ADHD, Alcoholism and Nutrient Deficiencies

This will probably be the last blog post on the ADHD and alcoholism connection. We have investigated the connection between ADHD and alcoholism with regards to:

• Size and function of specific brain regions, such as the corpus callosum.


• The prevalence of ADHD in children of male alcoholics


• The theory behind omega-3 fatty acids, which are often deficient in ADHD and maintain cell structure and function


• How specific genes which encode for desaturase enzymes, can actually interact with alcohol and and omega-3 fatty acids and all combine to influence the likelihood of ADHD.

Now we will investigate another potential connection between the disorders of ADHD and alcoholism, which involves alcohol-induced deficiencies of key vitamins and minerals which are often deficient in individuals with ADHD. We will list some of these key nutrients below:


Magnesium: (Here are recommended daily magnesium intake levels)

We have posted on this nutrient extensively in the past. For example, there is relatively strong evidence of a connection between magnesium deficiency and childhood ADHD. Additionally, there are a number of disorders which occur alongside of ADHD, which are called comorbid disorders. Magnesium levels are thought to influence some of these ADHD comorbid disorders as well. Co-treatment with vitamin B6 has been shown to boost magnesium's effects for ADHD treatment as well. Finally, I have outlined some other nutrient treatment combinations thought to boost the effectiveness of magnesium for ADHD.

Magnesium deficiencies are also common in chronic alcoholics. There are several potential reasons for this including decreased absorption and increased urinary loss of magnesium, dietary deficiencies as alcohol calorically replaces magnesium-rich foods, and decreased retention due to liver dysfunction. Unfortunately, the actual process of quitting alcohol use can also result in magnesium shortages. This is due to the alcohol withdrawal process in which results in fatty acid composition changes and the buildup of compounds in a process called ketoacidosis. These compositional changes during the alcohol withdrawal process can result in products which bind to magnesium and reduce its serum levels. A review by Krishnel and coworkers on the efficacy of intravenous vitamins for alcoholics in the emergency department touted the benefits of oral magnesium supplementation for admitted alcoholic patients.


Thiamine (also spelled "thiamin"): (Here are recommended daily thiamin intake levels).

There are several studies pointing towards a connection between chronic alcohol abuse and thiamine deficiency, although the scope of these effects is still under debate. Thiamine deficiency has been implicated for a disorder called Wernicke's encephalopathy. Wernicke's encephalopathy does have some overlap in symptoms with ADHD, such as impaired short-term memory, but beyond this, there is little connection between the two disorders. One thing to note about thiamine is that while there is minimal research done on the possible connection between its deficiency and ADHD, thiamine does play a major role in the process of glucose metabolism. Individuals with ADHD have often shown sub-average blood glucose levels to several key brain regions. Some studies have even implicated a potential risk of thiamine depletion caused by rapid glucose administration (such as through IV treatment).


Vitamin B-6: (Here are recommended daily vitamin B-6 intake levels)

Vitamin B-6 has had numerous implications for both the causes and treatment of ADHD. B6 has been shown to assist and boost the effects of magnesium in treating ADHD. Vitamin B6 has an "active form", which is often referred to as pyridoxal phosphate (PLP).

Chronic alcoholism can lead to a condition known as hyperhomocysteinemia. This disorder is the result of excessive buildup of the compound homocysteine. Homocysteine has been implicated as a major factor in a number of cardiovascular and inflammatory diseases and is a leading culprit of stroke and arterial damage. In addition to these disorders, high homocysteine levels are thought to play an indirect role in the onset of ADHD.

Vitamin B-6, vitamin B-12 and folic acid all play a role in regulating homocysteine levels. In fact, there is thought to be a minimal level for each of vitamin B6, B12 and folate to combat excessive homocysteine levels. Below is a rough sketch of how homocysteine is converted to the more benign and extremely important bodily antioxidant glutathione. This is important, because ADHD individuals have often been shown to have lower than normal levels of this ubiquitous antioxidant (as well as antioxidant levels in general). Upping the conversion of homocysteine to glutathione through B vitamin-dependent pathways therefore presents two different therapeutic measures for the ADHD sufferer.


