A large international research team has just released a detailed analysis of studies looking at the connection between parents' mental health conditions and their children's mental health, particularly focusing on ADHD (Attention Deficit Hyperactivity Disorder). This analysis, called a meta-analysis, involved carefully examining previous studies on the subject. By September 2022, they had found 211 studies, involving more than 23 million people, that could be combined for their analysis.
Most of the studies focused on mental disorders other than ADHD. However, when they specifically looked at ADHD, they found five studies with over 6.7 million participants. These studies showed that children of parents with ADHD were more than eight times as likely to have ADHD compared to children whose parents did not have ADHD. The likelihood of this result happening by chance was extremely low, meaning the connection between parental ADHD and child ADHD is strong.
The researchers wanted to figure out how common ADHD is among children of parents both with and without ADHD. To do this, they first analyzed 65 studies with about 2.9 million participants, focusing on children whose parents did not have ADHD. They found that around 3% of these children had ADHD.
Next, they analyzed five studies with over 44,000 cases where the parents did have ADHD. In this group, they found that 32% of the children also had ADHD, meaning about one in three. This is a significant difference—children of parents with ADHD are about ten times more likely to have the condition than children whose parents who do not have ADHD.
The researchers also wanted to see if other mental health issues in parents, besides ADHD, were linked to ADHD in their children. They analyzed four studies involving 1.5 million participants and found that if a parent had any mental health disorder (like anxiety, depression, or substance use issues), the child’s chances of having ADHD increased by 80%. However, this is far less than the 840% increase seen in children whose parents specifically had ADHD. In other words, ADHD is much more likely to be passed down in families compared to other mental disorders.
The study had a lot of strengths, mainly due to the large number of participants involved, which helps make the findings more reliable. However, there were also some limitations:
Despite these limitations, the research team concluded that their analysis provides strong evidence that children of parents with ADHD or other serious mental health disorders are at a higher risk of developing mental disorders themselves. While more research is needed to fill in the gaps, the findings suggest that it would be wise to carefully monitor the mental health of children whose parents have these conditions to provide support and early intervention if needed
Behavioral disinhibition is a trait associated with both ADHD and several genes that affect dopamine signaling. A new study by three American medical researchers set out to examine how these ADHD risk genes - DRD4 (dopamine 4 receptor density), DAT1 (dopamine 1 transporter), and DBH(dopamine beta-hydroxylase) - affect estimated life expectancy in young adulthood.
The method used was a longitudinal study of 131 hyperactive children and 71 matched controls through early adulthood. The original evaluations were done in 1979-1980, when both groups were children in the 4 to 12 age range. They were reevaluated in1987-1988 as adolescents aged 12 to 20. The next follow-up was in 1992-1996 in early adulthood, aged 19 to 25. The final follow-up was in 1998-2004, for adults aged 24 to 32. All agreed to physical examinations that formed the basis for calculating estimated life expectancy using actuarial tables that factor in the effects of smoking, body mass index, alcohol, and other risk factors of on expected longevity. Participants also provided blood samples that enabled gene typing.
For the DAT1 gene, participants who had the homozygous-repeat allele (9/9) had a five-year reduction in estimated life expectancy relative to those with the ten-repeat allele (10/10). Those with the intermediate (9/10) configuration had a three-year reduction in estimated life expectancy.
For the DBH Taq1 gene, those with a heterozygous (A1/A2) combination had almost a three-year reduction in estimated life expectancy relative to those with homozygous (A1/A1 or A2/A2)configurations.
For DRD4, on the other hand, no significant differences were found in estimated life expectancy.
In a related study, several background traits were found to be significantly predictive of variance estimated life expectancy. The largest of these was behavioral disinhibition, followed by verbal IQ, self-rated hostility, and a nonverbal fluency test. But no significant differences were found between any of the gene polymorphisms on any of these four measures, indicating that the present gene associations were independent of the background traits.
The researchers next sought to determine which variables used in the estimated life expectancy calculations were associated with the two significant genes. For DBH, one variable stood out. Those with the A1/A2 heterozygous pairings had almost twice the alcohol consumption of those with homozygous pairings (p = 0.023).
For DAT1, two variables stood out. Overall, the 9/9 pairings smoked two and a half times as much as the 10/10pairings, with the 9/10 pairings midway between the extremes (p = 0.036). They were also 73 percent more likely to be smokers relative to the 10/10 pairings, and 61 percent more likely relative to the 9/10 pairings. They also had significantly less education than the 10/10 pairings, with the 9/10 pairings again being intermediate (p = 0.027).
