter to the Times Magazine [42], that some “sugar critics” were motivated merely by wanting “to keep the heat off saturated fats.”) This was the brainchild of nutritionist Ancel Keys, whose University of Minnesota laboratory had received financial support from the sugar industry as early as 1944. From the 1950s through the 1980s, Keys remained the most outspoken proponent of the fat hypothesis, often clashing publicly with Yudkin, the most vocal supporter of the sugar hypothesis—the two men “shared a good deal of loathing,” recalled one of Yudkin’s colleagues.

On federal panels, industry-funded scientists cited industry-funded studies to dismiss sugar as a culprit.

So when the Sugar Association needed a heart disease expert for its Food & Nutrition Advisory Council, it approached Francisco Grande, one of Keys’ closest colleagues. Another panelist was University of Oregon nutritionist William Connor, the leading purveyor of the notion that it is dietary cholesterol that causes heart disease. As its top diabetes expert, the industry recruited Edwin Bierman [43] of the University of Washington, who believed that diabetics need not pay strict attention to their sugar intake so long as they maintained a healthy weight by burning off the calories they consumed. Bierman also professed an apparently unconditional faith that it was dietary fat (and being fat) that caused heart disease, with sugar having no meaningful effect.

It is hard to overestimate Bierman’s role in shifting the diabetes conversation away from sugar. It was primarily Bierman who convinced the American Diabetes Association to liberalize the amount of carbohydrates (including sugar) it recommended in the diets of diabetics, and focus more on urging diabetics to lower their fat intake, since diabetics are particularly likely to die from heart disease. Bierman also presented industry-funded studies when he coauthored a section on potential causes for a National Commission on Diabetes report in 1976; the document influences the federal diabetes research agenda to this day. Some researchers, he acknowledged, had “argued eloquently” that consumption of refined carbohydrates (such as sugar) is a precipitating factor in diabetes. But then Bierman cited five studies—two of them bankrolled by the ISRF—that were “inconsistent” with that hypothesis. “A review of all available laboratory and epidemiologic evidence,” he concluded, “suggests that the most important dietary factor in increasing the risk of diabetes is total calorie intake, irrespective of source.”

Big Sugar found a reliable advocate in Frederick Stare, whose department at Harvard was bankrolled by the likes of Kellogg, Kraft, and Coca-Cola.

The point man on the industry’s food and nutrition panel was Frederick Stare [44], founder and chairman of the department of nutrition at the Harvard School of Public Health. Stare and his department had a long history of ties to Big Sugar. An ISRF internal research review credited the sugar industry with funding some 30 papers in his department from 1952 through 1956 alone. In 1960, the department broke ground on a new $5 million building funded largely by private donations, including a $1 million gift from General Foods, the maker of Kool-Aid and Tang.

By the early 1970s, Stare ranked among the industry’s most reliable advocates, testifying in Congress about the wholesomeness of sugar even as his department kept raking in funding from sugar producers and food and beverage giants such as Carnation, Coca-Cola, Gerber, Kellogg, and Oscar Mayer. His name also appears in tobacco documents, which show that he procured [45] industry funding for a study [46] aimed at exonerating cigarettes as a cause of heart disease.

The first act of the Food & Nutrition Advisory Council was to compile “Sugar in the Diet of Man,” an 88-page white paper edited by Stare and published in 1975 to “organize existing scientific facts concerning sugar.” It was a compilation of historical evidence and arguments that sugar companies could use to counter the claims of Yudkin, Stare’s Harvard colleague Jean Mayer, and other researchers whom Tatem called “enemies of sugar. [47]” The document was sent to reporters—the Sugar Association circulated 25,000 copies—along with a press release [48] headlined “Scientists dispel sugar fears.” The report neglected to mention that it was funded by the sugar industry, but internal documents confirm that it was [49].

Leading the panel that evaluated sugar for the FDA: George Irving, a former chair of the scientific advisory board for the International Sugar Research Foundation, an industry group.

The Sugar Association also relied on Stare to take its message to the people: “Place Dr. Stare on the AM America Show” and “Do a 3 ½ minute interview with Dr. Stare for 200 radio stations,” note the association’s meeting minutes. Using Stare as a proxy, internal documents explained [50], would help the association “make friends with the networks” and “keep the sugar industry in the background.” By the time Stare’s copious conflicts of interest were finally revealed—in “Professors on the Take, [51]” a 1976 exposé by the Center for Science in the Public Interest—Big Sugar no longer needed his assistance. The industry could turn to an FDA document to continue where he’d left off.

While Stare and his colleagues had been drafting “Sugar in the Diet of Man,” the FDA was launching its first review of whether sugar was, in the official jargon, generally recognized as safe (GRAS), part of a series of food-additive reviews [52] the Nixon administration had requested of the agency. The FDA subcontracted the task to the Federation of American Societies of Experimental Biology, which created an 11-member committee to vet hundreds of food additives from acacia to zinc sulfate. While the mission of the GRAS committee was to conduct unbiased reviews of the existing science for each additive, it was led by biochemist George W. Irving Jr., who had previously served two years as chairman of the scientific advisory board of the International Sugar Research Foundation. Industry documents show that another committee member, Samuel Fomon, had received sugar-industry funding for three of the five years prior to the sugar review.

The FDA’s instructions were clear: To label a substance as a potential health hazard, there had to be “credible evidence of, or reasonable grounds to suspect, adverse biological effects”—which certainly existed for sugar at the time. But the GRAS committee’s review would depend heavily on “Sugar in the Diet of Man” and other work by its authors. In the section on heart disease, committee members cited 14 studies whose results were “conflicting,” but 6 of those bore industry fingerprints, including Francisco Grande’s chapter from “Sugar in the Diet of Man” and 5 others that came from Grande’s lab or were otherwise funded by the sugar industry.

The sugar review panel cited five reports to contradict the notion that sugar consumption leads to diabetes—all had industry ties.

The diabetes chapter of the review acknowledged studies suggesting that “long term consumption of sucrose can result in a functional change in the capacity to metabolize carbohydrates and thus lead to diabetes mellitus,” but it went on to cite five reports contradicting that notion. All had industry ties, and three were authored by Ed Bierman, including his chapter in “Sugar in the Diet of Man.”