At this point, there is no need to familiarize yourself with the intermediate steps in the process, just note that the "active" form of vitamin B-6, Pyridoxal phosphate or PLP is needed in not one, but two different steps of this conversion process. Low levels of this key nutrient can lead to a backup of homocysteine as this process is severely hampered.

Vitamin B-12: (Here are recommended daily vitamin B-12 intake levels)

As mentioned above, vitamin B-12 also plays a critical role in maintaining homocysteine levels. It, along with folate (the "nutritionally active" form of folic acid), actually work together, along with a third compound called betaine) in converting potentially dangerously high levels of homocysteine back to the amino acid methionine. Keep in mind that deficiencies of vitamin B-12 can cause problems with regards to homocysteine buildup as an under balance of vitamin B12 with respect to folate can boost homocysteine levels. Keep this in mind when we proceed to the folic acid discussion, as isolated supplementation with folate can offset the desired B12/folate balance and be counterproductive. A brief diagram of this process can be seen below:

A quick note: If you look at the diagram above, you can see that the process of removing homocysteine by converting it to methionine can actually continue on to another important compound, S-Adenosylmethionine (SAMe). There has been a lot of discussion surrounding SAMe as a possible supplement used to treat ADHD. We will save this discussion for a later time, but it is at least worth mentioning that there have been some very positive things said about this nutrient. Additionally, SAMe has been shown to help protect against liver damage (even to the point of reversing the process), which, as we know, is extremely common in alcoholics. Also note that betaine supplementation can also help offset alcohol-induced liver damage, so the betaine mentioned in the above process is multifunctional with regards to ADHD and alcoholism.

In addition, there may be a connection between vitamin B-12 deficiencies and food allergies (which are often associated with a rise in ADHD-like behaviors themselves). This is in part, due to the connection between B-12 deficiencies and pernicious anemia. This is characterized by a reduction of gastric acid secretion through damage to cells in the stomach called parietal cells. Food allergies, which have been associated with ADHD, can be exacerbated by weak stomach acid levels, as food allergens which are normally broken down by sufficient acid are now present at higher levels. We have seen the effects of damage to the stomach and other digestive organs in the case of our earlier post on celiac disease and its correlation with ADHD symptoms.

***Keep in mind that this B-12/food allergy and ADHD connection is more hypothetical at this point, relatively little published information is available to confirm this indirect connection. Nevertheless, I personally believe that this possible association is at least worth mentioning.

Folic Acid/Folate: (Here are recommended daily folate intake levels)

As alluded to above, we have seen the intricate connection between vitamin B-12 and folate (folic acid is the synthetic form of folate used in food fortification. Within the scope of this post, I am using the two terms interchangeably). With regards to cognitive function and relevant disorders such as ADHD, there is also an important relationship regarding the balance of these two nutrients. For example, a relatively recent study found that for vitamin B-12 deficient individuals, folate is actually connected to folate and reduced cognitive function. However, when ample B-12 levels were available, higher folate levels were protective against cognitive impairment. Thus we see that folate can potentially be a double-edged sword in the war against high homocysteine levels and reduced cognitive function, and that folate's effectiveness is grossly dependent on an adequate vitamin B-12 balance.

Aside from the homocysteine/B-12 connection, it also appears that folate plays other critical roles which can indirectly affect the severity of negative symptoms associated with ADHD. Additionally, folic acid has been found to have a protective effect against formic acid, a neurotoxin. This relationship actually stems from the neurotoxic effects of methanol, which is often found in alcoholic beverages either as a congener (essentially a side product in alcoholic beverages, which actually play a factor in the hangover process), or through endogenous formation (within the body). One of the problems with methanol is that it shares the same enzyme system as ethanol (the main form of alcohol in beverages), but is slower to clear due to a less-efficient metabolic process and can build up to toxic levels in heavy drinkers. However, adequate folate levels in the liver can expedite the methanol metabolism and clearance and reduce levels of the neurotoxin formic acid. In addition to the liver, there is some evidence that folate-derived formic acid metabolism occurs in the mammalian brain as well. Folate is also thought to be connected to the key compound in regulating levels of SAMe (S-Adenosylmethionine). Folate deficiency can lead to reduced levels of SAMe. This is of importance, because in numerous studies S-Adenosylmethionine has been implicated as a potential treatment option for ADHD.


