Meta-analysis shows significant association
between dopamine system genes and attention
deficit hyperactivity disorder (ADHD)
Dawei Li1,3, Pak C. Sham4,5, Michael J. Owen6and Lin He2,3,*
1Bio-X Life Science Research Center and2NHGG Bio-X Center, Shanghai Jiao Tong University, Hao Ran Building,
1954 Hua Shan Road, Shanghai 200030, China,3Institute for Nutritional Sciences, Shanghai Institutes of Biological
Sciences, Chinese Academy of Sciences, 294 Taiyuan Road, Shanghai 200031, China,4SGDP Centre, Institute of
Psychiatry, King’s College London, UK,5Genome Research Center, The University of Hong Kong, Hong Kong SAR,
China and6Department of Psychological Medicine, Wales College of Medicine, Biology, Life and Health Science,
Cardiff University, Cardiff, UK
Received April 5, 2006; Revised May 25, 2006; Accepted June 7, 2006
Molecular genetic investigations of attention deficit hyperactivity disorder (ADHD) have found associations
with a variable number of tandem repeat (VNTR) situated in the 30-untranslated region of dopamine transpor-
ter gene (DAT1), a VNTR in exon 3 of dopamine receptor 4 gene (DRD4) and a microsatellite polymorphism
located at 18.5 kb from the 50end of dopamine receptor 5 gene (DRD5). A number of independent studies
have attempted to replicate these findings but the results have been mixed, possibly reflecting inadequate
statistical power and the use of different populations and methodologies. In an attempt to clarify this incon-
sistency, we have combined all the published studies of European and Asian populations up to October 2005
in a meta-analysis to give a comprehensive picture of the role of the three dopamine-related genes using mul-
tiple research methods and models. The DRD4 7-repeat (OR 5 1.34, 95% CI 1.23–1.45, P 5 2 3 10212) and
5-repeat (OR 5 1.68, 95% CI 1.17–2.41, P 5 0.005) alleles as well as the DRD5 148-bp allele (OR 5 1.34, 95%
CI 1.21–1.49, P 5 8 3 1028) confer increased risk of ADHD, whereas the DRD4 4-repeat (OR 5 0.90, 95% CI
0.84–0.97, P 5 0.004) and DRD5 136-bp (OR 5 0.57, 95% CI 0.34–0.96, P 5 0.022) alleles have protective
effects. In contrast, we found no compelling evidence for association with the 480-bp allele of DAT
(OR 5 1.04, 95% CI 0.98–1.11, P 5 0.20). No significant publication bias was detected in current studies. In
conclusion, there is a statistically significant association between ADHD and dopamine system genes,
especially DRD4 and DRD5. These findings strongly implicate the involvement of brain dopamine systems
in the pathogenesis of ADHD.
Evidence from family, twin and adoption data suggests that
attention deficit hyperactivity disorder (ADHD) is familial
and heritable (75–91%) (1–3). It is a common, highly disrup-
tive, disabling neurodevelopmental disorder that affects up to
6% of children (3). Subjects with ADHD have, compared with
controls, a higher frequency of course failures, fewer friends
(4), greater risk of substance abuse (5) and more traffic
citations including speeding, vehicular crashes and license
At least 20 potential susceptibility genes have so far been
studied in relation to ADHD (7). Evidence from pharmaco-
logical, neuroimaging and animal studies have suggested the
involvement of specific neurotransmitter systems, notably
dopaminergic pathways, in ADHD (3). Stimulant drugs,
which for half-a-century have provided the primary pharmaco-
logical treatment for ADHD, have their site of action in the
dopaminergic system (8). Thus, the genes encoding the dopa-
mine transporter and receptors have been the most attractive
candidate genes for ADHD. The most extensively studied
have been the dopamine transporter gene (DAT1), the
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Human Molecular Genetics, 2006, Vol. 15, No. 14
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by guest on June 2, 2013
dopamine receptor 4 gene (DRD4) and the dopamine receptor
5 gene (DRD5).
The 52.6 kb human DAT1 gene (SLC6A3) is located on
chromosome 5p15.3 and codes for a transmembrane protein
responsible for the presynaptic reuptake of dopamine (8).