In January 1976, the GRAS committee published its preliminary conclusions, noting that while sugar probably contributed to tooth decay, it was not a “hazard to the public.” The draft review dismissed the diabetes link as “circumstantial” and called the connection to cardiovascular disease “less than clear,” with fat playing a greater role. The only cautionary note, besides cavities, was that all bets were off if sugar consumption were to increase significantly. The committee then thanked the Sugar Association for contributing “information and data.” (Tatem would later remark [53] that while he was “proud of the credit line…we would probably be better off without it.”)

The committee’s perspective was shared by many researchers, but certainly not all. For a public hearing on the draft review, scientists from the USDA’s Carbohydrate Nutrition Laboratory submitted what they considered “abundant evidence that sucrose is one of the dietary factors responsible for obesity, diabetes, and heart disease.” As they later explained [54] in the American Journal of Clinical Nutrition, some portion of the public—perhaps 15 million Americans at that time—clearly could not tolerate a diet rich in sugar and other carbohydrates. Sugar consumption, they said, should come down by “a minimum of 60 percent,” and the government should launch a national campaign “to inform the populace of the hazards of excessive sugar consumption.” But the committee stood by its conclusions in the final version [55] of its report presented to the FDA in October 1976.

“The next time you hear a promoter attacking sugar, beware the ripoff,” warned a sugar industry ad. “Remember he can’t substantiate his charges.”

For the sugar industry, the report was gospel. The findings “should be memorized” by the staff of every company associated with the sugar industry, Tatem told his membership [53]. “In the long run,” he said [56], the document “cannot be sidetracked, and you may be sure we will push its exposure to all corners of the country.”

The association promptly produced an ad for newspapers and magazines exclaiming “Sugar is Safe!” It “does not cause death-dealing diseases,” the ad declared, and “there is no substantiated scientific evidence indicating that sugar causes diabetes, heart disease or any other malady…The next time you hear a promoter attacking sugar, beware the ripoff. Remember he can’t substantiate his charges. Ask yourself what he’s promoting or what he is seeking to cover up. If you get a chance, ask him about the GRAS Review Report. Odds are you won’t get an answer. Nothing stings a nutritional liar like scientific facts.”

The Sugar Association would soon get its chance to put the committee’s sugar review to the test. In 1977, McGovern’s select committee—the one that had held the 1973 hearings on sugar and diabetes—blindsided the industry with a report titled “Dietary Goals for the United States,” recommending that Americans lower their sugar intake by 40 percent (PDF) [57]. The association “hammered away” at the McGovern report using the GRAS review “as our scientific Bible,” Tatem told sugar executives [58].

McGovern held fast, but Big Sugar would prevail in the end. In 1980, when the USDA first published [59] its own set of dietary guidelines, it relied heavily [60] on a review written for the American Society of Clinical Nutrition by none other than Bierman [61], who used the GRAS committee’s findings to bolster his own. “Contrary to widespread opinion, too much sugar does not seem to cause diabetes,” the USDA guidelines concluded. They went on to counsel that people should “avoid too much sugar,” without bothering to explain what that meant.

In 1982, the FDA once again took up the GRAS committee’s conclusion that sugar was safe, proposing to make it official. The announcement resulted in a swarm of public criticism, prompting the agency to reopen its case. Four years later, an agency task force concluded [62], again leaning on industry-sponsored studies, that “there is no conclusive evidence…that demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.” (Walter Glinsmann, the task force’s lead administrator, would later become a consultant [63] to the Corn Refiners Association, which represents producers of high-fructose corn syrup.)

By 1999, the average American would be eating more than double the amount of sugar the FDA had deemed safe in 1986.

The USDA, meanwhile, had updated its own dietary guidelines. With Fred Stare now on the advisory committee, the 1985 guidelines [64] retained the previous edition’s vague recommendation to “avoid too much” sugar but stated unambiguously that “too much sugar in your diet does not cause diabetes.” At the time, the USDA’s own Carbohydrate Nutrition Laboratory was still generating evidence [65] to the contrary and supporting the notion that “even low sucrose intake” might be contributing to heart disease in 10 percent of Americans.

By the early 1990s, the USDA’s research into sugar’s health effects had ceased, and the FDA’s take on sugar had become conventional wisdom, influencing a generation’s worth of key publications on diet and health. Reports from the surgeon general [66] and the National Academy of Sciences [67] repeated the mantra that the evidence linking sugar to chronic disease was inconclusive, and then went on to equate “inconclusive” with “nonexistent.” They also ignored a crucial caveat: The FDA reviewers had deemed added sugars—those in excess of what occurs naturally in our diets—safe at “current” 1986 consumption levels. But the FDA’s consumption estimate was 43 percent lower than that of its sister agency, the USDA. By 1999, the average American would be eating more than double the amount [9] the FDA had deemed safe­—although we have cut back by 13 percent since then.

Asked to comment on some of the documents described in this article, a Sugar Association spokeswoman responded that they are “at this point historical in nature and do not necessarily reflect the current mission or function” of the association. But it is clear enough that the industry still operates behind the scenes to make sure regulators never officially set a limit on the amount of sugar Americans can safely consume. The authors of the 2010 USDA dietary guidelines, for instance, cited two scientific reviews [68] as evidence that sugary drinks don’t make adults fat. The first was written by Sigrid Gibson [69], a nutrition consultant whose clients included the Sugar Bureau (England’s version of the Sugar Association) and the World Sugar Research Organization (formerly the ISRF). The second review was authored by Carrie Ruxton [70], who served as research manager of the Sugar Bureau from 1995 to 2000.

The Sugar Association has also worked its connections to assure that the government panels making dietary recommendations—the USDA’s Dietary Guidelines Advisory Committee, for instance—include researchers sympathetic to its position. One internal newsletter [71] boasted in 2003 that for the USDA panel, the association had “worked diligently to achieve the nomination of another expert wholly through third-party endorsements.”

When world health experts dared to recommend that people eat less sugar, the industry asked federal officials to intervene.

