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- •Contents
- •1.1 Introduction
- •1.2.1 Antidepressants
- •1.2.3.2 Second-Generation Antipsychotics (SGAs)
- •1.2.4 Mood Stabilizers
- •1.2.5 Stimulants
- •1.3 Conclusion
- •References
- •1.2.1.1 Selective Serotonin Reuptake Inhibitors
- •1.2.1.2 Bupropion
- •1.2.1.3 Other Less Commonly Used Antidepressants
- •1.2.2 Anxiolytics
- •1.2.3 Antipsychotics
- •1.2.3.1 First Generation Antipsychotics (FGAs)
- •2.2.8 Opioid Pharmacokinetics During Lactation
- •2.3 Conclusions
- •References
- •3.1 Introduction
- •3.2 Pregnancy Risk Categories
- •3.4.1.4 Monotherapy Versus Polytherapy
- •3.4.2.1 Experimental Studies
- •Animal Studies
- •3.4.2.2 Human Studies
- •Case Reports
- •Epidemiologic Studies
- •Meta-Analysis
- •3.4.2.3 Methodological Issues
- •Sample Size, Characteristics, Follow-Up
- •Recall Bias
- •Confounders
- •Confounding by Indication
- •Meta-Analysis
- •3.5 Lactation
- •3.5.1.4 Lipid Solubility
- •3.5.1.5 Pharmacogenomics
- •3.5.1.6 Oral Bioavailability
- •3.5.3.1 Milk Plasma Ratio (M/P Ratio)
- •3.5.3.2 Relative Infant Dose
- •3.5.3.3 Infant Plasma Concentration
- •3.5.3.5 Lactation Categories
- •3.7 Conclusion
- •References
- •4.1 Introduction
- •4.5 Conclusions
- •References
- •5.1 Introduction
- •5.2 Paternal Mental Health
- •5.2.1 Paternal Mental Health: Depressive Disorders
- •5.2.2 Paternal Mental Health: Anxiety Disorders
- •5.2.3 Paternal Mental Health: Bipolar Disorders
- •5.2.4 Paternal Mental Health: Posttraumatic Stress Disorders
- •5.2.5 Paternal Mental Health: Obsessive-Compulsive Disorders
- •5.2.6 Paternal Mental Health: Substance Use Disorders
- •5.4 Management Strategies
- •5.5 Conclusions
- •References
- •6.1 Introduction
- •6.5.1.1 Congenital Malformations
- •6.5.1.2 Preterm Birth
- •6.5.1.3 Low Birth Weight
- •6.5.1.4 Stillbirth
- •6.5.1.5 Low APGAR Scores
- •6.5.1.7 Neonatal Adaptation Syndrome
- •6.5.2.2 Neurodevelopmental Disorders
- •6.5.3 Maternal Outcomes
- •6.5.3.1 Postpartum Hemorrhage
- •6.5.3.2 Eclampsia, Hypertension
- •6.6.1 SSRIs
- •6.6.1.1 Sertraline
- •6.6.1.2 Paroxetine
- •6.6.1.3 Fluoxetine
- •6.6.1.5 Fluvoxamine
- •6.6.2 SNRIs
- •6.6.2.1 Duloxetine
- •6.6.2.2 Venlafaxine
- •6.6.3 TCAs
- •6.6.4 Atypical/Other Antidepressants
- •6.6.4.1 Vortioxetine
- •6.6.4.2 Bupropion
- •6.6.4.3 Mirtazapine
- •6.7 Statistical Significance Versus Clinical Significance
- •6.8 Conclusion
- •References
- •7: Antidepressants During Lactation
- •7.1 Introduction
- •7.2.2 Discussion
- •7.3.1 The Safety Scoring System
- •7.3.2 Methods
- •7.3.3 Safety Scores
- •7.3.3.1 Selective Serotonin Reuptake Inhibitors (SSRIs)
- •7.3.3.3 Tricyclic Antidepressants (TCAs)
- •7.3.3.4 Other Antidepressant Drugs
- •7.3.3.5 Neurosteroids Antidepressants
- •7.3.4 Discussion
- •7.4 General Discussion
- •7.5 Conclusion
- •Bibliography
- •8.1 Introduction
- •8.6 Gestational Diabetes
- •8.9.8 Special Cases
- •8.9.8.1 Risperidone
- •8.9.8.2 Aripiprazole
- •8.9.8.3 Clozapine
- •8.9.8.4 Olanzapine
- •8.11 Premature Infants/Low Birth Weight Infants
- •8.13.1 Definitions
- •8.15 Conclusion
- •References
- •Suggested Reading
- •9: Antipsychotics During Lactation
- •9.1 Introduction
- •9.3.2 Medication Risk Category Classifications
