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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
J Clin Hypertens (Greenwich). Author manuscript; available in PMC 2017 May 1.
Published in final edited form as:
PMCID: PMC4821812

Childhood Onset Essential Hypertension and the Family Structure


The prevalence and effect of single parent families in childhood onset essential hypertension (EH) is unknown. Children with EH and age, gender- 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 prospectively enrolled in the study. A single parent status was seen in 42% of the families; with and without EH (38% vs. 46%, p=0.41; OR: 0.7, 95%CI: 0.4–1.4). Upon multivariable analysis we did not identify a statistically significant socio-familial contributor to the development of childhood onset EH. A significant numbers of single parent families (42%), majority with single mothers were found in our pedigree study. Sociofamilial factors are known to contribute to the expression of the adult onset EH, but findings in our study suggest that they appear to contribute less in the expression of childhood onset EH.

Keywords: primary hypertension, pediatrics, single parent, pedigree, marital, socioeconomic


Genetic studies using a family-based design remain a powerful tool in determining the heritability of complex diseases1. However, the presence of single parent families can make enrollment of a triad for a family-based design a challenge. The family structure or family status relates to being in a parent and 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. The parent-child relationships may be formed either by marriage or common-law relationships. Sociofamilial factors such as a single parent family status may influence certain aspects of human health. Several studies among normotensive populations have linked childhood sociofamilial status as a predictor of future adult cardiovascular disease24 including adult essential hypertension, but not to hypertension in childhood58.

Although secondary causes of hypertension are more prevalent in childhood, an increasing number of children are being diagnosed with primary or essential hypertension (EH)9. Human EH is an age-dependent and multifactorial disease with both genetic and environmental contributors. In childhood, the genetic factors such as ethnicity and family history, appear to play a larger role than adulthood in the development of EH. 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 31–34%11. The contribution by genetic factors to hypertension is demonstrated by the fact that the level of hypertension shows a strong familial aggregation1214. In addition, there is stronger concordance of blood pressure in monozygotic versus dizygotic twins1517. The heritability estimates of blood pressure 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 twins1618. There is also familial aggregation of response to antihypertensive medications19. Furthermore, EH has contribution from hypertensinogenic environmental exposures such as alcohol, smoking, illicit drug use, stress, sedentary lifestyle etc. and aging which are higher among 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 play a role in the development of childhood onset EH is unknown. Thus, the secondary aim was to determine association of sociofamilial factors, including single-parent status, to 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 subjects 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 subjects, in a confidential manner, of the results obtained from the study. All families were given compensation of $20 per clinic visit for 3 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 family history and family structure was obtained by using a questionnaire and an in-person interview. Subjects, aged 19 years or younger, with either an established or a new diagnosis of EH were enrolled. Both treated and un-treated patients seen at the Pediatric Hypertension Clinic at the University of Texas Medical School that fit the enrollment criteria were eligible for inclusion in the study.

Blood Pressure Protocol

The BP was measured by a standard protocol and hypertension status 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 subjects at the first visit to the hypertension clinic by averaging the last 3 of 4 BP measurements performed by oscillometric method and confirmed by manual auscultation with a mercury sphygmomanometer by trained personnel using methods recommended by the Fourth Report20. Hypertension was diagnosed when 3 separate measurements of systolic and/or diastolic BP were recorded >95th% percentile for post-conceptual age, adjusted for height, age and gender per Fourth Report 20 were documented in the medical record. All children who were above the age of 5 years of age except those admitted with a hypertensive emergency underwent an 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 the ABPM. While on ABPM, the BP was automatically measured every 20 minutes for 24 hours. Subjects 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) greater than 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 greater than the 95th percentile and BP load greater than 50%. Children with hypertension in clinic but a 24-hour systolic BP and diastolic BP less than the pediatric 95th percentile and BP load less than 25% were considered to have White Coat hypertension and were excluded from the study.

