Recently, the World Health Organization (WHO) called for an international tax on sales of sugar-sweetened beverages. The thinking behind such a tax is that the growing epidemic of obesity in the world is caused by sugar-sweetened soda. However, this is contrary to the WHO Medical Officer that stated, “The decrease in soda sales in Mexico (who recently imposed a sugar tax on soda) is good news, but we don’t have conclusive evidence yet on whether this is actually reducing obesity and type 2 diabetes.”
Swapping Out Soda for Water May Not Impact Long-term Obesity
Harvard Medical School did a comprehensive study on reducing the use of sugar-sweetened soda in obese children by replacing them with free bottled water and intensive dietary consulting 1. The result after two years of extensive intervention was that there was no change in the levels of obesity in these children.
This is why nutrition is so complicated, and yet we try to make it too simple. Let’s start with obesity. Calories do count. If you consume more calories than you immediately need, you will store the excess (usually in your fat cells) for later use.
The Two Reasons We Overeat
There are two reasons why people overeat. One is apparent, and the other is less apparent.
- Tasty food – More palatable food activates the hedonic reward system, which makes you eat more food. The more palatable the food, the more dopamine the hedonic reward releases which overrides your calorie thermostat. This is why sugar is more palatable than non-starchy vegetables even when both supply the same levels of carbohydrates to the body.
- Inflammation in the energy-balance system in the hypothalamus – This is basically a “calorie thermostat” in the brain that balances the intake and burning of calories with great precision. This is explained more in my book, Toxic Fat 2 and also addressed within Our Brains Control Why We Eat – But You’re Much Smarter. One of the best ways to cause hypothalamic inflammation to generate an increase in calorie intake is to consume a high fat diet rich in palmitic acid (3-5).
Why We Can’t Solely Blame Sugar for Our Weight Issues
Added sugar makes soda, a snack, or any meal more palatable. This is why it is so prevalent in processed foods. The more palatable a food is, the more likely you are to eat it. In addition, added sugar also has a metabolic effect as it can stimulate insulin release to lower blood sugar and that will also make you hungry. Since it is very difficult to separate one mechanism from another, it’s easier just to make sugar the “evil one” and call it a day as the WHO has suggested. This same type of thinking was also used in Middle Ages to burn witches to order to get rid of the Black Plague.
Palatability May Be A Clue To Overconsumption
Genetic manipulation in mice has allowed the separation of the impact of sugar on the two mechanisms in the brain that control our intake of food 6. In this experiment, the sugar taste receptor was genetically knocked out in mice. When these mice were fed a high-sugar diet (by adding extra sugar to their water like a soda), they didn’t gain weight because it didn’t taste sweet. The metabolic effect of the sugar was still present, but the lack of palatability of the added sugar prevented any weight gain.
Then they added some fat to the sugar-sweetened water. Now the mice without the sweet taste receptors quickly become obese as the combination of the fat and the sugar in the water was affecting the hedonic reward system in the brain.
This is the secret that the food industry and dessert makers learned many years ago: the combination of sugar and fat is irresistible. This also helps explains why you have weight regain on high-fat, low-carbohydrate diets. First, they are rich in saturated fats (like palmitic acid) to distort the energy-balance thermostat in the hypothalamus so you eventually end up eating more calories than you need. Second, the fat activates the hedonic reward system so you eat more calories because the food is more palatable. End result is that you gain weight.
So let’s go back to the Harvard study on reducing the use of sugar-sweetened sodas. It was successful (the children drank less soda), but it didn’t reduce their obesity after two years. It doesn’t matter if you reduce the sugar unless you are also reducing the fat at the same time. This is why McDonald’s sells the combo package of the sugar-sweetened soda and fatty hamburger. Maybe this is why they call it a Happy (for our bottom line) Meal.
The Key To Avoid Weight Gain Is To Limit Both Sugar and Fat
The secret to treating obesity is to eat the least amount of calories without being hungry or tired. You do this by reducing diet-induced inflammation in the brain (by reducing omega-6 and saturated fats), and from bypassing the sweet receptors in the tongue (using low-glycemic carbohydrates such as non-starchy vegetables).
You still need the right balance of protein, carbohydrate, and fat to control the metabolic response of meal in the blood and the gut. Also, consider Zone PastaRx as your primary protein source. PastaRx is our patented protein-rich food product designed to stabilize blood sugar and curb hunger for hours.
If you can do everything I’ve recommended at each meal, you can restrict calories without hunger or fatigue for a lifetime. That is the promise of the Zone Diet.
Need additional support? Check out Zone Lifestyle Tips: 6 Ways to Tame Your Sweet Tooth to see how you can kick your sugar habit for good, despite how rewarding it may taste.
- Ebbeling CB et al. “A randomized trial of sugar-sweetened beverages and adolescent body weight.” N Engl J Med 367:1407-1416 (2012).
- Sears B. Toxic Fat. Thomas Nelson. Nashville, TN (2008).
- Kleinridders A et al. “MyD88 signaling in the CNS is required for development of fatty acid-induced leptin resistance and diet-induced obesity.” Cell Metab 10:249-259 (2009).
- Cintra DE et al. “Unsaturated fatty acids revert diet-induced hypothalamic inflammation in obesity.” PLoS One 7:30571 (2012).
- Sears B and Perry M. “The role of fatty acids in insulin resistance.” Lipids Health Disease 14:121 (2015).
- Glendinning et al. “The role of T1r3 and Trpm5 in carbohydrate-induced obesity in mice.” Physiol Behav 107: 50-58 (2012).