Adult ADHD is a Risk Factor for Broken Bones

Although some people view the impulsivity and inattentiveness of ADHD adults as a normal trait, these symptoms have adverse consequences, which is why doctors consider ADHD to be a disorder. The list of adverse consequences is long and now we can add another: broken bones.   A recent study by Komurcu and colleagues examined 40 patients who were seen by doctors because of broken bones and forty people who had not broken a bone.  After measuring ADHD symptoms in these patients, the study found that the patients with broken bones were more impulsive and inattentive than those without broken bones.  These data suggest that, compared with others, adults with ADHD symptoms put themselves in situations that lead to broken bones.  What could those situations be?  Well, we know for starters that ADHD adults are more likely to have traffic accidents.   They are also more likely to get into fights due to their impulsivity.   As a general observation, it makes sense that people who are inattentive are more likely to have accidents that lead to injuriers.  When we don’t pay attention, we can put ourselves in dangerous situations.  Who should care about these results?  ADHD patients need to know about this so that they understand the potential consequences of their disorder.  They are exposed to so much media attention to the dangers of drug treatment that it can be easy to forget that non-treatment also has consequences.  Cognitive behavior therapy is also useful for helping patients learn how to avoid situations that might lead to accidents and broken bones.    This study also has an important message for administrators how make decisions about subsidizing or reimbursing treatment for ADHD.  They need to know that treating ADHD can prevent outcomes that are costly to the healthcare system, such as broken bones.   For example, in a study of children and adolescents, Leibson and colleagues showed that healthcare costs for ADHD patients were twice the cost for other youth, partly due to more hospitalizations and more emergency room visits.  Do these data mean that every ADHD patient is doomed to a life of injury and hospital visits?   Certainly not.  But they do mean that patients and their loved ones need to be cautious and need to seek treatments that can limit the possibility of accidents and injury.

REFERENCES

Komurcu, E., Bilgic, A. & Herguner, S. (2014). Relationship between extremity fractures and attention-deficit/hyperactivity disorder symptomatology in adults. Int J Psychiatry Med 47, 55-63.

Leibson, C. L., S. K. Katusic, et al. (2001). “Use and Costs of Medical Care for Children and Adolescents With and Without Attention-Deficit/Hyperactivity Disorder.” Journal of the American Medical Association 285(1): 60-66.

Does Acetaminophen use During Pregnancy Cause ADHD in Offspring?

Many media outlets have reported on a study suggesting that mothers who use acetaminophen during pregnancy may put their unborn child at risk for ADHD.   Given that acetaminophen is used in many over-the-counter pain killers, correctly reporting such information is crucial.  As usual, rather than relying on one study, looking at the big picture using all available studies is best.  Because it is not possible to examine this issue with a randomized trial, we must rely on naturalistic studies.

One registry study (http://www.ncbi.nlm.nih.gov/pubmed/24566677) reported that fetal exposure to acetaminophen predicted an increased risk of ADHD with a risk ratio of 1.37.  The risk was dose-dependent in the sense that it increased with increased maternal use of acetaminophen.  Of particular note, the authors made sure that their results were not accounted for by potential confounds (e.g., maternal fever, inflammation and infection).  Similar results were reported by another group (http://www.ncbi.nlm.nih.gov/pubmed/25251831), which also showed that risk for ADHD was not predicted by maternal use of aspirin, antacids, or antibiotics.  But that study only found an increased risk at age 7 (risk ratio = 2.0) not at age 11.  In a Spanish study, (http://www.ncbi.nlm.nih.gov/pubmed/27353198), children exposed prenatally to acetaminophen were more likely to show symptoms of hyperactivity and impulsivity later in life.  The risk ratio was small (1.1) but it increased with the frequency of prenatal acetaminophen use by their mothers.

We can draw a few conclusions from these studies.  There does seem to be a weak, yet real, association between maternal use of acetaminophen while pregnant and subsequent ADHD or ADHD symptoms in the exposed child.  The association is weak in several ways: there are not many studies, they are all naturalistic and the risk ratios are small.   So mothers that have used acetaminophen during pregnancy and have an ADHD child should not conclude that their acetaminophen use caused their child’s ADHD.  On the other hand, pregnant women who are considering the use of acetaminophen for fever or pain should discuss other options with their physician.  As with many medical decisions, one must balance competing risks to make an informed decision.

Find more evidenced-based blogs at www.adhdinaduls.com.

 

 

Do Some Foods Cause ADHD? Does Dieting Help?

