International Journal of Epidemiology, 2017, 409–420

doi: 10.1093/ije/dyw073
Advance Access Publication Date: 10 May 2016
Original article

Neurocognitive Development and Mental Health

Parental age and attention-deficit/hyperactivity

disorder (ADHD)

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Susanne Hvolgaard Mikkelsen,1,* Jørn Olsen,2,3 Bodil Hammer Bech4
and Carsten Obel1,5
1
Department of Public Health, Section for General Medical Practice, 2Department of Clinical Medicine,
Clinical Epidemiolgy, Aarhus University, Aarhus, Denmark, 3Department of Epidemiology, Fielding
School of Public Health, University of California, Los Angeles, CA, USA, 4Department of Public Health,
Section for Epidemiology and 5Center of Collaborative Health, Aarhus University, Aarhus, Denmark
*Corresponding author. Susanne Hvolgaard Mikkelsen, Ph.d. Student, MHSc., RN, Institute of public health, Department of gen-
eral medical practice, Aarhus University, Bartholins Allé 2, 8000 Aarhus C, Denmark. Email:susanne.hvolgaard.mikkelsen@ph.au.dk
Accepted 16 March 2016

Abstract
Background: Previous studies have suggested that young mothers more often have chil-
dren with ADHD. We used sibling comparisons to examine the nature of this association
and to investigate if this association is explained by early environment or genetic and
socioeconomic factors.
Methods: A large population-based cohort including all singletons born in Denmark
from 1 January 1991 through 31 December 2005 was followed from birth until 30 April
2011. Data were available for 94% (N ¼ 943 785) of the population. Offspring ADHD was
identified by an ICD-10 diagnosis of Hyperkinetic Disorder (HKD). We used sibling-
matched Cox regression to control for genetic and socioeconomic factors.
Results: In the population cohort we found that children born by parents aged 20 years
or younger had more than twice the risk of being diagnosed with ADHD compared with
children with parents between 26 and 30 years of age. When comparing full siblings the
associations were attenuated, but we found a trend of increased risk of ADHD with
decreasing maternal age, which was not seen for paternal age.
Conclusions: Sibling comparisons suggested that the associations between both mater-
nal and paternal age and ADHD are partly explained by common genetic and socioeco-
nomic factors. The trend of increased risk of ADHD with decreasing maternal age, but
not with paternal age, may be linked to pregnancy or early-life environmental factors.
Even though only a smaller part of the association can be attributed to environmental
factors, there is a public health interest to support young parents through their first years
of parenthood.

Key words: Maternal age, paternal age, parental age, hyperkinetic disorder, attention-deficit/hyperactivity
disorder, sibling design

C The Author 2016; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association
V 409
410 International Journal of Epidemiology, 2017, Vol. 46, No. 2

Key messages

• Children diagnosed with ADHD were more likely to have younger parents than children without ADHD.
• The highest risk of ADHD was found when both parents were very young.
• Sibling comparisons suggested that the association between both young maternal and paternal ages and ADHD

mainly can be accounted for by genetic and socioeconomic factors.

• In the area of public health, focus on delaying fertility without ameliorating the background risks experienced by

young parents and their children may not be fully effective in reducing offspring ADHD. Public policy initiatives
should be targeted at attention to young parents and individual support of at-risk parents and their children.