In the few instances when governmental authorities have sought to reduce people’s sugar consumption, the industry has attacked openly. In 2003, after an expert panel convened by the World Health Organization recommended that no more than 10 percent of all calories in people’s diets should come from added sugars—nearly 40 percent less than the USDA’s estimate [72]] for the average American—current Sugar Association president Andrew Briscoe wrote [73] the WHO’s director general warning that the association would “exercise every avenue available to expose the dubious nature” of the report and urge “congressional appropriators to challenge future funding” for the WHO. Larry Craig (R-Idaho, sugar beets) and John Breaux (D-La., sugarcane), then co-chairs of the Senate Sweetener Caucus, wrote a letter [74] to Secretary of Health and Human Services Tommy Thompson, urging his “prompt and favorable attention” to prevent the report from becoming official WHO policy. (Craig had received more than $36,000 [75] in sugar industry contributions in the previous election cycle.) Thompson’s people responded with a 28-page letter [76] detailing “where the US Government’s policy recommendations and interpretation of the science differ” with the WHO report. Not surprisingly, the organization left its experts’ recommendation on sugar intake out of its official dietary strategy [77].

In recent years the scientific tide has begun to turn against sugar. Despite the industry’s best efforts, researchers and public health authorities have come to accept that the primary risk factor for both heart disease and type 2 diabetes is a condition called metabolic syndrome, which now affects more than 75 million Americans [78], according to the Centers for Disease Control and Prevention. Metabolic syndrome [79] is characterized by a cluster of abnormalities—some of which Yudkin and others associated with sugar almost 50 years ago—including weight gain, increased insulin levels, and elevated triglycerides. It also has been linked to cancer [80] and Alzheimer’s disease [81]. “Scientists have now established causation,” Lustig said recently. “Sugar causes metabolic syndrome.”

“The science is in,” Lustig says. But the industry is going to fight tooth and nail to prevent that science from translating into public policy.”

Newer studies [82] from the University of California-Davis have even reported that LDL cholesterol, the classic risk factor for heart disease, can be raised significantly in just two weeks by drinking sugary beverages at a rate well within the upper range of what Americans consume—four 12-ounce glasses a day of beverages like soda, Snapple, or Red Bull. The result is a new wave of researchers coming out publicly against Big Sugar.

During the battle over the 2005 USDA guidelines, an internal Sugar Association newsletter [83] described its strategy toward anyone who had the temerity to link sugar consumption with chronic disease and premature death: “Any disparagement of sugar,” it read, “will be met with forceful, strategic public comments and the supporting science.” But since the latest science is anything but supportive of the industry, what happens next?

“At present,” Lustig ventures, “they have absolutely no reason to alter any of their practices. The science is in—the medical and economic problems with excessive sugar consumption are clear. But the industry is going to fight tooth and nail to prevent that science from translating into public policy.”

Like the tobacco industry before it, the sugar industry may be facing the inexorable exposure of its product as a killer—science will ultimately settle the matter one way or the other—but as Big Tobacco learned a long time ago, even the inexorable can be held up for a very long time.

Additional Link:
Sugar Industry Internal Documents Revealed
How a Young Dentist Drilled into the Sugar Industry

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7: NY Times Article…It’s the Sugar…

Posted on March 4, 2013 by Stanley Roth

The New York Times reported a recent study in the prestigious PLoS One Journal (a peer-reviewed publication of the Public Library of Science) conclusively linked a rise in sugar consumption to a rise in diabetes in 175 countries:

NY TIMES
Mark Bittman
February 27, 2013

Sugar is indeed toxic. It may not be the only problem with the Standard American Diet, but it’s fast becoming clear that it’s the major one.

A study published in the Feb. 27 issue of the journal PLoS One links increased consumption of sugar with increased rates of diabetes by examining the data on sugar availability and the rate of diabetes in 175 countries over the past decade. And after accounting for many other factors, the researchers found that increased sugar in a population’s food supply was linked to higher diabetes rates independent of rates of obesity.

In other words, according to this study, it’s not just obesity that can cause diabetes: sugar can cause it, too, irrespective of obesity. And obesity does not always lead to diabetes.

The study demonstrates this with the same level of confidence that linked cigarettes and lung cancer in the 1960s. As Rob Lustig, one of the study’s authors and a pediatric endocrinologist at the University of California, San Francisco, said to me, “You could not enact a real-world study that would be more conclusive than this one.”

The study controlled for poverty, urbanization, aging, obesity and physical activity. It controlled for other foods and total calories. In short, it controlled for everything controllable, and it satisfied the longstanding “Bradford Hill” criteria for what’s called medical inference of causation by linking dose (the more sugar that’s available, the more occurrences of diabetes); duration (if sugar is available longer, the prevalence of diabetes increases); directionality (not only does diabetes increase with more sugar, it decreases with less sugar); and precedence (diabetics don’t start consuming more sugar; people who consume more sugar are more likely to become diabetics).

The key point in the article is this: “Each 150 kilocalories/person/day increase in total calorie availability related to a 0.1 percent rise in diabetes prevalence (not significant), whereas a 150 kilocalories/person/day rise in sugar availability (one 12-ounce can of soft drink) was associated with a 1.1 percent rise in diabetes prevalence.” Thus: for every 12 ounces of sugar-sweetened beverage introduced per person per day into a country’s food system, the rate of diabetes goes up 1 percent. (The study found no significant difference in results between those countries that rely more heavily on high-fructose corn syrup and those that rely primarily on cane sugar.)

This is as good (or bad) as it gets, the closest thing to causation and a smoking gun that we will see. (To prove “scientific” causality you’d have to completely control the diets of thousands of people for decades. It’s as technically impossible as “proving” climate change or football-related head injuries or, for that matter, tobacco-caused cancers.) And just as tobacco companies fought, ignored, lied and obfuscated in the ’60s (and, indeed, through the ’90s), the pushers of sugar will do the same now.

But as Lustig says, “This study is proof enough that sugar is toxic. Now it’s time to do something about it.”

The next steps are obvious, logical, clear and up to the Food and Drug Administration. To fulfill its mission, the agency must respond to this information by re-evaluating the toxicity of sugar, arriving at a daily value — how much added sugar is safe? — and ideally removing fructose (the “sweet” molecule in sugar that causes the damage) from the “generally recognized as safe” list, because that’s what gives the industry license to contaminate our food supply.

On another front, a coalition of scientists and health advocates led by the Center for Science in the Public Interest petitioned the F.D.A. to both set safe limits for sugar consumption and acknowledge that added sugars, rather than lingering on the “safe” list, should be declared unsafe at the levels at which they’re typically consumed. (The F.D.A. has not yet responded to the petition.)

Allow me to summarize a couple of things that the PLoS One study clarifies. Perhaps most important, as a number of scientists have been insisting in recent years, all calories are not created equal. By definition, all calories give off the same amount of energy when burned, but your body treats sugar calories differently, and that difference is damaging.