An obvious limitation of the study was its small sample size. The authors cautioned, our findings should be considered quite preliminary and in need of much greater research before being given much weight in the literature or public policy.
"With these limitations in mind, they concluded, the present study demonstrated that two ADHD risk genes (DB Hand DAT1) independently contributed to a reduction in ELE [estimated life expectancy] beyond the second-order variables of behavioral disinhibition, IQ, hostility, and nonverbal fluency that contributed in the related study to variation in ELE. The gene polymorphisms seemed to be influencing ELE through their affiliation with first-order or more proximal factors related to ELE such as education, smoking, alcohol use, and possibly exercise."
ADHD, especially when untreated, impairs patients and creates difficulties in families.
Although these are the proximal targets of treatment, ADHD also burdens society due, for example, to underemployment and the use of health resources. A recent study assessed the economic burden using the Danish population registries, researchers, which link medical information with employment, education, crime, and social care registers while maintaining confidentiality. They identified 5,269 adults with adult ADHD who had not been diagnosed with ADHD in childhood and, we can assume, were probably not treated for the disorder. They excluded patients with other psychiatric diagnoses and cases without a same-sex sibling free of any diagnosed psychiatric diagnoses. That left 460 pairs of same-sex siblings, one with an adult with ADHD and the other with no psychiatric diagnosis. They selected the non-ADHD sibling closest in age to the ADHD sibling. Using siblings mitigated the effects of genetics and upbringing between the ADHD group and normally developing controls.
Looking at personal income (combining work income and public transfers), adults with ADHD on average brought home about 12,000 Euros less - almost a third less - than their sibling counterparts. They also paid 40% less tax. Balancing that out, their after-tax income was roughly 7,500 Euros less than their siblings. With the additional personal cost of prescribed medication(prescriptions are relatively inexpensive in Denmark, and co-payments even more so) the net personal cost to adults with ADHD was 7,700 Euros.
The net public costs were considerably greater. That was primarily due to the reduction in taxes paid (about 4,500 Euros) and the increase in income replacement transfers (just over 5,500 Euros). The cost of additional crimes committed by adults with ADHD added another 1,000 Euros. Additional primary and secondary health care costs contributed another 1,000 Euros. Subsidies for prescribed medicines added 661 Euros, but that was partly counterbalanced by a reduction of 344 Euros in education costs. There were no significant differences in costs from traffic accidents or adult continuation of foster care. Overall, the net per capita public cost of adults with ADHD was just over 12,400 Euros each year.
Combining public and private costs, the per capita economic burden of adult ADHD was just over 20,000 Euros each year.
The study could not evaluate the extent to which ADHD treatment may reduce the economic burden, but given many studies that show treatment for ADHD reduces impairments, we would expect treatment to have a positive impact on the economic burden. These results are extremely important for policymakers and for those who control the allocation of treatment in healthcare systems. Although treating ADHD incurs costs, not treating it incurs even greater costs in the long run
Drivers with ADHD are far more likely to be involved in crashes, to be at fault in crashes, to be in severe crashes, and to be killed in crashes. The more severe the ADHD symptoms, the higher the risk. Moreover, ADHD is often accompanied by comorbid conditions such as oppositional-defiant disorder, depression, and anxiety that further increase the risk.
What can be done to reduce this risk? A group of experts has offered the following consensus recommendations:
· Use stimulant medications. While there is no reliable evidence on whether-stimulant medications are of any benefit for driving, there is solid evidence that stimulant medications are effective in reducing risk. But there is also a “rebound effect” in many individuals after the medication wears off, in which performance becomes worse than it had been before medication. It is therefore important to time the taking of medication so that its period of effectiveness corresponds with driving times. If one has to drive right after waking up, it makes sense to take a rapid-acting form. The same holds for late-night driving that may require a quick boost.
· Use a stick shift vehicle wherever possible. Stick shifts make drivers pay closer attention than automatic transmissions. The benefits of alertness are most notable in city traffic. But using a stick shift is far less beneficial in highway driving, where shifting is less frequent.
· Avoid cruise control. Highways can be monotonous, making drivers more prone to boredom and distraction. That is even more true for those with ADHD, so it is best to keep cruise control turned off.