- •9.4 First-Generation Antipsychotics (FGAs)
- •9.4.1 Haloperidol
- •9.4.2 Chlorpromazine
- •9.5 Second-Generation Antipsychotics (SGAs)
- •9.5.1 Olanzapine
- •9.5.3 Quetiapine
- •9.5.4 Aripiprazole
- •9.5.5 Clozapine
- •9.5.6 Amisulpride
- •9.5.7 Ziprasidone
- •9.5.8 Newer Second-Generation Antipsychotics
- •9.6 Comprehensive Risk-Benefit Assessment Framework
- •References
- •10.1 Introduction
- •10.2 Lithium
- •10.2.1 Placental Transfer
- •10.2.2 Embryonic Period: Organogenesis
- •10.2.4 Child Development
- •10.2.5 Maternal Management
- •10.4 Antiepileptic Drugs
- •10.4.1 Placental Transfer
- •10.4.2 Carbamazepine
- •10.4.2.1 Embryonic Period: Organogenesis
- •10.4.3 Valproates
- •10.4.3.1 Embryonic Period: Organogenesis
- •10.4.4 Lamotrigine
- •10.4.4.1 Embryonic Period: Organogenesis
- •10.5 Conclusion
- •References
- •11: Mood Stabilizers During Lactation
- •11.1 Introduction
- •11.4.1 Lithium
- •11.4.2 Valproate
- •11.4.3 Carbamazepine
- •11.4.4 Oxcarbazepine
- •11.4.5 Lamotrigine
- •11.4.6 Topiramate
- •11.4.7 Gabapentin
- •11.6 Conclusion
- •References
- •12.1 Introduction
- •12.4.1 Benzodiazepines
- •12.4.2 Z-Drugs
- •12.5 Perinatal Complications
- •12.6 Conclusions
- •References
- •13.1 Introduction
- •13.2 Benzodiazepines
- •13.2.1 Diazepam
- •13.2.2 Clonazepam
- •13.2.3 Alprazolam
- •13.2.4 Lorazepam
- •13.2.5 Oxazepam
- •13.2.6 Midazolam
- •13.3 Z-Drugs
- •13.4 Conclusion
- •References
- •14.1 Introduction
- •14.2 Methadone, Buprenorphine, Buprenorphine/Naloxone
- •14.3 Naltrexone
- •14.4 Buspirone
- •14.5 Gabapentinoids
- •14.5.1 Pregabalin
- •14.5.2 Gabapentin
- •14.6 Pramipexole
- •14.7 Methylphenidate
- •14.8 Acamprosate
- •14.9 Disulfiram
- •14.10 Baclofen
- •14.11 Other Medicines
- •14.11.1 Nalmefene
- •14.11.2 Biperiden
- •14.12 Conclusions
- •References
- •15: Major Depression
- •15.1 Introduction
- •15.5.2 Safety Profile
- •15.5.3 Symptom Profile
- •15.5.5 Dosing
- •References
- •16: Bipolar Disorder
- •16.1 Introduction
- •16.2 Identifying Perinatal Bipolar Disorder
- •16.6.1 Acute Treatment
- •16.6.3 Maintenance Treatment
- •16.9 Conclusions
- •References
- •17.1 Introduction
- •17.5.1 Pregnancy
- •17.5.2 Postpartum Period
- •17.6 Conclusion
- •References
- •18: Obsessive-Compulsive Disorder
- •18.1 Introduction
- •18.3 Pharmacological Treatment
- •18.3.1 General Considerations
- •18.3.2.1 First-Line Treatment
- •Switch Between Antidepressants
- •SSRI Treatment at Supratherapeutic Doses
- •18.3.3 Prophylactic Treatment
- •18.3.3.1 Pre-conceptional Phase
- •18.3.3.2 Pregnancy
- •18.3.3.3 Postpartum Period
- •18.4 Conclusion
- •References
- •19: Anxiety Disorders
- •19.1 Introduction
- •19.6 Pharmacological Treatment
- •19.6.1 General Considerations
- •19.10 Conclusion
- •References
- •20: Posttraumatic Stress Disorder
- •20.1 Introduction
- •20.3 Pharmacological Treatment
- •20.3.1 General Considerations
- •20.4 Conclusion
- •References
- •21: Alcohol Use Disorders
- •21.1 Introduction
- •21.2 Epidemiology
- •21.7.1 Naltrexone Use
- •21.7.2 Disulfiram Use
- •21.7.3 Acamprosate Use
- •21.7.4 Nalmefene Use
- •21.7.5 Baclofen Use
- •21.7.6 Other Medications
- •21.8 Conclusions
- •References
- •22: Substance Use Disorders
- •22.1 Introduction
- •22.7 Conclusions
- •References