Diagnosis of Essential Hypertension

Once hypertension was confirmed, all children underwent further evaluation for secondary hypertension per recommendations by the Fourth Working Group20. The diagnosis of secondary hypertension was made by extensive evaluation per recommendations by the Fourth Working Group20 including a urinary evaluation, blood tests, renal ultrasound and echocardiogram in all children; renal magnetic resonance imaging for evaluation for renal artery stenosis in all those with stage II hypertension or resistant hypertension; sleep study for those with obesity and/or symptoms, and so on. Criteria for the diagnosis of EH were: (a) BP elevation in the clinic above the 95th percentile on 3 previous occasions, (b) positive 24 hour ambulatory BP monitoring (except in those who with history of hypertensive emergency requiring admission or those who were less than 5 years old), (c) absence of secondary causes of hypertension and (d) no concurrent medication with the potential to raise BP (e.g., steroids, central stimulants).

Recruitment Criteria for Study Population

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

Inclusion criteria

(a) history of diagnosis of EH per protocol described above 20 (b) no known underlying medical conditions predisposing to hypertension. (c) no concurrent medication with the potential to raise BP at the time of diagnosis (e.g., steroids or stimulant medication) (c) no evidence of white-coat hypertension after an ambulatory BP monitoring (d) living with at least one of their biological parent (e) at least one parent spoke and wrote English or Spanish and (f) age less than 19 years at the time of diagnosis of EH.

Exclusion criteria

(a) adopted or custody with extended relatives without involvement of either biological parent (b) parents without ability to read or speak English or Spanish language (c) children with white coat hypertension and prehypertension (d) children involved in custody issues (e) children with complete evaluation for hypertension pending or lost to follow-up (f) children born by donor egg or sperm were not enrolled in this study. 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), gender and ethnicity. Their normotensive status was confirmed by averaging the last 3 of 4 BP measurements performed by trained personnel using methods recommended by the Fourth Report20.

Inclusion criteria were as follows (a) age less than 19 years at the time of enrollment (b) no history of elevated BP, or prehypertension/hypertension established upon BP measurements in the child (c) no known underlying medical conditions predisposing to hypertension and (d) no concurrent medication with the potential to raise the BP (e.g., steroids or stimulant medications) (e) living with at least one of their biological parents, (f) at least one parent 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 3-generational pedigree was drawn for each family based on the in-person interview. A pedigree was constructed and all data was store in a computerized database using Progeny software (version 7, Progeny software LLC, Delray Beach, Florida, USA.). Probands with a one first-degree relative or two second-degree relatives with hypertension diagnosed before age of 50 years were defined as having familial hypertension. Those probands with normotensive parents and grandparents (without history of consanguinity) were defined to have non-familial 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 the marital status, the number of household members, their relationship to the child (whether biological or not), and the education level and occupation of the parents. A single-parent family was defined as a family with the absence of either a biologically or non-biologically-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 (a) Single parent household when the child lived with only a single parent, biological in relation, regardless of any doses of interaction with the other birth parent (regular basis to no interaction with and without prior contact established and (b) A two-parent household when the child lived with at least one birth parent and another biologically or non-biologically-related parent regardless of parental marital status. The marital status for biological parents that were married and living together or separated was coded as “married”. A “non-marital” 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 subjects and parents at study entry. Phenotyping of EH was nuclear family based. 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 co-morbid 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, 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 less than 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, ANOVA with posthoc Tukey) and non-parametric (Mann-Whitney, 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 to normal controls and to describe the odds ratios (OR) and 95 % confidence intervals (CI). All analysis was performed in STATA (v.10, College Station). Statistical significance was assumed at a Type I error rate of 0.05.


