Children who experienced parental divorce are found to have low levels of oxytocin in adulthood


People who were children when their parents were divorced showed lower levels of oxytocin — the so-called “love hormone” — when they were adults than those whose parents remained married, according to a study led by Baylor University. That lower level may play a role in having trouble forming attachments when they are grown.

Oxytocin — secreted in the brain and released during bonding experiences such as delivery of a baby or sexual interaction or nursing, even being hugged by a romantic partner — has been shown in previous research to be important for social behavior and emotional attachments in early life.

The oxytocin system also has been linked to parenting, attachment and anxiety.

The new study, published in the Journal of Comparative Psychology, delves into an area that has not been well researched — a link between oxytocin, early experience and adult outcomes.

“Since the rates of divorce in our society began to increase, there has been concern about the effects of divorce on the children,” said lead author Maria Boccia, Ph.D., professor of child and family studies at Baylor University in the Robbins College of Health and Human Sciences.

“Most research has focused on short-term effects, like academic performance, or longer-term outcomes like the impact on relationships. How divorce causes these effects, however, is unknown.

Oxytocin is a neurohormone that is important in regulating these behaviors and is also sensitive to the impact of stressful life events in early life,” she said. “This is a first step towards understanding what mechanisms might be involved.”

Previous studies of children whose parents were divorced have found that the experience was associated with mood disorders and substance abuse — behaviors found to be related to oxytocin, Boccia said.

Additionally, such childhood experiences as divorce or death of a parent are associated with depression and anxiety in adolescents and adults, as well as with poorer parenting in adulthood, less parental sensitivity and warmth, overreaction and increased use of punishment.

Researchers in the Baylor study examined the effect of the experience of parental divorce in childhood on later adult oxytocin levels.

They also asked participants to complete a set of questionnaires on attachment style and other measures.

“What we found was that oxytocin was substantially lower in people who experienced parental divorce compared to those who did not and correlated with responses on several measures of attachment,” Boccia said.

“These results suggest that oxytocin levels are adversely affected by parental divorce and may be related to other effects that have been documented in people who experience parental divorce.”

Animal studies also suggest that one mechanism contributing to the negative effects of early parental separation may be suppression of oxytocin activity.

For the latest study, researchers recruited 128 individuals ages 18 to 62 at two institutions of higher learning in the Southeast United States. Of those, 27.3% indicated their parents were divorced.

The average age for participants when their parents divorced was 9 years.

Upon arriving at the study site, participants were asked to empty their bladders, then given a 16-ounce bottle of water to drink before filling out questionnaires about their parents and peers during childhood, as well as their current social functioning.

The questions addressed their parents’ style, including affection, protection, indifference, over-control and abuse; and their own levels of confidence, discomfort with closeness, need for approval and their styles of relationships and caregiving.

After participants completed the questionnaires, urine samples were collected, and researchers analyzed oxytocin concentrations. The levels were substantially lower in individuals whose childhood experience included their parents’ divorce.

Further analysis showed that those individuals rated their parents as less caring and more indifferent. They also rated their fathers as more abusive.

Those who experienced parental divorce during childhood were less confident, more uncomfortable with closeness and less secure in relationships. They rated their own caregiving style as less sensitive and close than did the participants whose parents had not divorced.

“One of the first questions I am asked when presenting this research to other scientists is ‘does how old the child is when the divorce occurs matter?’ That is the most pressing question that we need to explore,” Boccia said.

Funding: This study was supported with a grant from the National Institutes of Health. Co-researchers included Gordon-Conwell Theological Seminary in Charlotte, N.C., and the departments of surgery and psychiatry at the University of North Carolina-Chapel Hill.

Psychobiological effects on infant health linked to parental separation and other childhood adversities

Although the most known effects of the divorce process are commonly evident in the behavioral and emotional fields, physical morbidity of the children was also described in situations of parental loss and often correlated childhood adversities. For example, a study from Taiwan (Juang et al., 2004) found a clear link between parental divorce and children’s daily headache (chronic daily headache-CDH).