- •23.1 Introduction
- •23.3 Most Common Sleep Disorders During Peripartum
- •23.3.1 Insomnia
- •23.3.1.2 Pathophysiology
- •Hypnotic Benzodiazepines

4 General Approach toPsychopharmacological Treatment During thePerinatal Period
77
As reported by an editorial published many years ago by Robinow, but still quite
truthful: “The stark reality is that pregnancy in the context of a history of mental
illness often leaves the mother, the baby, and their doctors between Scylla and
Charybdis” (Robinow 2006).
It would be desirable as well as appropriate that both the investments in clinical
psychopharmacological research programs and the dissemination of reliable information on fetal and gestational safety of PDs were seen also as an essential tool for
the improvement of women’s mental health care during the perinatal period.
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impact of medication. A systematic review. J Affect Disorders. 2019;249:96–103.
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Cohen LS, Altshuler L, Harlow BL, Nonacs R, Newport DJ, Viguera AC, Suri R, Burt VK,
Hendrick V, Reminick AM.Relapse of major depression during pregnancy in women who
maintain or discontinue antidepressant treatment. JAMA. 2006;295(5):499–507. Erratum in:
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Eleftheriou G, Zandonella Gallagher R, Butera R, etal. Consensus panel recommendations for
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Grigoriadis S, Vonder Porten EH, Mamisashvili L, Roerecke M, Rehm J, Dennis CL, Koren G,
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Grigoriadis S, Wilton AS, Kurdyak PA, etal. Perinatal suicide in Ontario, Canada: a 15-year pop-
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C. Bellantuono

The Role ofPaternal Mental Health
During thePerinatal Period:
FromPreconception toPostpartum
GiuliaFrancesconi, RosaVolgare, UmbertoVolpe,
andLauraOrsolini
5.1 Introduction
Paternal health and lifestyle behaviors are critically unrepresented in reproductive
health discussions. Despite being formally acknowledged as a vital component of
reproductive health, paternal involvement in clinical practice and assessment is
often overlooked (Montagnoli etal. 2021). Paternal traits and behaviors may inuence offspring’s physical and mental health through both direct genetic inheritance
and epigenetic modications, as well as through indirect mechanisms that overly
affect the maternal environment. Direct effects include epigenetic changes in sperm
caused by lifestyle choices such as diet and smoking, which can alter gene expression patterns and affect offspring’s phenotypes across generations (Donkin and
Barrès 2018; Sharp etal. 2019) impacting on the behavioral and cognitive characteristics (Yeshurun and Hannan 2019). Indirect paternal effects inuence the maternal environment through behaviors such as smoking, alcohol consumption, and
stress, which can harm both the mother and the child or affect maternal behaviors
that are important for the child’s health (Scheffers-van Schayck etal. 2019; Braun
etal. 2020). These modications can affect offspring phenotypes, including susceptibility to chronic diseases such as obesity and diabetes (Fleming etal. 2018).
