Childhood‐Onset Essential Hypertension and the Family Structure

Abstract

The prevalence and effect of single‐parent families in childhood‐onset essential hypertension (EH) is unknown. Children with EH and age‐, sex‐, and ethnicity‐matched controls were enrolled. Family structure data were obtained by in‐person interview. A total of 148 families (76 hypertension probands, 72 control probands; median 14 years) were prospective‐ly enrolled in the study. Single‐parent status was seen in 42% of the families––with and without EH (38% vs 46%, P=.41; odds ratio, 0.7; 95% confidence interval, 0.4–1.4). After multivariable analysis, a statistically significant sociofamilial contributor to the development of childhood‐onset EH was not identified. A significant number of single‐parent families (42%), the majority with single mothers, were found in our pedigree study. Sociofamilial factors are known to contribute to the expression of adult‐onset EH, but findings in our study suggest that they appear to contribute less in the expression of childhood‐onset EH.

Genetic studies using a family‐based design remain a powerful tool in determining the heritability of complex diseases.1 However, the presence of single‐parent families can make enrollment of a triad for a family‐based design a challenge. The family structure or status relates to being in a parent‐child relationship, usually the biological parents, but can also include situations in which someone is acting in the position of a parent to a child such as a legal guardian or an adult otherwise functioning as a parent. Parent‐child relationships may be formed either by marriage or common‐law relationships. Sociofamilial factors such as single‐parent family status may influence certain aspects of human health. Several studies among normotensive populations have linked childhood sociofamilial status with future adult cardiovascular disease,2, 3, 4 including adult essential hypertension (EH), but not hypertension in childhood.5, 6, 7, 8

Although secondary causes of hypertension are more prevalent in childhood, an increasing number of children are being diagnosed with primary or essential hypertension.9 Human EH is an age‐dependent and multifactorial disease with both genetic and environmental contributors. In childhood, genetic factors such as ethnicity and family history appear to play a larger role in the development of EH than that in adulthood. The heritability for childhood‐onset EH has been reported at 80%,10 indicating a high genetic contribution for manifestation of the phenotype at this early age. Whereas, the heritability of adult‐onset EH has been reported between 31% and 34%.11 The contribution of genetic factors to hypertension is demonstrated by the fact that the level of hypertension shows a strong familial aggregation.12, 13, 14 In addition, there is stronger concordance of blood pressure (BP) in monozygotic vs dizygotic twins.15, 16, 17 The heritability estimates of BP do not change after adjustment for dietary intake, smoking, alcohol and caffeine consumption, fatness and physical activity and fitness, despite the greater lifestyle concordance in monozygotic twins.16, 17, 18 There is also familial aggregation of response to antihypertensive medications.19 Furthermore, hypertensinogenic environmental exposures such as alcohol, smoking, illicit drug use, stress, sedentary lifestyle, and aging contribute to EH, which are more common in adults than children.

The primary aim of this study was to determine the prevalence of single‐parent families in a pedigree study in children. Whether childhood sociofamilial status plays a role in the development of childhood onset EH is unknown. Thus, the secondary aim was to determine the association of sociofamilial factors, including single‐parent status, with childhood‐onset EH.

Study Design

Institutional Approval

The study was approved by the institutional Committee for the Protection of Human Subjects at the University of Texas Health Science Center and Children's Memorial Hermann Hospital, Texas Medical Center. All participants and parents gave informed assent and consent, respectively, for this study. We were careful in maintaining full patient confidentiality, safeguarding the rights and welfare of human subjects, and informing participants, in a confidential manner, of the results obtained from the study. All families were given compensation of $20 per clinic visit for three visits for their participation in order to enroll all first‐degree relatives.

Patient Population

Patients were enrolled in this case‐control single‐center observational pedigree study from 2011 until 2014. Detailed information on family history and family structure was obtained by using a questionnaire and an in‐person interview. Participants aged 19 years or younger with either an established or a new diagnosis of EH were enrolled. Both treated and untreated patients seen at the Pediatric Hypertension Clinic at the University of Texas Medical School who fit the enrollment criteria were eligible for inclusion in the study.