And as Lustig lucidly wrote in “Fat Chance,” his compelling 2012 book that looked at the causes of our diet-induced health crisis, it’s become clear that obesity itself is not the cause of our dramatic upswing in chronic disease. Rather, it’s metabolic syndrome, which can strike those of “normal” weight as well as those who are obese. Metabolic syndrome is a result of insulin resistance, which appears to be a direct result of consumption of added sugars. This explains why there’s little argument from scientific quarters about the “obesity won’t kill you” studies; technically, they’re correct, because obesity is a marker for metabolic syndrome, not a cause.

The take-away: it isn’t simply overeating that can make you sick; it’s overeating sugar. We finally have the proof we need for a verdict: sugar is toxic.

Next Article: How the Sugar Industry Was Able to Suppress Information on the Dangers of Sugar

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6: Harvard Study Confirms Low-Glycemic Diet is Healthiest Way to Eat

Posted on February 19, 2013 by Stanley Roth

FROM HARVARD SCIENCE MAGAZINE

A new study published Tuesday in the Journal of the American Medical Association (JAMA) challenges the notion that “a calorie is a calorie.”

The study, led by Harvard Medical School (HMS) Assistant Professor of Pediatrics Cara Ebbeling and Professor of Pediatrics David Ludwig, finds diets that reduce the surge in blood sugar after a meal — either low-glycemic index or very-low carbohydrate — may be preferable to a low-fat diet for those trying to achieve lasting weight loss. Furthermore, the study finds that the low-glycemic index diet had similar metabolic benefits to the very low-carb diet without negative effects of stress and inflammation as seen by participants consuming the very low-carb diet.

The research was conducted at the New Balance Foundation Obesity Prevention Center at Harvard-affiliated Boston Children’s Hospital, where Ludwig is director and Ebbeling is associate director.

Weight re-gain is often attributed to a decline in motivation or adherence to diet and exercise, but biology also plays an important role. After weight loss, the rate at which people burn calories (known as energy expenditure) decreases, reflecting slower metabolism. Lower energy expenditure adds to the difficulty of weight maintenance and helps explain why people tend to re-gain lost weight.

Prior research by Ebbeling and Ludwig has shown the advantages of a low-glycemic load diet for weight loss and diabetes prevention, but the effects of these diets during weight loss maintenance has not been well studied. Research shows that only one in six overweight people will maintain even 10 percent of their weight loss over the long term.

The study suggests that a low-glycemic load diet is more effective than conventional approaches at burning calories (and keeping energy expenditure) at a higher rate after weight loss. “We’ve found that, contrary to nutritional dogma, all calories are not created equal,” says Ludwig, who is also director of the Optimal Weight for Life Clinic at Boston Children’s Hospital. “Total calories burned plummeted by 300 calories on the low-fat diet compared to the low-carbohydrate diet, which would equal the number of calories typically burned in an hour of moderate-intensity physical activity,” he says.

Each of the study’s 21 adult participants (ages 18-40) first had to lose 10 to 15 percent of their body weight, and after weight stabilization, completed all three of the following diets in random order, each for four weeks at a time. The randomized crossover design allowed for rigorous observation of how each diet affected all participants, regardless of the order in which they were consumed:

  • The low-fat diet, which reduces dietary fat and emphasizes whole grain products and a variety of fruits and vegetables, was based on 60 percent of daily calories from carbohydrates, 20 percent from fat, and 20 percent from protein.
  • The low-glycemic index diet, made up of minimally processed grains, vegetables, healthy fats, legumes and fruits, gathered 40 percent of daily calories from carbohydrates, 40 percent from fat, and 20 percent from protein. Low-glycemic index carbohydrates digest slowly, helping to keep blood sugar and hormones stable after the meal.
  • The low-carbohydrate diet, modeled after the Atkins diet, was based on 10 percent of daily calories from carbohydrates, 60 percent from fat, and 30 percent from protein.

The study used state-of-the-art methods, such as stable isotopes to measure participants’ total energy expenditure, as they followed each diet.

Each of the three diets fell within the normal healthy range of 10 to 35 percent of daily calories from protein. The very-low-carbohydrate diet produced the greatest improvements in metabolism, but with an important caveat: This diet increased participants’ cortisol levels, which can lead to insulin resistance and cardiovascular disease. The very-low-carbohydrate diet also raised C-reactive protein levels, which may also increase risk of cardiovascular disease.

Though a low-fat diet is traditionally recommended by the U.S. government and American Heart Association, it caused the greatest decrease in energy expenditure, an unhealthy lipid pattern, and insulin resistance.

“In addition to the benefits noted in this study, we believe that low-glycemic-index diets are easier to stick to on a day-to-day basis, compared to low-carb and low-fat diets, which many people find limiting,” says Ebbeling. “Unlike low-fat and very-low-carbohydrate diets, a low-glycemic-index diet doesn’t eliminate entire classes of food, likely making it easier to follow and more sustainable.”

Other co-authors of the study include Henry Feldman and Erica Garcia-Lago from Boston Children’s Hospital, Janis Swain from Brigham and Women’s Hospital, William Wong from Baylor College of Medicine, and David Hachey from Vanderbilt University. The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Center for Research Resources, the National Institutes of Health, and the New Balance Foundation.

LudwigLowGlycemicStudyOverview_380

Next Article: New York Times Article: It’s the Sugar

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5: “60 Minutes” Segment – New Research Links Sugar to Cancer and Metabolic Sydrome

Posted on April 2, 2012 by Stanley Roth

From Sunday, April 1, 2012’s airing of “60 Minutes”:  New research supports the argument that sugar is addictive, toxic, and contributes to obesity, hypertension, increases in harmful LDL cholesterol, and diabetes.  In addition, researchers at Harvard are discovering that almost a third of all cancers (particularly breast and colon cancer) have increased insulin receptors on their cell surfaces, leading researchers to believe that high sugar consumption directly feeds opportunistic cancer cells.  Sugar binds to the cancer cell insulin receptors and is absorbed into the cancer cells, providing the fuel necessary for rapid cell growth.