Recently, increasing attention has been given to paternal mental health. Evidence
from several human studies suggested that preconception paternal mental health
may be associated with adverse health outcomes in their offspring through both
genetic and non-genetic mechanisms (Coleman etal. 2020). Depression in fathers
before conception is linked to late preterm births, excessive infant crying, and
potential changes in newborn’s brain structure, such as accelerated white matter
5
G. Francesconi · R. Volgare · U. Volpe · L. Orsolini (*)
Unit of Clinical Psychiatry, Department of Experimental and Clinical Medicine (DIMSC),
Polytechnic University of Marche, Ancona, Italy
e-mail: l.orsolini@staff.univpm.it
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2025
F. Uguz, L. Orsolini (eds.), Perinatal Psychopharmacology,
https://doi.org/10.1007/978-3-031-99720-4_5
79

80
G. Francesconi et al.
development (van den Berg etal. 2009; Karlsson etal. 2020; Spry etal. 2020). A
recent study revealed that men diagnosed with depression before pregnancy had
offspring with increased attention-decit/hyperactivity disorder (ADHD) and
autism spectrum disorder (ASD) risks (Chen etal. 2020). It is possible that preconceptional paternal depression persisted to the postnatal stage to affect children via
altered parenting styles with fewer positive activities, such as reading, singing, and
hugging, and a higher level of conict in the father-child relationships making it
difcult to satisfy the child’s attachment in their early years and potentially affecting the development of a psychopathology later in childhood or adulthood. Family
factors, such as maternal depression and couple conicts, could also mediate the
association between paternal postnatal depression and child outcomes (Tan et al.
2023). The underlying biological mechanisms are still unclear. Special attention
should also be paid to the use of psychoactive drugs, with selective serotonin reuptake inhibitors (SSRIs) and valproic acid among the most studied substances, that
have been hypothesized to be associated with the occurrence of neurodevelopmental disorders in children born from fathers who used these substances in the preconception period (Evans-Hoeker et al. 2018; Yang et al. 2018; Montagnoli
etal. 2021).
5.2 Paternal Mental Health
Fathers have become increasingly more involved in parenting due to mothers’ growing active roles in the workforce, cultural changes regarding masculinity and fatherhood, and greater equality in gender roles. While maternal mental health issues such
as depression, stress, and anxiety are well-documented contributors to adverse child
outcomes (Barona etal. 2017; Cook etal. 2018; Tuovinen etal. 2018; Vehmeijer
etal. 2019), the impact of paternal mental health remains less clear (Sweeney and
MacBeth 2016; Gentile and Fusco 2017; Cui etal. 2020; Challacombe etal. 2023).
Several studies indicated that preconception paternal mental health may signicantly impact offspring’s mental, cognitive, and behavioral health through genetic
and non-genetic mechanisms (Yeshurun and Hannan 2019; Coleman etal. 2020).
Preconception paternal mental health, including depression and anxiety, seemed to
correlate with offspring risks for mental health conditions such as ADHD, ASD, and
emotional disturbances. These effects could be due to altered parenting styles (e.g.,
fewer positive interactions, and increased conicts) due to psychiatric pathologies
(Chen etal. 2020; Tan etal. 2023). Maternal mental health appears to correlate with
paternal mental health. Paulson and Bazemore (2010) reported a correlation between
paternal and maternal depression during the prenatal and postnatal periods, suggesting that paternal depression could inuence maternal depression, which could
adversely affect fetal and infant development through a spillover effect. Additionally,
females mated with stressed males exhibit altered maternal care, further impacting
offspring health, suggesting a bidirectional inuence on child outcomes (Chen etal.
2020; Zutshi etal. 2021; Tan etal. 2023). Paternal mental health is also important
when considering fertility. Depression has been diagnosed in up to 49% of male

5 The Role of Paternal Mental Health During the Perinatal Period…
81
partners suffering from infertility, while female partners of depressed men are less
likely to conceive. Although human and animal studies have demonstrated the association between father’s mental health and an increased risk of adverse health outcomes in their offspring, the underlying biological mechanisms are unclear. Further
research is therefore needed, although recently paternal mental health has become
an emerging area of research interest, with a special focus on depression.
5.2.1 Paternal Mental Health: Depressive Disorders
Approximately 10% of fathers have symptoms that meet the criteria for depressive
episodes of varying severity in the perinatal period (Fisher 2016) which is approximately half the rate of maternal postpartum depression (14–18%) (Liu etal. 2022).
