How to Become Smarter (25 page)

We can conclude that further studies are necessary to confirm the beneficial effects of elimination diets on mental performance and mental health. On the other hand, investigation of the effects of individual food additives at realistic doses is unlikely to yield significant results. Simultaneous administration of many food additives may be easier to study. In summary, existing evidence suggests that food additives alone are not responsible for the symptoms of ADHD [
63
,
64
,
929
,
1000
].

• ADHD is a complex disorder characterized by core symptoms of inattention, hyperactivity, or impulsivity.
  
• The Feingold hypothesis suggests that food additives cause symptoms of ADHD.
  
• Elimination diets are beneficial for some but not all ADHD patients.
  
• Addition of cocktails of food additives to the diet reproduces some symptoms of ADHD in healthy children. Yet the size of this effect is too small to explain the magnitude of symptoms in ADHD.
  [
  Previous
  ][
  Next Key Points
  ]
  

A number of studies have attempted to identify abnormal physiological changes in ADHD patients (the study of pathophysiology). These data can help to identify possible causes and lead to new treatments. These studies have produced a lot of useful information about ADHD, but this chapter discusses only the findings related to nutrition. Some of these studies have uncovered abnormalities that are similar to the changes that can result from low-protein diets. In particular, a study on ADHD patients in Taiwan revealed lowered concentration of protein in blood [
302
]. Two other studies, from North America, showed that ADHD patients, on average, have a lower than normal concentration of the amino acids phenylalanine and tyrosine in blood [
303
,
304
]. (Amino acids are building blocks of proteins and are the byproducts of digestion of proteins in your stomach.) Low-protein diets cause a drop of the level of phenylalanine and tyrosine in the blood. High-protein diets have the opposite effect; that is, they increase the blood levels of these amino acids [
305
,
306
].

Studies on laboratory monkeys have shown that if young monkeys consume a low-protein diet, this causes retardation of growth of the brain [
307
]. Several studies of ADHD children have shown that these kids have a somewhat smaller brain volume compared to their healthy peers [
308
-
310
]. The brain size of ADHD children catches up to the normal size when the kids grow up [
311
]. These findings also suggest that protein malnutrition may be linked to ADHD.

Another relevant finding is that dietary iron deficiency (low level of iron in blood) is more frequent among ADHD patients compared to the general population [
312
,
313
]. Iron supplementation of the diet can be beneficial for ADHD patients, according to some studies [
314
,
315
]. On the other hand, research suggests that the blood level of iron correlates with consumption of meat [
316
]. Meat is a protein-rich food product and low consumption of meat may be responsible for both protein malnutrition and iron deficiency. In light of the above observations, it is reasonable to suppose that the more frequent occurrence of iron deficiency among ADHD patients may be the result of low consumption or impaired digestion of meat. On the other hand, the aforementioned Taiwanese study [
302
] showed a
higher
blood iron level in ADHD patients compared to healthy controls. Another recent study showed that the iron status of ADHD patients is not different from that of healthy controls [
879
]. Further research is necessary to resolve these discrepancies.

To summarize, the above studies point to one of these possible causes of ADHD:

1. low consumption of protein by ADHD patients;
   
2. low quality of dietary protein;
   
3. alternatively, ADHD patients may have deficiencies in the digestion of protein-rich foods.
   

These pathological changes can be responsible for lower protein levels in blood, lowered blood levels of tyrosine and phenylalanine, and slightly smaller brain size in ADHD. The potential flaw in the above “protein malnutrition theory” of ADHD is that ADHD drugs (psychostimulants) suppress appetite and thereby can reduce intake of dietary protein. If this is the case, then the low quality of dietary protein is not the cause of ADHD but a consequence of pharmacological treatment. In actuality, this possible flaw most likely is not valid. Many of the above studies deal with unmedicated ADHD patients separately from medicated patients and controls. Many of these studies found the signs of dietary protein deficiency in
unmedicated
patients. The studies of blood levels of phenylalanine and tyrosine included unmedicated patients only [
303
,
304
]. The brain imaging studies used separate groups of medicated and unmedicated ADHD patients [
308
]. The above studies found somewhat smaller brain volumes and lowered blood levels of phenylalanine and tyrosine in unmedicated ADHD patients compared to healthy controls. Another recent study [
317
] compared body measurements among three groups: medicated ADHD children, unmedicated ADHD children, and age-matched controls from the general population. Both medicated and unmedicated children with ADHD have shorter height and somewhat smaller head circumference compared to age-matched controls. Head circumference correlates with brain volume. The only statistically significant difference between medicated and unmedicated ADHD children is the amount of body fat and thigh circumference. Both are smaller in medicated children. Parents often blame stunted growth of ADHD children on stimulant drugs, yet the above studies suggest that this problem is unrelated to ADHD medication.

The aforementioned Taiwanese study by Dr. Jiun-Rong Chen and colleagues [
302
] found that ADHD patients consume the same amount of protein compared to healthy controls. Yet these patients have a lower total blood concentration of protein. This observation suggests that ADHD patients either consume lower quality protein (e.g., plant rather than animal protein [
318
]) or protein assimilation is impaired in these patients, or both. A recent report out of Australia showed that, on average, ADHD patients consume 50% less meat, fish, and eggs compared to the general population [
889
]. These data support the hypothesis of low quality of dietary protein in ADHD patients.