Various studies have, moreover, described increased prevalence of attention deficit and hyperactivity disorder (ADHD) in children in situations of divorce and abuse (and not always for a selection effect); for example, (Cohen et al., 2002) interactional effects of marital disruption and abuse were found for risk for lifetime ADHD, with parental marital disruption and having been physically abused combining to increase the risk indeed 15 times for diagnosis of lifetime ADHD.

In this study, parental marital status alone was not a significant risk factor for adolescent psychopathology, but a childhood adversity as physical abuse was a significant risk factor for several diagnostic categories.

Much research (but all conducted in monoparental countries, where shared parenting is uncommon and divorce is often linked to the increasing adverse effect of parental loss, high rates of family conflict, etc.) found a correlation between parental divorce and eating disorders and excessive weight (Igoin-Apfelbaum, 1985Johnson et al., 2002Yannakoulia et al., 2008).

Another study from France (Roustit et al., 2011) examined the relationship between adverse family environments during childhood and self-perceived health in adulthood. It was found that exposure to separation and divorce in childhood was associated with worse health perception in older age. The study referred to mental health as well as to physical status. Moreover, a study of almost 1 million children in Sweden observed that children growing up with single parents were more than twice as likely to experience a serious psychiatric disorder, commit or attempt suicide, or develop an alcohol addiction (Ringsback-Weitoft et al., 2003).

Similarly, Hailey Maier and Lachman (2000) found in a sample of 4242 adults who responded to the survey of Midlife Development in the United States that loss or separation from parents in childhood does have a negative impact on health problems and psychological adjustment in midlife, and that the effects are more pronounced for divorce. It appears that parental divorce leads to lower education and income attainment, an increase in drug use, and lower levels of family support which may result in a greater number of health problems later in life, while parental death was also related to lower educational attainment but showed no relationship with adult health.

Although both experiences (parental loss as consequence of divorce and as consequence of parental death) can impact economic resources, social resources may be more affected by parental divorce, but parental divorce can result in changes in the child’s relationship with both parents, whereas parental death is less likely to disrupt the child’s relationship with the remaining parent.

In further research, Tyrka et al. (2008) found that participants with separation/desertion and those with parental death were significantly more likely than the control subjects to report the subsequent onset of symptoms of a depressive or anxiety disorder but Otowa et al. (2014) went beyond finding that early parental separation has stronger and wider effects on adult psychopathology than parental death.

Going into details, parental separation was associated with a wide range of adult psychopathology, whereas parental death was specifically associated with phobia and alcohol dependence. Maternal and paternal separations were almost equally associated with most forms of psychopathology.

Structural equation modeling suggested that parental loss accounted for about 10 percent of the variance of adult psychopathology, of which parental separation had the strongest impacts on risk for depression and drug abuse/dependence (11% of the total variance).

Finally, a key body of research in Israel (Agid et al., 1999) has drawn several conclusions:

  1. Increased overall rates of early parental loss are observed in major depression, bipolar disorder, and schizophrenia, but the finding is most striking in major depression followed by schizophrenia. The finding in regard to major depression is consistent with the majority of published studies in which loss is not broken down into categories, while the literature on bipolar disorder and schizophrenia is insufficient for comparison.
  2. Patients with major depression manifest a significantly increased rate of early parental loss due to permanent separation but not due to death, as observed by a number of methodologically rigorous case–control and epidemiological studies.
  3. Loss of mother may be more significant than loss of father; although in this analysis, this observation was at a trend level only.
  4. Loss at an early age (less than 9 years) is of greater significance than later loss, as previously observed by several researchers.
  5. A specific sensitivity of females rather than males to loss in major depression and bipolar disorder is suggested by this research but cannot be regarded as definitive because of sample size.
  6. Genetic predisposition may influence the degree of susceptibility of the individual to the effects of early environmental stress and may also determine the psychopathological entity to which the individual is rendered vulnerable as a consequence of the stress.

Biological consequences of parental loss and other childhood adversities: latest knowledge

By a more biological point of view, we have a lot of evidence too; for instance, Nicolson (2004) showed that cortisol levels in adult men are increased if in their childhood they were subject to parental loss or other adversities.