A quick word on homocysteine: We have spent a fair amount of time highlighting the connection between alcohol consumption and homocysteine levels. In fact, chronic alcoholics reported double the serum homocysteine levels as nondrinkers. Hyperhomocysteinemia has also been associated as a major culprit in the process of alcoholism-induced brain shrinkage.

However, it is worth noting that the source of the alcohol may play a critical role with regards to homocysteine levels. A study found that beer consumers had notably lower levels of homocysteine than did consumers of wine or other spirits. While this association was not thoroughly addressed, this is possibly due to the relatively high levels of B vitamins in certain forms of brewer's yeast (which is used in the beer-making process). This is right in line with our study on vitamins B-6 and B-12.

In addition to the nutrients listed above, there are thought to be other nutritional factors at play. For example, chronic alcoholics who are faced with alcohol withdrawal are at increased risk of omega-3 fatty acid oxidation. This oxidative damage can disrupt the omega-6/omega-3 fatty acid balance, which we addressed in an earlier post as being a critical factor in cell membrane integrity. Additionally, alcoholism has been linked to deficiencies in antioxidants such as vitamin C (remember that individuals with ADHD generally have lower total antioxidant levels than their non-ADHD peers). Alcoholic liver damage has also been linked to zinc deficiency. We have investigated the zinc connection to ADHD earlier, namely in the potential ability of zinc to boost the effectiveness of Ritalin, a common ADHD stimulant medication.

Finally, I have alluded a bit to the compound S-Adenosylmethionine (SAMe) in this post. It is an ADHD treatment method of great potential interest. We will be discussing the possible merits of SAMe in the near-future.

Genes, Omega-3's, Alcohol and ADHD

In our last discussion, we were exploring the theory behind omega-3 fatty acid supplementation for ADHD, and alluded to the fact that there may be some genes at work involving this process. Additionally, there is some evidence that alcohol use can inhibit the effectiveness of some of the enzymes that are coded for by these genes, and possibly be a factor in the onset of ADHD. We will be exploring these associations in this blog post.

Omega-3 fatty acids are crucial for our overall well being for a number of reasons, with many of them being tied to maintaining the structure of all different types of cells in our bodies. Among these omega-3's are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). ALA converts to EPA (and eventually DHA) through a series of steps, several of which use the enzymes governed by the genes listed above. A summary of this process is highlighted below (original file source here):

The diagram above may look quite complicated, but we're just focusing on a few of the objects listed above.

As a quick side note: a lot of the other objects on this diagram above are showing the role these omega-3's and omega-6's play in the inflammatory process of immune reactions. This discussion is beyond the range of this post, but I have included it to illustrate that omega-3 and omega-6 fatty acids play a critical role in regulating a number of different functions and systems. Omega-3 imbalances can lead to immune dysfunction, which is thought to be one of the reasons why individuals with ADHD, who often have lower blood levels of omega-3's than their peers, are also more likely to have immune system disorders such as allergies. This ADHD/allergy connection will be explored in the future. Also, notice that omega-3's and omega-6's use the same enzymes. This is important, and was discussed at length in the previous post.

The section on the left of the above diagram describes how one omega-3 fatty acid is converted to another, for example, the a-linolenic acid (top left) eventually makes its way to forming EPA (fourth one down on the left), which eventually is converted to DHA (last one in the left column). Bringing our attention to the center, we see a series of enzymes with names like ∆6 desaturase, elongase, etc. These enzymes play a major role in the actual chemical conversion process of one type of omega-3 fatty acid to another.