· Avoid alcohol. Drinking and driving is a bad idea for everyone, but, once again, it’s even worse for those with ADHD. Parents should consider the no-questions-asked policy of either picking up their teenager anytime and anywhere or setting up an account with a ride-sharing service.
· Place the smartphone out of reach and hearing. Cell phone use is as about as likely to impair as alcohol. Hands-free devices only reduce this risk moderately, because they continue to distract. Texting can be deadly. Sending a short text or emoticon can be the equivalent of driving 100 yards with one’s eyes closed. Either turn on Do Not Disturb mode or, for even greater effectiveness, place the smartphone in the trunk.
· Make use of automotive performance monitors. These can keep track of maximum speeds and sudden acceleration and braking, to verify that a teenager is not engaging in risky behaviors.
· Take advantage of “graduated driver’s licensing laws” wherever available. These laws forbid the presence of peers in the vehicle for the first several (for example, six) months of driving. Parents can extend that period for teenagers with ADHD, or set it as a condition in states that lack such laws.
· Encourage practicing after obtaining a learner’s permit. Teenagers with ADHD generally require more practice than those without. A “pre-drive checklist” can be a good place to start. For example: check the gas, check the mirrors, make sure the view through the windows is unobstructed, put your cell phone in Do not disturb mode and place it out of reach, put on a seatbelt, and scan for obstacles.
· Consider outsourcing. Look for a driving school with a professional to teach good driving skills and habits.
Experts do not agree on whether to delay licensing for those with ADHD. On the one hand, teenagers with ADHD are 3-4 years behind in the development of brain areas responsible for executive functions that help control impulses and better guide behavior. Delaying licensing can reduce risk by about 20 percent. On the other hand, teens with ADHD are more likely to drive without a license, and no one wants to encourage that, however inadvertently. Moreover, graduated driver’s licensing laws only have a legal effect on teens who get their licenses at the customary age.
An international team of mental health professionals used a nationally representative sample of English adults over age 16 to explore this question. Of 13,671 households selected, 7,461 were a little more than half participated.
Participants used the Adult ADHD Self-Report Scale (ASRS) Screener to assess symptoms of ADHD on a scale ranging from 0 to 24. Those scoring ≥ 14 were considered as having high levels of ADHD symptoms. They also responded to a computer-assisted self-interview that asked, "Have you been unfairly treated in the last 12 months … because of your mental health," requiring a yes or no answer.
The raw data showed an exponential relationship between levels of ADHD symptoms and mental health discrimination. Respondents scoring0-9 on the ASRS reported negligible discrimination (prevalence of 0.3%). Among those scoring 10-13, the prevalence was 2.3%, rising to 5.5% of those with scores in the 14-17 range, and 18.8% among those in the 18-24 range.
After adjusting for sociodemographic variables (sex, age, ethnicity, marital status, educational attainment, and income), those with high levels of ADHD symptoms were nearly 10 times more likely to have experienced discrimination than others. After adjusting for other psychopathology and stressful life events, this increased risk fell to 2.8.
The authors concluded, "This is an important finding given that mental health discrimination has been associated with detrimental consequences in individuals with mental health disorders and therefore might also be a factor in the negative outcomes that have been noted in adults with ADHD/ADHD symptomatology. As ADHD continues to be underdiagnosed and untreated in adults, the results of this study highlight the importance of identifying and treating these individuals and suggest that interventions to inform the public about ADHD may be important for reducing the stigma and discrimination associated with this condition."
Many college students truly have ADHD and deserve to be treated, but some attempt to fake ADHD symptoms to get stimulant medications for nonmedical uses, such as studying and getting high. Some students who fake ADHD also seek to gain accommodations that would give them additional time to complete exams. To address this issue, two psychologists examined data from 514 university students being assessed for ADHD to evaluate the ability of assessment tools to detect students who fake ADHD symptoms.
All participants had asked to be assessed to determine whether they could qualify for disability services. This was therefore by no means a random sample of university students, and could be expected to include some non-ADHD individuals seeking the benefits of an ADHD diagnosis. But this offered a good opportunity to explore which combination of tools would yield the best accuracy, and be best at excluding malingerers.
That was achieved by using both multiple informants and multiple assessment tools and comparing results. Self-assessment was supplemented by assessment by other informants (e.g. parent, partner, friend, or another relative). These were supplemented with symptom validity tests to check for telltale highly inconsistent symptom reporting, or symptom exaggeration, which could signal false positives.
