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May 15, 2021
Myth: ADHD medications "anesthetize" ADHD children.
The idea here is that the drug treatment of ADHD is no more than a chemical straightjacket intended to control a child's behavior to be less bothersome to parents and teachers. After all, everyone knows that if you shoot up a person with tranquilizers, they will calm down.
Fact: ADHD medications are neither anesthetics nor tranquilizers.
The truth of the matter is that most ADHD medications are stimulants. They don't anesthetize the brain; they stimulate it. By speeding up the transmission of dopamine signals in the brain, ADHD medications improve brain functioning, which in turn leads to an increased ability to pay attention and control behavior. The non-stimulant medications improve signaling by norepinephrine. They also improve the brain's ability to process signals. They are not sedatives or anesthetics. When taking their medication, ADHD patients can focus and control their behavior to be more effective in school, work, and relationships. They are not "drugged" into submission.
Myth: ADHD medications cause drug and alcohol abuse
We know from many long-term studies of ADHD children that when they reach adolescence and adulthood, they are at high risk for alcohol and drug use disorders. Because of this fact, some media reports have implied that their drug use was caused by treatment of their ADHD with stimulant medications.
Fact: ADHD medications do not cause drug and alcohol abuse
Some ADHD medications indeed use the same chemicals that are found in street drugs, such as amphetamine. But there is a very big difference between these medications and street drugs. When street drugs are injected or snorted, they can lead to addiction, but when they are taken in pill form as prescribed by a doctor, they do not cause addiction. When my colleagues and I examined the world literature on this topic, we found that rather than causing drug and alcohol abuse, stimulant medicine protected ADHD children from these problems later in life. One study from researchers at Harvard University and the Massachusetts General Hospital found that the drug treatment of ADHD reduced the risk for illicit drug use by84 a percent. These findings make intuitive sense. These medicines reduce the symptoms of the disorder that lead to illicit drug use. For example, an impulsive ADHD teenager who acts without thinking is much more likely to use drugs than an ADHD teen whose symptoms are controlled by medical drug treatment. After we published our study, other work appeared. Some of these studies did not agree that ADHD medications protected ADHD people from drug abuse, but they did not find that they caused drug abuse.
Myth: Psychological or behavioral therapies should be tried before medication.
Many people are cautious about taking medications, and that caution is even stronger when parents consider treatment options for their children. Because medications can have side effects, shouldn't people with ADHD try to talk therapy before taking medicine?
Fact: Treatment guidelines suggest that medication is the first-line treatment.
The problem with trying talk or behavior therapy before medication is that medication works much better. For ADHD adults, one type of talk therapy(cognitive behavioral therapy) is recommended, but only when the patient is also taking medication. The multimodal treatment of ADHD (MTA) study examined this issue in ADHD children from several academic medical centers in the United States. That study found that treating ADHD with medication was better than treating it with behavior therapy. Importantly, behavior therapy plus medication was no more effective than medication alone. That is why treatment guidelines from the American Academy of Pediatrics and the American Academy of Children and Adolescents recommend medicine as a first-line treatment for ADHD, except for preschool children. ADHD medications indeed have side effects, but these are usually mild and typically do not interfere with treatment. And don't forget about the risks that a patient faces when they do not use medications for ADHD. These untreated patients are at risk for worsening ADHD symptoms and complications.
Myth: Brain abnormalities of ADHD patients are caused by psychiatric medications
A large scientific literature shows that ADHD people have subtle problems with the structure and function of their brains. Scientists believe that these problems are the cause of ADHD symptoms. Critics of ADHD claim that these brain problems are caused by the medications used to treat ADHD. Who is right?
Fact: Brain abnormalities are found in never medicated ADHD patients.
Alan Zametkin, a scientist at the US National Institute of Mental Health, was the first to show brain abnormalities in ADHD patients who had never been treated for their ADHD. He found that some parts of the brains of ADHD patients were underactive. His findings could not be due to medication because the patients had never been medicated. Since his study, many other researchers have used neuroimaging to examine the brains of ADHD patients. This work confirmed Dr. Zametkin’s observation of abnormal brain findings in unmediated patients. Reviews of the brain imaging literature have concluded that the brain abnormalities seen in ADHD cannot be attributed to ADHD medications.
Wilens, T., Faraone, S. V.,Biederman, J. &Gunawardene, S. (2003). Does Stimulant Therapy of Attention-Deficit hyperactivity disorder Beget Later Substance Abuse? Aneta-Analytic Review of the Literature.Pediatrics111, 179-185.
Humphreys, K. L., Eng, T. &Lee, S. S. (2013).Stimulant Medication and Substance Use Outcomes: A Meta-analysis. JAMA psychiatry, 1-9.
Chang, Z., Lichtenstein, P., Halldner,L., D'Onofrio, B., Serlachius, E., Fazel, S., Langstrom, N. & Larsson, H. (2014). Stimulant ADHD medication and risk for substance abuse. J Child Psychol Psychiatry55,878-85.