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Introduction
Attention-deficit/hyperactivity disorder (ADHD) is one of
the most common psychiatric disorders in childhood.1,2
During recent decades a trend towards an increase in
ADHD diagnosis has been observed,36 with a current esti-
mated prevalence of 3–7% among children and adoles-
cents.1,7,8 This trend may to some extent be related to
changes in diagnostic criteria, earlier age at diagnosis,
increased clinical awareness and media attention.1,4,9–11
There is robust evidence from a wide range of study de-
signs that the development of ADHD has a strong genetic
component.12 First-degree relatives of those with ADHD
are two to eight times more likely than relatives of un-
affected individuals to also show ADHD symptoms.13
Twin studies have found higher concordance rates for
ADHD among monozygotic twin than dizygotic twin
pairs, with a heritability estimate around 80%.13,14
However, heritability estimates include not only genetic in-
fluences, but also the effects of gene-environment inter-
action. Genetic predisposition in parents may lead to
inherited predisposition in children with expression trig-
gered by environmental factors.15.
ADHD constitutes a major social and economic chal-
lenge, and identification of potentially preventable envir-
onmental factors is of major public health interest.
Environmental exposures in utero as well as in early life
have been shown to be important for lifetime health, but to
date only few plausible environmental causes have been
identified for the development of ADHD, leaving limited
room for prevention.
There is an increasing focus on potential perinatal fac-
tors related to mental health in offspring.16,17 A systematic
review of pre- and perinatal risk factors for ADHD impli-
cated exposure to tobacco smoke in utero as a suspected
risk factor18 although recent research questions this con-
clusion.19,20 Also, exposure to other substances during
pregnancy has been linked to ADHD. Moderate maternal
alcohol use during pregnancy and exposure to illicit sub-
stances have been associated with increased risk of ADHD
in some, but not all, studies.18 The probably most robust
associations so far are the links between intrauterine
growth retardation and prematurity and subsequent
ADHD in the offspring.18.21,22 Another consistently found
association is that children with ADHD have younger par-
ents compared with children without ADHD,23–28 but sur-
prisingly few studies have aimed to explore the nature of
this association by including both parents in their
analyses.27
Although the association has not been studied in depth,
a number of biological hypotheses have been suggested. An
imbalance between the competing nutritional needs of the
mother and child may play a role; and, further, children
of young mothers are exposed to different amounts of sex-
related hormones compared with children of older
mothers.29,30 A likely alternative explanation is that the as-
sociation simply reflects genetic and socioeconomic factors
accompanying young parenthood.31–36 A recent Swedish
study using sibling and cousin comparisons to partly con-
trol for unmeasured genetic and environmental confound-
ing, supported that the association is mainly explained by
genetic factors contributing to both young maternal age at
childbirth and ADHD in offspring.37 If this is the case, a
mother may confer risk to her children regardless of
whether she gives birth as a teenager or later in life, which
has been supported by studies finding that maternal age at
first birth was more predictive of later-born children’s psy-
chiatric problems than maternal age at the child’s own
birth.35,37,38 Maternal age at her first birth could be seen
as a marker of genetic and social factors related to ADHD
in young mothers.
The crucial question is whether this higher risk in off-
spring of younger mothers constitutes a potential for pre-
vention by delaying fertility, or whether focus should be on
supportive interventions in young parents to improve the
upbringing environment and thereby reduce symptoms in
offspring with a genetic predisposition.
If the association between young maternal age and off-
spring ADHD is caused by familial factors, a similar
International Journal of Epidemiology, 2017, Vol. 46, No. 2
association is to be expected between young paternal age
and ADHD and, further, an additional risk is to be ex-
pected when both parents are very young. Few studies
have reported on associations between paternal age and
ADHD, and results have been conflicting.23,27,39,40 A study
from Sweden reported advanced paternal age to be associ-
ated with an increased risk of ADHD.40 In contrast, an-
other study from Israel found that the paternal age
distribution among children with ADHD was similar to
what we see in the general population.39
We studied offspring ADHD according to maternal as
well as paternal age, and combined parental age in a large
population-based cohort. We did comparisons of risk be-
tween full and half siblings to control for unmeasured gen-
etic and socioeconomic factors and other shared family
characteristics.
Methods
Setting
All citizens in Denmark are given a unique civil registration
number at birth or immigration, by the Danish Central
Population Registry (DCPR). This registry includes infor-
mation on date of birth and biological relationships for all
citizens in Denmark since 1968. Using the civil registration
number we linked data from the Danish Medical Birth
Figure 1. Flowchart.
411
Registry (DMBR) and the Danish Psychiatric Central
Research Register (DPCR) with psychiatric outcome.
We defined a cohort study with follow-up of singletons
born in Denmark from 1 January 1991 to 31 December
2005. All births by women with permanent residence in
Denmark (N ¼ 999 713) were identified in the Danish
Medical Birth Registry, DMBR. We excluded multiple
births (n ¼ 37 406) and, after linkage with the DCPR, we
excluded additionally 18 522 children with insufficient or
missing data for the biological father; this left 943 785
children in the cohort (Figure 1). The study was approved
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by the Danish Health Authority and the Danish Data
Protection Agency.
Maternal and paternal ages at birth were calculated
based on the civil registration numbers of mothers, fathers
and children, and was then divided into five age groups
ranging from 20 years or younger to older than 35 years,
in 5-year intervals.
Outcome definition
We defined offspring ADHD as children with an ICD-10
diagnosis of Hyperkinetic Disorder (F90x) after the age of
5 years, identified in the DPCR. The ICD-10 classification
system has been used since 1994. The DPCR provides indi-
vidual-level data on clinical diagnoses and admission dates
for all inpatient psychiatric hospital admissions since 1969
412
and outpatient visits at psychiatric hospitals and clinics
since 1995.
Statistical analyses
Maternal and paternal ages were studied separately. We
used maternal or paternal age between 26 and 30 years as
the reference group. In a subanalysis, maternal and pater-
nal ages were further divided into three age groups— < 26,
26–30, > 30 years—to study parental age combining both
maternal and paternal age. We used maternal and paternal
ages > 30 years as the reference group. Finally, to examine
the full childbearing age range, maternal and paternal ages
were studied as continuous variables using cubic splines.41
Measured covariates included: gender (girls, boys); parity
(1, > 1); maternal smoking during pregnancy (yes, no); and
birth-year groups (1-year intervals).
We examined the relative risk (RR) of being diagnosed
with ADHD associated with the exposure variable of inter-
est, using Cox regression. Cox regression estimates hazard
rate ratios comparing the different exposure groups,
assuming the hazard ratio remains constant over time. We
evaluated the proportional hazard assumption by graphical
assessment of log-log plots, and the assumption was ac-
ceptable. Results are reported as hazard ratios (HR) with
95% confidence intervals (CIs). The Cox regression
allowed us to control for entry at different time points,
varying length of follow-up and changing rates of ADHD
over time. Since ADHD is a rare outcome resulting in low
hazard rates, the relative HR will approximate RR and
hazard ratios can be interpreted in terms of additional cu-
mulative risk. Each child contributed with risk time begin-
ning at the age of 5 years old and ending at diagnosis,
immigration, death or end of follow-up on 30 April 2011,
whichever came first. To control for the lack of independ-
ence of children within the same family, we used robust
variance estimation in the population cohort analyses. We
did regular cohort analyses and then compared results with
both full and half sibling-matched analyses. All statistical
analyses were performed with Stata/SE 12.
Population cohort analyses
To adjust for changing diagnostic criteria, differences in as-
sessment methods over time, changing age at first child-
birth and the changing prevalence of ADHD during the
study period, we adjusted for calendar time by including
separate baseline diagnostic rates (strata) for each birth
year.1,10,42
We estimated crude and adjusted HR within the popula-
tion cohort. Maternal and paternal age were studied cat-
egorically and as continuous variables expressed as cubic
International Journal of Epidemiology, 2017, Vol. 46, No. 2
splines with five knots, which are the default knot values
based on Harrell’s recommended percentiles.41 The adjusted
HR was in addition adjusted for parity, maternal smoking
during pregnancy and gender. As maternal and paternal
ages are highly correlated, we adjusted for the other parent’s
age by including the age difference between parents in the
model; this covered both the parental age difference and the
age of the other parent as a confounder.43
Gestational age and birthweight are assumed to be po-
tential intermediate factors and were therefore not ad-
justed for in the final models,44 but in subanalyses we
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examined if the association between maternal age and
ADHD was modified by gestational age or birthweight.
Further, we examined whether associations of interest
were modified by parity, gender or birth year.
Sibling-matched analyses
Two sibling subcohorts were identified as children born in
the time period 1 January 1991 to 31 December 2005. One
included full siblings; the other included half siblings with
the same biological mother. Full sibling comparisons pro-
vide stronger adjustment for shared genetic and time-stable
environmental factors compared with half sibling compari-
sons. Only families with at least two siblings, of which at
least one child was diagnosed with ADHD, were included,
corresponding to 6436 families in the full sibling cohort
and 1795 families in the half sibling cohort.
The sibling-matched design extends the Cox regression
model by stratifying on the set of either full or half siblings.
In the stratified Cox regression model, each family has its
own baseline rate function reflecting the family’s shared
genetic and environmental factors and thus adjustment for
all factors that are shared within each sibling set.
Additionally, the sibling comparisons allow us to control
for the age difference between parents among full siblings
and maternal age at birth of first child among both full and
half siblings. Only families with at least two siblings dis-
cordant for parental age group contributed with informa-
tion on the association between parental age and ADHD.
The adjusted sibling-matched analyses were controlled for
the same covariates as in the population cohort and, in
addition, adjustment for the increasing prevalence of
ADHD was achieved by including calendar time in a cubic
spline with five knots.41
Results
Population cohort
In the population cohort, 1.30% of the children had a hos-
pital diagnosis of ADHD (1.99% boys and 0.58% girls,
International Journal of Epidemiology, 2017, Vol. 46, No. 2 413