On the other hand, some individuals with ADHD have executive functioning problems that may make it difficult for them to reliably appraise their symptoms on self-assessment tests, which can lead to false negatives. Performance validity tests were therefore also administered, to detect poor effort during evaluation, which could lead to false negatives.
Observer reporting was found to be more reliable than self-reporting, with significantly lower inconsistency scores (p < .001), and significantly higher exaggeration scores (p < .001). More than twice as many self-reports showed evidence of symptom exaggeration as did observer reports. This probably understates the problem when one considers that the observer reports were performed not by clinicians but by parents and partners who may themselves have had reasons to game the tests in favor of an ADHD diagnosis.
Even so, the authors noted, "External incentives such as procurement of a desired controlled substance or eligibility for the desired disability accommodation are likely to be of more perceived value to those who directly obtain them." They suggested compensating for this by making ADHD diagnoses only based on positive observer tests in addition to self-reports: "Applying an 'and' rule-one where both self-and observers reports were required to meet the diagnostic threshold-generally cut the proportions meeting various thresholds at least in half and washed out the differences between the adequate and inadequate symptom validity groups."
They also recommended including formal tests of response validity, using both symptom validity tests and performance validity tests. Overall, they found that just over half of the sub-sample of 410 students administered performance validity tests demonstrated either inadequate symptom or performance validity.
Finally, they recommended "that clinicians give considerable weight to direct, objective evidence of functional impairment when making decisions about the presence of ADHD in adults. The degree to which symptoms cause significant difficulty functioning in day-to-day life is a core element of the ADHD diagnostic criteria (American Psychiatric Association,2013), and it cannot be assumed that significant symptoms cause such difficulty, as symptoms are only moderately associated with such functional impairment. ... we urge clinicians to procure objective records (e.g., grade transcripts, work performance evaluations, disciplinary and legal records) to aid in determining functional impairment in adults assessed for ADHD."
Treating ADHD With Methylphenidate in Adults With Autism
A team from Harvard Medical School and Massachusetts General Hospital conducted a six-week open-label trial of liquid-formulation extended-release methylphenidate (MPH-ER) to treat ADHD in adults with high-functioning autism spectrum disorder (HF-ASD). ASD is a lifelong disorder with deficits in social communication and interaction and restricted, repetitive behaviors. Roughly half of those diagnosed with ASD also are diagnosed with ADHD.
This was the first stimulant trial in adults with both ASD and ADHD. There were twelve males and three female participants, all with moderate to severe ADHD, and in their twenties, with IQ scores of at least 85.
The use of a liquid formulation enabled doses to be raised very gradually, starting with a daily dose of 5 mg(1mL) and titrating up to 60 mg over the first three weeks, then maintaining that level through the sixth week. Participants were reevaluated for ADHD symptoms every week during the six-week trial. The severity of ASD was assessed at the start, midpoint, and conclusion of the trial, as were other psychiatric symptoms.
Before the trial, researchers agreed on a combination of targets on two clinician-rated scoring systems that would have to be reached for treatment to be considered successful. One is a score of 2 or less on the CGI-S, a measure of illness severity, with scores ranging from 1 (normal, not at all ill) to 7 (most extremely ill). The other is a reduction of at least 30 percent in the AIS RS score, which combines each of 18 symptoms of ADHD on a severity grid (0=not present; 3=severe; overall minimum score: 0; overall maximum score: 54).
After the trial, twelve of the fifteen patients (80 percent) met the preset conditions for success. Fully fourteen (93 percent) saw a ≥ 30 percent reduction in their AISRS score, while twelve scored ≤ 2 on illness severity.
However, when using the patient-rated ASRS scoring system, only five (33 percent) saw a ≥ 30 percent reduction in ADHD severity.
Thirteen participants (87percent) reported at least one adverse event, and nine (60 percent) reported two or more. One reported a serious adverse event (attempted suicide) in a patient with multiple prior attempts. Because the attempt was not deemed due to medication, they continued and completed the trial. Seven participants experienced titration-limiting adverse events (headaches, palpitations, jaw pain, and insomnia). Headache was most frequent (53%), followed by insomnia and anxiety(33% each), and decreased appetite (27%).
During the trial, weight significantly decreased, while pulse significantly increased. There were no significant differences in other vital and cardiovascular measurements.
The authors concluded, "this OLT of short-term MPH-ER therapy documents that acute treatment with MPH-ER in young adults with ASD was associated with significant improvement in ADHD symptoms, mirroring the typically-expected magnitude of response observed in adults with only ADHD. Treatment with MPH-ER was well-tolerated, though associated with a higher than expected frequency of adverse events."
