Cookie Preferences
By clicking, you agree to store cookies on your device to enhance navigation, analyze usage, and support marketing. More Info
Thank you! Your submission has been received!
Oops! Something went wrong while submitting the form.
January 26, 2022
This systematic review of the literature identified seven studies addressing ADHD and sexuality.
Sexual function
A Dutch study compared 136 persons with ADHD with two large surveys of the general Dutch population. They used both a self-report questionnaire, the Questionnaire for screening Sexual Dysfunction and a non-validated questionnaire especially constructed for the study. They found that males with ADHD reported a 50 percent higher rate of frequent masturbation than males in the general population. Both males and females were less than half as likely to be satisfied with their sex life. That was almost certainly linked to the fact that ADHD participants in the sample were less likely to be in a relationship.
A second study compared 79 ADHD participants with controls. Using a validated questionnaire, the Diagnostic Interview Schedule, to assess sexual function, they found a significant positive correlation between ADHD and the items "sex drive more than the average" and "recurrent thoughts about sex' by comparison with the control group.
A third study used two validated inventories “ the Derogates Sexual Functioning Inventory and the Social Sexual Orientation Inventory“ to assess sexual function among 27 young adult males. They found their sex drive to be higher than in the control group.
Another study, also with 27 ADHD patients, compared them with two other groups, one with fiber mitosis (benign connective tissue cancers), and the other with both ADHD and fibromatosis. They used the validated Life Satisfaction Questionnaire to assess sexual function and found that those with ADHD reported lower sex life satisfaction.
On the other hand, the only large study, with over 14,000 participants, using a non-validated questionnaire to assess sexual function, found negligible associations between ADHD and the number of sexual partners, the frequency of having sex with one's partner, and the frequency of masturbation.
Sexual dysfunctions
The Dutch study mentioned above, comparing 136 ADHD outpatients with two large surveys of the general Dutch population, used a validated self-report questionnaire, the Questionnaire for screening Sexual Dysfunctions, and a non-validated questionnaire, specially designed for the study, the Questionnaire for screening Sexual Problems. It found the rate of sexual dysfunction among both males and females with ADHD to be over twice the level in the general population. Men were four times as likely to report problems with orgasm, 50 percent more likely to report premature ejaculation, and over ten times as likely to report sexual aversion. Women were over three times as likely to report sexual excitement problems, over twice as likely to report problems with orgasm, and over three times as likely to report sexual aversion. No significant differences existed between patients treated with psychostimulants and those without such treatment.
A second study, which used a validated questionnaire to compare 79 ADHD participants with controls, found significant correlations between ADHD and aversion to sex for men but none for women.
On the other hand, a third study, comparing 32 subjects with ADHD with 293 controls, found no significant difference in the prevalence of sexual dysfunctions. It used clinical interviews to assess ADHD, and a non-validated questionnaire to assess sexual dysfunctions.
A fourth study took a very different approach. It compared 38 individuals with premature ejaculation to 27 controls. It found more than ten times the rate of ADHD symptoms among those with premature ejaculation than in the control group. Significantly, it measures premature ejaculation directly, with a stopwatch.
Conclusion
The authors concluded, "This article provides the first systematic review of sexual health among subjects with ADHD and shows that the quality of sexual health among subjects with ADHD seems poor," but acknowledged "several limitations to our review. There are only a few studies for the topics we reviewed. For many studies, the sample size was small. The methodology and measurement instruments differed, which created a potential bias."
Indeed, the study with the largest sample size found negligible associations between ADHD and sexual function, contradicting studies with small sample sizes.
Only four of the studies, all with small sample sizes, examined sexual dysfunctions. Two found strong associations with ADHD, one found none, and the fourth had mixed results.
This points to a compelling need for further research on ADHD and sexuality, with larger sample sizes.
Lorenzo Soldati, MD, Francesco Bianchi-Demicheli, MD, Pauline Schockaert, MAS, John Köhl, MAS, MylèneBolmont, Ph.D., Roland Hasler, Ph.D., and Nader Perroud, MD, “SexualFunction, Sexual Dysfunctions, and ADHD: A Systematic Literature Review,” Journal of Sexual Medicine(2020),https://doi.org/10.1016/j.jsxm.2020.03.019.
