Does ADHD improve your sense of smell?

Due to a high degree of overlap in symptoms with other disorders, finding accurate ways of differentiating ADHD is of utmost importance. Based on a recent study by Romanos and coworkers, it appears that individuals with ADHD may be able to "sniff out" their disorder. In a publication on Improved Odor Sensitivity in ADHD, Romanos and others found that children with ADHD had significantly better sensitivity for particular odors when compared to their non-ADHD peers. In other words, children with ADHD may be able to better detect minute or trace levels of certain smells when compared to other children. As an interesting aside, the study noted that boys actually had a slight advantage as far as odor detection when compared to girls (which goes against many other study findings which indicate that females have better senses of smell).

However, when these children were investigated in two other "smell" categories, which included discrimination between different smells, and the actual identification of particular agents causing the smell, they should no advantages over their non-ADHD peers. Similar studies have also been done on adults with ADHD, and have shown little to no effect between ADHD and sense of smell. These findings seem to agree with another recent report on olfactory impairments in children with ADHD. This study found that children with ADHD were worse at identifying the nature of particular odors than non-ADHD children. It appears that these deficits are tied to a specific brain region called the orbitofrontal region, the outer section which is approximated by the green region in the diagram below (original file source can be found here). Note that this region has numerous implications with regards to the disorder of ADHD.

To throw another wrinkle into the mix, it appears that stimulant medication treatments for ADHD may negate these olfactory advantages (with regards to the increased ability of ADHD children to detect minute levels of odors better than their peers). The Romanos study also investigated another group of similar age and gendered individuals with ADHD who were on the medication methylphenidate (Ritalin, Concerta, Daytrana, etc.). Like the non-medicated ADHD children, this group all had the combined subtype of ADHD (meaning that both hyperactive/impulsive as well as inattentive symptoms were present to a large extent). They found that the medicated children did not have the improved smell sensitivity that their non-medicated ADHD peers did, but rather had an odor detectability level similar to that of the non-ADHD group. In other words, it appeared that methylphenidate (as well as other ADHD stimulant medications, potentially), may offset any improvements in smell detection in ADHD individuals.

It is believed that the dopamine system and pathways play a critical role in smell differences between ADHD children and their peers. Keep in mind that methylphenidate and most other stimulants for ADHD work by increasing the concentration of the neurotransmitter dopamine in the areas between neuronal cells, by reducing the transport of this important brain chemical into the cells themselves (individuals with ADHD often have an imbalance between the dopamine levels inside and outside of these neurons, and often have insufficient dopamine levels in the surrounding areas outside the neuron cells). Dopamine levels have been shown to have a protective effect on olfactory neurons (neurons related to smell). Chemical alterations of dopamine levels, such as those introduced by methylphenidate or other ADHD stimulants may therefore interfere with odor sensitivities in key regions of smell such as the olfactory bulb region of the brain.

On a final note, the findings by Romanos and coworkers are of potential interest because of the fact that many neuropsychiatric disorders are accompanied by a sharp decrease in odor detection and sense of smell. These include Parkinson's Disease, obsessive-compulsive disorder (OCD), schizophrenia, autism, and depression. Because of this, it may be possible to use odor sensitivity tests to help differentiate between ADHD and other neuropsychiatric disorders, at least in children. Although we have seen that there is some conflicting evidence surrounding studies, it appears that we could, at least in theory, administer some type of smell test of trace levels of specific odorous chemical agents that are undetectable to the majority of the child population and see whether the potential ADHD candidate could detect these minute traces. Furthermore, it would be interesting to see whether other stimulant medications besides methylphenidate have the same effects on curbing the increased odor sensitivities exhibited in ADHD children.

Do ADHD Stimulant Drugs Stunt Growth?