Perinatal paternal depression (PPD) can begin as early as the rst trimester of pregnancy to 1 year after the birth of the child, though it most commonly emerges around
4 weeks postpartum (DSM-5-TR) (APA 2013). Several paternal factors may
increase the risk of depression during the peripartum period. These include unemployment, legal problems, addiction, neurotic personality traits, nancial strain, an
unplanned pregnancy, and distress related to the imminent birth. Additionally, a lack
of social support, avoidant coping strategies, low self-esteem, exposure to negative
life events, poor sleep quality, and perceived stress can further contribute to this risk
(Wang etal. 2021). Among these, maternal depression emerged as the most signicant factor inuencing paternal peripartum depression, with severe depression in
the partner appearing to increase the father’s risk of major depressive disorder
(MDD) up to 50% (Wee etal. 2011). Similarly, a positive family and/or personal
history of depression appears to inuence the occurrence of depression (Goodman
2004). Several studies conrmed that marital dissatisfaction is a robust risk factor
for paternal perinatal depression. There is also some evidence suggesting that infant
factors, such as difcult temperament and feeding challenges, may play a role in
increasing the risk of paternal depression, though research in this area is less extensive. The mechanisms determining the onset of perinatal depression in fathers are
currently not completely dened. Certainly, the disruption of the circadian rhythm
and sleep deprivation for childcare represent potential determinants. The nightly
activities and care needs of the child can negatively impact fathers’ productivity in
their work, which is typically uninterrupted. This dynamic makes it challenging for
fathers to adjust to their new role, often leading to increased frustration (Sokół-
Szawłowska 2020).
Depression in men may manifest differently compared to the female counterpart.
Clinical studies reported that men usually display increased irritability, impulsivity,
persistent sadness, anxiety, dysphoria, low self-esteem, stiffness of affect, feelings
of isolation, social withdrawal, disrupted eating patterns, insomnia, tendency to
abuse substances (sometimes as part of autotherapy), self-harm ideation, and, in
some cases, suicidal thoughts (Addis 2008; Da Costa etal. 2019; Bruno etal. 2020).
The different clinical picture can make diagnosis difcult as well as man’s tendency
to downplay his mental state. It is important to consider that when comparing men

82
G. Francesconi et al.
and women, men are less likely to report their experiences of depression in the same
way that women do and they also less likely seek treatment, mainly due to poor
social support, inability to express feelings of sadness/depression for the fear to be
judged and/or for internal stigma (Carlberg etal. 2018). As a result, paternal perinatal depression has been underreported, underrecognized, underdiagnosed, and
undertreated.
The most common assessment screening tool is the Edinburgh Postnatal
Depression Scale (EPDS) (Kozinszky and Dudas 2015). Other tools available to
assess paternal depression are represented by the Gotland Male Depression Scale
(GMDS) (Sigurdsson etal. 2015), the Masculine Depression Scale (Magovcevic
and Addis 2008), the Male Depression Risk Scale (Herreen et al. 2022), and the
Beck Depression Inventory-II (BDI-II). Diagnosis is needed since depressive symptomatology may signicantly alter the father-infant relationship modifying the
child’s development and response to stress, with studies showing an association
between a father’s depressed mood and negative temperament in the child, a higher
emotional dysregulation (Ramchandani etal. 2008), and a higher occurrence of
both internalizing (sadness, anxiety, or physical symptoms like stomachaches) and
externalizing (aggression, oppositional behavior, property destruction, or misbehavior like stealing) problems (Cross etal. 2024). Furthermore, it has also been demonstrated an association between a father’s depressed mood and the emergence of
reduced social skills, and higher rates of psychiatric disorders in children, particularly at school age (Gentile and Fusco 2017). There is also evidence that fathers’
depression during their offspring’s childhood can be associated with offspring’s
mental health problems, most frequently anxiety and depression, during the transition to adulthood (Fisher 2016). Furthermore, depressed fathers display a worse
quality in the interaction with their children. They are less prone to play face-to-face
with the child, impairing the child’s communication skills. Depressed fathers more
likely manifest their violence toward family members compared to healthy fathers
and tend to be less engaged in offering a cognitive stimulation for their children
(Sweeney et al. 2016; Sundstom et al. 2017; Sokół-Szawłowska 2020; Cross
etal. 2024).