respectively) (Table 1). We found that both decreasing ma-
ternal and paternal ages were associated with higher risk of
being diagnosed with ADHD; the associations were margin-
ally attenuated after adjustment for the measured covariates.
Children with mothers or fathers 20 years of age or younger
had more than twice the risk of ADHD (HR ¼ 2.24, 95% CI
2.07–2.42 and HR ¼ 2.28, 95% CI 2.03–2.57, respectively)
(Table 2) compared with children with parents between 26
and 30 years of age. The associations between the catego-
rized maternal as well as paternal age and ADHD followed a
‘dose-response’ relation with increasing risk of ADHD with
children with mothers aged 29 years or fathers aged 32
years, a higher risk of ADHD was found with decreasing
maternal or paternal age (Figures 2 and 3) For children
with an older father (> 30 years), the younger the mother
the higher risk of ADHD. The risk increased by 25%
(HR ¼ 1.25, 95% CI 1.18–1.33) among children born to
mothers aged 26–30 years and by 98% (HR ¼ 1.98, 95%
CI 1.81-2.15) among children born to mothers aged below
26 years (Table 3). Among children born to mothers older
than 30 years, the risk of ADHD was also affected by pa-
ternal age (Table 3). The combination of both a young

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decreasing parental age (test for trend P-value < 0.001). mother and a young father resulted in the highest risk for
Additionally, we found almost similar associations ADHD (HR ¼ 2.31, 95% CI 2.16–2.46). In the population
when maternal and paternal ages were studied as continu- cohort, we did not find interaction by gestational age,
ous variables expressed as cubic splines. Compared with birthweight, gender, parity or birth year.