Here are seven questions or factors we need to address to assess the validity of studies on ADHD stimulant medications and their effects on growth:

1. Is there a history of prior stimulant medication use? Surprisingly, a number of studies on the inhibitory effects of ADHD stimulant medications either neglect or downplay the fact that children in their studies had a previous history of stimulant medication usage for their conditions. This can seriously confound effects, for if a child was taking a stimulant medication previously, he or she may still be on track for a lower baseline growth rate. Furthermore, if a child was taken off stimulant medications recently, there remains the possibility that his or her system is beginning to play "catch-up" by displaying a greater-than-normal increase in growth following a medication "holiday". In either case, baseline readings are skewed, and these effects muddy the accuracy of current stimulant medication studies on growth effects. Poulton and Nanan make this observation in their article on prior treatments with stimulant medication and growth in children with ADHD. They go on to say that growth is an accurate indicator of prior treatment with stimulant medication.
   
   
2. Beware of the pretreatment bias with regards to effectiveness of stimulant medications: Poulton and Nanan also warned about the natural bias of individuals with a previous treatment history of stimulants in that they have already proven to have a greater tolerance to potential side effects (otherwise they would have likely discontinued earlier stimulant treatments) and an overall higher levels of compliance and positive response to stimulant medications. This too, can give a potential "false positive" with regards to evaluating the effectiveness of current stimulant medication treatments for ADHD.
   
   
3. Do untreated children and adolescents with ADHD have different growth patterns than non-affected children? This is also a much-neglected consideration. Spencer and coworkers performed a study in which they saw a slower growth rate in the earlier years for children with ADHD, which was followed by a significantly later "catch" up period. In other words, compared to non-ADHD children, individuals with ADHD may be more predisposed to being "late bloomers", even when they are unmedicated. This potential difference in growth patterns between ADHD'ers and non-ADHD'ers, while still highly debatable, should at least raise the question as to whether delays in growth patterns for medicated individuals with ADHD can actually be attributed to the medications or to the nature of the disorder itself (or a combination of both).
   
   
4. Do "drug holidays" work? This is actually comprised of several questions and considerations. It is not uncommon for parents or prescribing physicians to allow for "drug holidays" for unmedicated ADHD children. These holidays can vary from a few days to longer periods such as an entire summer vacation. If the period of these drug holidays is long enough, such as in a summer-long study by Gittleman-Klein and coworkers on methylphenidate and growth, significant changes may be seen. This study saw a relative increase in weight but not in height following a summer off of medication of the stimulant methylphenidate (Ritalin). Of potential interest was the observation that following a second holiday from medication the following summer, a relative increase in height but not in weight was observed. It is entirely possible that the duration and frequency of drug holidays may effect the two parameters (height and weight) in slightly different fashions. Another article by Poulton suggests the possibility that height gains may take longer to remedy because gains in weight may drive subsequent growth in height.
   
   
5. Does the type of stimulant medication make a difference? In a preliminary sense, it appears that the answer would be "yes". For example, it appears that the stimulant drug dexamphetamine (d-amphetamine, also called by common name Dexedrine) has a greater inhibitory effect on growth during the first year of treatment than does methylphenidate (Ritalin, Concerta, Daytrana).
   
   
6. What is the typical extent of growth impairments due to stimulant medications? We need to be careful on this one, especially with regards to some of the earlier factors and considerations mentioned above. Nevertheless, a review of the literature seems to indicate a relative deficit in growth of around 1 cm per year for up to about 3 years which can be attributed to stimulant medication treatment. Furthermore, it appears that weight may be even more affected than height due to stimulant medication treatment, although it also appears that weight differences are easier to remediate than height differences and therefore pose less of a concern.
   
   
7. Are the growth changes due to stimulant medication temporary or permanent? Although hotly debatable, it appears that growth impairments due to prescribed stimulant medication usage is more of a short-term effect. A follow-up study of medicated ADHD children into adulthood indicated that even at moderately-high doses of the stimulant medication methylphenidate (45 mg/day average), medicated children with ADHD eventually reached normal final heights when compared to controls. It is worth mentioning, however, that these children eventually discontinued their medications. It is unclear as to what the effects may have been had they continued on with the methylphenidate usage into adulthood (especially since there has been a sharp trend towards continuing stimulant medication treatment into adulthood for adult ADHD).

Ritalin vs. Cocaine: Addiction Potential of Methylphenidate

If you were to read the opening couple of pages of most natural or alternative treatment books on ADHD, you would likely find some version of the following argument: "Ritalin is chemically similar to cocaine and amphetamines and studies have shown it has a high addiction potential". There actually is a fair amount of truth to that statement, but the latter half leaves out some equally important information concerning the nature of these studies.