Moreover, one should argue that depression is often accompanied by poor nutrition, substance use, stress, and lack of exercise, which may also lead to alterations
in sperm that can, in turn, adversely affect offspring (Yeshurun etal. 2019; Hoek
etal. 2020). Conversely, the involvement of a non-depressed father may protect
against some of the offspring risks associated with maternal depression
(Melrose 2010).
Relatedly, paternal depression puts the mother at increased risk for depression as
well, indirectly contributing to a further increased childhood risk for psychopathology. This can result in a higher prevalence of psychopathological symptoms during
preschool years and an increase in psychiatric diagnoses by the time they reach
school age (Cross etal. 2024). Interestingly, some ndings contradict these associations. Higher paternal depressive symptoms during the prenatal period were associated with fewer child behavioral difculties, particularly lower externalizing
symptoms like conduct and hyperactivity problems. Interestingly, indeed, greater

5 The Role of Paternal Mental Health During the Perinatal Period…
83
paternal depression and anxiety symptoms measured during childhood seemed to
correlate with higher child Intelligence Quotient (IQ) (Jones etal. 2023). Therefore,
one should argue that there are complex and nuanced relationships between paternal
mental health and child development, mostly still not fully investigated and understood, which suggests a careful approach and the need for more longitudinal studies
to fully understand these dynamics. Finally, a recent study showed evidence of an
association between preconception parental mental health disorders and preterm
birth, with persistent common mental disorder symptoms across adolescence and
young adulthood showing the greatest impact. Little evidence of an association
between paternal antenatal mental health disorders and small for gestational age
was found. The underlying process has not yet been identied (Spry etal. 2020).
5.2.2 Paternal Mental Health: Anxiety Disorders
Anxiety appears to be more prevalent than depression among new fathers. A systematic review conducted by Leach etal. (2016) found that anxiety seemed to affect
around 4–16% of fathers during the prenatal period and around 2–18% in the postnatal period. Paternal anxiety is highly comorbid with depression, and it may
include a variable set of symptoms including worries, fear, physical complaints, and
cognitive symptoms. Fathers are at risk for increased anxiety levels during pregnancy, postpartum, and throughout child development, with levels comparable to
mothers. Risk factors include having children with chronic illnesses, low- birthweight
infants, or co-parents with mental health issues, as well as low social support and
poor marital quality (Luoma etal. 2013; Cimino etal. 2015). Paternal anxiety correlates with child internalizing and externalizing behaviors and other psychiatric
conditions, highlighting a clear longitudinal connection between paternal anxiety
and adverse child outcomes. Anxious fathers often exhibit overprotective, overinvolved parenting styles, which can model and reinforce anxiety in children. These
behaviors, even occurring in infancy, may hinder children’s development of independence and increase their risk of psychopathology (Breaux etal. 2014; Möller
et al. 2015; Fisher 2016). A recent study showed that fathers’ prenatal anxiety
symptoms are associated with lower dehydroepiandrosterone (DHEA) levels and
higher rates of internalizing symptoms in children. In conclusion, these ndings
highlight the often overlooked importance of paternal factors during pregnancy in
child development, suggesting that prenatal paternal anxiety symptoms may be
associated with the child’s neuroendocrine function and, in turn, with internalizing
symptoms that occur at least until middle childhood (Jones etal. 2024).
5.2.3 Paternal Mental Health: Bipolar Disorders
Bipolar disorder in fathers, characterized by episodes of mania, hypomania, and
depression, impacts interparental and parent-child relationships and, ultimately, the
child’s emotional health. Research mainly found higher rates of manic, hypomanic,

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and mixed episodes in fathers during the postpartum period, compared to the general population (Pinheiro etal. 2011). Children of fathers with bipolar disorder face
a signicantly increased risk of bipolar and other mood, anxiety, and externalizing
disorders. While bipolar disorder affects parenting behaviors and self-efcacy, gender-specic impacts on fathers’ parenting styles remain under-investigated.