If we are to read what we believe on the Internet, dieting can cure many of the ills faced by humans.  Much of what is written is true. Changes in dieting can be good for heart disease, diabetes, high blood pressure and kidney stones to name just a few examples. But what about ADHD?  Food elimination diets have been extensively studied for their ability to treat ADHD.  They are based on the very reasonable idea that allergies or toxic reactions to foods can have effects on the brain and could lead to ADHD symptoms.

Although the idea is reasonable, it is not such an easy task to figure out what foods might cause allergic reactions that could lead to ADHD symptoms.   Some proponents of elimination diets have proposed eliminating a single food, others include multiple foods and some go as far to allow only a few foods to be eaten so as to avoid all potential allergies.  Most readers will wonder if such restrictive diets, even if they did work, are feasible.  That is certainly a concern for very restrictive diets.

Perhaps the most well-known ADHD diet is the Feingold diet (named after its creator).  This diet eliminates artificial food colorings and preservatives that have become so common in the western diet.   Some have claimed that the increasing use of colorings and preservatives explains why the prevalence of ADHD is greater in Western countries and has been increasing over time.   But those people have it wrong.  The prevalence of ADHD is similar around the world and has not been increasing over time.   That has been well documented but details must wait for another blog.

The Feingold and other elimination diets have been studied by meta-analysis.  This means that someone analyzed several well controlled trials published by other people.  Passing the test of meta-analysis is the strongest test of any treatment effect.    When this test is applied to the best studies available, there is evidence that exclusion of fool colorings helps reduce ADHD symptoms.  But more restrictive diets are not effective.  So removing artificial food colors seems like a good idea that will help reduce ADHD symptoms.   But although such diets ‘work’, they don’t work very well.  On a scale of one to 10 where 10 is the best effect, drug therapy scores 9 to 10 but eliminating food colorings scores only 3 or 4.   Some patients or parents of patients might want to this diet change first in the hopes that it will work well for them.  That is a possibility, but if that is your choice, you should not delay the more effective drug treatments for too long in the likely event that eliminating food colorings is not sufficient.  You can learn more about elimination diets from: Nigg, J. T. and K. Holton (2014). “Restriction and elimination diets in ADHD treatment.” Child Adolesc Psychiatr Clin N Am 23(4): 937-953.

Keep in mind that the treatment guidelines from professional organization point to ADHD drugs as the first line treatment for ADHD.  The only exception is for preschool children where medication is only the first line treatment for severe ADHD; the guidelines recommend that other preschoolers with ADHD be treated with non-pharmacologic treatments, when available.  You can learn more about non-pharmacologic treatments for ADHD from a book I recently edited: Faraone, S. V. & Antshel, K. M. (2014). ADHD: Non-Pharmacologic Interventions. Child Adolesc Psychiatr Clin N Am 23, xiii-xiv.

Adult ADHD is a Risk Factor for Broken Bones

Although some people view the impulsivity and inattentiveness of ADHD adults as a normal trait, these symptoms have adverse consequences, which is why doctors consider ADHD to be a disorder. The list of adverse consequences is long and now we can add another: broken bones.   A recent study by Komurcu and colleagues examined 40 patients who were seen by doctors because of broken bones and forty people who had not broken a bone.  After measuring ADHD symptoms in these patients, the study found that the patients with broken bones were more impulsive and inattentive than those without broken bones.  These data suggest that, compared with others, adults with ADHD symptoms put themselves in situations that lead to broken bones.  What could those situations be?  Well, we know for starters that ADHD adults are more likely to have traffic accidents.   They are also more likely to get into fights due to their impulsivity.   As a general observation, it makes sense that people who are inattentive are more likely to have accidents that lead to injuriers.  When we don’t pay attention, we can put ourselves in dangerous situations.  Who should care about these results?  ADHD patients need to know about this so that they understand the potential consequences of their disorder.  They are exposed to so much media attention to the dangers of drug treatment that it can be easy to forget that non-treatment also has consequences.  Cognitive behavior therapy is also useful for helping patients learn how to avoid situations that might lead to accidents and broken bones.    This study also has an important message for administrators how make decisions about subsidizing or reimbursing treatment for ADHD.  They need to know that treating ADHD can prevent outcomes that are costly to the healthcare system, such as broken bones.   For example, in a study of children and adolescents, Leibson and colleagues showed that healthcare costs for ADHD patients were twice the cost for other youth, partly due to more hospitalizations and more emergency room visits.  Do these data mean that every ADHD patient is doomed to a life of injury and hospital visits?   Certainly not.  But they do mean that patients and their loved ones need to be cautious and need to seek treatments that can limit the possibility of accidents and injury.