A total of 148 families, 76 hypertension probands, 72 control probands, males 53%, median age of 14 years (range 1–19 years) with a mean age 12.2 years (SD: 4.3), were prospectively enrolled in the study. Out of the eligible children with EH, 14% families refused to participate in the study. The demographics and family structure at detailed in Table 1. For family structure we evaluated (a) parental marital status, (b) non-biological parent status, and (c) single parent status (see 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 socio-familial distribution among all pedigrees

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%). Biological parent who was married but separated was analyzed as married and the parent who was widowed or divorced was analyzed as 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 non-biological 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 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 regular basis (n = 1, 1%), and dead (n = 1, 1%). For probands, the study was not designed to quantify the duration that the child’s contact with the biological parent. Therefore, the analysis could not control for that parameter.

A single parent status was seen in 42% of the families in our pedigree study; with and without EH (38% vs. 46%, p=0.41; 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 father 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 father was in continuous contact with the child (Table 1). Upon multivariable analysis (Table 2) we did not identify a statistically significant socio-familial 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 socio-familial risk factors for childhood onset essential hypertension


Childhood onset EH has a lower prevalence (2%)22 and is a much more difficult diagnostic challenge20 than adult onset EH where the prevalence is 30% 23. Since it is a difficult phenotype to ascertain amongst 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 to age, gender and ethnicity matched controls from similar clinical setting. Due to 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, non-biological parent status, and parental education status under the childhood sociofamilial status as risk factors for childhood onset EH. Overall, a single parent status was seen in 42% of the families, 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 in comparison to 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 families24, 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 has 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 ( A single-parent household has been considered a vulnerable family status25 associated with an increase in psychosocial stressors26, 27 and medical conditions27, both in the single parent28 and the child25. 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 poverty29, 30 behavioral problems3133, depression34, 35, earlier-onset of sexual activity36, substance abuse37, 38, suicide attempt39, obesity40 asthma41 and lower scholastic achievement31 in the child. In one study, single parent household did not show significant effect on systolic BP but did affect diastolic BP in children42. Since chronic stress is a major player in essential hypertension (EH) in adults43, stress reduction strategies have demonstrated reduction in BP in both normotensive44 and hypertensive adults 44, 45 and reduction in their 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 if their parents were more educated in comparison to less educated47. However the research related to only evaluating neighborhood socioeconomic status without evaluating family structure amongst youth for contribution to BP reactivity has been controversial48, 49 with one study showing a higher BP reactivity in black adolescents from a higher socioeconomic status in comparison to ones from a lower socioeconomic status49. On the other hand, a family history of EH has been linked positively to increase in BP reactivity amongst children, indicating a strong genetic contribution to this reactivity at an early stage5052. These findings again suggest that a family history or 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 disease24. In 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 a higher BP in adulthood53, 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 amongst the three major ethnicities. Our findings are supported by other studies reported in the literature demonstrating that childhood sociofamilial status does not affect the hypertension status in childhood57. 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 childhood7. A study of a cohort of men followed for over 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 EH5. In another study of a 1000 children, all physical health measures in early adulthood except for systolic BP showed a relationship to childhood socioeconomic status6. Although none of the previously reported studies were on childhood onset EH, our findings are reflected in several other BP studies amongst children as well57.

We evaluated the absence of contact or negligible contact with the biological father and found no contribution to childhood onset EH when we controlled for confounding variables. The physical presence of a father who is involved in the nurturing of the child has been demonstrated to contribute towards improved emotional and social outcome5557. We also evaluated for the “Cinderella effect” whereby having a step-parent or a non-biological parent would be related to more stress and abuse. In our study, we found no significant difference between children living with two biological parents versus one biological parent and a non-biological parent in the development of EH during childhood. A Swedish study of children ages 16 years or younger demonstrated that those living with their natural parents have a lower prevalence of cardiovascular illnesses, including hypertension as an adult58. 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 by the Fragile Families and Child Wellbeing Study with higher family instability in the latter situation 29. A marital life in comparison to unmarried status has been associated with improved parental functioning25 and improved BP profile in adults 5961. 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 adults4. We evaluated paternal or maternal education status in our families and did not find any significant difference in the childhood sociofamilial status in those with and without childhood onset EH

Since EH appears to be a time related disease, the environmental exposures possibly require several years before the disease manifests. Although adult onset EH may have a contribution 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, aging and so on. Thus, childhood-onset EH may have a relatively higher genetic contribution10 and it may be more fruitful to identify genetic contribution in childhood-onset EH as opposed to adult-onset EH.