We can conclude that:

1. the adverse effects of stimulant medication are smaller than what many people assume;
   
2. stimulant medication is not the cause of the hypothetical protein malnutrition in ADHD children;
   
3. the hypothetical protein malnutrition in ADHD may be the result of low quality of dietary protein, insufficient assimilation of dietary protein, or both.
   

These observations suggest that increased consumption of high-quality protein such as meat [
120
,
318
,
319
,
835
,
836
,
853
,
912
] should be beneficial for ADHD patients, as we will see in the next section.

• A recent study out of Australia shows that ADHD patients consume 50% less meat, fish, and eggs than the general population does. The total amount of protein that ADHD patients consume is normal. These data suggest that people with ADHD tend to consume dietary protein of lower quality.
  
• Several pathological changes observed in ADHD patients are similar to the effects of low-protein diets.
  
• These changes include: {1} lowered levels of the amino acids tyrosine and phenylalanine in blood, {2} lowered total level of protein in blood, and {3} a somewhat smaller brain size in afflicted children than in their healthy peers.
  
• ADHD drugs (amphetamine-like stimulants such as
  Ritalin
  ®) reduce appetite, but researchers find most of the above changes in both medicated and unmedicated patients. Therefore, the appetite-reducing effects of ADHD medication cannot explain the low consumption or poor digestion of protein-rich foods by ADHD patients.
  [
  Previous
  ][
  Next Key Points
  ]
  

An introduction to some basics of neuroscience will be helpful at this point, in order to make the discussion in this section more comprehensible to lay readers. (Readers can skip the technical details by pressing the skip button or
this link
.) The readers curious about fine details of how neurons communicate with each other can read articles “neuron” and “chemical synapse” on Wikipedia.org. Most people know that brain cells are called neurons. There are roughly a hundred billion neurons in the brain and they form numerous and complex connections among each other. A single neuron can send electrical signals to tens and hundreds of other neurons via its long and branched “sprouts” called
axons
. Each neuron can also receive signals from many other neurons via its shorter “sprouts” called
dendrites
. There are many different types of neurons. The type of neural cells relevant in this context is the neurons that use a chemical called
dopamine
to send signals to other neurons. The ends (terminals) of an axon of such a neuron can release dopamine. This causes propagation of an electrical signal from this neuron to its target neuron (from the axon of the signaling neuron to the dendrite of the target neuron). This is because the receiving end (dendrite) of the target neuron is responsive to dopamine. The connection point between two neurons, i.e. the junction between an axon and a dendrite, is called a
synapse
. The signaling neuron releases dopamine into the synapse, and the recipient neuron detects the presence of dopamine in the synapse. Dopamine and other chemicals, such as serotonin, that neurons use to communicate with other neurons are called
neurotransmitters
. Neurons are not the only type of cells in the brain. There are numerous supporting cells called
glia
, which in most cases do not conduct electrical signals and do not participate in the neural networks of the brain. The so-called
interstitial fluid
fills the spaces between neurons and glial cells. Local concentration of neurotransmitters in the interstitial fluid can change when neurons are sending and receiving signals within a given region of the brain. This is because neurotransmitters can leak out of synapses (connections between neurons) into the interstitial fluid and vice versa.

Neurons that send signals to other neurons by means of the neurotransmitter dopamine are called dopaminergic neurons. The dopaminergic neurons are concentrated in several discrete regions of the brain. Since axons can be long, up to one meter (about three feet) and longer, dopaminergic neurons can send signals to target neurons in a distant area of the brain. Dopaminergic neurons send signals to neurons that are responsive to dopamine. Whether a neuron is responsive to dopamine depends on the properties of the dendrites or “receiving terminals” of these target neurons.

Suppose the concentration of dopamine increases or decreases in an area of the brain where the neurons are responsive to dopamine. These changes will affect the firing activity of those neurons. This in turn can have subjective and objective effects on a person’s mood, motivation, and attentional performance.
Drugs that psychiatrists prescribe for attention deficit hyperactivity disorder (ADHD), such as
Adderall
®, increase the level of the chemical dopamine in several brain regions that participate in attention control. In particular, these drugs can increase the level of dopamine in the frontal part of the brain (called
prefrontal cortex
). They also increase the concentration of dopamine in a central region of the brain called the
striatum
(translated from Latin as “a striped body”) [
294
,
297
,
320
]. Research shows that these changes are essential for the attention-enhancing effects of psychostimulant drugs such as
Ritalin
® and
Adderall
® [
294
,
297
,
320
].

These same drugs can improve attention control and attention span in healthy people as well [
321
-
328
]. People whose attention function is average or below average benefit most from these drugs. The minority of people who have excellent or optimal attention function do not benefit from psychostimulant drugs and their attentional performance can deteriorate with these drugs [
294
]. Healthy people, such as college students and some professors, increasingly use psychostimulant drugs without prescription (illegally) as a study aid or vocational aid. This practice carries a risk of abuse and addiction [
9
-
18
]. This risk is small when patients use prescription stimulants at therapeutic doses under a physician’s supervision.