Using a family-based association study, Cook et al. (9) first
reported an association between ADHD and the 480-bp
allele of a variable number of tandem repeat (VNTR) poly-
morphism situated in the 30-untranslated region. Subsequent
findings have been mixed, but a meta-analysis (10) of family-
based studies in 2001 showed a statistically significant effect,
and a recent analysis (2) also found a small but significant
The DRD4 gene of size 3400 bp, at chromosome 11p15.5, is
one of the most variable human genes known. A VNTR poly-
morphism in exon III consists of a 48-bp repeat unit and codes
for an amino-acid sequence located in the third intracellular
cytoplasmic loop of the receptor. Ten alleles (2–11 repeats)
have been identified in the global population, and allele fre-
quencies vary considerably between populations. An early
study (11) suggested that the 7-repeat allele conferred
increased risk of ADHD, a finding which was confirmed by
meta-analysis (12) in 2001.
The DRD5 gene, of size 2031 bp, maps to chromosome
4p15.1-p15.3. Daly et al. (13) first reported a risk effect of
the 148-bp allele of a microsatellite polymorphism (CT/GT/
GA)n located 18.5 kb from the 50end of the gene. A
meta-analysis (14) of five studies and a joint analysis (15) of
14 groups also showed association with the 148-bp allele. Hap-
lotype analysis (16) has also revealed a significant association.
The polymorphism was also reported to be associated with
oppositional defiant disorder, which was diagnosed in more
than half of the children clinically referred with ADHD (17).
The positive findings with each of the three candidate genes
have been independently replicated by other groups using
either case–control or family-based association designs.
However, a proportion of subsequent studies have produced
contrary results. The association data has increased sharply
in recent years in both European and, more particularly,
Asian populations. To reconcile the conflicting findings and
elucidate the genetic architecture of ADHD, the current
meta-analysis combines results from all case–control and
family-based association studies published up to October
The combined search yielded 885 references. Among these 36,
50 and 13 studies were found to be association studies on the
DAT1, DRD4 and DRD5 genes, respectively. These references
were then filtered to ensure conformity with the inclusion cri-
teria. Some studies were excluded although we tried to contact
authors in cases where there were queries regarding their
studies. For the DAT1 gene, one study (18) was discarded
because of insufficient data; two studies (19,20) because the
identity of the risk allele was uncertain [although we tried to
contact the authors to query the data (18–20)]; one haplotype
relative risk (HRR) (21) because the risk alleles (440-, 480-
and 520-bp) were combined; one (22) because the sample
overlapped with that of another study [case–control and trans-
mission disequilibrium test (TDT)] (21); and one (23) because
it is used as a trait measure design. For the DRD4 gene, one
study (24) was discarded because of insufficient data; one
(20) because the identity of the risk allele was uncertain;
two (25,26) because the risk alleles (2–7-repeat) were com-
bined; two (27,28) for overlapping samples with other
studies (29,30), respectively; one (23) for trait measure
design; and one (case–control) (31) for using non-healthy sub-
jects as controls. For the DRD5 gene, two studies (15,32) were
discarded because of insufficient data and one (19) because the
identity of the risk allele was uncertain. As a result, 26, 38 and
9 studies were included for the DAT1, DRD4 and DRD5 genes,
respectively. These studies included 2576 cases, 3453 controls
and 6592 parent–offspring trios.
DAT1 VNTR polymorphism
The included studies comprised eight case–control (21,33–
39), two HRR (36,40), three haplotype-based haplotype
relativerisk (HHRR) (9,13,16)
(21,33,41–50). The 480-bp allele was the most common
allele, having higher frequency in Asians than in Europeans,
and the frequency differences between cases and controls
varied among different populations. Overall, the results for
all three putative risk alleles (480, 520 and 440-bp) were
either very weak or non-significant (Table 1). However,
there was evidence of heterogeneity in all combined studies
for the 480-bp allele, because of greater evidence for positive
association results from the family-based studies and Euro-
pean studies than from the case–control studies and Asian
studies, respectively (Tables 2 and 3).
and13 TDT studies
DRD4 VNTR polymorphism
HHRR (29,54) and 18 TDT studies (21,29,30,33,44–
46,52,55,59–66). For the 7-repeat allele, the frequency
varied widely across normal populations, being abundant in
Europeans (9.1–25.6%), but undetectable in Asians (21,38).
In the 12 European case–control studies, 10 studies showed
higher frequency in cases than in controls. In the 21 European
family-based studies, 19 showed preferential transmission.
