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10.1007/s00213-021-05989-3

However, there was insufficient evidence for the association between antibiotic intake after birth and ADHD risk.

Antibiotic exposure and childhood attention-deficit/hyperactivity disorder: systematic review and meta-analysis.

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10.1177/1087054720914352

Quantifying early health services use among children later diagnosed with ADHD could help us understand the early life impact of the disorder and uncover health care utilization patterns associated with higher ADHD risk.

Patterns of Health Services Use Before Age 1 in Children Later Diagnosed With ADHD

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10.1017/CTS.2021.707

5-methoxytryptophol (5-MTX), a neuroendocrine molecule which also has antioxidant and immunomodulatory properties, was inversely associated with acetaminophen and ADHD risk.

22566 Identifying metabolic mechanisms linking prenatal acetaminophen exposure to childhood attention-deficit hyperactivity disorder

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10.1101/2021.02.16.21251737

If confirmed, these findings support previous evidence that maternal ASD or neuroticism may be possible targets for intervention to help break the chain of the intergenerational transmission of ADHD risk.

Identifying intergenerational risk factors for ADHD symptoms using polygenic scores in the Norwegian Mother, Father and Child Cohort

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10.1016/j.envint.2021.106549

Simultaneously decreasing all constituents of common-detect OPE-phthalate mixture, specifically DPHP, DNBP, and 6 phthalate metabolites, by a quartile resulted in an ADHD risk ratio of 0.

Pregnancy exposure to organophosphate esters and the risk of attention-deficit hyperactivity disorder in the Norwegian mother, father and child cohort study

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10.1007/s00787-021-01860-0

Increased ADHD risk in children in terms of hazard ratios (HRs) and 95% confidence intervals (CIs) was associated with prenatal exposure to paternal autoimmune diseases, including Sjögren’s syndrome (HR: 8.

Risk of attention deficit hyperactivity and autism spectrum disorders among the children of parents with autoimmune diseases: a nationwide birth cohort study

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10.1101/2021.08.06.21261679

In analyses of the polygenic architecture, we found higher polygenic score (PGS) of ADHD risk variants in persistent ADHD (mean PGS=0.

Differences in the genetic architecture of common and rare variants in childhood, persistent and late-diagnosed attention deficit hyperactivity disorder

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10.1002/ajmg.b.32844

Interestingly, a causal effect from cannabis use to ADHD risk was also observed for the first time.

Genomics and epigenomics of substance use disorders: An introduction

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10.1101/2021.03.30.21254492

We used genetic variants from alcohol metabolising genes (alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)) as proxies for fetal alcohol exposure to investigate their association with offspring ADHD risk around age 7-8.

Maternal and offspring genetic risk score (GRS) analyses of fetal alcohol exposure and ADHD risk in offspring

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10.1093/ACREFORE/9780190632366.013.181

While genetic factors contribute to ASD and ADHD risk, the environmental contribution to ASD and ADHD has been recognized as having potentially equal importance, which raises the hope for early prevention and intervention.

Early Life Origins of ASD and ADHD

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10.3390/ijerph18094939

Dose–response analysis for parental age and ADHD risk was performed.

Parental Age and the Risk of ADHD in Offspring: A Systematic Review and Meta-Analysis

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10.1101/2021.03.25.21254087

We investigated associations between maternal prenatal smoking, alcohol and caffeine consumption with childhood ADHD risk accounting for shared familial factors.

Prenatal smoking, alcohol and caffeine exposure and ADHD risk in childhood: parental comparisons and polygenic risk score (PRS) analyses

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10.33774/COE-2021-XZ72R

Although ADHD is highly heritable, environmental factors also appear to contribute to ADHD risk.

Environmental risks and ADHD: An update on the evidence

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10.1101/2021.08.18.21262211

We derived ADHD-PRS and identified 25 ADHD risk-factors in Danish national registers.

Interplay of ADHD polygenic liability with birth-related, somatic and psychosocial factors in ADHD - a nationwide study

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10.25972/OPUS-23626

The study of ADHD risk genes such as ADGRL3 requires the gene to be first identified using human studies.

ADHD Genetics in Mouse and Man

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Adhd Risk - However, there was insufficient evidence for the association between antibiotic intake after birth and ADHD risk. [1] Quantifying early health services use among children later diagnosed with ADHD could help us understand the early life impact of the disorder and uncover health care utilization patterns associated with higher ADHD risk. [2] 5-methoxytryptophol (5-MTX), a neuroendocrine molecule which also has antioxidant and immunomodulatory properties, was inversely associated with acetaminophen and ADHD risk. [3] If confirmed, these findings support previous evidence that maternal ASD or neuroticism may be possible targets for intervention to help break the chain of the intergenerational transmission of ADHD risk. [4] Simultaneously decreasing all constituents of common-detect OPE-phthalate mixture, specifically DPHP, DNBP, and 6 phthalate metabolites, by a quartile resulted in an ADHD risk ratio of 0. [5] Increased ADHD risk in children in terms of hazard ratios (HRs) and 95% confidence intervals (CIs) was associated with prenatal exposure to paternal autoimmune diseases, including Sjögren’s syndrome (HR: 8. [6] In analyses of the polygenic architecture, we found higher polygenic score (PGS) of ADHD risk variants in persistent ADHD (mean PGS=0. [7] Interestingly, a causal effect from cannabis use to ADHD risk was also observed for the first time. [8] We used genetic variants from alcohol metabolising genes (alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)) as proxies for fetal alcohol exposure to investigate their association with offspring ADHD risk around age 7-8. [9] While genetic factors contribute to ASD and ADHD risk, the environmental contribution to ASD and ADHD has been recognized as having potentially equal importance, which raises the hope for early prevention and intervention. [10] Dose–response analysis for parental age and ADHD risk was performed. [11] We investigated associations between maternal prenatal smoking, alcohol and caffeine consumption with childhood ADHD risk accounting for shared familial factors. [12] Although ADHD is highly heritable, environmental factors also appear to contribute to ADHD risk. [13] We derived ADHD-PRS and identified 25 ADHD risk-factors in Danish national registers. [14] The study of ADHD risk genes such as ADGRL3 requires the gene to be first identified using human studies. [15]