Table 1. Descriptive statistics of the population cohort

Variable All births No. (%) ADHD-diagnose Maternal age, mean Paternal age, mean
No. (%) (95% CI) (95% CI)

Total no. (%) 943 785 (100) 12 294 (1.30) 29.43 (29.42–29.44) 32.32 (32.31–32.34)
Gender no. (%)
Female 458 749 (48.61) 2647 (0.58) 29.63 (29.61–29.64) 32.32 (32.30–32.34)
Male 485 036 (51.39) 9647 (1.99) 29.64 (29.62–29.65) 32.33 (32.31–32.34)
Birthweight, no. (%), grams
 2000 13 224 (1.40) 281 (2.12) 29.74 (29.65–29.83) 32.50 (32.39–32.61)
2001–2500 23 953 (2.54) 467 (1.95) 29.36 (29.29–29.42) 32.03 (31.95–32.11)
2501–3000 111 746 (11.84) 1723 (1.54) 29.09 (29.06–29.12) 31.91 (31.87–31.94)
3001–3500 307 588 (32.59) 3827 (1.24) 29.35 (29.33–29.37) 32.10 (32.08–32.12)
3501–4000 318 112 (33.71) 3845 (1.21) 29.78 (29.76–29.80) 32.43 (32.41–32.45)
>4000 158 909 (16.84) 2013 (1.27) 30.27 (30.25–30.29) 32.81 (32.78–32.83)
Missing 10 253 (1.09) 138 (1.35) 30.08 (29.99–30.17) 32.99 (32.87–33.10)
Gestational age, no. (%), full weeks
< 32 6581 (0.70) 144 (2.19) 29.86 (29.74–29.99) 32.58 (32.43–32.73)
32–36 38 441 (4.07) 708 (1.84) 29.52 (29.47–29.57) 32.18 (32.12–32.24)
37–40 634 759 (67.26) 8218 (1.29) 29.66 (29.65–29.67) 32.35 (32.34–32.37)
> 40 250 395 (26.53) 3015 (1.20) 29.59 (29–57.29.60) 32.27 (32.25–32.29)
Missing 13 609 (1.44) 209 (1.54) 29.27 (29.19–29.35) 32.22 (32.11–32.32)
Apgarscore 5 min
9 67 232 (7.12) 1070 (1.59) 29.59 (29.56–29.63) 32.16 (32.12–32.21)
10 86 3277 (91.47) 11 031 (1.28) 29.63 (29.62–29.64) 32.33 (32.32–32.34)
Missing 13 276 (1.41) 193 (1.45) 29.70 (29.61–29.78) 32.69 (32.59–32.80)
Parity
1 406 476 (43.07) 5565 (1.37) 27.76 (27.75–27.78) 30.54 (30.53–30.56)
2 342 850 (36.33) 4245 (1.24) 30.22 (30.21–30.23) 32.85(32.84–32.87)
>2 177 717 (18.83) 2255 (1.27) 32.82 (32.80–32.84) 35.40 (35.38–35.43)
Missing 16 742 (1.77) 229 (1.37) 29.10 (29.03–29.18) 32.02 (31.93–32.11)
Smoking during pregnancy
Non smoker 676 117 (71.64) 6661 (0.99) 29.89 (29.88–29.90) 32.56 (32.55–32.57)
Smoker 219 876 (23.30) 4957 (2.25) 28.85 (28.83–28.87) 31.59 (31.56–31.61)
Missing 47 792 (5.06) 676 (1.41) 29.54 (29.50–29.58) 32.37 (32.32–32.42)
Birthyear
1991–95 318 085 (33.70) 4839 (1.52) 28.87 (28.86–28.89) 31.63 (31.61–31.65)
1996–2000 318 521 (33.75) 5025 (1.58) 29.67 (29.65–29.68) 32.36 (32.34–32.38)
2001–2005 307 179 (32.55) 2430 (0.79) 30.38 (30.37–30.40) 33.01 (32.99–33.03)
414 International Journal of Epidemiology, 2017, Vol. 46, No. 2

Table 2. Population cohort;crude and adjusted associations between maternal and paternal age and ADHD

Population cohort: risk of ADHD, HR (95%CI)

Maternal age Paternal age

Age groups, years Crude HR*1 Adjusted HR*2 Crude HR*1 Adjusted HR*2
No. ¼ 943 785 No. ¼ 883 933 No. ¼ 943 785 No. ¼ 883 933