They also cautioned, "The results of this study need to be considered in light of some methodological limitations. This was an open-label study; therefore, assessments were not blind to treatment. We did not employ a placebo control group and, therefore, cannot separate the effects of treatment from time or placebo effects. ... firmer conclusions regarding the safety and efficacy of MPH-ER for the treatment of ADHD in HF-ASD populations await results from larger, randomized, placebo-controlled clinical trials."
ADHD is far more prevalent among persons with AUD (roughly20 percent) than it is in the general population. The most accurate way of identifying ADHD is through structured clinical interviews. Given that this is not feasible in routine clinical settings, ADHD self-report scales offer a less reliable but much less resource-intensive alternative. Could the latter be calibrated in a way that would yield diagnoses that better correspond with the former?
A German team compared the outcomes of both methods on 404 adults undergoing residential treatment for AUD. All were abstinent while undergoing evaluations. First, to obtain reliable ADHD diagnoses, each underwent the Diagnostic Interview for ADHD in Adults, DIVA. If DIVA indicated probable ADHD, two expert clinicians conducted successive follow-up interviews. ADHD was only diagnosed when both experts concurred with the DIVA outcome.
Participants were then asked to use two adult ADHD self-report scales, the six-item Adult ADHD Self Report Scale v1.1 (ASRS) and the 30-item Conner's Adult ADHD Rating Scale (CAARS-S-SR). The outcomes were then compared with the expert interview diagnoses.
Using established cut-off values for the ASRS, less than two-thirds of patients known to have ADHD were scored as having ADHD by the test. In other words, there was a very high rate of false negatives. Lowering the cut-off to a sum score ≥ 11 resulted in an incorrect diagnosis of more than seven out of eight. But the rate of false positives shared to almost two in five. Similarly, the CAARS-S-SR had its greatest sensitivity (ability to accurately identify those with ADHD) at the lowest threshold of ≥ 60, but at a similarly high cost in false positives (more than a third).
The authors found it was impossible to come anywhere near the precision of the expert clinical interviews. Nevertheless, they judged the best compromise to be to use the lowest thresholds on both tests and then require positive determinations from both. That led to successfully diagnosing more than three out of four individuals known to have ADHD, with a false positive rate of just over one in five.
Using this combination of the two self-reporting questionnaires with lower thresholds, they suggest, could substantially reduce the under-diagnosis of ADHD in alcohol-dependent patients.
Autism spectrum disorder (ASD) is frequently comorbid with ADHD. Among adults with ADHD, as many as half are reported to also have ASD.
A Dutch team set out to answer two questions:
1) Do adults with ADHD and comorbid ASD experience less effectiveness in pharmacological treatment for ADHD than adults with only ADHD
2) Do adults with ADHD and comorbid ASD experience different or more severe side effects of pharmacological treatment for ADHD than adults with only ADHD, as measured in side effect scores, blood pressure, heart rate, and weight?
This was a retrospective study, using well-documented medical records, of the effects of drug treatment with methylphenidate (MPH), dexamphetamine (DEX), atomoxetine (ATX), bupropion, or modafinil.
The researchers compared 60 adults with comorbid ASD and ADHD to 226 adults with only ADHD. ADHD symptoms were scored using the Conner's ADHD Rating Scale: Self Report-Short Version (CAA RS: S-S). Side effects of ADHD medication were measured using either a 13-item or 20-item checklist with 4-point scales for item response. Researchers also tracked changes in body weight, blood pressure, and heart rate.
Following treatment, ADHD symptoms among the comorbid group declined by a quarter, and among the ADHD-only group by almost a third. There was no significant difference between men and women. Controlling for age, gender, and ADHD subtype, a comorbid diagnosis of ASD also did not significantly affect ADHD symptom reduction.
Turning to side effects, in the ADHD+ASD group, there were significant increases in decreased appetite and weight loss, and decreases in agitation, anxiety, and sadness/unhappiness. In the ADHD-only group, there were significant increases in decreased appetite, weight loss, and dry mouth, and decreases in sleeping disorder, nervousness, agitation, anxiety, and sadness/unhappiness. Yet there were no significant differences between the two groups. Side effects increased and decreased similarly in both. Likewise, there were no significant differences between the groups in changes in heart rate and blood pressure. The only significant difference in medication dosage was for bupropion, which was higher in the ADHD+ASD group, though without any sign of the difference in side effects.
