3. My Theory for the Cause of ADHD

It appears to me that at least two complementary coping mechanisms have been developed in different segments of the population to adjust metabolism for dietary fat deficiency. One coping mechanism, which I described in my essay on obesity, involves storing a steadily expanding "silo" of fat reserves on the body. The alternative mechanism, which I now believe is the one adopted by children with ADHD, is to implement a fat conservation mode: to manipulate the body's energy requirements towards favoring glucose over fat, while simultaneously stunting growth and compromising brain development.

While in my essay on obesity I argued that the obese suffer from defective glucose metabolism in the muscles, it appears that children with ADHD suffer from the exact opposite problem: very efficient glucose metabolism. Insulin is critical for the metabolism of glucose. When insulin levels are high, body fat cells are unable to release their fat stores, as shown in the figure at the right [lipolysis = breakdown of fat tissue]. I have proposed that obesity is protective against ADHD because the abundant fat cells can release plenty of triglycerides into the blood early in the morning, before the first meal. This fat supply can tide the person over through the long fatty-acid drought that occurs during the day, while an abundance of high-glycemic index low-fat foods are consumed. A further advantage is that obese people typically have reduced insulin production (due to insufficient calcium, which I explain later), so the levels of insulin in the blood are never excessively high. Their muscle cells have been programmed to prefer fat metabolism, but there is also plenty of fat available from the triglycerides (released before the meal began) to supply the brain's raw materials to enhance communication through neural pathways. Furthermore, the glucose that is not consumed by the muscles is readily available

It seems that ADHD children have adopted an entirely different strategy for coping with insufficient fats in the food sources. Research has shown that many of them suffer from hypoglycemia (low blood sugar), because their insulin is extremely efficient -- the opposite of diabetes [19]. In direct contrast with obese people, the fat cells of ADHD children program the muscles to prefer glucose over fat as a fuel source. This reduces the burden placed on the fat cells to convert glucose to fat, which is a very inefficient process. Furthermore, unlike the obese, ADHD children typically have no shortage of insulin, produced by the pancreas in response to glucose. Insulin enables the muscles to readily consume the glucose, but also unfortunately supresses the ability of the fat cells and the liver to release stored fats. If there is plenty of glucose in the consumed foods, and very little fat, then the muscles and brain consume the glucose, but the brain is deprived of sufficient fats to construct high quality long-distance neural connections. ADHD children have been found to have shrunken white matter in parts of the brain that are involved with focus of attention and learning new knowledge. I believe this is a direct consequence of a lack of a supply of fats, critically, when the neural pathways that make up the white matter are actively being formed.

The body with inadequate fat supply in the food sources is essentially like a car engine running on only two cylinders. While it has been argued that the body can manufacture all the fats it needs from other sources such as glucose, this is not actually true. The body uses fats not only as an energy source, but also, crucially, as a component of cell walls and as the insulation that covers all nerve fibers, i.e., the myelin sheath, not just in the brain but everywhere in the body. Two specific kinds of fats, omega-3 fats and omega-6 fats, are called "essential fatty acids" (EFA's) because the body cannot manufacture them. It is essential to obtain them from food sources such as meat, eggs, and fish.

Furthermore, the body cannot produce fat supply in the blood stream "at will." As I have mentioned previously, when insulin levels are high, the subcutaneous fat cells and the abdominal fat cells, as well as the liver, are suppressed from releasing their stored fats. When glucose is available, the fat cells are otherwise engaged in the task of taking up the glucose and converting it into additional fat supplies. The presence of insulin disables the process of lipolysis that is necessary before the stored fats can be released into the blood stream.