The combined European studies produced a significant
P-value of 2 ? 10212, with only weak evidence for heterogen-
eity between studies (P ¼ 0.03) (Table 1). No evidence for
publication bias was found. The overall OR was 1.34 (1.23,
1.45). The significant results were consistent between case–
control and family-based studies although heterogeneity was
found between design types (P ¼ 0.002), with a larger odds
ratio estimate in case–control than in family-based studies
For the 4-repeat allele, in the 13 case–control studies, 11
showed lower frequency in cases. In the 14 family-based
The 4-repeat allele was the most prevalent allele, ranging from
60.8–77% across normal populations, and appears to confer a
protective effect. All studies together showed a significant
P-value of 0.004 [OR ¼ 0.90 (0.84, 0.97)] without evidence
Human Molecular Genetics, 2006, Vol. 15, No. 142277
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for heterogeneity or for publication bias (P . 0.05) (Table 1).
However, there was weak evidence for heterogeneity between
design types (P ¼ 0.01).
The 5-repeat allele also appears to confer an increased risk.
Combining all studies showed a significant P-value of 0.005
[OR ¼ 1.68 (1.17, 2.41)], without evidence for heterogeneity or
for publication bias (Table 1). Also there was no heterogeneity
between design types and sample ethnicities (Tables 2 and 3).
For the 3- and 2-repeat alleles, the results were non-
Figures 1 and 2 show the forest plots and funnel plots for
the 7-repeat allele. The forest/funnel plots for other alleles
are shown as supplements.
The selected studies comprised two HHRR (13,16) and seven
TDT studies (44–46,64,67–69), all of European origin. For
the 148-bp risk allele, combining all studies showed a signifi-
cant P-value of 8 ? 1028[OR ¼ 1.34 (1.21, 1.5)] with evi-
dence of heterogeneity (P ¼ 0.0008) and weak evidence for
publication bias (P ¼ 0.01) (Table 1). For the 136-bp allele,
the results were weak [P ¼ 0.02, OR ¼ 0.57 (0.34, 0.96),
respectively] without evidence of heterogeneity or publication
bias. The 148-bp allele has a risk effect on ADHD, whereas
the 136-bp allele has a protective effect. For the 146-bp
allele, no preferential transmission was found (Table 1).
Sensitivity and retrospective analyses
The results of the DRD4 7-repeat allele and the DRD5 148-bp
allele were consistent, and were not changed substantially by
the removal of any data set. For the 7-repeat allele, the
P-values were never .2 ? 10210; for the 148-bp allele, the
largest P-value was 6 ? 1026. For the 5-repeat allele, which
has a low frequency (0–8%), the P-value became non-
significant (P . 0.05) after study by Comings (51) was
removed. This study accounted for more than one-third of
the total sample size.
Analysis in retrospect based on the publication year (70),
showed that the cumulative results tended to be stable after
2001 for the DRD4 long alleles, but not for the DRD5 gene,
Table 2. Heterogeneity analyses by design types
Alleles/Types Overall OR
1.14 (0.91, 1.43)
1 (0.89, 1.12)
0.91 (0.76, 1.09)
1.06 (0.99, 1.14)
1.81 (1.06, 3.08)
1.18 (0.67, 2.09)
0.97 (0.82, 1.15)
0.97 (0.82, 1.14)
1.07 (0.79, 1.44)
0.95 (0.7, 1.28)
0.8 (0.71, 0.9)
0.97 (0.89, 1.05)
1.92 (1.21, 3.03)
1.32 (0.75, 2.35)
1.65 (1.41, 1.92)
1.23 (1.12, 1.36)
2 ? 10210
Family-based ¼ HRR þ HHRR þ TDT.
aHeterogeneity test between design types (case–control versus family-
Table 1. Results of all combined studies
DAT1 440-bp (11)a
DAT1 480-bp (26)
DAT1 520-bp (7)
DRD4 2-repeat (28)
DRD4 3-repeat (24)
DRD4 4-repeat (27)
DRD4 5-repeat (21)
DRD4 7-repeat (33)
DRD5 148-bp (9)
DRD5 136-bp (3)
DRD5 146-bp (3)
1.02 (0.93, 1.13)
1.04 (0.98, 1.11)
1.48 (1, 2.18)
0.97 (0.86, 1.09)
0.99 (0.8, 1.23)
0.90 (0.84, 0.97)
1.68 (1.17, 2.41)
1.34 (1.23, 1.45)
1.34 (1.21, 1.5)
0.57 (0.34, 0.96)
0.84 (0.6, 1.15)
2 ? 10212
8 ? 1028
1 ? 1026
P(Z): Z test used to determine the significance of the overall OR.