 

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4: Understanding the Glycemic Load

Posted on November 17, 2011 by Stanley Roth

One of the most misunderstood and confusing parts of a low-glycemic diet is the difference between the “glycemic index” and the “glycemic load” of a food.  Most glycemic food charts list both the “GI” and the “GL” of each food.  Understanding the difference between the glycemic index and glycemic load can broaden the different kinds of foods you can eat.

The GI is a system of measuring the body’s blood sugar response to equal amounts of  carbohydrate in foods such as bread, pasta, rice, fruits, peas, beans, yogurt, milk, and vegetables.  Note the GI is calculated for a food portion containing 50 grams of carbohydrate in each food.  That isn’t a serving size of 50 grams of food (about 2 ounces). It’s a serving size of however much food it would take to contain 50 grams of carbohydrate in that particular food.  Foods vary widely in how much carbohydrate they contain, and sometimes the resulting glycemic index number can be a little deceptive.

Take watermelon for example.  Watermelon has a GI of 75, a very high glycemic index.  Based on that GI alone, you might never eat watermelon.  But the GI is based on eating 50 grams of carbohydrates in watermelon.  How much watermelon is that?  It turns out to be a lot of watermelon.

A normal slice of watermelon only has about 6 grams of carbohydrate.  Most of watermelon is water.  So while eating 50 grams of watermelon carbs would quickly spike your blood sugar, you would have to consume 8-9 good size slices of watermelon…more than a pound of watermelon and more than the average person eats.

So the glycemic load was developed to predict blood sugar spikes based on normal serving sizes.  In the case of watermelon, that serving size is calculated to be 120 grams of watermelon…about 4 ounces, or one slice.  When watermelon is viewed from the point of view of eating a single slice, the effect on blood sugar is low.  Thus, the glycemic load of watermelon is 4…a very low GL and a food that is OK to eat.

Another example is carrots.

Cooked carrots have a GI of 92…about as much as raw sugar.  Again, based on the GI alone, carrots would be a food most people would avoid.  But the GI is based on eating enough carrots to consume 50 grams of carbohydrates.  Thus the question is, how many carrots would that be?

In order to eat 50 grams of carbohydrate in carrots, you would have to eat over a pound and a half of carrots, because each carrot is very low in carbohydrates.  Very few people would eat that many carrots.  Therefore, the normal serving size of carrots was estimated to be 80 grams, or about 3 ounces…the weight of 1-2 carrots.  If you eat one carrot, the glycemic load (the actual effect on blood sugar) is very low, because individual carrots are low in carbohydrates.  It takes a lot of carrots to get 50 grams of carbohydrates to spike your blood sugar.

Now lets compare those numbers to a bagel.  A bagel has a GI of 72, just a few points below watermelon.  But you’ll get 50 grams of carbohydrate eating just one bagel, so eating a “normal” serving of bagel will give you the full blood sugar spike that a GI of 72 predicts.  That’s why a bagel has a glycemic load of 25, which is high.

A GL greater than 20 is considered high, a GL of 11-19 is considered medium, and a GL of 10 or less is considered low.

So here’s what you need to remember.  Foods that have a low GI almost always have a low GL.  But foods with an intermediate or high GI may range from low to high GL—it all depends on the suggested serving size.  So peas have a glycemic index of 54.  Left with only that GI number, you would avoid peas.  But peas are low in carbohydrates, so you’d have to eat a ton of peas to spike your blood sugar.  That’s why the GL, the glycemic load, is so important.  For peas, the GL is listed as “4” for a 3-ounce serving.  You can have peas.  You can even eat 6-ounces of peas and have a GL of 8…still well below the low rating of 10 or below.

Again, low GI foods almost always have a low GL.  But learning to check the GL of intermediate to high GI foods will only expand the types of foods you can eat.  That’s why ice cream, which has a GI of 80, is OK to eat on a low-glycemic diet.  Ice cream is high in fat and stocked full of a lot of good milk proteins.  It does have sugar, but a relatively small amount in relation to its other ingredients.  So if you look at the serving size on a glycemic load chart, ice cream is listed as an 80 gram serving…about 4 ounces.  If you keep to this serving size, the glycemic load is only 10.  You can enjoy ice cream as a healthy, low-glycemic treat in satisfying, manageable quantities.

I hope this makes sense.  Here is a list of some other intermediate and high GI foods that have few carbohydrates in a normal serving, and therefore have a low glycemic load and are OK to eat on a low-glycemic diet:

Pumpernickel bread, glycemic index 50, glycemic load 6
Whole wheat bread, glycemic index 71, glycemic load 9
Apple, glycemic index 38, glycemic load 6
Peach, glycemic index 42, glycemic load 5
Microwave popcorn, glycemic index 55, glycemic load 6 (serving size about 1 ounce popped corn)
Honey, glycemic index 60, glycemic load 10 (serving size about 1 ounce honey)
Whole grain baguette (like Semifreddi’s), glycemic index 73, glycemic load 9
Cherries, glycemic index 63, glycemic load 9

You get the point. Low GI foods are a no-brainer. Intermediate and high-GI foods can be added to a low-glycemic diet if they are naturally low in carbohydrates and have a low GL number for a specific portion size.

Next article: 60 Minutes: New Research Links Sugar to Cancer and Metabolic Syndrome

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3: The Low Glycemic Diet

Posted on November 8, 2011 by Stanley Roth

Note: a word of caution.  Everyone is different.  Before undertaking any change in your dietary habits, it is always wise to consult your doctor or nutritionist.  The low-glycemic diet is healthy and safe for 99.9% of the people on it, but if you have a unique health condition or you’re taking medications for an existing health condition, you should be supervised.  Medications frequently need to be adjusted to accommodate changes in weight, blood pressure, sugar levels, and cholesterol/triglyceride numbers achieved on a low-glycemic diet. It’s also a good idea for everyone to get their blood numbers tested before starting so improved health scores can be tracked.