The authors concluded that this retrospective study "showed pharmacological treatment of adults with diagnoses of ADHD and ASD to be just as successful as the pharmacological treatment of adults with only ADHD," but cautioned that "randomized controlled trial should be conducted to evaluate the effectiveness and possible side effects of pharmacological treatment for ADHD in patients with ASD more reliably."
In this study, researchers found subtle differences in the cortex of the brains of children with ADHD.
The ENIGMA-ADHD Working Group published a second large study on the brains of people with ADHD in the American Journal of Psychiatry this month. In this second study, the focus was on the cerebral cortex, which is the outer layer of the brain.
ADHD symptoms include inattention and/or hyperactivity and acting impulsively. The disorder affects more than one in twenty (5.3%) children, and two-thirds of those diagnosed continue to experience symptoms as adults.
In this study, researchers found subtle differences in the brain's cortex when they combined brain imaging data on almost 4,000 participants from 37 research groups worldwide. The differences were only significant for children and did not hold for adolescents or adults. The childhood effects were most prominent and widespread for the surface area of the cortex. More focal changes were found in the thickness of the cortex. All differences were subtle and detected only at a group level, and thus these brain images cannot be used to diagnose ADHD or guide its treatment.
These subtle differences in the brain's cortex were not limited to people with the clinical diagnosis of ADHD: they were also present - in a less marked form - in youth with some ADHD symptoms. This second finding results from a collaboration between the ENIGMA-ADHD Working Group and the Generation Study from Rotterdam, which has brain images of, 2700 children aged 9-11 years from the general population. The researchers found more symptoms of inattention to be associated with a decrease in cortical surface area. Furthermore, siblings of those with ADHD showed changes to their cortical surface area that resembled their affected sibling. This suggests that familial factors such as genetics or shared environment may play a role in brain cortical characteristics.
This is the largest study to date to look at the cortex of people with ADHD. It included 2246 people with a diagnosis of ADHD and 1713 people without, aged between 4 and 63 years old. This is the second study published by the ENIGMA-ADHD Working Group; the first examined structures that are deep in the brain. The ADHD Working Group is one of over 50 working groups of the ENIGMA Consortium, in which international researchers pull together to understand the brain alterations associated with different disorders and the role of genetic and environmental factors in those alterations.
The authors say the findings could help improve understanding of the disorder. 'We identify cortical differences that are consistently associated with ADHD, by combining data from many research groups internationally. We find that the differences extend beyond narrowly-defined clinical diagnoses and are seen, in a less marked manner, in those with some ADHD symptoms and unaffected siblings of people with ADHD. This finding supports the idea that the symptoms underlying ADHD may be a continuous trait in the population, which has already been reported by other behavioral and genetic studies.'. In the future, the ADHD Working Group hopes to look at additional key features in the brain - such as the structural connections between brain areas - and to increase the representation of adults affected by ADHD, on whom limited research has been performed to date.
A team of Iranian researchers recently published a meta-analysis seeking to determine what, if any, association there may be between low vitamin D levels and ADHD in children and adolescents.
Combining the results from thirteen studies with 10,334participants, they found that youth with ADHD had "modest but significant" lower serum concentrations of 25-hydroxyvitamin D than normally developing children. The weighted mean difference was just under 7 nanograms per milliliter. The odds of obtaining such a result by chance would be less than one in a thousand(p < .001). There was little to no sign of publication bias. Between-study heterogeneity, however, was very high (I2 = 94).
These results suggest an association. But are low serum levels of vitamin D a cause or effect of ADHD? Causation is vastly more difficult to establish than an association. To begin to tease this out, the researchers identified four prospective studies that compared maternal vitamin D levels with the subsequent development of ADHD symptoms in their children. Two of these used maternal serum levels, and two used umbilical cord serum levels. Together, these studies found that low maternal vitamin D levels were associated with a 40% higher risk of ADHD in their children. Whether maternal serum or umbilical cord serum measurements were used had little or no effect on the outcome. Study heterogeneity was negligible. But the authors noted that this result "should be considered with caution" because it was heavily dependent on one of the prospective studies included in the analysis. All of which suggest a need for further prospective studies
In the meantime, the authors suggest it would be prudent to increase sun exposure and vitamin D supplementation, given the prevalence of vitamin D deficiency.