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May 17, 2021
There are several very effective drugs for ADHD, and those treatment guidelines from professional organizations view these drugs as the first line of treatment for people with ADHD. The only exception is for preschool children where medication is only the first line of treatment for severe ADHD; the guidelines recommend that other preschoolers with ADHD be treated with non-pharmacologic treatments, when available. Despite these guidelines, some parents and patients have been persuaded by the media or the Internet that ADHD drugs are dangerous and that non-drug alternative are as good or even better. Parents and patients may also be influenced by media reports that doctors overprescribe ADHD drugs or that these drugs have serious side effects. Such reports typically simplify and/or exaggerate results from the scientific literature. Thus, many patients and parents of ADHD children are seeking non-drug treatments for ADHD. What are these non-pharmacologic treatments and do they work? My next series of blogs will discuss each of these treatments in detail. Here I'll give an overview of my evidenced-based taxonomy of non-pharmacologic treatments for ADHD described in more detail in a book I recently edited (Faraone, S. V. &Antshel, K. M. (2014). ADHD: Non-Pharmacologic Interventions. Child Adolesc Psychiatry Clin N Am 23, xiii-xiv.). I use the term "evidence-based" in the strict sense applied by the Oxford Center for Evidenced Based Medicine (OCEBM; http://www.cebm.net/). Most of the non-drug treatments for ADHD fall into three categories: behavioral, dietary, and neurocognitive. Behavioral interventions include training parents to optimize methods of reward and punishment for their ADHD child, teaching ADHD children social skills, and helping teachers apply principles of behavior management in their classrooms. Cognitive behavior therapy is a method that teaches behavioral and cognitive skills to adolescent and adult ADHD patients. Dietary interventions include special diets that exclude food coloring or eliminate foods believed to cause ADHD symptoms. Other dietary interventions provide supplements such as iron, zinc, or omega-3 fatty acids. The neurocognitive interventions typically use a computer-based learning setup to teach ADHD patients cognitive skills that will help reduce ADHD symptoms. There are two metrics to consider when thinking about the evidence base for these methods. The first is the quality of the evidence. For example, a study of 10 patients with no control group would be a low-quality study, but a study of 100 patients randomized to either a treatment or control group would be of high quality and the quality would be even higher if the people's rating patient outcomes did not know who was in each group. The second metric is the magnitude of the treatment effect. Does the treatment dramatically reduce ADHD symptoms, or does it have only a small effect? This metric is only available for high-quality studies that compare people treated with the method and people treated with a 'control' method that is not expected to affect ADHD. I used a statistical metric to quantify the magnitude of the effect. Zero means no effect, and larger numbers indicate better effects on treating ADHD symptoms. For comparison, the effect of stimulant drugs for ADHD is about 0.9, which is derived from a very strong evidence base. The effects of dietary treatments are smaller, about 0.4 to 0.5, but because the quality of the evidence is not strong, these results are not certain and the studies of food color exclusions apply primarily to children who have high intakes of such colorants. In contrast to the dietary studies, the evidence base for behavioral treatments is excellent, but the effects of these treatments on ADHD symptoms are very small, less than 0.1. Supplementation with omega-3 fatty acids also has a strong evidence base, but the magnitude of the effect is also small (0.1 to 0.2). The neurocognitive treatments have modest effects on ADHD symptoms (0.2 to 0.4) but their evidence base is weak. This review of non-drug treatments explains why ADHD drug treatments are usually used first. The evidence base is stronger, and they are more effective in reducing ADHD symptoms. There is, however, a role for some non-drug treatments. I'll be discussing that in subsequent blog posts. See more evidence-based information about ADHD at www.adhdinadults.com
Faraone, S. V.&Antshel, K. M. (2014). ADHD: Non-Pharmacologic Interventions. ChildAdolescPsychiatr Clin N Am 23, xiii-xiv.
Faraone, S. V. &Antshel, K. M. (2014).Towards an evidence-based taxonomy of nonpharmacologic treatments for ADHD.Child AdolescPsychiatr Clin N Am 23, 965-72.
The Background:
Previous research has suggested that people with ADHD have higher rates of death than those without the condition. Until now, many of those studies lacked the detail needed to untangle why this might be the case. A recent meta-analysis of eight separate studies reported that ADHD roughly doubled the risk of death, and it hinted that factors like socioeconomic status and other mental illnesses might help explain the link.
The Study:
To explore this in more detail, researchers used the US National Health Interview Survey, a nationally representative prospective cohort of just over 52,000 adults. Survey records were linked with the National Death Index, and participants were followed from the date of interview until death or December 31, 2019, whichever came first. The main outcome was death from any cause. With a median follow-up of just under eight years, there were 6,024 deaths recorded.
When the team adjusted their analysis for age, sex, ethnicity, and the year of the survey, having ADHD was associated with a 58% higher risk of death. Controlling further for family income and educational level reduced that increased risk slightly, to 50%.