Here is a summary of the ground rules of a low-glycemic diet…

  • When you eat foods containing sugars (breads, pastas, grains, fruits, beans, vegetables), try to choose foods that have a low-glycemic index and are absorbed more slowly into the bloodstream.  There’s a link in the sidebar to the Mendosa GI database; other lists are available via Google search, along with glycemic-index apps for iPhones, Blackberry, and Android phones;
  • Read the labels of processed foods you buy.   Avoid products with added sugar, honey, fruit juice, fruit concentrate, etc.  The words “syrup”, “sweetener”, and anything ending in “ose” can usually be assumed to be a sugar.  There’s no such thing as a “good” sugar;
  • Do not eat foods containing high-fructose corn syrup;
  • Eat plenty of unprocessed, carb-free protein foods like fresh meats, chicken, pork, fish, eggs, and cheese.  Protein is the cornerstone of your diet;
  • Choose foods that are high in fiber such as fruits, legumes, and vegetables: avocados, pearl barley, beans of all kinds, steel cut oatmeal, whole grain breads and pastas;
  • Breads and pastas should only be whole wheat or whole grain;
  • Avoid “low-fat” processed foods, sauces, and salad dressings.  They are high in sugar;
  • Eat lots and lots of fruits and vegetables;
  • Eat lots of olive oil and foods rich in omega-3 and omega-6 fatty acids such as: avocados, cauliflower, broccoli, cabbage; dark leafy green vegetables like kale, spinach, Swiss chard, collards, etc.; fish including salmon, scallops, halibut, shrimp, cod, sardines, anchovies, and albacore tuna; nuts of all kinds including almonds, sunflower seeds, walnuts, pumpkin seeds, pine nuts, and sesame seeds; healthy oils like olive oil, canola, and flaxseed oil;
  • Eat eggs, with yolks, 4-5 times a week;
  • Don’t drink fruit juice.  Eat the fruit (with the fiber) instead;
  • Don’t drink sugared drinks of any kind: sodas, sports drinks, Red Bull, sweetened teas, etc.;
  • Eat only fresh, unprocessed, natural fats.  Eat real butter, not margarine.  Use real half-and-half or cream and not non-dairy coffee creamers (loaded with sugars).  Low- or non-fat milk and cottage cheese are fine, but avoid low-fat hard cheeses;
  • Do not eat foods containing trans-fats.  Avoid anything that contains the word “hydrogenated”, including “partially hydrogenated oils,” “hydrogenated oils,” or “mono-dyglicerides.”  (Note: the term “0% trans fats” on a label means nothing…the FDA allows up to 2.2 grams of trans fats per serving before the trans fat needs to be disclosed to the consumer);
  • Unless it’s a special occasion, limit alcohol consumption to one glass of wine per day with a meal (preferably red wine…contains less sugar than white).  This has nothing to do with calories.  The ethanol in alcoholic beverages metabolizes in the liver similar to fructose and creates by-products that, over time, cause cirrhosis and fatty-liver disease.  Remember the motto: “one drink- good for the heart; two drinks- bad for the liver.”
  • Avoid beer (high in carbs).  One hard liquor drink with a meal is OK, but make sure the “mixer” is low-sugar;
  • EAT A HIGH-PROTEIN BREAKFAST EVERY DAY.  It will curb your hunger all day long;
  • Drink lots and lots of water.

Much of the above may seem counter-intuitive to everything you’ve been told about how we should eat (eat carbs, avoid fat), but please remember that before I started eating like this, I was a card-carrying member of the metabolic syndrome club.   Eating low-glycemic, I’ve lost 43 pounds in months, not years, and my blood pressure, cholesterol, and blood sugars are now all normal.

What do I now typically eat?

Four to five times a week, I’ll have eggs for breakfast.  Sometimes I’ll make one of my favorite breakfasts, heuvos rancheros.  I’ll mix black beans with salsa and heat them both in a pan, then pour the mixture over a whole wheat tortilla.  Next I’ll fry two eggs in real butter and top them both with slices of real cheddar cheese.  When the cheese is melted, I’ll put the eggs/cheese atop the bean/salsa mix and top the whole thing with slices of fresh avocado.  Slice up an orange and I’m good to go…usually until the late afternoon without a drop of hunger.

Why no hunger?  Because the fat releases hormones that tell my body I’m satiated, so I’m not hungry.  Everything on the plate is low-glycemic, so my blood sugar doesn’t rise.  Without a rise in blood sugar, insulin doesn’t kick in to lower my blood sugar level and make me ravenously hungry.   Going all day without an ounce of hunger is a feeling I never experienced until I started eating low-glycemic.  How many calories are in that meal?  I’m sure more than any weight loss plan would allow, yet I was averaging a 10-pound a month weight reduction.

Other mornings I’ll scramble eggs with onions and vegetables, put the entire mixture in a whole wheat pita pocket, and then top the pita with cheese and melt the whole thing in the microwave.  This I’ll often serve with a slice of ham or sausage.  Fruit is always included in my breakfasts; toast and hash browns are not.

When I’m not eating eggs for breakfast, I’ll make a quesadilla with cheese, salsa, avocado, and tomato, or I’ll cook up some Aidell’s chicken-Italian sausages and eat them with a slice of whole wheat toast, and fruit.  Other mornings I’ll cook up steelcut oatmeal, which unlike ordinary oatmeal has a low-glycemic index.  For sweetener, I’ll use a little honey or artificial sweetener (more about honey in a moment).  If I’m making oatmeal for breakfast, I’ll always cook up a protein with it like ham, bacon, or sausage to contain my appetite later in the day.

I often skip lunch because I’m just not hungry.  That’s the amazing thing about eating this way…you can go hours and hours and not be hungry or even think about food.  But if I do eat lunch, it’s usually a salad with some protein (grilled chicken, fish, etc.).  On this diet, you can eat a Cobb Salad that provides protein in eggs, bacon, and cheese, or you can have a bacon, lettuce, and tomato sandwich, which I’ll have on whole wheat bread or whole wheat pita.

Other favorite lunches include a simple Caprese salad…I slice up fresh mozzarella cheese, fresh tomato, and fresh basil, and then top the plate with olive oil and balsamic vinegar.  The cheese provides fat and protein and is very filling.  It also provides lots of calcium, phosphorus, and vitamin B-12.

One of my favorite (and most nutritionally complete meals) is a Caesar Salad: a can of anchovies, olive oil, garlic, lemon juice, tabasco sauce, Worcestershire sauce, and Parmesan cheese tossed with romaine lettuce.  It has everything– the olive oil and anchovies are high in both omega-3 and omega-6 fatty acids and antioxidants, and the anchovies provide calcium, iron, phosphorus, niacin and selenium…as well as being a good source of protein. The romaine lettuce is a good source of riboflavin, vitamin B6, calcium, magnesium, phosphorus and copper, vitamin A, vitamin C, vitamin K, thiamin, folate, iron, potassium and manganese, as well as being a good source of dietary fiber.  The cheese adds more calcium and protein, along with enough fat to keep you satiated.  Most times the salad alone is a complete meal, but you can always add a piece of grilled or baked chicken or fish.  We eat a Caesar salad 3-4 times a week. I’ve included the recipe in the “Dinner” section of the top header bar.