Similarly, Luecken (1998) found that both childhood loss of a parent and poor quality of care are associated with long-term increases in blood pressure and altered neuro-hormonal responses to stress. More in detail, repeated-measures analysis of covariance revealed significant main effects on blood pressure of both parental loss and low quality of family relationships (all p values < 0.05) such that subjects who lost a parent or reported poor-quality family relationships (FR) showed higher blood pressure across all periods.

The loss by FR by period interaction was not significant. An FR by period interaction was found for cortisol during the trial, in which poor-quality FR subjects showed increased cortisol, whereas all others showed decreases. A loss by period interaction was found for cortisol during the speech, in which cortisol increased in loss subjects and decreased in non-loss subjects.

We must highlight that chronic augmentation of cortisol due to influence on hypothalamo–hypophysis–adrenocortical axis is linked to several disease in adulthood and senescence like psychopathology (e.g. depression), diabetes II, obesity, and osteoporosis.

It is noteworthy that through the action of glucocorticoids on the central nervous system, repeated or chronical psychological stress can inhibit the thyroid-stimulating hormone (TSH) secretion (Helmreich et al., 2005).

In psychological stress, conversely, growth hormone (GH) responses are rarely seen. Rather, there is GH secretory defect with prolonged psychosocial stress causing a wide pattern of clinical situations toward the rare condition called psychosocial dwarfism (PD) (Delitala et al., 1987Magner et al., 1984Skuse et al., 1996)

PD is a term describing severe childhood or adolescent short stature and/or delayed puberty due to emotional deprivation, inadequate parenting, or psychological harassment. Decreased GH secretion, that is reversible after separation of the child from the responsible environment, is a characteristic finding in this condition (Albanese et al., 1994).

The treatment with GH is not usually of benefit until the psychosocial situation is improved. PD is also associated with a variety of behavioral abnormalities, such as depression and bizarre eating PD were first studied in infants in foundling homes or orphanages who failed to thrive, had decreased growth, and even died.

It was hypothesized that this failure to thrive resulted from lack of attention and stimulation and/or deficient nutrition. Later, it was shown that weight gain was independent of food intake, whereas with a caring and attentive environment, growth advanced and the psychological profile improved. In addition to low GH secretion, these patients had a dysfunctional thyroid axis, resembling the “euthyroid sick” syndrome (Dom et al., 1993Green et al., 1984).

Battaglia et al. (2009) showed that childhood separation anxiety can cause, in genetically prepared people, panic disorders.

More in detail shared genetic determinants appeared to be the major underlying cause of the developmental continuity of childhood separation anxiety disorder into adult panic disorder and the association of both disorders with heightened sensitivity to CO(2). Inasmuch as childhood parental loss is a truly environmental risk factor, it can account for a significant additional proportion of the covariation of these three developmentally related phenotypes.

In the area of childhood adversities, Lacey et al. (2013) found (but in the United Kingdom, a monoparental country where parental loss after divorce is common: it would be interesting to know whether the researchers would have obtained the same outcome in a biparental country such as Sweden, where shared parenting is common and parental loss rare) that parental separation increases C Reactive Protein (CRP) levels (correlated with type II diabetes, coronary heart disease, depression, inflammatory diseases, etc.) in adulthood via chains of disadvantage across the life course.

Hartwell et al. (2013) found an important association of elevated basal cytokines with childhood adversity in a sample of healthy adults demonstrating the long-term impact of childhood trauma and stress on homeostatic systems. Importantly, this association was found in healthy adults, suggesting that these alterations may precede the development of significant stress-related psychiatric disorder or disease.

Moreover, Kiecolt-Glaser et al. (2011) demonstrated that childhood adversity heightens the impact of later-life caregiving stress on telomere length and inflammation and are so related to continued vulnerability among older adults enhancing the impact of chronic stress factors: it means more psychiatric disorders (for abuse has been demonstrated to lead to an increase in metabolic diseases, cancers, and lung diseases).