Maladaptive parenting style associated with bipolar disorder seems to be linked
with the emergence of children’s internalizing and externalizing problems, despite
more studies being needed to clarify this relationship (Fisher 2016).
5.2.4 Paternal Mental Health: Posttraumatic Stress Disorders
Research on posttraumatic stress disorder (PTSD) in fathers found that traumatic
experiences, such as witnessing a difcult birth, dealing with a child’s serious illness, or exposure to natural disasters and war, can lead to intrusive memories, avoidance, negative mood, and heightened arousal. These symptoms impair paternal
functioning and parenting, negatively affecting children’s mental health (Nicholls
and Ayers 2007). Fathers who develop PTSD from childbirth trauma may struggle
with bonding and interparental relationships, affecting infant outcomes (Ribi etal.
2007). Fathers with PTSD often exhibit externalizing parenting behaviors, such as
irritability and detachment, contributing to their children’s anxiety, depression, and
behavioral problems. One study showed that the child’s gender and age may be
determinants of the type of behavioral problems resulting from paternal PTSD: preadolescent girls had somatic complaints and aggression, while adolescent girls
showed more depressive symptoms; pre-adolescent boys were more anxious, while
adolescent boys had somatic complaints and hyperactivity. Overall, paternal PTSD,
regardless of its cause, signicantly hinders functional parenting and poses a risk to
children’s emotional and behavioral health (Fisher 2016).
5.2.5 Paternal Mental Health: Obsessive-Compulsive Disorders
Obsessive-compulsive disorder (OCD) in fathers is one of the least explored paternal mental health conditions. This disorder is characterized by intrusive and recurrent thoughts or images (obsessions) and/or ritualistic and repetitive behaviors that
relieve anxiety (compulsions), causing signicant distress and being difcult to
control. Currently, there is no data available on the prevalence of OCD in fathers,
but it seems to be linked to maladaptive parenting styles. A study conducted by
Yoshida etal. found that fathers with OCD or depression with severe obsessive traits
tended to be signicantly more overprotective of their children than fathers without
obsessive traits or with mild obsessive traits (Yoshida etal. 2005). However, the
available evidence is insufcient to determine with certainty the impact of paternal
OCD on parenting behavior and children’s mental health (Fisher 2016).

5 The Role of Paternal Mental Health During the Perinatal Period…
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5.2.6 Paternal Mental Health: Substance Use Disorders
Alcohol and other substances, such as tobacco, cannabis, alcohol, and recreational
drugs, have been extensively demonstrated to exert teratogenic effects when consumed prenatally by the mother, contributing to developmental delays, physical
anomalies, and growth defects in offspring. Paternal substance use seems to signicantly affect fertility, pregnancy outcomes, and offspring health through genetic and
epigenetic mechanisms or via social, psychological, or behavioral inuences on the
maternal environment (Abel 2004; Thomas etal. 2023).
Paternal smoking is a modiable risk factor that signicantly inuences pregnancy and infant health. It is important to consider that paternal smoking has a
direct effect on fetal development through secondhand smoke. While no studies
report a direct association between paternal smoking and small for gestational age
or decreased birth weight of the offspring, it is known that paternal smoking, even
light smoking, increases the risk of heart defects. The father’s smoking habit is also
associated with an increased risk of overweight and obesity (odds ratio [OR]=1.41,
95% condence interval [CI]=1.17–1.85), the development of childhood leukemia,
and appears to negatively impact offspring lung function. It has also been linked to
higher rates of ADHD in offspring (Carter etal. 2023).
Regular cannabis use during adolescence, a critical period for testicular development, has been linked to reduced sperm concentration, lower total sperm count,
signicant testicular atrophy, impaired reproductive hormones, and male infertility
(Durairajanayagam 2018; Montagnoli etal. 2021). Cannabis use before conception
has also been associated with increased pregnancy loss, decreased birth weight in
children, and behavioral and neurodevelopmental problems in offspring. These
effects are thought to result from changes in cholinergic synaptic function and
related behavioral outcomes (Slotkin etal. 2020).
