Carbs and carbs alone, not fat, increase body weight. It doesn't matter whether the carbs are from sugar, bread, fruit, or vegetables: They’re all rapidly digested and quickly converted to blood glucose.  A short time after a carb-rich meal, the glucose in your bloodstream rises rapidly, and your pancreas produces a large amount of insulin to take the excess glucose out.

Just as eating fat doesn’t raise blood glucose, it doesn't raise insulin levels either. This is important because insulin is the hormone responsible for body fat storage. Because fats do not elicit an insulin response, they cannot be stored as body fat.
Insulin takes glucose out of the bloodstream. It is converted first into a starch called glycogen, which is stored in the liver and in muscles. But the body can store only a limited amount of glycogen, so the excess glucose is stored as body fat. This is the process of putting on weight.

When your blood glucose level returns to normal, after about 90 minutes, the insulin level in your bloodstream is still near maximum.  As a result, the insulin continues to stack glucose away in the form of fat.  Ultimately, the level of glucose in your blood falls below normal, and you feel hungry again. So you have a snack of more carbohydrates, and the whole process starts over again. You're getting fatter, but feeling hungry at the same time. Ultimately, insulin resistance caused by continually high insulin levels in your bloodstream impairs your ability to switch on a satiety center in the brain. You enter a vicious cycle of continuous weight gain combined with hunger. Under such circumstances, it is almost impossible not to overeat.

Taking Off Weight:  Only Cutting Carbs Can Do It

So you've put the weight on–now you need to take it off again. Here again,  “healthy eating” hampers your attempts because a carbohydrate-based diet prevents you from losing excess fat. 

To lose fat, your body must use that fat as fuel.  It will only use its stored fat as fuel if you deprive it of its present supply of fuel:  blood glucose.

There are two ways to cut your body's glucose supply.  You can starve, which is what low-calorie, low-fat dieting is.  Alternatively, you can reduce the starches and sugars from which glucose is made, and make up the difference with another fuel:  fat.

The latter approach has two advantages over the traditional calorie-controlled diet.  First, you don’t have to go hungry.  Second, by feeding your body on fats, your body will stop trying to find glucose and will naturally begin using its own stored fat.

When you eat carbs, your capacity to use fat is limited. Increasing blood glucose during dieting stimulates insulin release. Even at very low concentrations of insulin, fat synthesis is activated and break-up of fat is inhibited.  This means that if you eat a carbohydrate-based low-fat diet, you force your body into a fat-making mode, not a fat-using mode.

Insulin inhibits the production of fat-burning enzymes, thereby preventing your body's fat cells from releasing their fat. This stops your body from burning your stored fat and makes it impossible for you to lose the weight you have put on.

References:

1. Robertson MD, Henderson RA, Vist GE, Rumsey RDE. Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism. Am J Clin Nutr 2002; 75: 505-510.

2. Bruning JC, Gautam D, Burks DJ, et al. Role of brain insulin receptor in control of body weight and reproduction. Science 2000; 289: 2122-5.

3. Odeleye OE, de Courten M, Pettitt DJ, Ravussin E. Fasting hyperinsulinemia is a predictor of increased body weight gain and obesity in Pima Indian children. Diabetes 1997; 46: 1341-5.

4. Sigal RJ, El-Hashimy M, Martin BC, et al. Acute postchallenge hyperinsulinemia predicts weight gain: a prospective study. Diabetes 1997; 46:1025-9.

5. Kreitzman SN. Factors influencing body composition during very-low-calorie diets. Am J Clin Nutr 1992; 56: 217S-223S

6. Meijssen S, Cabezas MC, Ballieux CG, et al. Insulin mediated inhibition of hormone sensitive lipase activity in vivo in relation to endogenous catecholamines in healthy subjects. J Clin Endocrinol Metab 2001; 86: 4193-7.

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