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. Additionally, our case and control populations were clinic based and 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, co-parenting 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.


A significant number of single parent families, 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 the adult onset EH.


Funding Resources: The project described was supported by Grant Number K23HL089391 for “Determination of genetics of childhood onset hypertension” (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.

We would like to thank Dr. Jon Tyson, Dr. Eric Boerwinkle and Dr. Jacqueline Hecht for mentorship of Dr. Monesha Gupta during her career development award by National Institutes of Health. We would like to thank Dr. Jon Tyson and Dr. Joshua Samuels for the review of the manuscript. We would also like to thank the families who donated their data and time for this study.


Conflict of Interest Disclosures: Disclosures none


1. Ott J, Kamatani Y, Lathrop M. Family-based designs for genome-wide association studies. Nat Rev Genet. 2011;12:465–474. [PubMed]
2. Cohen S, Janicki-Deverts D, Turner RB, Marsland AL, Casselbrant ML, Li-Korotky HS, Epel ES, Doyle WJ. Childhood socioeconomic status, telomere length, and susceptibility to upper respiratory infection. Brain Behav Immun. 2013;34:31–38. [PMC free article] [PubMed]
3. Galobardes B, Smith GD, Lynch JW. Systematic review of the influence of childhood socioeconomic circumstances on risk for cardiovascular disease in adulthood. Ann Epidemiol. 2006;16:91–104. [PubMed]
4. Janicki-Deverts D, Cohen S, Matthews KA, Jacobs DR., Jr Sex differences in the association of childhood socioeconomic status with adult blood pressure change: The cardia study. Psychosom Med. 2012;74:728–735. [PMC free article] [PubMed]
5. Lindgarde F, Furu M, Ljung BO. A longitudinal study on the significance of environmental and individual factors associated with the development of essential hypertension. J Epidemiol Community Health. 1987;41:220–226. [PMC free article] [PubMed]
6. Poulton R, Caspi A, Milne BJ, Thomson WM, Taylor A, Sears MR, Moffitt TE. Association between children’s experience of socioeconomic disadvantage and adult health: A life-course study. Lancet. 2002;360:1640–1645. [PMC free article] [PubMed]
7. Su S, Wang X, Pollock JS, Treiber FA, Xu X, Snieder H, McCall WV, Stefanek M, Harshfield GA. Adverse childhood experiences and blood pressure trajectories from childhood to young adulthood: The georgia stress and heart study. Circulation. 2015 [PMC free article] [PubMed]
8. Riley EH, Wright RJ, Jun HJ, Hibert EN, Rich-Edwards JW. Hypertension in adult survivors of child abuse: Observations from the nurses’ health study ii. J Epidemiol Community Health. 2010;64:413–418. [PMC free article] [PubMed]
9. Gupta-Malhotra M, Banker A, Shete S, Hashmi SS, Tyson JE, Barratt MS, Hecht JT, Milewicz DM, Boerwinkle E. Essential hypertension vs. Secondary hypertension among children. Am J Hypertens. 2015;28:73–80. [PMC free article] [PubMed]
10. Robinson RF, Batisky DL, Hayes JR, Nahata MC, Mahan JD. Significance of heritability in primary and secondary pediatric hypertension. Am J Hypertens. 2005;18:917–921. [PubMed]
11. Ehret GB. Genome-wide association studies: Contribution of genomics to understanding blood pressure and essential hypertension. Curr Hypertens Rep. 2010;12:17–25. [PMC free article] [PubMed]