 20 2.43 (2.27–2.61) 2.24 (2.07–2.42) 2.42 (2.16–2.71) 2.28 (2.03–2.57)

21–25 1.54 (1.47–1.61) 1.49 (1.42–1.56) 1.52 (1.44–1.60) 1.49 (1.40–1.57)
26–30 1.00 (ref.) 1.00 (ref.) 1.00 (ref.) 1.00 (ref.)
31–35 0.83 (0.79–0.88) 0.80 (0.76–0.85) 0.83 (0.79–0.87) 0.78 (0.74–0.82)
> 35 0.84 (0.78–0.90) 0.78 (0.72–0.84) 0.79 (0.75–0.83) 0.61 (0.57–0.65)

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P-value*3 < 0.001 < 0.001 < 0.001 < 0.001

*1Crude estimate stratified by birth year.

*2Adjusted estimate (parity 1/> 1; smoking no/yes; parental age difference; gender), stratified by birth year.
*3Test for trend.

Figure 2. Population cohort; crude and adjusted association between maternal age as a continuous variable expressed as cubic spline and ADHD.

Sibling cohort
In the full sibling cohort we found a weaker ‘dose-
response’ relation with higher risk of ADHD with decreas-
ing maternal age (P-value < 0.05). Compared with children
born to mothers aged between 26 and 30 years, the risk of
ADHD was increased by 28% (HR ¼ 1.28, 95% CI 0.94–
1.73) among children born to mothers aged 20 years or
younger (Table 4). Maternal age above 30 years remained
associated with lower risk of ADHD in the offspring
(Table 4). In the half sibling cohort, the same tendency of a
‘dose-response’ relation was seen(P-value 0.30). We
found no indication of a ‘dose-response’ relation be-
tween paternal age and ADHD either in the full sibling or
in the half sibling cohort (P-value 0.21 and 0.56,
respectively).
Further, results from the full sibling cohort suggested
that a sibling born when both parents were < 26 years old
had 61% (HR ¼ 1.61, 95% CI 1.13–2.30) higher risk of
ADHD compared with a later-born sibling with both par-
ents being older than 30 years old. Compared with a sib-
ling with both parents above 30 years, a sibling born
earlier in the parents’ lifespan with only a father above 30
years had a 32% (HR ¼ 1.32, 95% CI 1.12–1.56) and a
70% (HR ¼ 1.70, 95% CI 1.26–2.29) higher risk of
ADHD if the mother was 26–30 years old or younger than
26 years, respectively (Table 5). Conversely, in full siblings,
International Journal of Epidemiology, 2017, Vol. 46, No. 2 415

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Figure 3. Population cohort; crude and adjusted association between paternal age as a continuous variable expressed as cubic spline and ADHD.

Table 3. Population cohort; crude and adjusted combined effect of parental age on risk of ADHD

Population cohort: risk of ADHD, HR (95%CI)

Maternal age, years Paternal age, years

Crude HR*1 No.: 943 785 < 26 26–30 >30 P-value*3

< 26 2.40 (2.27–2.54) 1.83 (1.72–1.95) 1.98 (1.82–2.14)
26–30 1.69 (1.51–1.89) 1.23 (1.17–1.30) 1.21 (1.14–1.28)
> 30 2.02 (1.59–2.57) 1.25 (1.14–1.38) 1.00 (ref.) <0.001
Adjusted HR*2 No.: 883 933
< 26 2.31 (2.16–2.46) 1.85 (1.73–1.97) 1.98 (1.81–2.15)
26–30 1.63 (1.45–1.84) 1.29 (1.22–1.37) 1.25 (1.18–1.33)
> 30 1.76 (1.38–2.26) 1.23 (1.11–1.36) 1.00 (ref.) <0.001

*1Crude estimate stratified by birth year.

*2Adjusted estimate (parity 1/> 1; smoking no/yes; gender), stratified by birth year.
*Test for trend.

born to mothers aged above 30 years, decreasing paternal
age was no longer associated with an additional risk for
ADHD. (Table 5).
Discussion
In the population-based cohort we found that young ma-
ternal age as well as young paternal age were associated
with offspring ADHD, with the highest risk found when
both parents were younger than 26 years old. In the sibling
comparison, the association between maternal age and
ADHD was weaker, with the weakest association observed
in full siblings. We found no association between
paternal age and ADHD in full or half siblings. The results
including comparisons between children with different de-
grees of genetic similarity support the hypothesis that
part of the population-wide association between young
maternal age as well as young paternal age and offspring
ADHD may be explained by family-related factors. The as-
sociation may partly be caused by genetic risk factors, as
we observed the weakest association in the full sibling
comparison, which provides a stronger adjustment for
shared genetics than the half sibling comparison. Initiating
parenting at a young age may be a proxy for behavioural
genetic risk factors shared among members of the same
family and transmitted from parents to their offspring,
contributing to young parental age as well as offspring
ADHD.
416 International Journal of Epidemiology, 2017, Vol. 46, No. 2