Although ADHD was conceived as a childhood disorder, we now know that many cases persist into adulthood. My colleagues and I charted the progression of ADHD through childhood, adolescence, and adulthood in our "Primer" about ADHD,http://rdcu.be/gYyV. Although the lifetime course of ADHD varies among adults with the disorder, there are many consistent themes, which we described in the accompanying infographic. Most cases of ADHD startin uterobefore the child is born. As a fetus, the future ADHD person carries versions of genes that increase the risk for the disorder. At the same time, they are exposed to toxic environments. These genetic and environmental risks change the developing brain, setting the foundation for the future emergence of ADHD.
In preschool, early signs of ADHD are seen in emotional lability, hyperactivity, disinhibited behavior, and speech, language, and coordination problems. The full-blown ADHD syndrome typically occurs in early childhood, but can be delayed until adolescence. In some cases, the future ADHD person is temporarily protected from the emergence of ADHD due to factors such as high intelligence or especially supportive family and/or school environments. But as the challenges of life increase, this social, emotional, and intellectual scaffolding is no longer sufficient to control the emergence of disabling ADHD symptoms. Throughout childhood and adolescence, the emergence and persistence of the disorder are regulated by additional environmental risk factors such as family chaos along with the age-dependent expression of risk genes that exert different effects at different stages of development. During adolescence, most cases of ADHD persist and by the teenage years, many youths with ADHD have onset with a mood, anxiety, or substance use disorder. Indeed, parents and clinicians need to monitor ADHD youth for early signs of these disorders. Prompt treatment can prevent years of distress and disability. By adulthood, the number of comorbid conditions has increased, including obesity, which likely has effects on future medical outcomes.
The ADHD adult tends to be very inattentive by showing fewer symptoms of hyperactivity and impulsivity. They remain at risk for substance abuse, low self-esteem, occupational failure, and social disability, especially if they are not treated for the disorder. Fortunately, there are several classes of medications available to treat ADHD that are safe and effective. And the effects of these medications are enhanced by cognitive behavior therapy, as I've written about in prior blogs.
Although there has been much research documenting that ADHD adults are at risk for other psychiatric and substance use disorders, relatively little is known about whether ADHD puts adults at risk specifically for somatic medical disorders.
Given that people with ADHD tend toward being disorganized and inattentive, and that they tend to favor short-term over long-term rewards, it seems logical that they should be at higher risk for adverse medical outcomes. But what does the data say?
In a systematic review of the literature, Instances and colleagues have provided a thorough overview of this issue. Although they found 126 studies, most were small and were of "modest quality". Thus, their results must be considered to be suggestive, not definitive for most of the somatic conditions they studied.
Also, they excluded articles about traumatic injuries because the association between ADHD and such injuries is well established. Using qualitative review methods, they classified associations as being a) well-established; b) tentative, or c) lacking sufficient data.
Only three conditions met their criteria for being a well-established association: asthma, sleep disorders, and obesity.
They found tentative evidence implicating ADHD as a risk factor for three conditions: migraine headaches, celiac disease, and diseases of the circulatory system.
These data are intriguing, but cannot tell us why ADHD people are at increased risk for somatic conditions. One possibility is that suffering from ADHD symptoms can lead to an unhealthy lifestyle, which leads to increased medical risk. Another possibility is that the biological systems that are dysregulated in ADHD are also dysregulated in some medical disorders. For example, we know that there is some overlap between the genes that increase the risk for ADHD and those that increase the risk for obesity. We also know that the dopamine system has been implicated in both disorders.
Instances and colleagues also point out that some medical conditions might lead to symptoms that mimic ADHD. They give sleep-disordered breathing as an example of a condition that can lead to the symptom of inattention.
But this seems to be the exception, not the rule. Other medical conditions co-occurring with ADHD seem to be true comorbidities, rather than the case of one disorder causing the other. Thus, primary care clinicians should be alert to the fact that many of their patients with obesity, asthma, or sleep disorders might also have ADHD.
By screening such patients for ADHD and treating that disorder, you may improve their medical outcomes indirectly via increased compliance with your treatment regime and an improvement in health behaviors. We don't yet have data to confirm these latter ideas, as the relevant studies have not yet been done.