12. Clarke WR, Schrott HG, Burns TL, Sing CF, Lauer RM. Aggregation of blood pressure in the families of children with labile high systolic blood pressure. The muscatine study. Am J Epidemiol. 1986;123:67–80. [PubMed]
13. Munger RG, Prineas RJ, Gomez-Marin O. Persistent elevation of blood pressure among children with a family history of hypertension: The minneapolis children’s blood pressure study. J Hypertens. 1988;6:647–653. [PubMed]
14. Falkner B, Kushner H, Onesti G, Angelakos ET. Cardiovascular characteristics in adolescents who develop essential hypertension. Hypertension. 1981;3:521–527. [PubMed]
15. Degaute JP, Van Cauter E, van de Borne P, Linkowski P. Twenty-four-hour blood pressure and heart rate profiles in humans. A twin study. Hypertension. 1994;23:244–253. [PubMed]
16. Fagard R, Brguljan J, Staessen J, Thijs L, Derom C, Thomis M, Vlietinck R. Heritability of conventional and ambulatory blood pressures. A study in twins. Hypertension. 1995;26:919–924. [PubMed]
17. Somes GW, Harshfield GA, Alpert BS, Goble MM, Schieken RM. Genetic influences on ambulatory blood pressure patterns. The medical college of virginia twin study. Am J Hypertens. 1995;8:474–478. [PubMed]
18. Slattery ML, Bishop DT, French TK, Hunt SC, Meikle AW, Williams RR. Lifestyle and blood pressure levels in male twins in utah. Genet Epidemiol. 1988;5:277–287. [PubMed]
19. Daniels PR, Kardia SL, Hanis CL, Brown CA, Hutchinson R, Boerwinkle E, Turner ST. Familial aggregation of hypertension treatment and control in the genetic epidemiology network of arteriopathy (genoa) study. Am J Med. 2004;116:676–681. [PubMed]
20. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics. 2004;114:555–576. [PubMed]
21. Urbina E, Alpert B, Flynn J, Hayman L, Harshfield GA, Jacobson M, Mahoney L, McCrindle B, Mietus-Snyder M, Steinberger J, Daniels S. Ambulatory blood pressure monitoring in children and adolescents: Recommendations for standard assessment: A scientific statement from the american heart association atherosclerosis, hypertension, and obesity in youth committee of the council on cardiovascular disease in the young and the council for high blood pressure research. Hypertension. 2008;52:433–451. [PubMed]
22. Koebnick C, Black MH, Wu J, Martinez MP, Smith N, Kuizon BD, Jacobsen SJ, Reynolds K. The prevalence of primary pediatric prehypertension and hypertension in a real-world managed care system. J Clin Hypertens (Greenwich) 2013;15:784–792. [PMC free article] [PubMed]
23. Keenan NL, Rosendorf KA. Prevalence of hypertension and controlled hypertension - united states, 2005–2008. MMWR Surveill Summ. 2011;60(Suppl):94–97.
24. Manichaikul A, Chen WM, Williams K, Wong Q, Sale MM, Pankow JS, Tsai MY, Rotter JI, Rich SS, Mychaleckyj JC. Analysis of family- and population-based samples in cohort genome-wide association studies. Hum Genet. 2012;131:275–287. [PMC free article] [PubMed]
25. Schor EL. Family pediatrics: Report of the task force on the family. Pediatrics. 2003;111:1541–1571. [PubMed]
26. Avison WR, Ali J, Walters D. Family structure, stress, and psychological distress: A demonstration of the impact of differential exposure. J Health Soc Behav. 2007;48:301–317. [PubMed]
27. Cairney J, Boyle M, Offord DR, Racine Y. Stress, social support and depression in single and married mothers. Soc Psychiatry Psychiatr Epidemiol. 2003;38:442–449. [PubMed]