Table 4. Sibling cohorts; crude and adjusted associations between parental age and ADHD

Cohorts: risk of ADHD, HR (95% CI)

Full siblings Half siblings

Age groups, years Crude HR*1 Adjusted HR*2 Crude HR*1 Adjusted HR*2

Maternal age No. ¼ 12 659 No. ¼ 11 853 No. ¼ 3549 No. ¼ 3281
20 1.16 (0.90–1.51) 1.28 (0.94–1.73) 1.33 (0.81–2.20) 1.38 (0.78–2.45)
21–25 1.10 (0.96–1.26) 1.15 (0.98–1.34) 1.16 (0.87–1.55) 1.24 (0.90–1.73)
26–30 1.00 (ref.) 1.00 (ref.) 1.00 (ref.) 1.00 (ref.)
31–35 0.77 (0.67–0.89) 0.73 (0.62–0.85) 0.80 (0.58–1.10) 0.89 (0.62–1.27)
> 35 0.65 (0.49–0.87) 0.61 (0.44–0.85) 0.71 (0.39–1.29) 0.79 (0.41–1.54)

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P-value*3 < 0.05 < 0.05 0.22 0.30
Paternal age No. ¼ 12335 No. ¼ 11572 No. ¼ 3289 No. ¼ 3083
 20 0.83 (0.58–1.18) 0.91 (0.60–1.37) 1.01 (0.74–1.38) 0.93 (0.57–1.52)
21–25 0.92 (0.79–1.06) 1.03 (0.86–1.22) 1.07 (0.89–1.28) 1.02 (0.77–1.34)
26–30 1.00 (ref.) 1.00 (ref.) 1.00 (ref.) 1.00 (ref.)
31–35 0.97 (0.85–1.11) 0.90 (0.77–1.05) 1.01 (0.83–1.23) 1.14 (0.85–1.53)
> 35 0.79 (0.61–1.01) 0.74 (0.53–1.02) 1.06 (0.83–1.35) 1.34 (0.77–2.30)
P-value*3 0.37 0.21 0.95 0.56

*1Crude estimate (adjusting for birth date by cubic spline).

*2Adjusted estimate (birth date by cubic spline; parity 1/> 1; smoking no/yes; gender; other parents age).
*3Test for trend.

Table 5. Sibling cohorts; crude and adjustedcombined effects of parental age on risk of ADHD

Risk of ADHD; HR (95% CI)

Maternal age, years Paternal age, years

Full siblingcohort

Crude HR*1 No.: 12 769 < 26 26–30 >30 P-value*3

< 26 1.30 (0.96:1.77) 1.33 (1.04–1.70) 1.65 (1.28–2.14)
26–30 1.08 (0.78–1.50) 1.32 (1.10–1.58) 1.26 (1.09–1.45)
> 30 0.95 (0.40–2.27) 1.05 (0.83–1.33) 1.00 (ref.) 0.72
Adjusted HR*2 No.: 11 967
< 26 1.61 (1.13–2.30) 1.50 (1.13–1.99) 1.70 (1.26–2.29)
26–30 1.35 (0.93–1.96) 1.45 (1.18–1.79) 1.32 (1.12–1.56)
> 30 0.79 (0.29–2.13) 1.09 (0.84–1.42) 1.00 (ref.) 0.32
Half siblingcohort
Crude HR*1 No.: 3730
< 26 1.96 (1.00:3.84) 1.33 (1.04–1.70) 2.04 (1.06–3.94)
26–30 1.28 (0.70–2.33) 1.32 (1.10–1.58) 1.16 (0.75–1.81)
> 30 1.06 (0.40–2.82) 1.05 (0.83–1.33) 1.00 (ref.) 0.25
Adjusted HR*2 No.: 3683
< 26 1.80 (0.86–3.80) 1.34 (0.68–2.65) 1.85 (0.89–3.86)
26–30 1.18 (0.60–2.29) 1.43 (0.86–2.37) 1.01 (0.62–1.67)
> 30 1.50 (0.51–4.38) 0.82 (0.43–1.56) 1.00 (ref.) 0.16

*1Crude estimate(adjusting for birth date by cubic spline).

*2Adjusted estimate (birth date by cubic spline: parity 1/> 1; smoking no/yes; gender).
*3Test for trend.