Controlling for health conditions (like high blood pressure, diabetes, stroke, heart disease, and cancer) and lifestyle factors (smoking, alcohol use, physical activity, and body weight) also reduced the association to about 46%.
By contrast, when the researchers adjusted for two psychiatric conditions (anxiety and depression) commonly found alongside ADHD, the link between ADHD and higher mortality disappeared statistically. In other words, once anxiety and depression were taken into account, ADHD itself was no longer associated with a clearly measurable increase in the risk of death.
What Does This Mean?
The authors conclude that the apparent effect of ADHD on mortality seems to operate largely through accompanying mental illness, and to a lesser extent through lifestyle and physical health problems. They suggest that treating and managing these co-occurring issues (through medications, therapy, and behavioral interventions) might help reduce the risk of premature death in people with ADHD, although they note that further evidence is needed.
The Background:
Dementia is a rapidly growing public health problem affecting more than 50 million people worldwide. Nearly 10 million new cases are diagnosed each year, and that number is expected to almost triple by 2050. The most common form is Alzheimer’s disease, accounting for roughly 60–70% of cases, followed by vascular dementia at around 20%. Other types include dementia with Lewy bodies, Parkinson’s disease dementia, and frontotemporal dementia. While no cure exists, managing modifiable risk factors (such as high blood pressure, smoking, physical inactivity, and poorly controlled diabetes) can delay or slow both the onset and progression of the condition.
Several studies have reported an elevated dementia risk among people with ADHD, and a number of mechanisms may explain this association. These include shared genetic or neurobiological vulnerabilities, reduced cognitive reserve (leaving the brain less resilient to age-related damage), and greater lifetime exposure to other established dementia risk factors.
Earlier reviews explored the possible link between ADHD and dementia, but tended toward a broader scope (incorporating other neurodegenerative disorders or mixing study designs), which introduced substantial variability and precluded quantitative synthesis. The relevant research literature has also expanded considerably since those reviews appeared.
The Study:
This meta-analysis restricted inclusion to case-control and cohort studies, yielding five that met the criteria. One was a case-control study with 400 participants; the other four were cohort studies collectively covering 3.7 million individuals, two retrospective and two prospective.
The Results:
Pooling the four cohort studies, individuals with ADHD showed approximately two-and-a-half times the dementia risk of those without the diagnosis. There was no indication of publication bias.
The Take-Away:
The authors concluded that ADHD is associated with a significantly increased risk of all-cause dementia in later life, while noting that its relationship to specific dementia subtypes remains less clear and warrants attention in future research.
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The Background:
Women with polycystic ovary syndrome (PCOS) themselves show higher rates of ADHD. Because ADHD is partly heritable (meaning genes contribute to the condition), some of the increased ADHD seen in children of mothers with PCOS could come from shared genetic factors. In other words, a mother’s and her child’s increased risk might sometimes reflect common genes rather than an effect of the pregnancy itself.
Beyond genetics, growing evidence points to maternal metabolic problems during pregnancy as another important risk factor for neurodevelopmental outcomes. PCOS is one of these conditions and is considered both potentially modifiable (treatable or manageable) and biologically plausible as a contributor to risk. PCOS affects an estimated 5–10% of women of reproductive age worldwide and is characterized by signs such as hyperandrogenism (higher-than-normal levels of “male” hormones), insulin resistance (poorer ability to use the hormone insulin, which can affect blood sugar and metabolism), and chronic low-grade inflammation.
However, studies to date have not all reached the same conclusions. Some research suggests the association between maternal PCOS and offspring ADHD is stronger for girls, while other studies did not analyze results by child sex. Methodological differences make it harder to draw clear conclusions.
The Study:
It’s important to note that the studies included in this meta-analysis were observational (cohort studies and case-control studies). Observational studies can identify associations (that two things occur together) but cannot prove that one causes the other. A cohort study follows people over time, and a case-control study compares people with a condition to similar people without it.
The pooled results came from six studies that together included almost 1.4 million mother–child pairs and that adjusted for confounders (other factors that might influence the result, such as maternal age or socioeconomic status). After statistical adjustment, children of mothers with PCOS had about 40% greater odds of ADHD than children of mothers without PCOS. The analysis reported no evidence of publication bias (no clear sign that only positive studies were published) and zero heterogeneity (the results were consistent across the studies).
There was no meaningful difference in results between cohort and case-control studies, and the meta-analysis did not find a significant difference in the association when comparing male and female offspring.
The Take-Away:
The research team concluded that this large-scale synthesis found an association between maternal PCOS and higher odds of ADHD and other neuropsychiatric conditions in children. They suggested that children born to mothers with PCOS may benefit from developmental monitoring to identify and address problems early, while emphasizing that causal relationships have not been established. They called for further studies to confirm these findings and to investigate the biological and environmental mechanisms that might explain the association. Indeed, because women with PCOS show higher rates of ADHD than other women, we need genetically informed research designs to see if the reported association is confounded.
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