BP Protocol

BP was measured by a standard protocol and hypertension status was confirmed both by clinic measurements and by ambulatory BP monitoring for 24 hours in all children as follows: hypertensive status in the clinic was confirmed in all patients at the first visit to the hypertension clinic by averaging the last three of four BP measurements performed by oscillometric method and confirmed by manual auscultation with a mercury sphygmomanometer by trained personnel using methods recommended by the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents (Fourth Report).20 Hypertension was diagnosed when three separate measurements of systolic and/or diastolic BP were >95th percentile for postconceptual age, adjusted for height, age, and sex per the Fourth Report.20 All children who were older than 5 years, except those admitted with a hypertensive emergency, underwent ambulatory BP monitoring (ABPM) using Spacelabs oscillometric monitors (Spacelabs, Inc, Redmond, WA). The children along with their families were instructed on avoidance of caffeinated beverages or supplements, any medications, herbal or over‐the‐counter products, smoking, and alcohol for 24 hours prior to and during ABPM. While performing ABPM, BP was automatically measured every 20 minutes for 24 hours. Patients with 24‐hour systolic BP or diastolic BP greater than the pediatric 95th percentile or BP load (percentage of BP values exceeding the 95th percentile for the 24‐hour period) >25% were considered to have ambulatory hypertension.21 Both BP and BP load were used to define the severity of ambulatory hypertension. Specifically, more severe ambulatory hypertension was defined as mean systolic or diastolic BP >95th percentile and BP load >50%. Children with hypertension in the clinic but a 24‐hour systolic BP and diastolic BP less than the pediatric 95th percentile and BP load <25% were considered to have white‐coat hypertension and were excluded from the study.

Diagnosis of EH

Once hypertension was confirmed, all children underwent further evaluation for secondary hypertension per recommendations by the Fourth Report.20 The diagnosis of secondary hypertension was made by extensive evaluation per recommendations by the Fourth Report,20 including urinary evaluation, blood tests, renal ultrasound, and echocardiography in all children; renal magnetic resonance imaging for renal artery stenosis in all patients with stage II hypertension or resistant hypertension; and sleep study for those with obesity and/or symptoms. Criteria for the diagnosis of EH were: (1) BP elevation in the clinic >95th percentile on three previous occasions, (2) positive 24‐hour ambulatory BP monitoring (except in those with a history of hypertensive emergency requiring admission or those who were younger than 5 years), (3) absence of secondary causes of hypertension, and (4) no concurrent medication with the potential to raise BP (eg, steroids, central stimulants).

Recruitment Criteria for the Study Population

For our family‐based genetic study, to be considered for further analysis, criteria for recruitment of the study participants consisted of the following:

Inclusion criteria: (1) history of diagnosis of EH per protocol described above20; (2) no known underlying medical conditions predisposing to hypertension; (3) no concurrent medication with the potential to raise BP at the time of diagnosis (eg, steroids or stimulant medication); (4) no evidence of white‐coat hypertension after ambulatory BP monitoring; (5) living with at least one of their biological parents; (6) at least one parent who spoke and wrote English or Spanish; and (7) age younger than 19 years at the time of diagnosis of EH.

Exclusion criteria: (1) adopted or custody with extended relatives without involvement of either biological parent; (2) parents without the ability to read or speak English or Spanish; (3) children with white‐coat hypertension and prehypertension; (4) children involved in custody issues; (5) children with complete evaluation for hypertension pending or lost to follow‐up; and (6) children born by donor egg or sperm. The criteria were tailored to exclude children with unknown genetic contribution to their hypertension.

Recruitment Criteria for Control Population

Children who were unrelated to the study population were prospectively enrolled into the study along with their siblings and parents. We recruited the control population from the ambulatory pediatric clinics. We matched the control probands based on age (age of diagnosis of hypertension of the case probands), sex, and ethnicity. Their normotensive status was confirmed by averaging the last three of four BP measurements performed by trained personnel using methods recommended by the Fourth Report.20

Inclusion criteria were as follows (1) age younger than 19 years at the time of enrollment; (2) no history of elevated BP or prehypertension/hypertension established by BP measurements; (3) no known underlying medical conditions predisposing to hypertension; (4) no concurrent medication with the potential to raise BP (eg, steroids or stimulant medications); (5) living with at least one of their biological parents; and (6) at least one parent who spoke and wrote English or Spanish.