REFERENCES

Komurcu, E., Bilgic, A. & Herguner, S. (2014). Relationship between extremity fractures and attention-deficit/hyperactivity disorder symptomatology in adults. Int J Psychiatry Med 47, 55-63.

Leibson, C. L., S. K. Katusic, et al. (2001). “Use and Costs of Medical Care for Children and Adolescents With and Without Attention-Deficit/Hyperactivity Disorder.” Journal of the American Medical Association 285(1): 60-66.

Adult Onset ADHD: Does it Exist? Is it Distinct from Youth Onset ADHD?

 There is a growing interest (and controversy) about ‘adult’ onset ADHD. No current diagnostic system allows for the diagnosis of ADHD in adulthood, yet clinicians sometimes face adults, who meet all criteria for ADHD, except for age at onset. Although many of these clinically referred adult onset cases may reflect poor recall, several recent longitudinal population studies have claimed to detect cases of adult onset ADHD that showed no signs of ADHD as youth (Agnew-Blais, Polanczyk et al. 2016, Caye, Rocha et al. 2016). They conclude, not only that ADHD can onset in adulthood, but that childhood onset and adult onset ADHD may be distinct syndromes (Moffitt, Houts et al. 2015).

In each study, the prevalence of adult onset ADHD was much larger than the prevalence of childhood-onset adult ADHD. These estimates should be viewed with caution.  The adults in two of the studies were 18-19 years old.  That is too small a slice of adulthood to draw firm conclusions. As discussed elsewhere (Faraone and Biederman 2016), the claims for adult onset ADHD are all based on population as opposed to clinical studies. Population studies are plagued b the “false positive paradox”, which states that, even when false positive rates are low, many or even most diagnoses in a population study can be false.

Another problem is that the false positive rate is sensitive to the method of diagnosis.  The child diagnoses in the studies claiming the existence of adult onset ADHD used reports from parents and/or teachers but the adult diagnoses were based on self-report.  Self-reports of ADHD in adults are less reliable than informant reports, which raises concerns about measurement error.   Another longitudinal study found that current symptoms of ADHD were under-reported by adults who had had ADHD in childhood and over-reported by adults who did not have ADHD in childhood (Sibley, Pelham et al. 2012).   These issues strongly suggest that the studies claiming the existence of adult onset ADHD underestimated the prevalence of persistent ADHD and overestimated the prevalence of adult onset ADHD.  Thus, we cannot yet accept the conclusion that most adults referred to clinicians with ADHD symptoms will not have a history of ADHD in youth.

The new papers conclude that child and adult ADHD are “distinct syndromes”, “that adult ADHD is more complex than a straightforward continuation of the childhood disorder” and that that adult ADHD is “not a neurodevelopmental disorder”. These conclusions are provocative, suggesting a paradigm shift in how we view adulthood and childhood ADHD.   Yet they seem premature. In these studies, people were categorized as adult onset ADHD if full-threshold ADHD had not been diagnosed in childhood. Yet, in all of these population studies there was substantial evidence that the adult onset cases were not neurotypical in adulthood (Faraone and Biederman 2016). Notably, in a study of referred cases, one-third of late adolescent and adult onset cases had childhood histories of ODD, CD and school failure (Chandra, Biederman et al. 2016). Thus, many of the “adult onsets” of ADHD appear to have had neurodevelopmental roots.

Looking through a more parsimonious lens, Faraone and Biederman (2016) proposed that the putative cases of adult onset ADHD reflect the existence of subthreshold childhood ADHD that emerges with full threshold diagnostic criteria in adulthood. Other work shows that subthreshold ADHD in childhood predicts onsets of the full-threshold ADHD in adolescence (Lecendreux, Konofal et al. 2015). Why is onset delayed in subthreshold cases? One possibility is that intellectual and social supports help subthreshold ADHD youth compensate in early life, with decompensation occurring when supports are removed in adulthood or the challenges of life increase. A related possibility is that the subthreshold cases are at the lower end of a dimensional liability spectrum that indexes risk for onset of ADHD symptoms and impairments. This is consistent with the idea that ADHD is an extreme form of a dimensional trait, which is supported by twin and molecular genetic studies (Larsson, Anckarsater et al. 2012, Lee, Ripke et al. 2013).  These data suggest that disorders emerge when risk factors accumulate over time to exceed a threshold.  Those with lower levels of risk at birth will take longer to accumulate sufficient risk factors and longer to onset.

In conclusion, it is premature to accept the idea that there exists an adult onset form of ADHD that does not have its roots in neurodevelopment and is not expressed in childhood. It is, however, the right time to carefully study apparent cases of adult onset ADHD to test the idea that they are late manifestations of a subthreshold childhood condition.