There is a growing interest (and controversy) in '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 a 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 by 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 ADHDused 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 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 add 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 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.
The Background:
Concerns remain about how ADHD and methylphenidate (MPH) use might affect children's health and growth, and especially how it may affect their adult height. While some studies suggest disrupted growth and a possible biological mechanism, the impact of ADHD prevalence and MPH use is still unclear. Children with ADHD may develop unhealthy habits – irregular eating, low physical activity, and poor sleep – that can contribute to obesity and reduced height. MPH’s appetite-suppressing effect can lead to skipped meals or overeating. Since growth hormone is mainly released during deep sleep, chronic sleep deprivation could plausibly slow growth and impair height development; however, a clear link between ADHD, MPH use, overweight, and shorter stature has never been firmly established.
The Study:
South Korea has a single payer health insurance system that covers more than 97% of its population. A Korean research team used the National Health Insurance Service database to perform a nationwide population study to explore this topic further.
The study involved 34,850 children, of whom 12,866 were diagnosed with ADHD. Of these children, 6,816 (53%) had received methylphenidate treatment, while 6,050 (47%) had not. Each patient with ADHD was precisely matched 1:1 by age, sex, and income level to a control participant without ADHD. The sex ratio was comparable in all groups.The team used Body Mass Index (BMI) as an indicator of overweight and obesity.
The Results:
The researchers found that being diagnosed with ADHD was associated with 50% greater odds of being overweight or obese as young adults, and over 70% greater odds of severe obesity (BMI > 30) compared to matched non-ADHD controls, regardless of whether or not they were medicated.
Those diagnosed with ADHD, but not on methylphenidate, had 40% greater odds of being overweight or obese, and over 55% greater odds of becoming severely obese, relative to matched non-ADHD controls.
Methylphenidate users had 60% greater odds of being overweight or obese, and over 85% greater odds of becoming severely obese, relative to matched non-ADHD controls.
There were signs of a dose-response effect. Less than a year’s exposure to methylphenidate was associated with roughly 75% greater odds of becoming severely obese, whereas exposure over a year or more raised the odds 2.3-fold, relative to matched non-ADHD controls. Using MPH increased the prevalence of overweight from 43.2% to 46.5%, with a greater prevalence among those using MPH for more than one year (50.5%).
It is important to note that most of this effect was from ADHD itself, with methylphenidate only assuming a predominant role in severe obesity among those with longer-term exposure to the medicine.
As for height, children with ADHD were no more likely to be short of stature than matched non-ADHD controls. Being prescribed methylphenidate was associated with slightly greater odds (7%) of being short of stature, but there was no dose-response relationship.
Conclusion:
The team concluded, “patients with ADHD, particularly those treated with MPH, had a higher BMI and shorter height at adulthood than individuals without ADHD. Although the observed height difference was clinically small in both sexes and age groups, the findings suggest that long-term MPH exposure may be associated with growth and body composition, highlighting the need for regular monitoring of growth.” They also point out that “Despite these findings, the clinical relevance should be interpreted with caution. In our cohort, the mean difference in height was less than 1 cm (eg, maximum −0.6 cm in females) below commonly accepted thresholds for clinical significance.” Likewise, increases in overweight/BMI were small.
One problem with interpreting the BMI/obesity results is that some of the genetic variants that cause ADHD also cause obesity. If that genetic load increases with severity of ADHD than the results from this study are confounded because those with more severe ADHD are more likely to be treated than those with less severe ADHD.
Due to these small effects along with the many study limitations noted by the authors, these results should be considered alongside the well-established benefits of methylphenidate treatment.
What do we mean by expert? In simple terms, an expert possesses in-depth knowledge and specialized training in a particular field. In order to be considered an expert in any field, a person must have both deep knowledge of and competence in their specific area of expertise. Experts have a background that includes education, research, and experience. In the world of mental health and psychology, this typically means formal credentials (a PhD, MD, etc) in addition to years of study, peer-reviewed publications, and/or extensive clinical experience.
Experts are recognized by their peers (and often by the public) as reliable authorities on a specific topic. Experts usually don’t make big claims without evidence; instead, they cite studies and speak cautiously about what the evidence shows.