Keep your attention on the enzymes that have the key term desaturase in their title. These are the ones we need to be concerned about when dealing with the aforementioned genes and alcohol. Without these enzymes functioning at their highest level, the incorporation of dietary omega-3's into the actual structure of the cell membrane is significantly. Genetic differences and the presence of external factors (such as alcohol or other types of fats) can significantly impair the function of these enzymes and slow the conversion process (and ultimately uptake and incorporation into cell membranes) of these critical omega-3's.

A number of these desaturase enzymes are all coded from a specific genetic region located on the 11th chromosome in humans, located at the 11q25 region (chromosomes have 2 "arms", a "p" and a "q", the numbering refers to relative location on that arm, so "11q25" refers to the 25th region on the "q" arm on the 11th chromosome). Interestingly, this region is located near the 11q22 region, which has been linked to ADHD. The closer two genetic regions are, the higher the chances they will be co-transmitted (passed on together from parent to child). In other words, gene forms which are located near each other on a chromosome are more likely to be passed on together, suggesting the possibility that the 11q22 ADHD region may in fact be influenced by some of the genes from nearby 11q25 region.

Brookes and coworkers did a study on the association between these desaturase genes and ADHD (on a personal note, I would like to acknowledge the authors of this particular study. Much of the information in these past two posts is gleaned from their work, and this paper provided a great starting point for much of my research for this post). They found that the 11q25 region contained three genes which code for desaturase enzymes located next to each other: Fatty Acid Desaturase 1, Fatty Acid Desaturase 2, and Fatty Acid Desaturase 3 (abbreviated as FADS1, FADS2 and FADS3, respectively). These genes each exist in different forms, called alleles, which have slightly different DNA configurations (which can differ by as little as one letter in the DNA "code").

Key findings from the Brookes study: This group saw a significant difference in the prevalence of ADHD stemming from two different alleles in the FADS2 gene. It appears that a single point difference was all it took to boost the likelihood of association with ADHD. Individuals with ADHD were significantly more likely to have the "C" form of the FADS2 gene than the "T" form of the gene at marker 498793 (this number just gives the detailed location on which spot of the DNA this form can be found).

Additionally, it appears that the onset of ADHD stemming from prenatal alcohol exposure may be somewhat genetic as well. For individuals who were exposed to alcohol via maternal consumption during pregnancy, there is some nominal evidence linking "G" allele instead of the "C" allele at two different locations on the FADS1 gene was correlated with a higher likelihood of being diagnosed with ADHD. However, the authors concluded that this connection was only "speculative".

This possible ADHD/genetics/fatty acid consumption/alcohol exposure connection is somewhat intriguing. The study established a strong ADHD connection to a specific allele of the FADS2 gene on the 11th chromosome, and also cited a number of other studies on the effects of omega-3 consumption on ADHD symptoms, but the connections with alcohol are more strained. Nevertheless, the findings from other studies offer support for this possible alcohol association with these other factors:

1. We have seen before that omega-3 fatty acid deficiencies are more prevalent in individuals with ADHD. The previous post describes the process of how omega-3's affect cell membrane integrity, which, in turn, can effect the passage of key chemical signaling agents such as dopamine (which has repeatedly been found to deficient in specific brain regions of ADHD individuals). The desaturase enzymes, which are products of the genes listed above are partly responsible for the process of omega-3 metabolism and incorporation into the cell membranes.



2. Different alleles (alternate forms of a gene) can result in slightly different forms of these enzymes, some of which are more efficient than others. In other words, enzymes coded for by one form of a gene are somewhat better at metabolizing omega-3's and incorporating them into cells than the "alternate" enzymes coded for from the "alternate" forms of the gene. As a result, small changes in the gene code in these aforementioned regions can indirectly affect the efficiency of omega-3-to-membrane incorporation.



3. Several studies have pointed to the the connection between alcohol and fatty acid metabolism in animal models of ADHD.