This post is not meant to be a pro-stimulant drug message, I certainly do see some apparent risks for many ADHD medications, especially concerning young children and their developing nervous systems. However, I also feel that we should carefully examine the nature of many of these "anti-methylphenidate" studies and evaluate the relevancy of their findings. To facilitate this discussion, I have taken data from a serious of research articles on the topic of habit-forming potentials of methylphenidate (Ritalin, Concerta, Daytrana, etc.) and have attempted to box together some of the overlapping information with relevant conclusions that are, to the best of my ability, as unbiased as possible. Here are some key points worth noting:

• Chemical similarity to cocaine and amphetamines. The chemical structure of methylphenidate is given below. As a comparison, the structure of methamphetamine is also given. I realize that the majority of readers here are not organic chemists, so I have highlighted the similar regions of the two molecules (which is a relatively big overlap as far as chemical structure and function is concerned). The purple/red regions below highlight chemically similar regions between the two drugs, while the green/blue areas show chemical differences. For brevity and simplicity, I have not included the structure of cocaine, because there are fewer obvious similarities between the chemical structures of methylphenidate and cocaine. Just realize that there are chemical and functional similarities between the two drugs.

• A huge factor in a drug's addiction potential rests on how fast the drug can both enter and leave the brain. In short, the faster the entry and the faster the clearance of the drug from the brain, the greater the "high" and the greater the addiction potential. We have seen this before in earlier posts, such as the one on Vyvanse for ADHD treatment. The chart below summarizes some of the key comparisons between methylphenidate and cocaine (most of the data comes from studies by Volkow and coworkers on brain entry and clearance times of cocaine vs. methylphenidate:

We can see from the chart above that cocaine and methylphenidate show similarly quick routes of entry into the brain when administered intravenously (note that this is not the typical route for taking methylphenidate for ADHD patients). However, note that the clearance time from the brain is significantly longer for methylphenidate than cocaine (half-life is a common measuring tool, which refers to the amount of time it takes for half the drug to clear the system). Also note that when methylphenidate is taken in the appropriate manner (orally), the time to arrive at a peak concentration (based on a mammalian model) is significantly longer as well. Both the longer clearance time and times to peak concentrations play a crucial role in reducing the involved "high" and addiction potential for methylphenidate, when compared to drugs such as methamphetamines and cocaine.

• The type of methylphenidate administered may also play a role in the addiction potential. There is a general trend towards prescribing longer-lasting sustained release versions of methylphenidate over the original immediate-release version (although cost is also a factor, with the longer-release versions typically carrying a higher price tag). At the 20 and 40 mg levels, one study showed that the immediate-release version of methylphenidate produced a higher degree of addictive level effects than the longer-release version, although this was based on more qualitative subjective measurements than hard, concrete numerical data.

• On somewhat of an interesting note, it appears that the reinforcing effects of methylphenidate may be much more pronounced in the case of sleep deprivation. One study indicated that methylphenidate only produced reinforcing effects when study participants were limited to 4 hours of sleep the previous night. Given the fact that sleep problems and disturbances are remarkably common in individuals with ADHD, this may actually lend a fair amount of support to potential for abuse among ADHD individuals. However, I personally believe that, based on the other points regarding individuals with ADHD, this population is still relatively "safe" from stimulant medication abuse when the medication is administered and taken in a proper manner.

• We have spoken extensively on the role of Dopamine Transporter (DAT) proteins and their role on governing levels of dopamine, a key neuro-signaling agent which is thought to be critically involved with regards to the onset and symptoms of ADHD. In short, DAT proteins are responsible for shuttling dopamine into and out of neuronal cells and maintaining an overall balance of this important chemical. Individuals with ADHD are thought to have more of these DAT proteins in their brain systems, which results in lower levels of dopamine in the areas between nerve cells, a phenomena which is commonly seen in cases of ADHD and related disorders. DAT proteins are therefore common targets of many ADHD stimulant drugs, which typically act by binding to these DAT proteins and reduce their shuttling effects, which, in turn, helps restore higher dopamine levels in these key regions between nerve cells. It is hypothesized that drugs, even at low doses (such as 20 mg methylphenidate) which bind to and saturate these DAT proteins may contribute to some of the "high" associated with these drugs. However, other findings have contradicted this, with regards to the role of the DAT proteins on "highs" associated with stimulant medications such as methylphenidate.