Tip: Those looking for likes and clicks will often speak in absolutes (e.g., “refined sugar makes your ADHD worse, but the Keto Diet will eliminate ADHD symptoms”) while experts will use language that emphasizes evidence (e.g., “research has proven that there is no ‘ADHD Diet’, but some evidence has suggested that certain individuals with ADHD may benefit from such dietary interventions as limiting food coloring or increasing omega fatty acids.”)
Social media has created an incredible opportunity for those with ADHD to gain access to invaluable resources, including the creation of communities by and for those with ADHD. Many people with ADHD report feeling empowered and less alone by connecting with others online. These online social platforms provide a space for those with ADHD to share their own perspectives and their lived experience with the disorder. Both inside and outside of mental health-related communities, social media is a powerful tool for sharing information, reducing stigma, and helping people find community. When someone posts about their own ADHD challenges or tips, it can reassure others that they’re not the only ones facing these issues. This kind of peer support is valuable and affirming.
It is vital for those consuming this media, however, to remember that user-generated content on social media is not vetted or regulated. Short TikTok or Instagram videos are designed to grab attention, not to teach nuance or cite scientific studies. As it turns out, most popular ADHD posts are misleading or overly simplistic, at best. One analysis of ADHD TikTok videos found that over half were found to be “misleading” by professionals. Because social feeds reinforces what we already believe (the “echo chamber” effect, or confirmation bias), we can easily see only content that seems to confirm our own experiences, beliefs, or fears.
Stories aren’t a substitute for expert guidance.
It’s important to recognize the difference between personal experience and general expertise. Having ADHD makes you an expert on your ADHD, but it does not make you an expert on ADHD for everyone. Personal stories are not scientific facts. Even if someone’s personal journey is true, the same advice or experience may not apply to others. For instance, a strategy that helps one person focus might have no effect– or possibly even a negative effect– on someone else.
Researchers have found that most ADHD content on social media is based on creators’ own experiences, not on systematic research. In one study, almost every TikTok ADHD creator who listed credentials actually just cited their personal story. Worse, about 95% of those videos never noted that their tips might not apply to everyone (journals.plos.org.) In other words, they sound absolute even though they really only reflect one person’s situation. It’s easy to misunderstand the condition if we take those singular experiences as universal facts.
So how can you tell when someone is speaking from expertise rather than personal experience or hearsay? Experienced professionals usually speak cautiously, rather than in absolutes. They tend to say things like “research suggests,” “some studies show,” or “evidence indicates,” rather than claiming something always or never happens. As one health-communication guide puts it, a sign of a trustworthy source is that they do not speak in absolutes; instead, they use qualifiers like “may,” “might,” or refer to specific studies. For example, an expert might say, “Some people with ADHD may have difficulty with organization,” instead of “ADHD people always lose things.”
Real experts also cite evidence. In science and psychology, experts usually share knowledge through peer-reviewed articles, textbooks, or professional conferences – not just social media posts. Reliable health information is typically backed by references to studies published in reputable journals.
If someone makes a claim online, ask: Do they point to research, or is it just their own testimony? This is why it’s wise to prefer content where the author is a recognized authority (like a doctor or researcher) and where references to scientific studies or official guidelines are provided. In fact, advice from sites ending in “.gov”, “.edu”, or “.org” (government, university, or professional organizations) tends to be more reliable than random blogs. When in doubt, look up who wrote the material and whether it cites peer-reviewed research.
When navigating mental health information online, remember these key points:
If you see sweeping statements like “This one habit will predict if you have ADHD” or “Eliminating this one food will cure your ADHD symptoms”--- that’s a red flag. Instead, the hallmark of expert advice is a tone of humility (“evidence suggests,” “it appears that,” etc.), clear references to studies or consensus statements, and an acknowledgment that individual differences exist.
At the same time, we need to acknowledge that community voices are incredibly valuable – they help us feel understood and less alone. The goal is not to dismiss personal stories, but to balance them with facts and evidence-based information. Let lived experience spark questions, but verify important advice with credible sources. Follow trusted organizations (for example, the National Institutes of Health, CDC, or ADHD specialist groups) and mental health professionals who communicate carefully. Use the online ADHD community for support and sharing tips, but remember it’s just one piece of the puzzle.