P(Q): Cochran’s x2-based Q statistic test used to assess the heterogeneity.
P(T): T test used to evaluate the significance of publication bias.
For Tables 1–3, data in columns P(Z), P(Q) and P(T) are the P-values
for the corresponding tests.
aThe number of studies included are indicated in parentheses.
Table 3. Heterogeneity analyses by sample ethnicities
Alleles/Ethnicities Overall OR (95% CI)
1 (0.9, 1.11)
1.45 (0.98, 2.15)
1.07 (1, 1.15)
0.93 (0.81, 1.07)
1.15 (0.47, 2.78)
1.57 (1.02, 2.42)
0.96 (0.83, 1.11)
0.98 (0.8, 1.21)
0.98 (0.78, 1.23)
1.23 (0.64, 2.37)
0.88 (0.81, 0.95)
1 (0.86, 1.15)
1.7 (1.06, 2.71)
1.65 (0.93, 2.93)
The DRD4 7-repeat allele was not detected in Asian populations.
aHeterogeneity test between sample ethnicities (European versus Asian).
2278Human Molecular Genetics, 2006, Vol. 15, No. 14
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for which the rough asymptote line suggested that more
studies are needed (Fig. 3).
Sensitivity analyses and other meta-data/figures of each
individual study are available on request.
Compelling evidence for the involvement of dopamine
systems in ADHD derives from the fact that dopamine enhan-
cers such as amphetamine and methylphenidate improve beha-
vioral symptoms of most children with ADHD (71). This has
resulted in dopamine system genes being considered as candi-
date genes for the well established heritability of ADHD (72).
DAT1 initially was considered as a candidate because stimu-
lant medications are known to block the dopamine transporter
in achieving their therapeutic effects (73). In the present study
the results overall were weak or non-significant. However, a
negative result is only conclusive if the entire gene has been
adequately tagged by SNPs and/or microsatellite polymorph-
isms and that there is sufficient power and uniformity in the
studies. Indeed, there is evidence in the literature for DAT1
haplotypes that include the 480-bp allele, being associated
with ADHD (16,41,74,75). It is therefore possible that the
480-bp allele is in linkage disequilibrium with a risk allele
or alleles elsewhere in DAT1 or that susceptibility to ADHD
depends upon interaction between the 480-bp allele and
another DAT1 variant. This could explain the lack of signifi-
cant association but significant heterogeneity that was
observed infamily-based studies
studies. Evidence for heterogeneity with the 480-bp allele
could in principle also reflect subtle differences in ascertain-
ment, diagnostic criteria, or other methodological differences,
or the result from the fact that the 480-bp allele confers risk by
means of an interaction with another locus or with an environ-
mental factor. With regard to the latter suggestion, it is of
interest that a recent study (75) provided evidence that a haplo-
type involving the 480-bp allele might interact with maternal
use of alcohol during pregnancy to increase risk of ADHD.
In contrast to the weak effects observed for DAT1, strong evi-
dence (P ¼ 2 ? 10212) was obtained that the 7-repeat allele of
DRD4 confers increased risk, with evidence also obtained that
the 5-repeat allele confers increased risk (P ¼ 0.005) and that
the 4-repeat is protective (P ¼ 0.004). Weak evidence for het-
erogeneity was found in the effects of the 7-repeat allele
(P ¼ 0.03) and the 4-repeat allele in European populations
(P ¼ 0.04). Furthermore, for the two alleles, heterogeneity was
found between design types (P ¼ 0.002 and 0.01, respectively),
Figure 1. Forest plots of ln(OR) and overall ln(OR) with 95% CI for the
DRD4 7-repeat allele. Black squares indicate the ln(OR), with the size of
the square inversely proportional to its variance, and horizontal lines represent
the 95% CIs. The overall ln(OR) are indicated by the unshaded black diamond.