Fruit and nuts are always on the menu.  Between meals, or sometimes AS a meal, I’ll eat a bunch of fruit or have nuts and cheese.  If you’ve tried eating fruit, nuts, and cheese as part of a deprivation diet, you’d be hungry all the time, because the lack of fats and calories during the day would make your body think it’s starving.  But as part of the larger low-glycemic eating lifestyle, with enough calories, protein, and fat in your diet to quell your hunger, fruit, nuts, and cheese are a completely filling snack.

So we keep a bowl of assorted seeds and nuts on the kitchen counter, alongside a bowl of fresh fruits.  These are “free foods” to eat whenever you feel like a snack. The fruits provide lots of fiber and vitamin C, and by mixing the nuts and seeds together, you get all 9 essential amino acids in one snack (the essential amino acids are the 9 proteins the human body cannot make and which must be obtained in food).

My wife’s favorite breakfast, lunch, or snack is unsweetened yogurt, topped with toasted almonds and honey.  Like in the oatmeal breakfast, the honey is fructose, but eaten in such small quantities (you don’t need a lot of it because fructose is 78% sweeter than sugar) it’s harmless to the body.

One staple of our diet now is bean soups.  Saute an onion with garlic, add a can of diced tomatoes (or dice some tomatoes fresh), pour in some chicken stock, and then pick your “bean or beans du jour” — canned black beans, pintos, kidney, garbanzo, etc.  Choose one type of bean or any mixture of them.  Add Italian seasoning and some chicken or sausage and you have a hearty meal that you can store in your refrigerator for lunch, dinner, or a mid-day snack.

We no longer eat rice of any kind.  Instead, we eat pearl barley which has a low-glycemic index, a wonderful nutty flavor, and an amazing 8 grams of fiber per serving.  We cook up the barley and then mix it with assorted sauteed vegetables and some butter.  Wonderfully creamy and delicious, even without the veggies!

So here’s a summary list of some of the foods you’re NOT supposed to eat on a low-glycemic diet:

No white breads; no pastas or pasta products like couscous; no potatoes, potato products, or rice (not even brown rice); no corn or corn products like cornmeal, corn tortillas, or popcorn; no crackers, cookies, or cakes; no commercial cereals of any kind; no commercial salad dressings; no high-glycemic tropical fruits such as pineapple, cantaloupe, mangos, figs, kiwi, papaya, or bananas; no dried fruits; no high-sugar vegetables like beets, corn, pumpkin, or cooked carrots; no sugared drinks, teas, sport drinks; no coffee creamers (lots of sugar); no fruit juice (don’t panic…you can eat all the low-glycemic fruits you want, because the juice comes packaged with natural fiber); no commercial peanut butters containing sugar; no soy products except soybeans (edamame) and soy sauce; no commercial sauces (barbecue sauce, pasta sauces, steak sauce, gravies, etc.); no frozen desserts such as sorbets or frozen yogurts that are high in sugar.

That’s it.  Now here’s a summary of what you CAN have:

All meats, poultry, fish, shellfish, and eggs.  Being able to eat eggs has been my salvation because I hate egg whites;

Whole wheat or multigrain breads including rye, pumpernickel, whole wheat sourdough, and whole wheat pita; whole wheat pastas cooked al dente (overcooking increases the glycemic index); pearl barley, steelcut oats for oatmeal;

Olive oil, real butter, real mayonnaise, any nut/seed oil, canola oil, safflower oil, sunflower oil;

All cheeses (real, not low-fat!), real sour cream, cottage cheese;

Milk, half-and-half, cream;

All nuts and seeds including sunflower seeds, pumpkin seeds, almonds, walnuts, peanuts, pecans, etc.;

All beans, dried or canned;

Virtually all fruits including apples, blueberries, oranges, limes, lemons, honeydew melon, peaches, raspberries, cherries (my favorite!), pears, strawberries, plums, grapes, blackberries, and grapefruit (but no grapefruit if you’re taking a statin!).

Virtually all vegetables including artichokes, asparagus, brussels sprouts, broccoli, cabbage, cauliflower, celery, cucumber, eggplant, endive, greens (collard, mustard, bok choy), tomatoes, water chestnuts, lima beans, green beans, red/yellow/green bell peppers, leeks, mushrooms, olives, peas, pickles, radishes, spinach, sweet potatoes (not a potato!), arugula, lettuce, onions, swiss chard, snow peas, squash, yams, zucchini, and sauerkraut.  Avocados are one of the best foods you can eat;

Red wine (yippee!).  You can drink in moderation on a low-glycemic diet.  Follow the motto: “One drink, good for the heart; two drinks, bad for the liver…”  Red wine is preferred over white wine, as white wines tend to be higher in sugar.  Avoid beer (malt and barley are sugars).  Mixed drinks are OK providing the mixer isn’t fruit juice or high in sugar (like sugary tonic water).  Use a mixer that is artificially sweetened.

And finally, best of all….ICE CREAM!  I kid you not.  Ice cream is actually low in sugar and contains high-quality dairy proteins (milk, skim milk, non-fat milk, whole eggs).  It’s a wonderful treat every now and then.  Make sure the ice cream contains regular table sugar (sucrose) or plain fructose and not maltodextrins, dextrose, or high-fructose corn syrup.  Note high-fructose corn syrup is NOT the same product as plain fructose, which is low-glycemic in small quantities and is a good sweetening agent for ice cream and desserts.

The best thing is how satisfying all these foods are when put together.  Sometimes in the evenings my wife and I are just simply not hungry, and we’ll have a piece of chicken and call it dinner.  One night we just steamed some broccoli and put some melted cheddar cheese on top and called it dinner.  We’re just not that hungry any more.  My wife says we eat like 25-year old female roommates.

Welcome to the low-glycemic diet.  Here’s to your health!