This new epigenetic approach allowed the authors to observe that presence of multiple childhood adversities was related to both heightened interleukine-6 (IL-6) and shorter telomeres compared with the absence of adversity; the authors observed that the telomere difference could translate into a 7- to 15-year difference in life span. Abuse was associated with heightened IL-6 and tumor necrosis factor-alpha (TNF-α) levels; for TNF-α, this relationship was magnified in caregivers compared with controls. Moreover, abuse and caregiving status were associated significantly and independently with higher levels of depressive symptoms. Dysregulation of TNF production has been implicated in a variety of human diseases including Alzheimer’s disease, cancer, major depression, psoriasis, and inflammatory bowel disease (IBD) (Brynskov et al., 2002Dowlati et al., 2010Locksley et al., 2001Swardfager et al., 2010Victor and Gottlieb, 2002).

IL-6 stimulates the inflammatory and auto-immune processes in many diseases such as diabetes, atherosclerosis, depression, Alzheimer’s disease, systemic lupus erythematosus, multiple myeloma, prostate cancer, Behçet’s disease, and rheumatoid arthritis (Gadó et al., 2000Hirohata and Kikuchi, 2012Nishimoto, 2006Smith et al., 2001Tackey et al., 2004).

Opacka-Juffry and Mohiyeddini (2012) contributed with interesting research which showed evidence that adverse experience in early life (such as but not exclusively parental loss) is negatively associated with oxytocin system activity in adulthood (correlated with depression and anxious disorders) and offer further insight into mediator and moderator effects on this link. Gunther Meinlschmidt and Christine Heim (2007) found altered central sensitivity to the effects of oxytocin after early parental separation and suggest that future studies should replicate these results and scrutinize the role of oxytocin in mediating risk versus resilience to psychopathology after early social adversity.

A new topic is the possible correlation between height and familial disruption: Sheppard et al. (2015) argue that familial disruption during early childhood has far-reaching repercussions for the health of both men and women. Their study assesses adult height as one such health-relevant outcome.

For men, parental death and divorce during early childhood were associated with later puberty. Later puberty was associated with shorter adult height. Path analyses demonstrated that the relationship between parental divorce and height was completely mediated by age at puberty, although parental death was only partially mediated by age at puberty.

Among women, it was found that the father’s death during early childhood was associated with earlier puberty, which was in turn associated with shorter adult stature. The relationship between paternal death and height is entirely mediated by age at puberty; no evidence of a direct relationship between childhood family disruption and adult height.

Another link between parenting and human biology was found by Human Lauren et al. (2014). They observed that adolescents whose daily experiences were perceived more accurately by their parents reported better psychological adjustment (lower stress and depression) and a greater sensitivity of their immune cells to anti-inflammatory signals from cortisol (i.e. diminished production of inflammatory proteins when cells were stimulated with the combination of a bacterial product (lipopolysaccharide) and cortisol; |β| range, 0.38–0.53, all p values < 0.041).

The authors argued that more attentive parental care regarding adolescents’ daily experiences is associated with better adolescent psychological adjustment and a more sensitive anti-inflammatory response to cortisol. These results provide preliminary evidence that more attentive parental care regarding their adolescent’s daily experiences may be one specific daily parent factor that plays a role in adolescent health and well-being.

It is also noteworthy that Scott et al. (2008) found that childhood adversities predicted adult-onset asthma with risk increasing with the number of adversities experienced.

Another body of research found that all childhood adversity was associated with elevated markers of inflammation in breast cancer survivors, with potential negative implications for health and well-being. In particular, chaotic home environment showed unique links with inflammatory outcomes (Crosswell et al., 2014).

Finally, we recall that it is commonly known that adverse life events increase vulnerability to affective disorders later in life, possibly mediated by methylation of the serotonin transporter gene methylation. All that granted, Van der Knaap et al. (2014) demonstrate a higher level of serotonin transporter gene methylation after stressful life events in adolescents, with a more pronounced association for stressful events during adolescence than during childhood.

Source: Baylor University


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