Nakao, T., Radua, J., Rubia, K. &Mataix-Cols, D. (2011 ). Gray matter volume abnormalities in ADHD: voxel-based meta-analysis exploring the effects of age and stimulant medication. Am J Psychiatry168, 1154-63.
Rubia, K., Alegria, A. A., Cubillo, A. I., Smith, A. B., Brammer, M.J. &Radua, J. (2014). Effects of stimulants on brain function inattention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Biol Psychiatry76, 616-28.
Spencer, T. J., Brown, A., Seidman, L. J., Valera, E. M., Makris, N., Lomedico, A., Faraone, S. V. &Biederman,J. (2013).Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies. J Clin Psychiatry74, 902-17.
The Background:
Meta-analyses have previously suggested a link between maternal thyroid dysfunction and neurodevelopmental disorders (NDDs) in children, though some studies report no significant difference. Overweight and obesity are more common in children and adolescents with NDDs. Hypothyroidism is often associated with obesity, which may result from reduced energy expenditure or disrupted hormone signaling affecting growth and appetite. These hormone-related parameters could potentially serve as biomarkers for NDDs; however, research findings on these indicators vary.
The Study:
A Chinese research group recently released a meta-analysis examining the relationship between neurodevelopmental disorders (NDDs) and hormone levels – including thyroid, growth, and appetite hormones – in children and adolescents.
The analysis included peer-reviewed studies that compared hormone levels – such as thyroid hormones (FT3, FT4, TT3, TT4, TSH, TPO-Ab, or TG-Ab), growth hormones (IGF-1 or IGFBP-3), and appetite-related hormones (leptin, ghrelin, or adiponectin) – in children and adolescents with NDDs like ADHD, against matched healthy controls. To be included, NDD cases had to be first-diagnosis and medication-free, or have stopped medication before testing. Hormone measurements needed to come from blood, urine, or cerebrospinal fluid samples, and all studies were required to provide both means and standard deviations for these measurements.
Meta-analysis of nine studies encompassing over 5,700 participants reported a medium effect size increase in free triiodothyronine (FT3) in children and adolescents with ADHD relative to healthy controls. There was no indication of publication bias, but variation between individual study outcomes (heterogeneity) was very high. Further analysis showed FT3 was only significantly elevated in the predominantly inattentive form of ADHD (three studies), again with medium effect size, but not in the hyperactive/impulsive and combined forms.
Meta-analysis of two studies combining more than 4,800 participants found a small effect size increase in thyroid peroxidase antibody (TPO-Ab) in children and adolescents with ADHD relative to healthy controls. In this case, the two studies had consistent results. Because only two studies were involved, there was no way to evaluate publication bias.
The remaining thyroid hormone meta-analyses, involving 6 to 18 studies and over 5,000 participants in each instance, found no significant differences in levels between children and adolescents with ADHD and healthy controls.
Meta-analyses of six studies with 317 participants and two studies with 192 participants found no significant differences in growth hormone levels between children and adolescents with ADHD and healthy controls.
Finally, meta-analyses of nine studies with 333 participants, five studies with 311 participants, and three studies with 143 participants found no significant differences in appetite-related hormone levels between children and adolescents with ADHD and healthy controls.
The Conclusion:
The team concluded that FT3 and TPO-Ab might be useful biomarkers for predicting ADHD in youth. However, since FT3 was only linked to inattentive ADHD, and TPO-Ab’s evidence came from just two studies with small effects, this conclusion may overstate the meta-analysis results.
Our Take-Away:
Overall, this meta-analysis found only limited evidence that hormone differences are linked to ADHD. One thyroid hormone (FT3) was higher in children with ADHD—mainly in the inattentive presentation—but the findings varied widely across studies. Another marker, TPO-Ab, showed a small increase, but this came from only two studies, making the result less certain. For all other thyroid, growth, and appetite-related hormones, the researchers found no meaningful differences between children with ADHD and those without. While FT3 and TPO-Ab may be worth exploring in future research, the current evidence is not strong enough to consider them reliable biomarkers.
Background:
Recent progress in reproductive medicine has increased the number of children conceived via assisted reproductive techniques (ART). These include:
Although ART helps with infertility, there are concerns about its long-term effects on offspring, especially regarding neurodevelopment. Factors such as hormonal treatments, gamete manipulation, altered embryonic environments, as well as parental age and infertility, may influence brain development and raise the risk of neurodevelopmental and mental health disorders.
With previous studies finding conflicting results on a possible association between ART and increased risk of mental health disorders, an Indian research team has just published a new meta-analysis exploring this topic.
The Study:
Studies were eligible if they were observational (cohort, case-control, or cross-sectional), reported confounder-adjusted effect sizes for ADHD, and were published in English in peer-reviewed journals.
A meta-analysis of eight studies encompassing nearly twelve million individuals indicated a 7% higher prevalence of ADHD in offspring conceived via IVF/ICSI compared to those conceived naturally. The heterogeneity among studies was minimal, and no evidence of publication bias was observed.