4. It also appears that an individual may be able to "recover" from some of the negative effects on cognition due to alcohol exposure by an increase in dietary omega-3's. This includes increasing maternal dietary levels of omega-3's during pregnancy (based on animal model studies).
   

To summarize the whole post (as well as the previous one), it appears that omega-3 fatty acid metabolism plays a major role in ADHD. This is thought to be at least in part to the effects of omega-3's on maintaining cell membrane structure and integrity and their effects on regulating levels of the brain signaling agent dopamine (which is a crucial neurotransmitter and is often deficient in ADHD cases). However, properly functioning enzymes are required for these steps. Desaturase enzymes are coded for by a genetically "hot" region for ADHD on the 11th chromosome in humans. Different versions of these genes can result in a reduction in enzyme function and potentially affect the way these omega-3's are metabolized. In mammals, alcohol exposure can also lead to reduced desaturase enzyme activity. Additionally, there is at least some evidence that alcohol can increase the likelihood of specific forms of FADS1 gene giving rise to ADHD. This may be due to the two factors combining to reduce desaturase enzyme activity to a point where omega-3 metabolism falls past a hypothetical "break-point" resulting in a sharp increase in the onset of ADHD and other related disorders.

We have been focusing heavily on the ADHD and alcoholism connection for the past couple of weeks. We will be investigating a few more studies on this connection in the upcoming posts.

ADHD: A Precursor to Alcoholism? (Corpus Callosum part 2)

In the previous blog post on ADHD and alcoholism, we investigated some of the signs of overlap between the two disorders. One factor which both disorders appear to share in common is a reduction in volume of specific brain regions, including the corpus callosum, the genu, and the isthmus, when compared to similar individuals who do not exhibit either of the symptoms of ADHD or alcoholism. For a generalized location of these brain regions, please see the diagram below (which is a reprint of the figure from the last blog entry):

The corpus callosum is the tan band located inside of the gyrus cinguli, also known as the cingulate gyrus, a brain region whose role in ADHD we have discussed previously. The isthmus region is relatively small and is not labeled on this diagram. It is located to the right of the label "corpus callosum", and is just to the left of the area labeled "splenium".

**Please note my use of nomenclature here, I am continuing to use the same labeling as I did in the previous post. Here, we are considering the "genu" and "isthmus" as separate, distinct regions from the corpus callosum due, in part, to how they were classified in the studies I have been reviewing. However, many professionals label them all as one entity, with the genu and isthmus serving as sub-sections of the corpus callosum as a whole.

In today's blog, we will discuss the answers to two key questions:

1. Is there a hereditary factor at play for the size abnormalities for these three brain regions?


2. Does the outward expression of symptoms for one of these two disorders predate the other? In other words, is the appearance of ADHD symptoms a warning sign of impending alcohol abuse (or vice versa)?

For the answer to the first question, we turn to a journal article by Venkatasubramanian and coworkers in the journal Psychiatry Research: Neuroimaging. This group found that the relative size of the corpus callosum, genu and isthmus regions of the brain were correlated to an individual being at "high-risk" or "low-risk" for alcohol abuse. In this study, the "high-risk" group had a statistically significant reduction in size of multiple brain regions when compared to the "low-risk" group.

For comparison purposes, the "high-risk" group had approximately:

• a 9% reduction in corpus callosum volume
• a 13% reduction in the volume of the genu, and
• a 17% reduction in isthmus volume when compared to the low-risk group for these brain regions.

**Note: it worth mentioning that the comparative differences in relative brain sizes followed some sort of age-dependent trend. The subjects of study were boys and young men between the ages of 9 and 23. For the age 9-15 group, all three of the above brain regions were smaller. However, for the older group (over 15), only the isthmus region had a statistical size difference between the "high-risk" and "low-risk" groups. This suggests that either the isthmus region follows a much greater developmental delay in individuals identified as being "high-risk" for alcohol dependence than do the corpus callosum or the isthmus region never does fully "catch up" in size to the "low-risk group"

So what exactly constitutes "high" and "low" risk? In this study, the researchers studied males between the ages of 9 and 23 (sampling a relatively even distribution across this age range) who had male parents who both:

1. Developed an alcohol dependence before the age of 25 (average age of dependence around 20)
2. At least two relatives (first-degree), who also had alcohol dependence (average was 3 relatives).