Exclusion criteria were similar to the exclusion criteria for cases in addition to exclusion of the sibling of a study proband.

Pedigree and Family Structure

A three‐generational pedigree was drawn for each family based on the in‐person interview. A pedigree was constructed and all data were stored in a computerized database using Progeny software (version 7; Progeny software LLC, Delray Beach, FL). Probands with one first‐degree relative or two second‐degree relatives with hypertension diagnosed before the age of 50 were defined as having familial hypertension. Those probands with normotensive parents and grandparents (without history of consanguinity) were defined as having a nonfamilial form of hypertension. An extended pedigree chart was constructed for families with a history suggestive of a single‐gene disorder. Saliva, blood, and urine samples were collected from all the participating first‐degree members of the families.

The biological parent who participated in the study provided information regarding the living status and family structure of the proband. At enrollment, we assessed a parent's absence within a household via an in‐person interview with the biological parent of the child present at the clinic visit. The biological parent was asked about marital status, number of household members, their relationship to the child (whether biological or not), and education level and occupation of the parents. A single‐parent family was defined as a family with the absence of either a biologically or nonbiologically related parent in the residence due to any cause including never married, separation, divorce, incarceration, or death. We dichotomized our measure of parental absence into: (1) single‐parent household when the child lived with only a single parent, biological in relation, regardless of any interaction with the other birth parent (regular basis to no interaction with and without prior contact established; and (2) a two‐parent household when the child lived with at least one birth parent and another biologically or nonbiologically related parent regardless of parental marital status. The marital status for biological parents who were married and living together or separated was coded as “married.” A “nonmarital” status was given to divorced, widowed, or never married biological parents. The single‐parent status was further evaluated to determine whether the biological father was always absent or partially absent at the time of enrollment. The biological parent who was defined as always present was the one with contact with the child since birth. The biological parent who was defined as always absent was the one with no current contact with the child (contact not established, lost contact, separated, divorced, incarcerated, dead). The biological parent who was defined as partially absent was the one with current contact but who lived separately; however, the amount of contact was not ascertained.

Demographic and Anthropometric Data

All data were collected on all children and parents at study entry. Phenotyping of EH was on the nuclear family. After recruitment into the study, each family was evaluated and all information was recorded in a questionnaire along with demographic, sociofamilial including parental education and occupation, family history, and comorbid data. Anthropometric measurements along with BP measurements were made in proband and all first‐degree relatives. The ethnicity recorded was self‐reported and labeled as whites (non‐Hispanic white or European Americans), blacks (African Americans, non‐Hispanic blacks), Hispanics, Asians, American Indians, and others. The education recorded was self‐reported and categorized as high school, high school or GED, some college or technical school, and degree or postgraduate education. The residential urban or rural status was also per self‐report. Prematurity was defined as gestational age <37 weeks. The age of onset of hypertension and type of hypertension for each family member was determined along with history of end‐organ damage such as stroke, congestive heart failure, and renal failure.

Statistical Analysis

Data from the medical records was abstracted and tabulated. Continuous variables were compared between groups using parametric (t tests, analysis of variance with post hoc Tukey) and nonparametric (Mann‐Whitney U test, Kruskal Wallis) tests depending on the distribution of the variable. Chi‐square tests were used to compare categorical variables across groups. Kernel density curves were drawn to graphically depict the distribution of age of diagnosis of hypertension. Univariable and multivariable logistic regression analyses were performed to assess the odds of different factors among probands with EH compared with normal controls and to describe the odds ratios (ORs) and 95% confidence intervals (CIs). All analyses were performed using STATA version 10 (StataCorp, College Station, TX). Statistical significance was assumed at a type I error rate of 0.05.

