Gary Taubes—The Case Against Sugar

Award-winning journalist Gary Taubes is known for his acclaimed books on health and science, including Why We Get Fat; Good Calories, Bad Calories; and Bad Science. His latest, The Case Against Sugar, may be his most important book to date.

Can sugar properly be labeled a toxic substance? Taubes thinks that may well be the case. The fact is, obesity and diabetes are more prevalent in the US population than ever before, and about 10% of children suffer from nonalcoholic fatty liver disease. The scientific evidence indicates that sugar is at the root of these problems, and is therefore indirectly responsible for the serious, often fatal conditions that can arise from them, such as heart disease and cancer.

In his new book, Taubes outlines the history of sugar throughout human civilization. He examines its use as an additive in cigarettes and as a preservative, its relationship to weight gain and chronic disease, and the ways in which “legitimate” scientific researchers—being funded by the sugar industry—misled the public for decades about the serious health consequences of sugar consumption.

In his interview with Life Extension®, Taubes—a correspondent for the journal Science and cofounder and scientific advisor of the Nutrition Science Initiative (NuSI)—touches on these and other fascinating topics.

LE: The news media have recently exposed the shocking connection between the sugar industry’s nonprofit organization, founded in 1943, and academic research that was biased in its favor. Tell us about how that situation came about, if you would.

GT: By 1951, the Sugar Association, Inc. (originally the Sugar Research Foundation), had distributed three million dollars in research grants throughout the highest levels of academia—from Princeton and Harvard on the East Coast to the California Institute of Technology on the West. At a time when academic researchers were encouraged to work closely with industry, the Sugar Association grants went to some of the most prominent researchers in nutrition, carbohydrate chemistry, and metabolism. The program was exceptional, and the grants themselves would regularly be written up in Science and other influential scientific journals.

Among the many researchers that the sugar industry would begin supporting during the war years, two of them—Ancel Keys, at the University of Minnesota, and Fred Stare, founder of the department of nutrition at Harvard—would become lifelong friends of the industry. Drs. Stare and Keys would play critical roles in the 1960s and 1970s, defending the place of sugar in a healthy diet and arguing against the idea that it could be a cause of chronic disease.

LE: How did the Sugar Association, Inc., operate to achieve its goals?

GT: By the early 1950s, the Sugar Association would begin fighting public-relations battles on multiple fronts. If Americans were told that sugar caused dental caries, the Sugar Association, with the help of the researchers it was funding, would find a way to present the evidence that suggested Americans would be foolish to consume less sugar. When obesity became an issue, as it quickly did, and Americans turned to artificial sweeteners, the Sugar Association would take on artificial sweeteners directly.

LE: Nevertheless, independent research over the years has revealed more and more serious disease associations with sugar consumption, especially now that sugar has been established as one of the likely causes of diabetes, much to the industry’s chagrin. Can you touch on a few examples?

GT: In 2003, epidemiologists from the Centers for Disease Control, led by Eugenia Calle, published an analysis in The New England Journal of Medicine reporting that cancer mortality in the United States was clearly associated with obesity and overweight. They reported the heaviest men and women were 50% and 60% more likely, respectively, to die from cancer than the lean. This increased risk of death held true for a host of common cancers—esophageal, colorectal, liver, gallbladder, pancreatic, and kidney cancers, as well as, in women, cancers of the breast, uterus, cervix, and ovary.

In 2004, the CDC followed up with an analysis linking cancer to diabetes, particularly pancreatic, colorectal, liver, bladder, and breast cancers. Cancer researchers trying to make sense of this association would later say that something about cancer seems to thrive on the metabolic environment of the obese and the diabetic.

LE: What might that “something” be?

GT: One conspicuous clue…was that the same association was seen with people who weren’t obese and diabetic (or at least not yet) but suffered only from metabolic syndrome and thus were insulin-resistant. The higher their levels of circulating insulin, and that of a related hormone known as insulin-like growth factor, the greater the likelihood that they would get cancer.

This link between cancer and insulin was evident with antidiabetes drugs as well. In 2005, Scottish researchers reported that diabetic patients who took a drug called metformin, which works to reduce insulin resistance and therefore lower circulating levels of insulin, also had a significantly reduced risk of cancer compared with diabetics on other medications. That association has been confirmed multiple times, and has led researchers to test whether metformin acts as an anticancer drug, preventing or inhibiting cancer’s recurrence in randomized controlled trials.

These observations also served to focus the attention of cancer researchers further on the possibility that insulin and insulin-like growth factors are cancer promoters, and thus that abnormally elevated levels of insulin—caused by insulin resistance, for instance—would increase our cancer risk.

This was an area of research that had emerged in the 1960s, with laboratory work by some of the leading cancer researchers—including Howard Temin, who would later win the Nobel Prize—demonstrating that cancer cells require insulin to propagate; at least they do so outside the human body, growing as cell cultures in the laboratory.

LE: What does the current overall research indicate?

GT: The science on the link between insulin and insulin-like growth factor (IGF) and cancer now has been well worked out. A consensus has been forming, led by some of the most respected cancer researchers—in particular Lewis Cantley, who runs the cancer research program at Weill Cornell medical college, and Craig Thompson, president of the Memorial Sloan Kettering Cancer Center, both in New York City. These researchers believe that cancer is as much a metabolic disease as a “proliferative” disease, and that for cancer cells to procreate, they need to rewire their metabolic programs—how they fuel themselves—to drive their unfettered growth.