Opioids appeared to impair male fertility by altering reproductive hormones and
spermatogenesis. Their use is associated with reduced testicular volume and erectile
dysfunction. Additionally, cocaine and opioid addiction in fathers has been linked to
low birth weight, early mortality, and ADHD in children (Fang et al. 2018;
Montagnoli etal. 2021). Paternal morphine exposure has been shown to increase
behavioral vulnerability to addiction in male offspring through long-lasting neural
adaptations in reward pathways (Toussaint etal. 2022).
Paternal alcohol consumption also affects fertility and pregnancy outcomes
(Finelli etal. 2021). Alcohol consumption impairs the quality of spermatozoa by
reducing their number, motility, and morphology. These effects have been observed
even after 1 month of abstinence, suggesting that alcohol-induced changes in spermatozoa may last for weeks or months (Roach etal. 2024). In addition, preconception paternal alcohol consumption alters the hormone balance, essential for
reproduction (Bedi etal. 2022; American Addiction Centre 2025). The effects of
paternal alcohol use extend beyond the embryonic stage, negatively impacting pregnancy outcomes and the health of offspring. Paternal alcohol use has been linked to
higher rates of miscarriage, stillbirth, and low birth weight. Additionally, paternal
alcohol use disorder (AUD) has been associated with increased risks of congenital

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anomalies and infant mortality (Klonoff-Cohen etal. 2003). Children of fathers who
drank heavily before conception have also been found to exhibit higher rates of
behavioral and mental health problems, mostly represented by ADHD, hyperactivity, anxiety, depression, and sleep disorders (Easey and Sharp 2021; Lo etal. 2024;
Jansen etal. 2024). These effects often manifest early in life, with risks peaking at
ages 2, 4, and 6. Interestingly, girls appear to show higher rates of emotional reactivity and cognitive challenges compared to boys who are more likely to display
somatic complaints and rule-breaking behaviors (Luan etal. 2022). The association
between fathers’ alcohol consumption and an increased risk of neurodevelopmental
disorders is also signicant. A recent study by May etal. (2023) suggested that
paternal alcohol use may increase the risk of fetal alcohol spectrum disorders
(FASD)—a condition characterized by cognitive difculties (problems with learning, memory, attention, and problem-solving skills), behavioral disorders (impulsivity, hyperactivity, and difculty with self-regulation), problems in interpersonal
interactions, and physical abnormalities (distinctive facial features, growth delays,
and organ anomalies) (Berlina 2024). May etal. (2023) found that fathers of children with FASD are more likely to have a history of heavy drinking. On average,
these fathers consume 9.2 drinks per occasion, compared to 4.8 drinks in control
groups, and exhibit signicantly higher rates of AUD.Although the mechanisms
remain unclear, this association raises the possibility that paternal alcohol use may
inuence FASD risk through genetic or environmental factors, or by affecting family dynamics and maternal health. A recent Swedish study (Khemiri etal. 2023)
explored the impact of paternal AUD on the offspring’s risk of intellectual disability
(ID), a neurodevelopmental disorder with altered cognitive, social, and physical
development (DSM 2013). The exact mechanisms remain unclear, but probably the
paternal alcohol use near conception may induce genetic mutations or epigenetic
changes, contributing to ID risk. Moreover, the relationship between paternal alcohol consumption and child outcomes appears to be dose-dependent: the more a
father drinks, the greater the risks for his children (Luan etal. 2022).
5.3 The Impact ofPaternal Psychopharmacotherapy
Most studies evaluating the safety of parental drug exposure during pregnancy and
conception primarily focus on maternal exposure. However, recent publications
have also highlighted the potential impact of paternal drug exposure on pregnancy
outcomes. Antipsychotics, anxiolytics, hypnotics, sedatives, and antidepressants are
frequently prescribed to fathers (Wensink etal. 2021) with some studies showing an
association between the use of some of these medications and the occurrence of
negative changes in sperm quality, as well as an increased risk of fetal mortality and
impaired fetal growth (Baumgartner etal. 2001; Safarinejad 2008; Engeland etal.
2013; Akasheh etal. 2014). In a prospective study by Wensink etal. (2022), rates of
preterm births were slightly higher in the drug-exposed groups (>6%) than in the
unexposed group (5%). Birth defects were generally similar between the two groups
(3.3–3.9% exposed vs 3.3% unexposed). The only drug group that showed a slightly
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