Results

A total of 148 families (76 hypertension probands and 72 control probands), males 53%, with a median age of 14 years (range, 1–19 years) and a mean age of 12.2 years (standard deviation, 4.3), were prospectively enrolled in the study. Of the eligible children with EH, 14% families refused to participate in the study. The demographics and family structure are detailed in Table 1. For family structure we evaluated (1) parental marital status, (2) nonbiological parent status, and (3) single‐parent status (Table 1). Besides the family structure, we also evaluated parental education status and parental employment status under the childhood sociofamilial status as risk factors for childhood‐onset EH.

Table 1.

Demographic and Sociofamilial Distribution Among All Pedigrees

	Total	Parental Marital Status			Single‐Parent Status			Paternal Absence Status
		Parents not married	Parents married	P value	Living with one parent	Living with two parents	P value	No absence	Partial absence	Complete absence	P value
No.	148	63 (42)	85 (58)		62 (42)	86 (58)		74 (50)	31 (21)	43 (29)
Proband age, median (IQR range), y	12.2 (9.0–15.1)	11.9 (8.3–15.4)	12.3 (9.4–15.1)	.647	12.6 (9.0–15.4)	12.1 (9.0–15.1)	.806	12.2 (9.3–15.1)	13.2 (9.4–15.1)	12 (8.3–15.5)	.821
Proband male sex, No. (%)	78 (53)	26 (41)	52 (61)	.016	26 (42)	52 (60)	.026	45 (61)	13 (42)	20 (47)	.132
Proband ethnicity, No. (%)
African American	69 (47)	39 (62)	30 (35)	.012	40 (65)	29 (34)	.003	24 (32)	16 (52)	29 (67)	.009
Hispanic	51 (34)	17 (27)	34 (40)		14 (23)	37 (43)		29 (39)	11 (35)	11 (26)
Caucasian	22 (15)	5 (8)	17 (20)		6 (10)	16 (19)		17 (23)	3 (10)	2 (5)
Others	6 (4)	2 (3)	4 (5)		2 (3)	4 (5)		4 (5)	1 (3)	1 (2)
Mother's education, No. (%)
<High school	27 (19)	9 (15)	18 (22)	.134	8 (14)	19 (23)	.211	13 (18)	11 (37)	3 (7)	.001
High school or GED	38 (27)	19 (31)	19 (23)		17 (29)	21 (25)		20 (28)	7 (23)	11 (27)
Some college/technical school	52 (36)	26 (43)	26 (32)		26 (44)	26 (31)		20 (28)	8 (27)	24 (59)
College degree/postgraduate	26 (18)	7 (11)	19 (23)		8 (14)	18 (21)		19 (26)	4 (13)	3 (7)
Father's education, No. (%)
<High school	36 (26)	15 (26)	21 (26)	.135	14 (25)	22 (26)	.135	17 (24)	10 (33)	9 (24)	.058
High school or GED	60 (43)	31 (53)	29 (35)		30 (54)	30 (36)		24 (33)	13 (43)	23 (61)
Some college/technical school	24 (17)	7 (12)	17 (21)		7 (13)	17 (20)		16 (22)	5 (17)	3 (8)
College degree/postgraduate	20 (14)	5 (9)	15 (18)		5 (9)	15 (18)		15 (21)	2 (7)	3 (8)
Mother employed, No. (%)	89 (62)	43 (70)	46 (56)	.079	41 (69)	48 (57)	.134	44 (61)	15 (50)	30 (73)	.133
Father employed, No. (%)	103 (74)	33 (57)	70 (85)	<.001	33 (58)	70 (84)	<.001	62 (86)	22 (73)	19 (50)	<.001
Size of the family (first‐degree), No. (%)	4.5 (4–5)	4 (3–4)	4 (4–5)	<.001	4 (3–4)	4 (4–5)	<.001	4 (4–5)	4 (3–5)	3 (3–4)	<.001
Maternal age, median (IQR range), y	37.4 (32.9–42.2)	35.3 (31.6–40.1)	38.8 (35.1–44.0)	.002	35.2 (31.4–39.3)	38.8 (35.2–44)	.002	39.2 (35–44.3)	36.4 (32.1–41.3)	34.6 (31.8–38.9)	.003
Paternal age, median (IQR range), y	40.4 (36.0–45.5)	37.4 (34.2–45.1)	41.6 (36.7–45.8)	.214	37.4 (35.0–48.0)	41.6 (36.6–45.0)	.659	42.2 (37.6–45.7)	37.1 (29.4–45.2)	34.6 (31.8–38.9)	.313
Residential urban status, No. (%)	128 (90)	54 (90)	74 (90)	.962	52 (90)	76 (90)	.872	64 (89)	24 (83)	40 (98)	.096

