Food Processing and Obesity

By — Obesity Prevention Special Edition Contributor
Updated on May 17, 2010

It’s no secret that all of America weighs 25 pounds more than it did just 30 years ago. Just go to the mall or to Disneyworld, and see for yourself. And those extra pounds have led to skyrocketing increases in heart disease, hypertension, Type 2 diabetes, and many other adult conditions, even in children. Indeed, nowhere has this weight burden been more obvious than in our nation’s youth. We have 10% of preschoolers, 25% of elementary school children, and 33% of teenagers tipping the scales. The childhood obesity epidemic has disastrous consequences. Thirty years ago, no one ever heard of Type 2 diabetes in children, and now 1 out of every 4 children with diabetes is Type 2. [Type 2 is Diabetes that develops later in life, often related to obesity, and can improve with weight loss; Type 1 Diabetes is the more ‘classic type’ that develops earlier in life and is more typically and persistently dependent on insulin.] One-third of adult Americans by the year 2030 are predicted to be diabetic. This current generation is the first one in history that is predicted to die younger than their parents, mostly due to the problems associated with overweight.

So what happened? It is said that obesity is an interaction between genes and the environment. Well, our genes haven’t changed in the last 30 years, but the environment sure has. We all eat more, and exercise less. This isn’t news. But what is news is that our energy intake (what we eat and drink) and expenditure (what we use in everyday living – including normal activity and sports/exercise) are biochemically determined. So what in the environment changed our biochemistry?

To understand this dilemma, you have to understand a little biochemistry, but I’ll explain as simply as possible. The hypothalamus (the brain region which regulates hormones and energy balance) normally receives a signal from your fat cells (adipocytes) called leptin. Leptin is the fat cell hormone that tells your hypothalamus that you have enough energy stored in order to burn energy at a normal rate. Leptin levels can be too low (leptin deficiency, due to dieting or starvation) or too high (leptin resistance, if something blocks the leptin hormone from acting on those brain cells). In either case, the brain can’t see the leptin signal, and so the brain interprets it as a state of starvation. In this “starvation response”, two things happen: 1) the sympathetic nervous system (which controls your heart rate, blood pressure, and muscle metabolism) slows energy expenditure in order to conserve energy (which makes you feel bad), and 2) the vagus nerve (which controls your stomach, intestine, and pancreas) directs the body to store more energy as fat. Both of these “starvation responses” work to bring your leptin level higher. Obese people have high leptin levels, and therefore they are leptin resistant.

What blocks leptin signaling in obese people? Research over the past ten years suggests the following: leptin transport from fat cells to the brain is prevented by high triglyceride levels in the blood, and leptin release from fat cells is prevented by high insulin levels in the blood. This phenomenon is a normal response under some circumstances, such as the temporary blockage of leptin to promote weight gain during puberty and pregnancy, and is essential for reproduction and the survival of the species. But at other times, this phenomenon becomes a problem, as it causes the “starvation response” at a higher weight instead of a normal response at a lower weight. In addition, leptin resistance also fosters continued reward of food, which makes you eat more. These are the cardinal features of the obesity epidemic.

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