Sugar: The Ditch of American Health Care August 12, 2014 Public Health, San Francisco Medicine, UCSF Robert Lustig, San Francisco Medicine, Sugar 0 By Robert H. Lustig, MD, MSL Note: This article was originally published in the July/August 2014 issue of San Francisco Medicine. The individual food choices made by millions of Americans are individual, aren’t they? Each of us gets to choose what we eat and drink. Yet what I eat matters to you, and what you drink matters to me. Because the consequences of each of our “personal” dietary choices not only have consequences for our personal health but also for our public health and our public coffers. The toll that our collective diet has already placed on the American health care system has plunged us into a very deep ditch from which there appears no escape. The economic toll from our collective ill health, wastage of medical resources, costs of drugs for chronic disease, and loss of productivity is already catastrophic. At this rate, Medicare will be broke by 2026. We used to have the best health care in the world. Now we’re #38; we rank just below Slovenia. What happened? In the last thirty years, the nutritional composition of the average American diet has been radically changed—for the worse. Processed food and sweets accounted for 11.6 percent of our diet in 1982, yet by 2012 it accounted for 22.9 percent, a doubling in thirty years. Added sugar (that is, compounds containing the sweet monosaccharide fructose, including sucrose, high-fructose corn syrup, agave, maple syrup, honey, etc.) figures prominently in why processed food is such a problem. Added sugar is a proximate cause for obesity, diabetes, heart disease, and fatty liver disease. Health care of the obese costs double that of normal-weight people. Costs for diabetes alone jumped from $171 billion in 2007 to $245 billion in 2012 in the U.S. But these translate into costs for everyone. For instance, employers pay an extra $2,751 dollars per employee for obesity, whether the employee is obese or not. This is dragging down economic growth and jobs. This is unsustainable. Unless we reverse course, it is alarmingly clear where we are all going to end up. There are some who say how we got here is unimportant. On the contrary, in order to back out of the ditch, you need to know how you drove into it. Otherwise, you just spin your wheels and get stuck further in the mud, as we’ve done for the past thirty years. Of the various components of our processed food diet, added sugar has received the most attention. In part because this is the hook that the food industry uses to get you to buy more; and in part because science has now demonstrated causation for these chronic diseases. Let’s examine the science more closely. Metabolic Effects of Fructose Fructose (and sugar in general) is an energy source, but it is not a nutrient (similar to alcohol). There is not one human biochemical reaction that requires dietary fructose (or alcohol, for that matter). The only place in the body where fructose is of physiologic import is in semen, and the fructose is manufactured de novo from glucose using the aldose reductase/sorbitol pathway. Indeed, patients with hereditary fructose intolerance (HFI) who are missing the enzyme fructose-1-phosphate aldolase B and cannot consume fructose lest they become hypoglycemic not only have fewer dental caries but they are quite healthy provided they maintain their fructose restriction. 1. Hepatic insulin resistance and metabolic syndrome After a large fructose bolus is ingested, it is transported from the duodenum straight to the liver via the portal vein, where it overwhelms the capacity of mitochondria to metabolize it via the tricarboxylic acid cycle. The hepatocyte has no choice but to convert the excess energy substrate into fatty acids, through a process known as de novo lipogenesis. These excess fatty acids have one of two fates: to get packaged into very low-density lipoproteins (VLDL, measured in the triglyceride fraction of the lipid profile), which promote cardiovascular disease; or get stuck in the liver, where they lead to fatty liver disease and promote hepatic insulin resistance, which drives hyperinsulinemia, weight gain, and puts you at risk for type II diabetes. 2. Reactive oxygen species (ROS) formation and aging Any nutritional substrate with a free reactive aldehyde or ketone moiety can bind to proteins (the Maillard or “browning” reaction), which reduces protein flexibility (leading to cell dysfunction) and releases ROS’s, which, if not quenched by an antioxidant, lead to cell damage. This is why bananas brown. While glucose can undergo the Maillard reaction (this is why we all have a measurable hemoglobin A1c), fructose does it seven times faster due to its unique stereochemistry. Protein inflexibility and ROS generation together contribute to cell dysfunction and aging. 3. Central nervous system effects to increase consumption The hedonic pathway that motivates the “reward” of food intake uses the neurotransmitter dopamine. Sugar leads to dopamine release, which then binds to the dopamine D2 receptors in the nucleus accumbens to transduce pleasure. But dopamine down-regulates its own receptor. More sugar leads to more dopamine and fewer receptors, which means you need more sugar to get less effect. And after a while you’re consuming a whole lot to get nothing—this is the phenomenon of tolerance, which is one-half of addiction. Click here to read part 2 - Empiric Role of Sugar in Chronic Metabolic Disease. Robert H. Lustig, MD, MSL, is professor of pediatrics in the Division of Endocrinology at the University of California, San Francisco. He is also the president of the Institute for Responsible Nutrition, a nonprofit dedicated to improving the global food supply and eradicating type II diabetes and chronic metabolic disease in children. He is the author of Fat Chance: Beating the Odds against Sugar, Processed Food, Obesity, and Disease, Sugar Has 56 Names: A Shopper's Guide, and The Fat Chance Cookbook. Comments are closed.