Abbreviations: GED, General Educational Development test; IQR, interquartile range. Data missing for mother's education and employment status (5), father's education and employment status (8), maternal age (13), paternal age (75), and residential urban status (6).

The marital status of the biological parent was as follows: married (n=79, 53%), divorced (n=15, 10%), separated (n=6, 4%), widowed (n=1, 1%), and never married (n=47, 32%). The biological parent who was married but separated was analyzed as married and the parent who was widowed or divorced was analyzed as a single parent. The biological parent absence status was determined by living arrangement of the probands as follows: both biological parents (n=79, 54%), biological mother and nonbiological father (n=7, 5%), one biological mother alone (n=60, 40%), and one biological father alone (n=2, 1%). Mothers reported the status of a biological father in the household as follows: living with the child (n=74, 50%), no contact with the child (n=36, 24%), dead (n=1, 1%), incarcerated (n=6, 4%), and some contact with the child on a regular basis (n=31, 21%). The status of the biological mother of the probands was as follows: living with the child (n=146, 98%), some contact with the child on a regular basis (n=1, 1%), and dead (n=1, 1%). For probands, the study was not designed to quantify the duration of the child's contact with the biological parent. Therefore, the analysis could not control for that parameter.

Single‐parent status was seen in 42% of the families in our pedigree study––with and without EH (38% vs 46%, P=.41; OR, 0.7; 95% CI, 0.4–1.4). The composition of single‐parent families was as follows: one biological mother alone (n=60, 97%) and one biological father alone (n=2, 3%). In our pedigrees, male probands were more likely to have married parents or parents living together (Table 1). African Americans were more likely to have unmarried parents, biological parents not living together, or complete absence of paternal contact in comparison to other ethnicities (Table 1). Maternal education above high school level was more common among children with complete paternal absence. A higher maternal age was more likely in pedigrees where parents were married or living together or where fathers were in continuous contact with the child (Table 1). An employed father was more likely in pedigrees where parents were married or living together or where fathers were in continuous contact with the child (Table 1). After multivariable analysis (Table 2), we did not identify a statistically significant sociofamilial contributor to the development of childhood‐onset EH. We adjusted for family structure, parental education and employment status, size of the family, and self‐reported residential urban status.

Table 2.

Odds Ratios of Sociofamilial Risk Factors for Childhood‐Onset Essential Hypertension

	Unadjusted		Adjusted
	Odds Ratio	95% Confidence Interval	Odds Ratio	95% Confidence Interval
Single‐parent statusa	0.73	0.38–1.40	2.48	0.47–13.18
Maternal education >high schoola	0.58	0.30–1.14	0.60	0.14–2.62
Paternal education >high schoola	0.51	0.25–1.06	0.64	0.15–2.78
Mother employed	0.84	0.43–1.64	0.72	0.19–2.78
Father employed	1.10	0.52–2.32	0.61	0.13–2.72
Family size	1.05	0.91–1.21	0.98	0.55–1.73
Maternal age	1.00	0.96–1.03	1.01	0.94–1.07
Paternal age	0.99	0.95–1.03	1.00	0.94–1.05
Residential urban status	0.51	0.24–1.12	1.46	0.28–7.53

^aReferent: single‐parent status: living with both parents; education: ≤high school.