Figure 2. Egger’s funnel plots of the combined studies (case–control þ
HRR þ HHRR) for the DRD4 7-repeat allele. The larger deviation from
funnel curve of each study means the more pronounced asymmetry. Results
from small studies will scatter widely at the bottom of the graph, with the
spread narrowing among larger studies. The significance of the intercept
was evaluated using the t-test. Plots for other alleles were shown as
Human Molecular Genetics, 2006, Vol. 15, No. 14 2279
by guest on June 2, 2013
with case–control studies having higher ORs. This could
reflect stratification in the case–control design. This is consist-
ent with an inflation of significance in case–control studies
because of population stratification (76), but we suspect that
this is unlikely because of the large number of case–control
studies and the lack of significant evidence for heterogeneity
of OR among the case–control studies. A more likely expla-
nation is that there are quantitative or qualitative phenotypic
differences between the cases of ADHD in case–control and
in family-based samples, and that these have different levels
of association with DRD4 alleles. Indeed, there is preliminary
evidence that cases of ADHD from completely ascertained
trios have a more severe phenotype and are more likely to
have symptoms of conduct disorder than cases where one
parent is not available for genotyping (77).
We have pooled OR estimates from different designs to
obtain an overall OR for the association between an allele
and ADHD. The purpose of this is to obtain a single
summary of the overall level of evidence for an association.
However, we do appreciate that different designs may
capture subjects with different characteristics, and may be
subject to different biases, and the combination of ORs
across different study designs may obtain an average that is
not very meaningful. The tests of heterogeneity between
ORs from different study designs are to some extent helpful
for revealing important differences between designs.
(P ¼ 8 ? 1028) and heterogeneity was found (P ¼ 0.0008)
possibly because of differences in the diagnostic criteria,
subtype ascertainment and demographic characteristics. The
136-bp risk allele is protective (P ¼ 0.02).
In this study, we accessed as much of the literature as poss-
ible, in order to achieve a complete and unbiased represen-
tation of the relevant studies. Those studies with insufficient
or ambiguous data were excluded. This effort to take a
comprehensive and even-handed approach to the literature
inclusion may have strengthened the robustness of the find-
ings while it avoided publication bias and minimized hetero-
geneity (78). Compared with previous studies (12,14,15,79),
the current meta-analysis pooled larger sample sizes, ana-
lyzed them both combined and separately, generated even
more significant results with systematic design types and
analysis approaches and included tests of heterogeneity by
study design and ethnicity, as well as sensitivity analyses.
[The two previous meta-analyses (12,14) of the DRD4 gene
included only 9 and 11 studies, respectively (Supplementary
Material, Table S1).] The current results demonstrate the
robustness of the association between the 7-repeat allele of
DRD4 and ADHD, which was significant in multiple
studies, and in both case–control and family-based studies.
In order to improve the scope and validity of subsequent
meta-analyses, there are two important issues that individual
studies should address. First, there needs to be clear description
of ascertainment and selection of cases and controls. Second,
raw genotype counts in the different groups, preferably stratified
by ethnicity and other potential confounding variables, should
be presented. Indeed, the presentation of only allele counts in
some studies has restricted the meta-analysis to an allele-wise
analysis with the limitations that the assumptions of Hardy-
Weinberg equilibrium and multiplicative risks have to be made.
ADHD, which is polygenic, is caused by the combined
actions of many factors. For greater insight into its genetic
component, more work is required to confirm the role of
other genes that may have a small effect, and to identify
new genetic risk factors. The large samples required will
necessitate multi-site projects and meta-analyses on the basis
of national and international collaboration.
To conclude, the 4-, 5- and 7-repeat alleles of the DRD4
gene and 148-bp and 136-bp alleles of the DRD5 gene show
strongly consistent associations with ADHD, in which the
DRD4 7- and 5-repeat alleles and the DRD5 148-bp allele
have risk effects, whereas the DRD4 4-repeat and the DRD5
136-bp alleles have protective effects. In contrast, DAT1
shows at best only weak evidence for association. The
meta-analysis strongly suggests the involvement of the brain
dopamine system genes, especially DRD4 and DRD5, in the
pathogenesis of ADHD, which may have potentially important
scientific and public health implications.