The study’s 95% confidence interval ranged from 4% to 10%. Further analysis of five studies comprising almost nine million participants that distinguished outcomes by sex revealed that the increase in ADHD risk among female offspring was not statistically significant. In contrast, the elevated risk in male offspring persisted, though it was marginally significant, with the lower bound of the confidence limit at only 1%.
Results:
A meta-analysis of three studies (1.4 million participants) found a 13% higher rate of ADHD in children conceived via ovulation induction/intrauterine insemination (OI/IUI) compared to natural conception. The effect size, though doubled, remains small. Minimal heterogeneity and no publication bias were observed.
The team concluded, “The review found a small but statistically significant moderate certainty evidence of an increased risk of ADHD in those conceived through ART, compared to spontaneous conception. The magnitude of observed risk is small and is reassuring for parents and clinicians.”
Our Take-Away:
Overall, the meta-analysis points to a small, but measurable increase in ADHD diagnoses among children conceived through ART, but the effect sizes are modest and supported by moderate-certainty evidence. And we must always keep in mind that the researchers who wrote the original articles could not correct for all possible confounds. These findings suggest that while reproductive technologies may introduce slight variation in neurodevelopmental outcomes, the effects are small and uncertain. For families and clinicians, the results are generally reassuring: ART remains a safe and effective avenue to parenthood, and the results of this study should not be viewed as a prohibitive concern. Thoughtful developmental monitoring and open, evidence-based counseling can help ensure that ART-conceived children receive support that caters to their individual needs.
The Background:
Myopia is a growing global health concern linked to conditions like macular degeneration, glaucoma, and retinal detachment. Its prevalence has surged in recent decades; by 2050, an estimated 5 billion people will have myopia. The increase is especially marked in Asia – a survey in Taiwan reports that 84% of students aged 15 to 18 are myopic, with 24% severely affected.
Dopamine is an important neurotransmitter in the retina, involved in eye development, visual signaling, and refractive changes. The dopamine hypothesis, suggesting that retinal dopamine release helps prevent myopia, has emerged as a leading theory of myopia control.
Most studies show ADHD is highly heritable, often involving dopamine system genes. ADHD is strongly associated with dopaminergic abnormalities, especially in dopamine transporter function and release dynamics.
Medications for ADHD, like methylphenidate, atomoxetine, and clonidine, help regulate dopamine to reduce symptoms.
The Study:
Given dopamine’s critical involvement in both ADHD and myopia, a Taiwanese research team hypothesized that medications for ADHD that influence dopaminergic pathways may have a significant effect on myopia risk.
To evaluate this hypothesis, the team conducted a nationwide cohort study using data from Taiwan’s National Health Insurance (NHI) program, which covers 99% of the nation’s 23 million residents and provides access to comprehensive eye care and screenings. Taiwan requires visual acuity screenings beginning at age four, with annual examinations for school-aged children to promote the early detection of visual anomalies such as myopia.
Furthermore, ADHD medication and diagnosis are tracked through compulsory diagnostic codes. This permits an accurate assessment of the effects of dopaminergic medications on myopia risk.
Propensity score allocation using a multivariable logistic regression model was applied to reduce bias from confounding influences, pairing cohorts based on similar scores.
The Results:
Comparing 133,945 individuals with ADHD with an equal number without ADHD, untreated ADHD was associated with a 22% greater risk of myopia.
However, after adjusting for covariates (gender, age, insured premium, comorbidities, location, and urbanization level), the ADHD cohort receiving medication treatment showed a 39% decreased risk of myopia relative to the untreated ADHD cohort.
Narrowing this further to the ADHD cohort receiving dopaminergic medications reduced the risk of myopia by more than half (52%) relative to the untreated ADHD cohort.
Treatment with two dopaminergic medications reduced the risk by well over two-thirds (72%) relative to the untreated ADHD cohort.
There were no significant differences between methylphenidate, atomoxetine, and clonidine. Each reduced risk by about 50%.
The team did not directly compare the ADHD cohort receiving dopaminergic medications with the non-ADHD cohort. But if there were 122 cases of myopia in the ADHD cohort for every 100 cases in the non-ADHD cohort, and dopaminergic medications halved the cases in the ADHD cohort to about 60, that would represent a roughly 40% reduction in myopia risk relative to the non-ADHD cohort.
The team concluded, “our research indicates that pharmacologically treated ADHD children have a reduced risk of myopia. Conversely, untreated ADHD children are at a heightened risk relative to those without ADHD. Moreover, the cumulative effects of ADHD medications were found to notably decrease myopia incidence, emphasizing the protective influence of dopaminergic modulation in these interventions.”
The Take-Away:
Children with untreated ADHD are more likely to develop myopia, but those receiving dopaminergic medications had a substantially lower risk. The findings suggest that ADHD medications may help protect against myopia by boosting dopamine signaling. More research is needed before firmly drawing this conclusion, but this research could open the door to new approaches for preventing myopia in at-risk children.
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