Chapters (40)
- Cover Page
- Title Page
- Dedication
- Prologue A Brief History of Banting
- Part One
- Chapter 1
- Chapter 2
- Chapter 3
- Chapter 4
- Part Two
- Chapter 5
- Chapter 6
- Chapter 7
- Chapter 8
- Chapter 9
- Chapter 10
- Chapter 11
- Chapter 12
- Chapter 13
- Part Three
- Chapter 14
- Chapter 15
- Chapter 16
- Chapter 17
- Chapter 18
- Chapter 19
- Chapter 20
- Chapter 21
- Chapter 22
- Chapter 23
- Chapter 24
- Epilogue
- Notes
- Bibliography
- Acknowledgments
- Illustration Credits
- A Note About the Author
- Also by Gary Taubes
- Footnotes
- Copyright
All of this was then summed up in the single statement—echoing the sentiments of the FDA Task Force, the National Academy of Sciences Diet and Health report, and The Surgeon General’s Report on Nutrition and Health, which preceded it—that dietary sugar consumption could not be held responsible for causing disease: “The panel concluded that current consumption of sugars, particularly sucrose, played no direct causal role in the development of cardiovascular…disease, of essential hypertension, or of diabetes mellitus….”
Four years later, The American Journal of Clinical Nutrition dedicated an entire issue to the deleterious effects of dietary fructose. A common refrain throughout the issue was the need for research that would establish at what level of sugar consumption the effects discussed—the elevation of blood pressure and triglycerides, increased insulin resistance, and even accelerated formation of advanced glycation end-products—would lead to disease. “Further studies are clearly needed to determine the metabolic alteration that may take place during chronic fructose or sucrose feeding,” as the Swiss physiologists Luc Tappy and Eric Jéquier wrote.
In 2002, the Institute of Medicine of the National Academies of Science released its two-volume report on Dietary Reference Intakes (subtitled Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids), and spent twenty pages discussing the possible adverse effects of sucrose and high-fructose corn syrup. It then concluded that there was still “insufficient evidence” to set up an upper limit for sugar consumption in the healthy diet. Nor did the IOM perceive any reason to pursue further research on fructose or sucrose or high-fructose corn syrup and so, perhaps, discover sufficient evidence. In early 2007, the National Institutes of Health was funding at most half a dozen research projects that addressed, even peripherally, the health effects of dietary fructose, meaning sugar and high-fructose corn syrup in the diet.
Over the years, what little research has been done on fructose metabolism has been carried out primarily by biochemists, who have had little motivation, other than perhaps personal health, to pay attention to the nutrition literature—again, an effect of specialization. Their own articles, moreover, are published in biochemistry journals, and have little influence on the nutrition and public-health communities. For this reason, observations on the potential dangers of fructose have managed to remain dissociated from discussions of sugar itself and the role of sucrose and high-fructose corn syrup in modern diets. After the ridicule that John Yudkin received for the work that culminated in his anti-sugar polemic, Pure, White and Deadly—and after the FDA decided that “no conclusive evidence demonstrates a hazard” from sucrose—few researchers have appeared willing even to contemplate the possibility that sugar consumption could have harmful consequences beyond perhaps causing cavities and contributing to obesity.
Chapter 13
Chapter Thirteen
DEMENTIA, CANCER, AND AGING
The bottom line is pretty irrefutable: What is good for the heart is good for the brain.
RUDOLPH TANZI AND ANN PARSON, Decoding Darkness: The Search for the Genetic Causes of Alzheimer’s Disease, 2000