Next article: Understanding the Glycemic Load

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2: The Origin of the Low-Fat, High-Carbohydrate Diet

Posted on November 7, 2011 by Stanley Roth

If you saw a book cover entitled “Pure, White, and Deadly,” you’d likely think the book was about cocaine or heroin. But in 1972, Dr. John Yudkin, a medical doctor and a professor of Nutrition and Dietetics at the University of London, published a book with that exact title…a book that warned that the increasing consumption of sugar was closely associated with coronary heart disease and Type II diabetes. Studies Dr. Yudkin had been conducting for 15 years indicated that sugars and starches raised blood triglycerides and insulin levels. Dr. Yudkin warned that a diet high in carbohydrates was directly linked to what we now call the “metabolic syndrome”– obesity, diabetes, high blood pressure, cholesterol imbalances, and cardiovascular disease.  In Yudkin’s studies, fat played little or no role as the cause of metabolic syndrome.

In 1980, Ansel Keyes, an American epidemiologist and statistician, published the Seven Countries Study, which showed a correlation between cholesterol and cardiovascular disease in the populations of seven different nations. Keyes argued that the rise of serum cholesterol in countries such as England, the United States, Australia and Canada could be directly correlated to a rise in the consumption of dietary fat in these countries, and that the rise of such dietary fat consumption could therefore be linked to the rise of coronary artery disease. His findings were quickly embraced by the Department of Agriculture, the American Medical Association, and the American Heart Association.

Two years later, the USDA published new dietary guidelines encouraging a decrease in the consumption of dietary fats, while encouraging increased consumption of high-sugar carbohydrates such as grains, breads, and pastas. Ansel Keyes’ dietary recommendations had been officially vetted and approved by the United States government, and the “low-fat, high-carb” diet craze was on.  America’s (and the world’s) sugar consumption rose dramatically.

What has been the result of an entire society following Keyes dietary guidelines over the past 30 years?

According to the Center for Disease Control, metabolic syndrome is up 26% since 1988, and for the first time is increasing in overweight adolescents. Americans are now getting almost 25% of their daily caloric intake from sugar. As UCSF neuroendocrinologist Dr. Robert Lustig says in his lecture, Sugar: The Bitter Truth, “Fat’s are going down, sugar is going up, and we’re all getting sick.”

How did Keyes get it so wrong?  He failed to test the effects that increased sugar consumption was already having in the diets of the industrialized nations he tested.  Keyes was also accused of “skewing” his results to favor his hypothesis: while he accumulated data from 22 countries, he reported the results of only 7, leaving out the high-fat diets of countries like France, Switzerland, Iceland, and Austria that showed no increase in cardiovascular disease in correlation to their consumption of dietary fat.

Keyes never isolated sugar from his results– in other words, Keyes failed to test a control group that ate just high fats without increased sugar.  So while Keyes was attributing metabolic syndrome results to an increase in dietary fat, what many now postulate was really causing his results was the high concentrations of sugar already present in the industrialized diets that accompanied the fats.

As America (and much of the world) embraced Keyes’ dietary findings, fat consumption has dropped and sugar consumption has soared, especially consumption of a new, man-made sugar called “high-fructose corn syrup.”

In 1975, an industrially engineered sweetener came to the United States. Manufactured by an enzyme process developed in Japan by Dr. Y. Takasaki, this new inexpensive sweetener– called high-fructose corn syrup, or HFCS– converted the glucose of ordinary corn syrup into a much sweeter fructose sugar. As a result, companies that used cane or beet sugar (sucrose) in their products could now buy cheaper high-fructose corn syrup, and save even more money by having to use less of it in their recipes. Within 2-3 years, the sweeter and cheaper HFCS was being used in soft drinks, breads, cakes, peanut butter, ketchup, pastries, candies, breakfast cereals, pastas, juice drinks, and even baby formula.  By the mid-1980’s, HFCS was present in 50% of all the processed foods manufactured in the U.S.

Interestingly, before the introduction of HFCS, human beings had very little dietary exposure to fructose. Fructose in nature was mostly limited to fruits, honey, dates, raisins, grapes, and apples and thus consumed in small quantities.  With the introduction of HCFS, many scientists expressed concern that while glucose could be metabolized by every living cell in the body, fructose could only be metabolized by the liver,  and therefore the long-term effect of increased fructose exposure was unknown.  Yet, the USDA– without any studies– adopted the position put forth by the American Beverage Council and the National Corn Growers Association that HFCS was essentially a “similar sugar” that was being swapped for an existing sugar and therefore required no regulation.

The effect on sugar consumption has been dramatic.

In 1970, the per capita consumption of sugar in the United States was 73 pounds a year. In 1999, the USDA reported that number had increased to 146 pounds a year, of which 65 pounds was comprised of high-fructose corn syrup.  By 2010, annual per capita sugar consumption had risen to 160 pounds of sugar per year, of which 96 pounds was comprised of high-fructose corn syrup…almost half a pound of pure sugar per day for every man, woman, and child in the United States.

By comparison, in 1800, the average American only consumed about 18 pounds of sugar a year. The rise of sugar consumption over just the past three decades in the United States and around the world represents the largest, most drastic dietary change in the history of mankind.

Had Keyes isolated the sugar and tested for its effects without dietary fat, he would have discovered what we now know…that John Yudkin’s 1972 treatise on the dangers of sugar was correct. High levels of sugars and starches, not dietary fats, are the major cause of the medical disorders present in the metabolic syndrome.

Why haven’t we corrected this mistake?  U.S. industry currently exports billions of dollars of soft drinks and fast food around the globe– both products which use high levels of sugar as an integral part of their consumer demand, formulation, and profit. Breakfast cereals, which also rely heavily on sugared products, generate $6.5B in annual sales. Sugar production alone is a $10B industry in the United States.

The corn, food, and beverage industries spend millions of dollars a year lobbying congress to protect their interests, and have launched numerous public relations campaigns to convince the public that sugar– including HFCS– is healthy (see www.sweetsurprise.com, a website sponsored by the Corn Growers Association).  Currently, in an attempt to deal with consumers’ new reluctance to eat HFCS, the corn industry has a petition before the FDA to allow food and beverage labels to substitute the term “corn sugar” for the current “high-fructose corn syrup” name.

Institutional changes and beliefs happen slowly.  Companies are banning trans fats and eliminating HFCS from foods in response to consumer demand, and consumers are becoming more aware of the dangers of sugar.  I believe this trend will only continue. But getting sugar out of our individual diets is something each of us can begin to do right now, by eating a low-glycemic diet.

Next article: The Low-Glycemic Diet

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