• Finally, in what may be the most important piece of the puzzle with regards to addictions and ADHD stimulant medications, there was a review done by Kollins which examined the nature of pre-existing studies on the abuse potential of methylphenidate. Kollins noted that a large number of the studies which suggested high addiction potentials for methylphenidate and related subjects gathered their data from non-ADHD individuals. This is important to note, especially considering some of the aforementioned differences between ADHD individuals and non-ADHD individuals with regards to chemical balances (such as the dopamine levels) and hard-wiring issues (such as a higher density of Dopamine Transporter Proteins or DAT's in individuals with ADHD). While this should not be grounds for immediate dismissal of these findings, the lack of studies on actual ADHD patients should raise some serious questions as to whether methylphenidate deserves its "guilty" label with regards to addiction potential. Of course, these studies provide ample evidence to support the assertion that ADHD medications such as methylphenidate can be abused if they are taken by the wrong individuals (non-ADHD patients, such as healthy individuals with few to no signs of ADHD as well as generalized drug abusers), but there appears to be an overall lack of evidence to support the claim that needy patients who do suffer from ADHD will turn into stimulant abusers if they begin to take methylphenidate at prescription-based levels.

• Kollins does conclude with some more relevant (at least in this blogger's opinion) concerns surrounding the use of methylphenidate for ADHD. He questions the impact of methylphenidate and related drugs with regards to:

1. Their impact on brain development, especially in young children (a topic in which there is still relatively little conclusive data available).
2. How dopamine level changes due to these medications may alter the dopamine system, including the levels of dopamine transporter proteins (DAT proteins).
3. The role of early stimulant exposure on latter stimulant abuse (although Kollins notes that early treatment with appropriate stimulants may actually have a protective effect against latter stimulant abuse).

For the most part, I am in agreement with this line of thinking. It is my opinion that we should shift our focus away from the fears of addiction potentials with regards to stimulant medications taken via appropriate doses and methods for ADHD and related disorders, and instead shift our attentions to the effects of these substances on the developing nervous systems of young children. We have seen that methylphenidate has several built-in safety measures with regards to reducing its abuse potential. Furthermore, I personally believe that there are much greater potential risks of stimulant medications with regards to their effects on the critical early neural developmental stages (such as those in the first 5 years of life) than to overall addiction potentials of these substances, and that our research focuses with regards to overall safety of these medications should shift in this direction.

Genes and Low Birth Weight Combine to Increase Risk of Conduct Problems Alongside ADHD

In the past, we have investigated the role of the COMT gene and its effects on the onset and severity of ADHD cases. Now it appears that this gene may play a role not only in the ADHD itself, but conduct or behavior disorders which often occur alongside (or are comorbid to) of ADHD.

Recall from earlier posts that COMT (which is short for Catechol O-Methyltransferase) refers to both a gene and an enzyme protein encoded by the gene, which is responsible for maintaining a balance of neurotransmitters such as dopamine in key regions of the brain. In essence, the COMT enzyme is responsible for breaking down levels of free dopamine in the prefrontal cortex region of the brain (the area highlighted in orange). Keep in mind that in another key brain region, called the striatum, another series of enzymes called the dopamine transporter (DAT) proteins play a greater regulatory role in maintaining dopamine levels. However, in the prefrontal cortex region of the brain (see area below), the COMT gene and COMT enzymes play a much greater role in regulating the balance of key neurotransmitters necessary for communication between brain cells.

The prefrontal cortex region of the brain is approximated by the area in orange in the figure above. Note that we are looking from the left side of the brain of an individual facing to his or her left. The numbering system refers to a subseries of brain regions from which this original figure was taken.