By being a savvy reader (checking credentials, looking for cited evidence, and spotting overgeneralizations), you can make the most of online ADHD content. In doing so, you give yourself both the empathy of community and the accuracy of real expertise. That way, you’ll be well-equipped to separate helpful insights from hype and to keep learning from both personal stories and science-based experts.
Stimulant medications have long been considered the default first-line treatment for attention-deficit/hyperactivity disorder (ADHD). Clinical guidelines, prescribing practices, and public narratives all reinforce the idea that stimulants should be tried first, with non-stimulants reserved for cases where stimulants fail or are poorly tolerated.
I recently partnered with leading ADHD researcher Jeffrey Newcorn for a Nature Mental Health commentary on the subject. We argue that this hierarchy deserves reexamination. It is important to note that our position is not anti-stimulant. Rather, we call into question whether the evidence truly supports treating non-stimulants as secondary options, and we propose that both classes should be considered equal first-line treatments.
Stimulants have earned their reputation as the go-to drug of choice for ADHD. They are among the most effective medications in psychiatry, reliably reducing core ADHD symptoms and improving daily functioning when properly titrated and monitored. However, when stimulant and non-stimulant medications are compared more closely, the gap between them appears smaller than commonly assumed.
Meta-analyses often report slightly higher average response rates for stimulants, but head-to-head trials where patients are directly randomized to one medication versus another frequently find no statistically significant differences in symptom improvement or tolerability. Network meta-analyses similarly show that while some stimulant formulations have modest advantages, these differences are small and inconsistent, particularly in adults.
When translated into clinical terms, the advantage of stimulants becomes even more modest. Based on existing data, approximately eight patients would need to be treated with a stimulant rather than a non-stimulant for one additional person to experience a meaningful benefit. This corresponds to only a 56% probability that a given patient will respond better to a stimulant than to a non-stimulant. This difference is not what we would refer to as “clinically significant.”
One reason non-stimulants may appear less effective is the way efficacy is typically reported. Most comparisons rely on standardized mean differences, a method of averages that may mask heterogeneity of treatment effects. In reality, ADHD medications do not work uniformly across patients.
For example, evidence suggests that response to some non-stimulants, such as atomoxetine, is bimodal: this means that many patients respond extremely well, while others respond poorly, with few in between. When this happens, average effect sizes can obscure the fact that a substantial subgroup benefits just as much as they would from a stimulant. In other words, non-stimulants are not necessarily less effective across the board, but that they are simply different in who they help.
In our commentary, we also highlight structural issues in ADHD research. Stimulant trials are particularly vulnerable to unblinding, as their immediate and observable physiological effects can reveal treatment assignment, potentially inflating perceived efficacy. Non-stimulants, with slower onset and subtler effects, are less prone to this bias.
Additionally, many randomized trials exclude patients with common psychiatric comorbidities such as anxiety, depression, or substance-use disorders. Using co-diagnoses as exclusion criteria for clinical trials on ADHD medications is nonviable when considering the large number of ADHD patients who also have other diagnoses. Real-world data suggest that a large proportion of individuals with ADHD would not qualify for typical trials, limiting how well results generalize to everyday clinical practice.
Standard evaluations of medication tolerability focus on side effects experienced by patients, but this narrow lens misses broader societal consequences. Stimulants are Schedule II controlled substances, which introduces logistical barriers, regulatory burdens, supply vulnerabilities, and administrative strain for both patients and clinicians.
When used as directed, stimulant medications do not increase risk of substance-use disorders (and, in fact, tend to reduce these rates); however, as ADHD awareness has spread and stimulants are more widely prescribed, non-medical use of prescription stimulants has become more widespread, particularly among adolescents and young adults. Non-stimulants do not carry these risks.
Non-stimulants are not without drawbacks themselves, however. They typically take longer to work and have higher non-response rates, making them less suitable in situations where rapid results are essential. These limitations, however, do not justify relegating them to second-line status across the board.
This is a call for abandoning a one-size-fits-all approach. Instead, future guidelines should present stimulant and non-stimulant medications as equally valid starting points, clearly outlining trade-offs related to onset, efficacy, misuse risk, and practical burden.
The evidence already supports this shift. The remaining challenge is aligning clinical practice and policy with what the data, and patient-centered care, are increasingly telling us.
_logo%201.svg)