Discussion

Childhood‐onset EH has a lower prevalence (2%)22 and is a much more difficult diagnostic challenge20 than adult‐onset EH (prevalence of 30%).23 Since it is a difficult phenotype to ascertain among children, many aspects of childhood‐onset EH remain undetermined. Our study has the advantage of having a large number of well‐phenotyped children with EH who were evaluated in a rigorous manner in a large multiethnic population. These EH probands were compared with age‐, sex‐, and ethnicity‐matched controls from similar clinical setting. As a result of the role played by sociofamilial factors in the occurrence of various health problems in children, we assessed the same in our pedigrees. Specifically, we evaluated the role of single‐parent status, parental marital status, nonbiological parent status, and parental education status under the childhood sociofamilial status as risk factors for childhood‐onset EH. Overall, single‐parent status was seen in 42% of the families, the majority with single mothers and African American ethnicity. In our study, African Americans were more likely to have unmarried parents, biological parents not living together, or complete absence of paternal contact compared with other ethnicities. A higher maternal age was more likely in pedigrees where fathers were in contact with the child, either married or living together, or living apart but in contact with the family. Maternal education above high school level was more common among children with complete paternal absence in our study. An employed father was more likely in pedigrees where parents were married or living together.

Findings from our pedigree study in children demonstrate the difficulty in ascertaining complete pedigree data due to the presence of single‐parent families. The high rates of single‐parent households found in our study has implications not only in its influence on the financial aspects in these children but also for practical purposes in the application of family‐based or pedigree studies in the United States. Furthermore, as efforts are made to identify genetic factors that might contribute to the occurrence of hypertension, this increase in single‐family households may result in logistical difficulties in obtaining complete triads for complete genomic analysis. Although certain analytic techniques and protocols have been created to assess single‐parent families,24 it would not be possible to directly observe and assess the transmission of alleles within the family.

Among our children with EH, single‐parent status was seen in 38% of the families. The longitudinal data from the United States Census Bureau have shown a gradual increase in the number of single‐parent families, whereby more than a quarter (27%) of the children in the 2010 Census lived with only one parent (www.census.gov). A single‐parent household has been considered a vulnerable family status25 associated with an increase in psychosocial stressors26, 27 and medical conditions,27 both in the single parent28 and the child.25 Thus, a single‐parent household has implications on the child's psychosocial and health outcomes. A single‐parent in comparison to a two‐parent family has been associated with higher poverty,29, 30 behavioral problems,31, 32, 33 depression,34, 35 earlier onset of sexual activity,36 substance abuse,37, 38 suicide attempt,39 obesity,40 asthma,41 and lower scholastic achievement31 in the child. In one study, single‐parent households did not show a significant effect on systolic BP but did affect diastolic BP in children.42 Since chronic stress is a major player in EH in adults,43 stress reduction strategies have demonstrated reduction in BP in both normotensive44 and hypertensive adults44, 45 and reduction in mortality.46 An exaggerated BP reactivity and/or delayed recovery to acute stressors among normotensive children has been evaluated as a risk factor for EH. One study on BP reactivity reported that poorer black adolescents had lower diastolic BP values if their parents were more educated compared with less educated.47 However, the research related to evaluating only neighborhood socioeconomic status without evaluating family structure among youth for contribution to BP reactivity has been controversial,48, 49 with one study showing higher BP reactivity in black adolescents from a higher socioeconomic status compared with ones from a lower socioeconomic status.49 On the other hand, a family history of EH has been positively linked to increase in BP reactivity among children, indicating a strong genetic contribution to this reactivity at an early stage.50, 51, 52 These findings again suggest that family history or a genetic contribution plays a large role in the development of high BP in children.

The presence of incomplete families is of added concern when familial structure and socioeconomic factors, together sociofamilial factors, play a role in the disease of interest. It appears that the effect of early‐life sociofamilial factors may play a larger role in the development of adult‐onset EH rather than childhood‐onset EH. Childhood sociofamilial status has been found to have an effect on adult cardiovascular disease.2, 3, 4 A study in black adults in the United States showed that familial structure in childhood with a single‐parent household exerts an effect on the occurrence of higher BP in adulthood.53, 54