Further evidence to support this view is that the major genetic mutations that have been discovered over the years as seemingly responsible for a host of different cancers seem to play critical roles, not just in the proliferation of cells but in regulating the metabolism of cells.

From this perspective of cancer as a metabolic disease, insulin and IGF promote the cancer process through a series of steps. First, insulin resistance and elevated levels of insulin trigger an increased uptake of blood sugar (glucose) as fuel for precancerous cells. These cells then begin producing energy through a mechanism known as aerobic glycolysis that is similar to what bacteria do in oxygen-poor environments. Once cancer cells make this conversion, they burn enormous amounts of glucose as fuel, providing them, apparently, with the necessary raw materials to proliferate.

By metabolizing glucose at such a rapid rate…these cancer cells generate relatively enormous amounts of compounds known technically as “reactive oxygen species” and less technically as “free radicals,” and these, in turn, have the ability to mutate the DNA in the cell nucleus. The more glucose a cell metabolizes and the faster it does so, the more free radicals are generated to damage DNA…and the more DNA damage, the more mutations are generated, and the more likely it is that one of those mutations will bestow on the cells the ability to proliferate without being held in check by the cellular processes that work to prevent this pathological process in healthy cells.

The result is a fast-forward acceleration of tumor growth. With this happening, the insulin and IGF in the circulation both work to signal the cell to keep proliferating, and to inhibit the mechanism (technically known as apoptosis, or cell suicide) that would otherwise kick in to shut it down.

LE: What other serious illnesses can sugar lead to by way of diabetes?

GT: Alzheimer’s, like cancer, is associated with type II diabetes, an observation that began to emerge from studies in the mid-1990s of 800 elderly residents of Hisayama, Japan; of 7,000 senior citizens in Rotterdam, the Netherlands; and of 1,500 type II diabetics in Rochester, Minnesota. These observations have been confirmed repeatedly since. They suggest that type II diabetics have from one and a half to two times the risk of Alzheimer’s dementia of nondiabetics, suggesting in turn, as the Rotterdam investigators did in 1999, that “direct or indirect effects of insulin could contribute to the risk of dementia.”

Waist circumference is also associated with Alzheimer’s risk—the thicker your waist, the greater your risk—as is body mass index itself, although only in midlife, not afterward. Getting fatter (as many of us do) in our thirties and forties is associated with an increased risk. Several studies have shown that higher insulin levels—hyperinsulinemia—are associated with increased risk. Hypertension is also associated with increased risk of Alzheimer’s.

LE: What do researchers think is the explanation for these associations?

GT: Perhaps high blood sugar is responsible for the increased risk of Alzheimer’s disease; the higher the blood sugar, the greater the oxidative stress in the brain, and the greater the production of what are called advanced glycation end products, AGEs. These AGEs are associated with the accumulation of plaques and tangles that may have a causative role.

Here’s another way to think about the idea that a cluster of chronic Western diseases associate with insulin resistance, metabolic syndrome, obesity, and diabetes and hence sugar consumption: Diabetes, though a discrete diagnosis by our doctors, is not a discrete phenomenon in which bad things suddenly start happening that didn’t happen before. It’s part of a continuum from health to disease that is defined in large part by the worsening of the metabolic abnormalities—the homeostatic disruption in regulatory systems—that we’ve been discussing and that are associated with insulin resistance, if not caused by it, and so part and parcel of metabolic syndrome.

As we become ever more insulin-resistant and glucose intolerant, as our blood sugar gets higher along with our insulin levels, as our blood pressure elevates and we get fatter, we are more likely to be diagnosed as diabetic and manifest the diseases and conditions that associate with diabetes. These include not just heart disease, gout, cancer, Alzheimer’s…but all the conditions typically perceived as complications of diabetes: blood vessel (vascular) complications that lead to strokes, dementia, and kidney disease; retinopathy (blindness) and cataracts; neuropathies (nerve disorders); plaque deposits in the arteries of the heart (leading to heart attacks) or the legs and feet (leading to amputations); accumulation of advanced glycation end products, AGEs, in the collagen of our skin that can make diabetics look prematurely old, and that in joints, arteries, and the heart and lungs can cause the loss of elasticity as we age.

It’s this premature aging of the skin, arteries, and joints that has led some diabetes researchers to think of the disease as a form of accelerated aging. But increasing our risk of contracting all these other chronic conditions means we’re also likely to get these ailments at ever-younger ages and thus, effectively, age faster.

LE: In your book, you bring up the question, “How little sugar is still too much?”

GT: It’s impossible to say…the clinical trials necessary to begin to answer such a question were never pursued.

The traditional response is that we should eat sugar in moderation. But this is a tautology. We only know we’re consuming too much when we’re getting fatter or manifesting other symptoms of insulin resistance and metabolic syndrome. At that point, the assumption is that we can dial it back a little and be fine—drink one or two sugary beverages a day instead of three, or, if we’re parenting, allow our children ice cream on weekends, say, rather than as a daily treat.

But if it takes years or decades, or even generations, for us to get to the point where we manifest symptoms of metabolic syndrome, it’s quite possible that even these apparently moderate amounts of sugar will turn out to be too much to reverse the situation and return us to health. And if the symptom or complication of metabolic syndrome and insulin resistance that manifests first is something other than getting fatter, such as cancer, for instance, we’re truly out of luck.

If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.

To order a copy of The Case Against Sugar, call 1-800-544-4440.