As a reference, the striatum region of the brain can be seen in the green areas of the figure below (original file source here):

Returning to our discussion on the COMT gene and the prefrontal cortex region of the brain, it is important to note that there are two main "flavors" of this gene and subsequent enzyme, the "Val" and the "Met" (I've mentioned previously in other posts what "Val" and "Met" stand for, but as a quick summary: "Val" is short for valine, and "Met" is short for methionine, both of which are common amino acids found in almost every protein in our bodies. However, these two amino acids exhibit slightly different biochemical properties, and a simple substitution of one for the other can actually result in significant changes as to how a protein functions. For the COMT enzyme, which is a special type of protein, the simple change from a "Val" to a "Met" or vice versa can actually dictate how efficient the whole enzyme becomes). COMT enzymes comprised of the "Val" form are actually 3-4 times more efficient at breaking down dopamine in key brain regions such as the prefrontal cortex, which results in overall lower levels of neurotransmitters such as dopamine.

Since individuals with ADHD are often deficient in free levels of dopamine in the prefontal cortex region of the brain, having the "Val" form of the COMT gene often poses a greater risk of exhibiting ADHD behavior. We have seen the effects of this Met/Val difference with regards to cognitive tasks and even the effects of these different gene forms on the onset of alcoholism-related ADHD symptoms. For example, on a post on gene variations and attentional control, we saw that individuals with the "Met" form of the gene (and enzyme) had improved attention-related control than those with the "Val" form.

With regards to conduct disorders comorbid to ADHD, it also appears that the lower dopamine levels associated with the "Val" forms of these enzymes is also a major determining factor in the childhood onset of anti-social behavior and conduct disorders. Furthermore, it appears that environmental factors and this "Val" form genetic factor can actually interact and combine, to increase the risk of an individual with ADHD in developing some sort of conduct problem to go alongside his or her ADHD symptoms.

Low birth weight, which has a number of implications for other disorders, was found to be a good indicator of childhood conduct problems appearing alongside of ADHD in its own right. It is believed that low birth weight is a good indicator of a poor prenatal environment, which is why so many disorders and developmental issues are often associated with low birth weights. Statistically, it was noted that children with low birth weights (less than 2.5 kilograms or 5.5 pounds) were at an increased risk of developing co-existing behavioral problems (conduct disorders) alongside of an ADHD diagnosis. As mentioned before, individuals who were unfortunate enough to have one or more copies of the "Val" version of the COMT gene plus a low birth weight, were statistically more likely to exhibit problems associated with conduct-related disorders.

As a quick reference to the severity of the effects of low birth weight and the "Val" version of the COMT gene, please consult the table below. This data was taken from an article by Thapar and coworkers on the effects of COMT genes and low birth weight on the onset of antisocial behavior in children with ADHD.

Notes on the table above: Relative Conduct Symptom Score refers to the severity of conduct problems which are given a numerical value (higher being more problems). I have assigned the first group a value of 1 as a reference. This refers to individuals who have at least one copy of the "Met" (which, in the cases of ADHD appears to be the "good") form of the COMT gene and enzyme, as well as a normal birth weight. As we can see from the table, having either a low birth weight or both copies of the "Val" (the "bad" form of the COMT gene with regards to ADHD) form resulted in a roughly 50% increase in symptoms of conduct or behavioral problems. However, for individuals who possessed both "Val" forms of the COMT gene and enzyme and had a low birth weight, we can see that conduct symptoms associated with ADHD shot up to over three times the original level. This at least suggests that while both genes and developmental environments can play a significant role in the onset of behavioral problems associated with ADHD, it is when these two factors are combined, that remarkable differences in symptoms begin to appear. In other words, strong gene-environment interactions are associated with antisocial behaviors in individuals with ADHD.

Keep in mind that these findings are somewhat inconclusive. Another research group performed a similar experiment, but was unable to replicate these findings which associated low birth weight and the "Val" form of the COMT genes to an increase in antisocial behavior in children with ADHD. Nevertheless, an additional study tied the presence of "Val" forms of the COMT gene to increased aggressiveness, conduct problems, and criminal behavior in individuals with ADHD. Although the information and conclusions from different studies on these topics remains controversial, the fact that the "Val" form of the COMT gene has been implicated in so many other deficits associated with ADHD, I believe that we should take notice of some of these recent findings.