The "low-risk" control group of children and young adults consisted of individuals whose parents were not diagnosed with alcoholism or any other psychological disorders. To ensure that maternal genetic influences were not a factor, none of the mothers of the children (the 9 to 23 year-old group) in the study were diagnosed with alcohol abuse.

This study is of potential interest. While the sample size was small (only 20 "high-risk" and 20 "low-risk"), the choice of following only male parents and male children offered some clear-cut advantages over other similar studies. Among them were:

• It eliminated gender effects. While debatable, some studies have found brain regions like the corpus callosum to be larger in males than in females. Having an all-male study eliminated this potential factor.


• The ages of the two groups (high and low risk) followed similar distribution patterns, to rule out size increases in these brain regions due to aging.


• Since the alcoholism was restricted to the paternal side, physiological effects during pregnancy were eliminated. This is important, as several studies have shown that maternal alcohol consumption during pregnancy can affect the development process including relative sizes of these brain regions. In other words, confounding effects, such as fetal alcohol syndrome were significantly reduced, since none of the mothers in the study suffered from clinical alcohol abuse.


• None of the 9 to 23 year-old test subjects had already developed an alcohol dependence. This eliminates the effects that chronic alcoholism has on reducing the size of the corpus callosum, as reported in recent studies.


• Other than alcoholism for fathers of the "high risk" group, none of the parents of the study participants had any other psychological disorder. This is important, especially due to the effects of comorbidity (disorders or symptoms occurring alongside alcoholism, such as conduct disorders or abuse of other substances) on worsening the symptoms of alcoholism.

So how does ADHD tie in to all of this?

Based on this study's findings, it appears that the expression of ADHD (as well as other "externalizing symptoms", which are symptoms that can be seen outwardly, such as hyper-excitability, conduct disorders, substance abuse, etc.) may be a warning sign of impending alcohol abuse.

For example, it has been postulated that hyperexcitability, which is often seen in individuals with ADHD (especially of the hyperactive-impulsive or combined subtypes) is a genetic precursor to alcohol dependence. In this case, and ADHD-like trait predates alcohol abuse. In other cases, symptoms such as substance abuse, conduct disorders, impulse control problems and other antisocial behaviors have grouped under the umbrella term generalized disinhibitory complex. Here, these numerous symptoms are essentially "clumped together" as one generalized behavior.

Regardless of the "model" one subscribes to, please keep in mind that a reduction in size the corpus callosum, genu and isthmus regions of the brain have been associated with ADHD.

Additionally, the degree of overlap between the two disorders was definitely worth mentioning. Out of the 20 children and young adults of the "high-risk" group, 17 of them were diagnosed with ADHD. Out of the 20 "low-risk" children? Zero.

Keep in mind that the fathers of the high-risk group were not diagnosed with any other disorders, just alcoholism. Additionally, keep in mind that none of the high-risk children had developed an alcohol dependence as of yet. These facts give compelling evidence that fathers who suffer from early-onset alcohol dependence who are not even ADHD themselves, are much more likely to have male children with ADHD, with an onset which precedes alcohol dependence itself.

In essence, this study established a degree of linkage (but not necessarily a direct cause) between the expressed behaviors of ADHD and alcoholism and the physiological features of relative sizes of the isthmus, corpus callosum and genu.

Hopefully this provides evidence that there is in fact a strong underlying hereditary component surrounding both disorders of ADHD and alcoholism. In the next couple of posts, we will investigate some of the individual genes thought to be involved in both of these disorders.

ADHD and Alcoholism: The Corpus Callosum (part 1)

In our last post, we discussed some of the ties between ADHD and eating disorders such as bulimia. In this post, we will begin the first of a multi-part investigation on the connection between ADHD and alcoholism. In this session, we will see how these two disorders are both tied to improper function in a key brain region known as the corpus callosum.

