Is Gaining Weight Really Our Fault?

Obesity is ever-increasing in both prevalence and severity, despite the fact that we have all the information we need to prevent it, literally at our fingertips.

Obesity is increasing in all age groups, especially in children.

We go on diets to lose weight, only to slowly gain it all back. What is going on?

Do we eat too much and move too little?


Are we simply victims of the interaction of our genetic makeup with the foods that are readily available?

Why do we gain weight? The answer is to store excess energy for future periods when food may be scarce.

How does our body store excess energy? I have two answers for you: leptin resistance and insulin resistance.

What is leptin?  It is a hormone that plays a key role in regulating energy intake (appetite) and energy output (metabolism). Leptin acts on the brain to inhibit appetite. The absence of leptin (or its receptor) leads to uncontrolled food intake and obesity.

Leptin decreases with fasting, very low-calorie diets, and physical exercise. It is increased in times of stress and with the onset of sleep apnea. While high levels of leptin in the blood are associated with appetite suppression, obese individuals tend to have high circulating levels of leptin. How can this be?

The answer is that obese people tend to be “leptin-resistant.” When you have an excess amount of fat stores, your leptin is continuously elevated. This leads to the deceased effect of leptin on your brain. Let me put this in simpler terms. If you eat a cookie, your leptin goes up and you aren’t hungry anymore. If an obese person eats a cookie, their leptin goes up, but their brain doesn’t register it. They still feel hungry, so they eat another cookie.

How do we get high levels of leptin? Leptin resistance and insulin resistance go hand-in-hand. Insulin resistance is essentially the result of more insulin required to lower your blood sugar level.  Resistance to insulin is associated with metabolic syndrome (high cholesterol, high blood pressure, weight gain, and diabetes).

Insulin resistance originates from many sources (Trans fats, branched amino acids, alcohol), but the most common source is fructose.

Fructose is one of the types of sugar that we eat. 100 years ago, we consumed about 15 grams per person per day. Today the estimate is a whopping 73 grams per person per day! Fructose is not like regular sugar. When you eat excess sugar, it goes into your liver for storage. When you eat fructose, however, it bypasses your liver and goes straight into fat.

There can be no doubt that we are suffering from excessive fructose intake. Fructose has become the universal sweetener because it is cheap.  The major source of fructose in our diet comes from corn (liquid sugar, high fructose corn syrup).

We evolved to live not unlike bears. We would eat fructose from fruit when it was available– at harvest for one to two months per year. This period was followed by four to five months of winter and weight loss. Now, fructose is available through fruit 24/7/365 and consumed in unlimited amounts. Worst of all, we take in all this fructose without fiber to help absorb it.

To summarize, I would say that obesity is often the result of leptin resistance. Insulin appears to be important in counteracting the effects of leptin on the brain. An abundance of fructose induces insulin resistance and drives weight gain, which in turn leads to increased consumption. Gaining weight may not be “our fault,” but we have the knowledge and the tools we need to counteract it.


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