Dopamine is an incredibly important hormone that is released from the substantia nigra in the midbrain and relayed to other parts of the brain through three principal neural pathways: the nigrostriatal pathway to the cerebellum to control body movement, the mesolimbic tract to the reward center and seat of emotion, and the mesocortical tract to the frontal lobes of the cerebral cortex that control high level planning and reasoning. These pathways are part of the white matter that is shrunken in size in the ADHD child's brain. With poor transmission speeds and an inability to maintain a strong signal, these poorly insulated pathways dissipate the message that the dopamine is trying to send.
A recent study by Dr. Nora Volkow compared the brains of 53 nonmedicated ADHD adults with those of 44 healthy non-ADHD adults over the period from 2001 to 2009, using positron emission tomography (PET) brain imaging . The study focused on dopamine receptors, which propagate the signal to distant parts of the brain, and dopamine transporters, which recycle excess dopamine after the signal is transmitted. The study found that both receptors and transporters were reduced in number in the ADHD brains as compared with the normal controls. The receptor count is likely reduced as a consequence of the slow and inefficient transport across the networks. The transporters are reduced in turn in order to slow down the process that sends the dopamine back into storage. This allows the dopamine to stay in the synapse for a longer period of time. Ritalin achieves a similar effect, and this is believed to be the main reason why it is effective.
Research on rats has shown that dopamine release is severely impaired in the absence of insulin . This may be an intentional design as protection against releasing dopamine when there is insufficient glucose to fuel the resulting brain activities. However,the ADHD child, who has an efficient glucose metabolism, must deplete the excess insulin before fats from fat stores can be released. Meanwhile, the dopamine supply is exhausted while trying to send signals over faulty networks, and the release of fats comes too late to be effective.
The brain needs fats as well as glucose for acquiring new knowledge - to reconfigure and reinforce the neural connections. The ADHD child is trapped in a catch-22, because, in order to get at the fat stores, the insulin levels must be low, but if the insulin levels are low, glucose is also likely low (since the insulin is so efficient) and, as well, the dopamine release will be suppressed. A child who consumes a low-fat diet and has very efficient glucose metabolism will likely never have, simultaneously, sufficient blood levels of dopamine, fats and glucose. As soon as the insulin levels are sufficiently low to allow the fats to be released, the glucose and dopamine are likely already depleted. With little fat in the dietary sources, and with impoverished and insulin-suppressed fat cells, it is difficult to imagine where the fat supply for the brain is going to come from.