Note the relative position of the corpus callosum in the diagram below (source of image here):

A quick aside: Note the proximity of this corpus callosum brain region to the cingulate gyrus (labeled "Gyrus cinguli" in the diagram above), a region which we discussed in a recent post on attentional control. The cingulate region can be thought of as the brain's "gear shifter". If underactive, it leads to consistent lack of focus on one thought or task (a hallmark characteristic of ADHD), if overactive, the cingulate can result in overfocus (a characteristic of obsessive compulsive disorder, or OCD).

Returning to the corpus callosum area of the brain, which is layered inside the cingulate gyrus, we can see some sub-regions of note. These include the genu and the splenium. There is also a small region (not listed on the diagram above), called the isthmus, which is just to the left of the splenium. Of these regions, pay close attention to the isthmus, genu, and corpus callosum.

Note: the classification of these brain region sometimes varies, some methods classify the isthmus and genu as part of the corpus callosum, while others group them as seperate elements. No need to get any further into specifics, but when I refer to "corpus callosum" in the context of this post, I am referring to the region distinct from the isthmus, genu and splenium.

The corpus callosum is primarily responsible for connecting and integrating information from the left and right hemispheres of the brain. It is composed of millions of individual fibers and is necessary for the integration and processing of sensory information and expressing this information through verbal language. This is one of the later-developing regions of the brain, and continues to develop and become more efficient during adolescence (and even into early adulthood). Studies have shown that this prolonged developmental process leaves brain regions like the corpus callosum more prone to improper development. One of the reasons young children have trouble expressing visual images verbally is because speech control is typically on the left side of the brain and visual imaging and imagination is typically on the right.

Improper development of this corpus callosum region can lead to quirks such as split brain. Additionally, it has been reported that development of this brain region can be impeded by prenatal alcohol exposure and is entirely missing in around seven percent of children with fetal alcohol syndrome. Additionally, chronic alcohol abuse can result in thinning in the corpus callosum region.

In addition to the inhibition of this key brain region due to alcohol exposure listed above, it appears that there may be an underlying factor at play for this region for both ADHD and alcoholism. A reduction in size in the corpus callosum, genu and isthmus has been associated with ADHD in both children and adults. A study done by Venkatasubramanian and coworkers found a connection between smaller volumes in these same three regions of the brain and an increased risk of developing alcoholism.

Note that a reduction in size of the corpus callosum has been linked with a decreased functional ability in this region as well. This includes the processing of information between the left and right hemispheres of the brain in processes such as integrating information of visual images obtained from both eyes.

In addition to its role in expressing and processing ideas and thoughts from both sides of the brain, the corpus callosum is also integral in coordinating movements in different parts of the body. This includes governing motor inhibition (restricting unwanted or inappropriate movements) across the body. Interestingly, individuals with ADHD have been shown to have a decreased ability in utilizing the corpus callosum to control movements, which is often tied to the impulsive behavior of ADHD individuals with their actions (such as constantly grabbing or playing with objects at inappropriate times).

The corpus callosum is not the only brain region thought to be involved with both ADHD and alcoholism. For example, the prefrontal cortex (the brain region behind the forehead), which we have discussed extensively in other posts, has repeatedly been found to be underactive for individuals with ADHD. Additionally, Schweinsburg and coworkers found a decrease in activation of the prefrontal cortex correlates with a higher risk in suffering from alcoholism.

In the next few posts, we will examine some of the genes thought to be underlying factors in both ADHD and alcohol abuse. Additionally, we will examine some of the numbers to get a better understanding of the magnitude of overlap between the two disorders. Finally, we will examine some of the "warning sign" behaviors which youngsters might display before the onset of alcoholism occurs.

However, in the next entry, we will examine whether there is a hereditary factor in place surrounding brain volume, as well the prevalence of expressed outward symptoms of ADHD, and how these are both associated with an increased risk in developing alcoholism later in life.