28. Avison WR, Davies L. Family structure, gender, and health in the context of the life course. J Gerontol B Psychol Sci Soc Sci. 2005;60(Spec No 2):113–116. [PubMed]
29. Waldfogel J, Craigie TA, Brooks-Gunn J. Fragile families and child wellbeing. Future Child. 2010;20:87–112. [PMC free article] [PubMed]
30. Brown GW, Moran PM. Single mothers, poverty and depression. Psychol Med. 1997;27:21–33. [PubMed]
31. Magnuson K, Berger LM. Family structure states and transitions: Associations with children’s wellbeing during middle childhood. J Marriage Fam. 2009;71:575–591. [PMC free article] [PubMed]
32. Zeiders KH, Roosa MW, Tein JY. Family structure and family processes in mexican-american families. Fam Process. 2011;50:77–91. [PMC free article] [PubMed]
33. Jablonska B, Lindberg L. Risk behaviours, victimisation and mental distress among adolescents in different family structures. Soc Psychiatry Psychiatr Epidemiol. 2007;42:656–663. [PubMed]
34. Sieh DS, Visser-Meily JM, Meijer AM. The relationship between parental depressive symptoms, family type, and adolescent functioning. PLoS One. 2013;8:e80699. [PMC free article] [PubMed]
35. Barrett AE, Turner RJ. Family structure and mental health: The mediating effects of socioeconomic status, family process, and social stress. J Health Soc Behav. 2005;46:156–169. [PubMed]
36. Boothroyd LG, Craig PS, Crossman RJ, Perrett DI. Father absence and age at first birth in a western sample. Am J Hum Biol. 2013;25:366–369. [PubMed]
37. Hemovich V, Crano WD. Family structure and adolescent drug use: An exploration of single-parent families. Subst Use Misuse. 2009;44:2099–2113. [PMC free article] [PubMed]
38. Barrett AE, Turner RJ. Family structure and substance use problems in adolescence and early adulthood: Examining explanations for the relationship. Addiction. 2006;101:109–120. [PubMed]
39. Kokkevi A, Rotsika V, Arapaki A, Richardson C. Increasing self-reported suicide attempts by adolescents in greece between 1984 and 2007. Soc Psychiatry Psychiatr Epidemiol. 2011;46:231–237. [PubMed]
40. Gibson LY, Byrne SM, Davis EA, Blair E, Jacoby P, Zubrick SR. The role of family and maternal factors in childhood obesity. Med J Aust. 2007;186:591–595. [PubMed]
41. Moncrief T, Beck AF, Simmons JM, Huang B, Kahn RS. Single parent households and increased child asthma morbidity. J Asthma. 2014;51:260–266. [PMC free article] [PubMed]
42. Dekkers JC, Snieder H, Van Den Oord EJ, Treiber FA. Moderators of blood pressure development from childhood to adulthood: A 10-year longitudinal study. J Pediatr. 2002;141:770–779. [PubMed]
43. Sparrenberger F, Cichelero FT, Ascoli AM, Fonseca FP, Weiss G, Berwanger O, Fuchs SC, Moreira LB, Fuchs FD. Does psychosocial stress cause hypertension? A systematic review of observational studies. J Hum Hypertens. 2009;23:12–19. [PubMed]
44. Tyagi A, Cohen M. Yoga and hypertension: A systematic review. Altern Ther Health Med. 2014;20:32–59. [PubMed]
45. Schneider RH, Grim CE, Rainforth MV, Kotchen T, Nidich SI, Gaylord-King C, Salerno JW, Kotchen JM, Alexander CN. Stress reduction in the secondary prevention of cardiovascular disease: Randomized, controlled trial of transcendental meditation and health education in blacks. Circ Cardiovasc Qual Outcomes. 2012;5:750–758. [PubMed]
46. Schneider RH, Alexander CN, Staggers F, Rainforth M, Salerno JW, Hartz A, Arndt S, Barnes VA, Nidich SI. Long-term effects of stress reduction on mortality in persons > or = 55 years of age with systemic hypertension. Am J Cardiol. 2005;95:1060–1064. [PMC free article] [PubMed]