Young parents represent a selected group of young peo- history of hyperactivity problems32 and they may transmit
ple, and many of their characteristics may increase the risk the genetic susceptibility to ADHD in the offspring even
of ADHD in offspring. Compared with those who become though the severity of their own symptoms would not
parents at an older age, young parents more often have a reach the diagnostic threshold. This hypothesis is also
International Journal of Epidemiology, 2017, Vol. 46, No. 2
supported by research reporting that young people with
ADHD behaviour are found to have earlier sexual debut
and have more risky sexual behaviour with more sexual
partners, and thus a higher probability of becoming par-
ents at an earlier age.2,32,34,45–49
If the association between young maternal age and
ADHD is explained by a genetic predisposition, the timing
of the birth in the mothers life may not be the critical factor
in determining offspring ADHD.35,36,50–52 If such a mater-
nal disposition to initiate childbearing at a younger age ex-
plained the observed association in the population-based
cohort, we would not have expected to find an association
in the sibling comparisons, as the risk will be the same
among siblings. The early childbearing phenotype of the
mother will be the same for all siblings, and the attenua-
tion in the association between maternal age and ADHD
found in the sibling comparison may reflect that this phe-
notype is central in the association found in the population
cohort. Although young maternal age was not associated
with ADHD in full siblings, we did find a trend of increas-
ing risk of ADHD with decreasing maternal age.
Additionally, when studying the combined effect of paren-
tal ages in full siblings, we observed a tendency to maternal
age affecting the association between paternal age and
ADHD; the younger the mother, the higher the risk.
Paternal age did not modify the association between mater-
nal age and ADHD.
A study found that young mothers showed more nega-
tive responsiveness and were more restrictive in controlling
their children, less supportive, more inadequate in guiding
their children and generally less responsive compared with
older mothers.34,35 Further, children of young mothers
were found likely to experience higher levels of maternal
depression, marital conflict and family disruption com-
pared with children of older mothers,54 which has been
associated with ADHD.54–56 This trend observed with ma-
ternal age may be due to improved maternal parenting
skills and maturity resulting in a more accepting attitude
towards a second or third child’s behaviour, potentially
causing fewer symptoms and/or decreased impairment
among later-born siblings. Also, the first child’s behaviour
could have made the mother more robust and competent in
handling later-born children with similar behaviour.
Mother-child attachment will differ among siblings but,
explaining part of the increased risk of ADHD with
decreased maternal age, we would also have expected an
association between low paternal age and ADHD as a re-
sult of paternal immaturity. However, the finding of a
trend with only maternal age may reflect less paternal in-
volvement in early parenting. Even though there have been
cultural changes towards more gender equality, pregnancy
and breastfeeding keep mothers in closer contact with the
417
child especially in the first years, which may explain this
finding.
This study supports that the association between young
maternal age and offspring ADHD is due to risk factors at
a family level, mainly accounted for by genetic factors, but
environmental factors or gene-environment interactions
might also play a role in the aetiology of ADHD. It has
been suggested that children with some genetic vulnerabil-
ity to develop ADHD can be more susceptible to environ-
mental risk factors, for example adversities in the perinatal
environment, exposure to alcohol and cannabis, and ad-
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verse obstetric and postnatal events. Maternal lifestyle dur-
ing pregnancy might explain the trend of increasing risk of
ADHD with decreasing maternal age, observed in full sib-
lings, as young mothers more often tend to engage in risky
behaviours during pregnancy that have been associated
with mental problems in the offspring.24,34 Young mothers
are more likely to smoke during pregnancy, which affects
the developing fetus.57 .However, it is also possible that
they are involved with other kinds of risky behaviours such
as poor nutrition, alcohol and cannabis use. Prenatal ex-
posure to alcohol has been shown to be associated with
increased risk of ADHD, independently of the effects of
prenatal smoking exposure.57 Maternal lifestyle and risky
behaviour during pregnancy may explain why the trend of
increased risk of ADHD with decreased age only is
observed regarding maternal age. In addition, studies of
the relationship between maternal age and low birthweight
found that children born to very young mothers had a
higher risk of low birthweight,58 and low birthweight has
been found to be associated with ADHD. We also con-
ducted subanalyses stratified by gestational age and birth-
weight, but the estimates did not change significantly
either in the population-based cohort or in the sibling
cohorts.
If different amounts of sex-related hormones29 or gy-
naecological immaturity explained the association between
young maternal age and ADHD, we would have expected
almost similar associations in the sibling cohorts as in the
population cohort and, further, we would not have ex-
pected an additional risk also when the father was very
young.
The present study has a number of strengths. It is based
on a complete 20-year follow-up using established diagnos-
tic data obtained from highly reliable nationwide registers,
based on standardized diagnostic reporting procedures. In
addition, data on both inpatient and outpatient visits were
available for the whole study population. Furthermore, our
study was able to examine the associations in both a full
anda half sibling cohort, corresponding to 6436 and 1795
families, respectively. Finally, as an important
418
methodological strength, we controlled for time trends