The term conduct disorder itself has a relatively widespread range of meanings. With regards to ADHD and the content of this post, I consider conduct disorders to include behaviors such as oppositional behaviors towards parents, teachers and other authorities, negative peer interactions, pervasive negative attitudes and interactions towards peers and authorities, and, in more extreme cases, illegal substance abuse, cruelty to animals and other individuals, destruction of property, stealing, and other criminal behaviors (please not that the Thapar article highlighted more of the latter and more severe behaviors on the list when addressing the topic of conduct disorders). Of course, there is a fair degree of ambiguity and a wide range of severity in the behaviors from this list, but I think we can all begin to picture the difference between a child who is merely hyperactive, implulsive and inattentive versus one who has a pervasively antagonistic attitude and behavioral patterns to go along with the classic ADHD symptoms.

The unique thing about antisocial behaviors with regards to ADHD is that they appear to be more genetically heritable than generalized antisocial behaviors, and that ADHD-like hyperactivity can potentiate and worsen the severity of accompanying conduct problems. Furthermore, it appears that children may be much more susceptible to antisocial behaviors arising from damage to the prefrontal cortex than are adults. This article suggests that when two or more factors which each have notable effects on ADHD-related conduct problems or comorbid disorders, the combined effects of two or more of these factors can operate in a synergistic fashion. It is my opinion that many of these genetic and early developmental factors will take on an increasingly powerful role with regards to both the diagnosis and treatment of ADHD and accompanying comorbid disorders such as behavioral and conduct problems.

Cost Effectiveness of ADHD Treatments

In the previous post on the economic impact of ADHD, we examined some of the eye-opening numbers attached to the disorder of ADHD and its impact on society. We reviewed 4-5 publications on the subject, most of which attached an annual price tag of several thousand dollars to the direct and indirect costs of the disorder on individuals with ADHD and their families. These factors included loss of productivity at work (which can be up to almost a full month of the year less than non-ADHD counterparts), medical expenses from the disorder itself, as well as from the increase in risk-taking behaviors of ADHD patients, additional educational expenses, loss of work time for family members, and the increased cost of treatment for substance abuse (which is also much higher in ADHD individuals).

It is important to take these numbers and figures with a grain of salt, and see them more as projections as opposed to actual hard, concrete figures. However, they should begin to give us at least a ballpark estimate of the economic impact that ADHD has on our society. The natural question which should flow from this information is: what is the actual cost of treating ADHD? While the treatment options for ADHD vary immensely from individual to individual and treatment to treatment, a study by Jensen and coworkers has sought to investigate the approximate cost-effectiveness of different ADHD treatments. A summary of this study can be found here. I will highlight some of the key points from the article:

• Cost-effectiveness for ADHD treatment was studied in four different areas: medication treatment, behavioral management treatment, a combined medication/behavioral treatment, and community care-based treatment (this last one would include things like juvenile justice programs, community mental health services, etc) . These data were based off of an original 1999 study on children with ADHD called the MTA Cooperative Group.
• Treatment "effectiveness" was determined by the ability of a particular treatment to bring a child's behavior to a "normal" level. An outcome of "normal" was determined by using a cutoff score determined by a special psychological scale called the SNAP scale, which assigns numbers to behavioral improvements in multiple categories, and is determined by parents, teachers and clinicians. Although somewhat subjective in nature, this scale has been a good indicator of tracking improvements with regards to the disorder of ADHD.
• Different scenarios of ADHD with regards to comorbid (co-existing) disorders were also analyzed. These included both internalizing comorbid disorders (anxiety and depression), externalizing comorbid disorders (which include conduct disorders or oppositional behaviors), as well as a combination of both types of comorbid disorders.
• Costs were determined by average consulting fees of psychiatrists, psychologists and behavioral therapists from the American Medical Association Socioeconomic monitoring system surveys, the approximate costs of prescription drugs based on wholesale prices and common markup values (often around 40%), and wages of behavioral support staffs.
• Out of the different treatment methods available, medication alone provided the most bang for the buck, as far as the most cost-effective measures go. Behavioral therapy was found to be exceedingly costly in terms of its relative effectiveness, and in some cases, actually limited some of the improvements in the overall symptoms. Thus, from a strictly economic standpoint, medication treatment appears to win out as the most cost-effective treatment for ADHD.
• Interestingly, it appears that for children with more internalizing ADHD comorbid symptoms (anxiety and depression), the behavioral treatments were not only more costly, but reduced the overall effectiveness of the medication treatment option, when compared to the medication option alone. This was a bit surprising, and suggests, that behavioral therapy should be considered more for externalizing symptoms (such as oppositional behavior or conduct problems) than for internalizing ones.
• This report was not meant to knock the effectiveness of behavioral treatment for ADHD, it just sought to investigate the cost-effectiveness (or lack thereof) of this type of treatment. However, if cost is not a factor, a combined medication/behavioral treatment program led to much higher rates of "normalizing" childhood behaviors, especially in children who exhibited both internalizing and externalizing comorbid disorders. In other words, for children who have ADHD, anxiety or depression, as well as some type of oppositional behavior, combining medication with therapy can be much more effective than treatment via either medications or therapy alone. However, based on a cost-effectiveness model, for those on a tight budget or with limited resources, the medication treatment option still wins hands-down.
• It is also important to note that community-based care programs, while largely inexpensive, often, unfortunately, have little effectiveness in treating ADHD with or without these side disorders, even though medication managements and behavioral measures are often utilized. This suggests the importance of specialization of professionals outside of basic community resources for dealing with and treating these disorders, which, unfortunately, often carries a heftier price tag. However, the approximate increase in costs of medication management alone (including the cost of a qualified diagnosing professional outside of the typical "community" environment), was relatively small in comparison to the community care model. This again, supports the evidence of the cost-effectiveness of a predominantly medication-based treatment.
• The ineffectiveness of community-based care was explained in part by the relatively lower levels of dosing for medications as well as less follow up (community care physicians often followed up only twice per year in the study, while the individuals on the non-community care based medication treatment plan often got monthly visits).

I realize that some of these findings are confusing to interpret. There were sections of the paper which were difficult to follow at times, but I would just like to hammer home a few personal points with regards to my thoughts on the article:

• Given the pinch most of us are feeling with the economic situation, we want to seek out the best treatments possible for the dollar. Based on this study, it appears that treatment with medication is by far the most cost-effective option.
• If money (or insurance) is less of a problem, there are advantages to utilizing behavioral treatment methods for ADHD. However, based on the findings of the above study, it appears that behavioral treatment on its own is still largely cost-ineffective.
• The one exception to the above point is if a child exhibits both internalizing (anxiety, depression) symptoms and externalizing symptoms (oppositional behaviors or conduct issues) along with his or her ADHD symptoms. It appears that, based on the results of the study listed above, that a combined medication and therapy treatment may be advantageous, although the price still jumps once behavioral management treatments are introduced.
• I realize that the idea of "drugging" our children is inherently wrong in the minds of most individuals. While I personally have a natural bias against this treatment method, I have written extensively about the relative safety and lack of risk factors for most ADHD medications out there today. Given the fact that many of us are feeling the pinch economically, medication treatment is often the only cost-effective option to most people, and this study indicates how cost-effective this treatment method really is.
• By no means is this post meant to downplay the vital role of community-based programs and treatment options out there, for a number of individuals, these programs have been extremely beneficial. Additionally, I know that a number of children exhibit wonderful behvioral changes with regards to their ADHD and related disorders. Nevertheless, the purpose of this review was to simply investigate the cost-effectiveness of these treatment options, and, on the whole, these resources often provide less bang-for-the-buck than medication treatments.
• Finally, I acknowledge that this is just one major study, and that to attach an unquestionable certainty to these findings would be irresponsible. However, we should note that, from the previous post, that the cost of untreated ADHD poses as an enormous economic threat to our society. As a result, all of the measures addressed in the passage above offer at least some degree of advantage over leaving ADHD and its comorbid disorders untreated.

If I can find enough quality studies on the topic, I may post further discussions on the cost effectiveness of different specific medications for ADHD in the near future. In the meantime, we will be returning to more hard-science based articles for the next several posts.