47. Wilson DK, Kliewer W, Plybon L, Sica DA. Socioeconomic status and blood pressure reactivity in healthy black adolescents. Hypertension. 2000;35:496–500. [PubMed]
48. Gump BB, Matthews KA, Raikkonen K. Modeling relationships among socioeconomic status, hostility, cardiovascular reactivity, and left ventricular mass in african american and white children. Health Psychol. 1999;18:140–150. [PubMed]
49. Jackson RW, Treiber FA, Turner JR, Davis H, Strong WB. Effects of race, sex, and socioeconomic status upon cardiovascular stress responsivity and recovery in youth. Int J Psychophysiol. 1999;31:111–119. [PubMed]
50. Treiber FA, McCaffrey F, Musante L, Rhodes T, Davis H, Strong WB, Levy M. Ethnicity, family history of hypertension and patterns of hemodynamic reactivity in boys. Psychosom Med. 1993;55:70–77. [PubMed]
51. Gerin W, Pickering TG. Association between delayed recovery of blood pressure after acute mental stress and parental history of hypertension. J Hypertens. 1995;13:603–610. [PubMed]
52. Lambert EA, Schlaich MP. Reduced sympathoneural responses to the cold pressor test in individuals with essential hypertension and in those genetically predisposed to hypertension. No support for the “pressor reactor” hypothesis of hypertension development. Am J Hypertens. 2004;17:863–868. [PubMed]
53. Barrington DS, Adeyemo AA, Rotimi CN. Childhood family living arrangements and blood pressure in black men: The howard university family study. Hypertension. 2014;63:48–53. [PMC free article] [PubMed]
54. Lawlor DA, Smith GD. Early life determinants of adult blood pressure. Curr Opin Nephrol Hypertens. 2005;14:259–264. [PubMed]
55. Pruett MK, Pruett KD. Fathers, divorce, and their children. Child Adolesc Psychiatr Clin N Am. 1998;7:389–407. viii. [PubMed]
56. Harris KM, Furstenberg FF, Jr, Marmer JK. Paternal involvement with adolescents in intact families: The influence of fathers over the life course. Demography. 1998;35:201–216. [PubMed]
57. Yogman MW, Kindlon D, Earls F. Father involvement and cognitive/behavioral outcomes of preterm infants. J Am Acad Child Adolesc Psychiatry. 1995;34:58–66. [PubMed]
58. Ayres NA, Miller-Hance W, Fyfe DA, Stevenson JG, Sahn DJ, Young LT, Minich LL, Kimball TR, Geva T, Smith FC, Rychik J. Indications and guidelines for performance of transesophageal echocardiography in the patient with pediatric acquired or congenital heart disease: Report from the task force of the pediatric council of the american society of echocardiography. J Am Soc Echocardiogr. 2005;18:91–98. [PubMed]
59. Fortmann AL, Gallo LC. Social support and nocturnal blood pressure dipping: A systematic review. Am J Hypertens. 2013;26:302–310. [PMC free article] [PubMed]
60. Kamon Y, Okamura T, Tanaka T, Hozawa A, Yamagata Z, Takebayashi T, Kusaka Y, Urano S, Nakagawa H, Kadowaki T, Miyoshi Y, Yamato H, Okayama A, Ueshima H. Marital status and cardiovascular risk factors among middle-aged japanese male workers: The high-risk and population strategy for occupational health promotion (hipop-ohp) study. J Occup Health. 2008;50:348–356. [PubMed]
61. Causland FR, Sacks FM, Forman JP. Marital status, dipping and nocturnal blood pressure: Results from the dietary approaches to stop hypertension trial. J Hypertens. 2014;32:756–761. [PubMed]