MATERIALS AND METHODS
The publications included in the analysis were selected from
PubMed and from www.cnki.net/index.htm with keywords
‘attention deficit hyperactivity disorder’, ‘ADHD’, ‘dopamine
transporter’, ‘dopamine 4 receptor’, ‘dopamine 5 receptor’,
‘association’ and the specific names and abbreviations of each
gene (e.g. ‘dopamine receptor 4’and ‘DRD4’). All references
Figure 3. Cumulative syntheses of studies for the DRD4 7-repeat allele and
the DRD5 148-bp alleles shown by overall ln(OR), the 4-, 5-repeat alleles
and DAT1 480-bp allele (data not shown) were similar with the 7-repeat allele.
2280Human Molecular Genetics, 2006, Vol. 15, No. 14
by guest on June 2, 2013
cited in these studies and in published reviews were examined
in order to identify additional works not indexed by
MEDLINE. The analyzed data cover all English and
Chinese publications from April 1995 to October 2005.
Eligible studies had to meet all of the following criteria (1):
published in peer-reviewed journal (2), contained independent
data (3), presented sufficient data to calculate the OR with CI
and P-value (4), were association studies investigating one or
more of the three polymorphisms using either case–control or
family-based approaches (5), described the genotyping
primers, machines and protocols or provided reference of
them (6), diagnosed ADHD patients according to the World
Health Organization’s International Statistical Classification
of Diseases and Related Health Problems (ICD), American
Psychiatric Association’s Diagnostic and Statistical Manual
of Mental Disorders (DSM) or Chinese classification of
mental disorders (CCMD) systems and (7) used healthy indi-
viduals as controls in case–control studies.
Studies were classified according to design into case–control
and family-based, and the latter further subdivided according
to statistical methodology into HRR, HHRR and TDT.
Studies were also subdivided between those dealing with
European ethnic populations and those dealing with Asian
ethnic populations. A study that contained data from both
ethnic populations was considered effectively as two studies.
Data from the case–control, HRR and HHRR studies were
summarized by two-by-two tables (meta-analysis was con-
ducted based on allele data, i.e. HHRR methodology, for
studies that originally used HRR or HHRR for analysis) and
TDT studies were summarized by two-by-one tables. The
two types of studies were statistically combined by the
method used by Lohmueller et al. (80), Cho et al. (81) and
Li et al. (82) to join case–control and family-based studies
into a single meta-analysis. From each table, a log-odds
ratio and its sampling variance were calculated (81).
Cochran’s x2-based Q statistic test (83–85) was performed
in order to assess possible heterogeneity of OR between the
individual studies. Heterogeneity Q tests (83,84) were also
performed for differences in OR between design types
(case–control versus family-based), and between sample eth-
nicities (European versus Asian). A test for funnel plot asym-
metry, described by Egger et al. (86), was used to assess
evidence for publication bias. ORs were pooled using the
method of DerSimonian and Laird (87) and 95% CIs were
constructed using Woolf’s method (88). The significance of
the overall OR was determined by the Z-test. For the sensi-
tivity analysis, each study was removed in turn from the
total, and the remaining was re-analyzed. This procedure
was used to ensure that no individual study was entirely
responsible for a finding. The analysis was conducted by
Comprehensive Meta Analysis software (Version 1.0.23,
BIOSTAT, Englewood, NJ, USA). The type I error rate was
set at 0.05. P-values were two-tailed.
Accession numbers and URLs for data presented herein are as
follows: Genotype data, http://www.hapmap.org/ for DAT1,
DRD4 and DRD5; GenBank, http://www.ncbi.nlm.nih.gov/
Genbank/ for genomic structure of DAT1, DRD4 and DRD5;
Genome data, http://genome.ucsc.edu/ for DAT1, DRD4 and
DRD5; Online Mendelian Inheritance in Man (OMIM),
http://www.ncbi.nlm.nih.gov/Omim/ for DAT1, DRD4 and
Supplementary Material is available at HMG Online.
This work was supported by grants from the Ministry of Edu-
cation, PRC, the National 973 and 863 programs, the National
Natural Science Foundation of China and the Shanghai
Municipal Commission for Science and Technology. We
thank the investigators of the included studies who have
given assistance on the data that this research required. We
thank Mingqing Xu and Jinbo Fan for the discussion with
them on statistics issues at the initial stage of this research.
We thank Guang He for the discussion with her on genetics
Conflict of Interest statement. No conflicts of interest.
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