including the increase in ADHD diagnosis during the study
period.
Although the Danish register contains complete infor-
mation for inpatient as well as outpatient contacts since
1995 in the public health system, some children are unrec-
ognized and thus untreated or treated without contact with
the hospital system. Accordingly, ADHD is undiagnosed in
the hospital system and we have false-negatives, especially
for the oldest children in the cohort. Among siblings, false-
negatives might therefore be more likely among the oldest
siblings, which might have biased the estimates towards
the null. We controlled for time trends and do not expect
them to influence our estimates significantly. In contrast,
as the literature also reports ADHD being over-diagnosed
typically referring to false-positives, we cannot exclude
non-differential misclassification.10,59,60 If we expect
increased focus on families with young parents, the likeli-
hood of getting in contact with the paediatric psychiatry
system and of being diagnosed may differ between parental
age groups, resulting in diagnostic parental age bias. In this
case, an overestimation of the association between young
parental age and ADHD cannot be rejected.
Only 1.30% of the children had an ICD-10 diagnosis of
Hyperkinetic Disorder (F90x), which is lower than sug-
gested in other studies. In this study, the ICD-10 diagnosis
of Hyperkinetic Disorder mainly represents the more se-
vere cases of the Diagnostic and Statistical Manual of
Mental Disorders (DSM-5) definition of attention-deficit/
hyperactivity disorder (ADHD) with some of the less se-
vere cases being missing.
We excluded less than 2% off the children on the basis
of missing data on paternal age. As an association between
lonely parenthood and offspring ADHD has been
observed, we might have excluded a group of children with
higher prevalence of ADHD.54 Compared with the total
study population, we found that children with missing
data on paternal age had 0.1% higher prevalence of
ADHD, but including these children in the analysis did not
change the crude associations between maternal age and
offspring ADHD either in the population cohort or in the
half sibling cohort.
Although the sibling design can be a powerful tool for
accounting for confounding because of both measured and
unmeasured stable within-family factors,28,40,61–63 the sib-
ling comparisons face a limitation, as they cannot account
for uncontrolled confounding by unmeasured sibling-
varying within-family factors as carry-over effects from
one sibling to another. We should therefore carefully con-
sider factors that may affect the exposure and outcome
differently between siblings. A sibling being diagnosed
with ADHD could affect parental behaviour in relation to
International Journal of Epidemiology, 2017, Vol. 46, No. 2
the other siblings within the family. Parental perceptions,
experience and behaviour may impact on the associations
of interest at the level of an individual child or family, but
these factors may be difficult or impossible to measure and
control for. Also, birth order might play an important role
when comparing the risk of ADHD among siblings. It is
possible that a diagnosis given to a child will make it more
likely that an undiagnosed sibling with the disorder will be
diagnosed and probably also lower the threshold for diag-
nosing another. In the sibling design, this would generate
fewer discordant sibling pairs attenuating the estimates.
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Our results are much in line with the study from Sweden,
using sibling- and cousin-comparisons, indicating that the
association between maternal age and ADHD mainly could
be explained by genetic confounding,37 as we found the
weakest association among full siblings. Another Swedish
study reported that siblings with fathers aged 45 years or
older had a highly increased risk of ADHD (HR ¼ 13.13,
95% CI 6.85-25.16) compared with their siblings born
when the father was 20 to 24 years old,40 which they suggest
is consistent with the hypothesis that new genetic mutations
that occur during spermatogenesis are causally related to
offspring ADHD. In contrast, we did not find any associ-
ations between either young or advantaged paternal age and
ADHD. A potential explanation could be failure to control
for the trend of increase in ADHD diagnosis as well as in-
crease in parental childbearing age over time in the Swedish
study.64 In addition, inconsistencies between studies may be
due to variation in the demographics of the study partici-
pants, sample size and availability of data on potential con-
founders. Further, in the present study we were able to
include data on clinical diagnoses and admission dates for
all inpatient psychiatric hospital admissions since 1969 and
outpatient visits at psychiatric hospitals and clinics since
1995, comparing 1973 and 2001 in Sweden, respectively.
Conclusion
We found that children diagnosed with ADHD more often
had younger parents compared with children without a diag-
nosis of ADHD. The risk of ADHD was highest if both par-
ents were very young. However, the risk attenuated in the
sibling-comparisons, suggesting that the population-wide as-
sociation between young parental age and offspring ADHD is
due to risk factors at a family level, mainly accounted for by
genetic factors, or that sibling comparisons are too conserva-
tive. As we found a trend of increased risk of ADHD with
decreasing maternal age, which was not found according to
paternal age, we cannot exclude the early-life environment or
maternal behaviour related to young maternal age playing a
role in the aetiology of ADHD.
International Journal of Epidemiology, 2017, Vol. 46, No. 2
Our results suggest that young parenthood could be a
marker of genetic traits and, if so, delaying fertility will not
be fully effective in reducing offspring ADHD. Public pol-
icy initiatives should still be targeted at attention to young
parents to support parenting as well as guidance on healthy
lifestyle during pregnancy among young mothers.
Funding
Susanne Hvolgaard Mikkelsen was supported by a full PhD fellow-
ship at Aarhus University, Denmark.
Conflict of interest: None.
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