Do you ever eat a big meal and feel stuffed, yet still put down a dessert high in fat and sugar? Do you ever over-eat to the point that you need to unbuckle your belt a notch, or even unbutton your pants?
There are multiple systems within your body that are circuited to the brain that interact to determine your weight loss and gain: your energy-balance system, and your appetite control center. While these interactions may seem out of your control, with the right mindset, they can be managed, and even controlled.
Your body weight is predetermined by an internal system
Each person has an energy-balance system within their body that constantly measures incoming hormonal inputs from their gut and blood to determine whether or not they should eat. This system is called the hypothalamus. The hypothalamus is the foundation for determining a set-point for body weight.
If your weight goes up or down beyond your genetically defined range, your brain tells you whether or not you should eat. This makes it difficult to maintain significant weight loss, because you’re constantly fighting against your own brain.
Under normal circumstances, this energy-balance system is 99.5% precise to maintain a set-point for your weight, and appears to be genetically controlled. This is why the average American can eat close to 750,000 calories per year and still gain less than a pound of weight (usually fat). It’s all predetermined.
Is the thermostat on your weight out of control?
Consider your hypothalamus to be a high-tech biological weight control thermostat. It works by constantly monitoring your gut and blood hormone levels, including leptin and insulin. Leptin comes from the fat cells to indicate if you have enough stored fat for a future rainy day. Insulin comes from the pancreas to indicate if you have enough blood glucose to supply the brain right now.
Under normal circumstances, these two hormones reach the brain and interact with their receptors in the hypothalamus to stop hunger.
But what if conditions are not normal? What if you have developed resistance to both insulin and leptin in the hypothalamus?
Although your blood levels might be normal, the information may not reach the interior of the target cells in the hypothalamus. As far as the brain is concerned, the compromised insulin and leptin hormonal signals indicates to your energy-balance system to keep on eating (especially fat and carbs) because both your short-term (low blood sugar) and long-term (lack of sufficient body fat) survival may be at risk. The hypothalamus responds to these attenuated messages from leptin and insulin by generating hunger signals causing you eat more.
So what happens when you go on a diet? The levels of insulin and leptin drop in the blood, and you are constantly hungry. Why? Because your hypothalamus thinks your survival may be compromised and increasing the strength of the hunger signals.
Controlling your weight doesn’t need to be heavy
The most common way to solve this weight-loss induced constant hunger problem is to increase insulin and leptin levels in the blood by eating more carbohydrates and fat. This will cause both hormone levels to rise. Eventually the increased leptin and insulin levels in the blood become high enough so the hormonal signals finally overcome the hormone resistance in the hypothalamus and you stop having consistent hunger. Unfortunately, in the process the lost weight starts to return.
This helps explain why there is such a low percentage of long-term success with diet-induced weight loss. Much of what we attribute to lack of willpower in people who regain this lost weight is really due to disturbances in hormonal communication.
Recognizing that your internal energy-balance system is unique, there still remains an elegant approach to reduce hormone resistance in your hypothalamus. Of course, it is only possible if you know what causes insulin and leptin resistance in the first place.
Increased cellular inflammation in the hypothalamus makes it increasingly unresponsive to both insulin and leptin. Although insulin and leptin are structurally different hormones and have different receptors, they use essentially the same internal signaling pathways. This means that cellular inflammation in the hypothalamus will disrupt both signaling pathways. Unless you reduce cellular inflammation in the hypothalamus, your only option to avoid constant hunger is to continue eating sugar and fat. This will increase the levels of insulin and leptin in the blood so their signals reach the appetite control center in the hypothalamus.
Your brain rewards you. Bonus – you get to live!
The dopamine reward system is your brain also controls hunger. Whereas the energy-balance system in the hypothalamus is necessary for survival, the dopamine reward system in a nearby section (ventral tegmental area or VAT) of the brain determines the desirability of eating. If there is no reward for doing something important for survival (like sex or eating), then why do it? The dopamine reward system reinforces habits that are necessary for the survival of any species (like sex is good, food is good). It is the same dopamine reward system that can be hijacked by addictive drugs and behaviors.
What if you had a significant deficiency of dopamine production in your brain? Studies with genetically modified mice that don’t feel rewarded after eating do not eat. As a result, they die soon after birth. That’s why the dopamine reward system is critical. It establishes that the habit of eating is good for survival.
Insulin resistance also affects dopamine-producing cells. Therefore, if you have insulin resistance in the energy-balance system of the hypothalamus, you also have dopamine resistance. This inhibits the release of adequate levels of dopamine to give you pleasure from eating the food.
You have two choices to get adequate pleasure out of eating. Either you can increase your intake of palatable foods high in fat and sugar by having dessert at the end of a meal, or by binge eating. Or better idea: you can reduce insulin resistance so that eating less food actually generates more pleasure. This occurs through increased dopamine release.
Avoid overeating: Sync your energy-balance system and appetite control center
The reason you overeat is because you need an appropriate interaction between the energy-survival system (“I eat to live”) as well as the hedonic dopamine reward system (“I love to eat”). Optimal dietary control only happens if you lower hormone resistance in the hypothalamus. Since insulin and leptin resistance are similar in their pathways inside the cell, anyone with insulin resistance is likely to have leptin resistance.
If you have diabetes or metabolic syndrome (i.e., pre-diabetes), you definitely have insulin resistance, and not surprisingly, you are constantly hungry. According to the American Diabetes Association, more than 110 million Americans have either pre-diabetes or diabetes. However, about 16% of normal-weight Americans also have insulin resistance.
How do you know if you have insulin resistance? Take my Insulin Resistance Quiz. This quick questionnaire will provide your personal Insulin Resistance Score, along with personalized dietary recommendations. If these dietary recommendations are working, you will not be hungry or fatigued for five hours after meals.
The secret for a truly healthy diet is to maintain lack of hunger and fatigue for the rest of your life.
- Sears, Barry. “Gaining it Back: The Science behind The Biggest Loser’s Failure.” Dr. Sear’s Blog. (2016).
- Davis JF, Choi DL and Benoit S. “Insulin, leptin, and reward.” Trends Endocrin Metab 21:68-74 (2009).
- Daws LC, Avison MJ, Robertson SD, Niswender KD, Galli A, and Saunders C. “Insulin signaling and addiction.” Neuropharmacology 61:1123-1128 (2011).
- Sotak BN, Hnasko TS, Robinson S, Kremer EJ, and Palmiter RD. “Dysregulation of dopamine signaling in the dorsal striatum inhibits feeding.” Brain Res 1061:88-96 (2005).
- McLaughlin T, Allison G, Abbasi F, Lamendola C, and Reaven G. “Prevalence of insulin resistance and associated cardiovascular disease risk factors among normal weight, overweight, and obese individuals.” Metabolism 53:495-439 (2004).