Despite the high prevalence of single‐parent households in our study, there was not an increase in childhood‐onset EH among those children in single‐parent families in comparison to two‐parent families among the three major ethnicities. Our findings are supported by other studies reported in the literature demonstrating that childhood sociofamilial status does not affect hypertension status in childhood.5, 6, 7 A study of childhood socioeconomic status measured by Hollingshead Four Factor Social Status Index compared it with trajectories of measured BP over several decades showed that it can affect BP status in adulthood after age 30 years but not childhood.7 A study of a cohort of men followed for more than 40 years from childhood to adulthood found that the single status of the men in adulthood, and not the childhood sociofamilial factors, was linked with adult‐onset EH.5 In another study of 1000 children, all physical health measures in early adulthood except for systolic BP showed a relationship with childhood socioeconomic status.6 Although none of the previously reported studies were on childhood‐onset EH, our findings are reflected in several other BP studies among children as well.5, 6, 7

We evaluated the absence of contact or negligible contact with the biological father and found no contribution to childhood‐onset EH when controlling for confounding variables. The physical presence of a father who is involved in the nurturing of the child has been demonstrated to contribute to improved emotional and social outcome.55, 56, 57 We also evaluated the Cinderella effect, whereby having a step‐parent or a nonbiological parent would be related to more stress and abuse. In our study, we found no significant difference between children living with two biological parents vs one biological parent and a nonbiological parent in the development of EH during childhood. A Swedish study of children 16 years or younger demonstrated that those living with their natural parents had a lower prevalence rate of cardiovascular illnesses, including hypertension, as an adult.58 We evaluated marital status of the parent since it has been found to influence the exposure to stress in children; a difference between married and unmarried parents was shown in the Fragile Families and Child Wellbeing Study, with higher family instability in the latter situation.29 Married vs unmarried status has been associated with improved parental functioning25 and improved BP profile in adults.59, 60, 61 In our current study, we did not find any significant difference in the parental marital status between those with and without childhood‐onset EH. Higher parental education has been associated with lower BP over time among adults.4 We evaluated paternal or maternal education status in our families and did not find any significant difference in childhood sociofamilial status in those with and without childhood‐onset EH.

Since EH appears to be a time‐related disease, the environmental exposures likely require several years before the disease manifests. Although adult‐onset EH may partly result from environmental factors such as sociofamilial status, the findings from our study suggest that the contribution may be much less pronounced in the development of childhood‐onset EH. The longitudinal development of disease such as EH may not fully manifest at the young ages described in our study and the impact from numerous environmental, including sociofamilial risk factors, may be limited in childhood‐onset EH. It appears that the predominant contribution to childhood‐onset EH is from genetic factors such as ethnicity and family history at this early stage of the disease, with lower contribution from other factors such as substance abuse, sociofamilial factors, sedentary lifestyle, diabetes, and aging. Thus, childhood‐onset EH may have a relatively higher genetic contribution10 and it may be more useful to identify genetic contribution in childhood‐onset EH as opposed to adult‐onset EH.

Limitations

We did not enroll children who did not have at least one biological parent and hence the study results cannot be extrapolated to children in adopted families and families involving a grandparent as the primary caretaker of the child. In addition, our case and control populations were clinic not population based. The degree of parental contact, sexual preference of the parent, access to resources, financial status, community support, and psychological status were not investigated in this study. Furthermore, child birth order status, coparenting behaviors, timing of onset of parent absence, or the age of the children at parental separation was also not assessed in this study. Finally, we did not evaluate children with white‐coat hypertension or prehypertension in this study who may have the potential to develop EH in future.

Conclusions

A significant number of single‐parent families, the majority with single mothers, were found in our pedigree study. Thus, sociofamilial factors should be considered not only during patient counseling but also when designing genetic studies. The findings from our study suggest that sociofamilial factors may contribute less in the expression of childhood‐onset EH than in the expression of adult‐onset EH.

Funding Resources

The project described was supported by grant number K23HL089391 for “Determination of Genetics of Childhood‐Onset Hypertension” to PI Monesha Gupta from the National Heart, Lung, and Blood Institute. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Heart, Lung, and Blood Institute or the National Institutes of Health.

Disclosures

None.

J Clin Hypertens (Greenwich). 2016;18:431–438. DOI: 10.1111/jch.12701. © 2015 Wiley Periodicals, Inc.