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.
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.