Parental influences on cardiovascular risk factors in Swedish children aged 5-14 years
Precursors of cardiovascular diseases (CVD) may originate in childhood and track into adulthood1-4. The extent of the contribution of socioeconomic and psychosocial environments on the development of CVD risk factors in children is debated. No study has comprehensively investigated these influences on a range of CVD risk factors in children. We investigated associations of:
- Parental Socioeconomic Position (SEP),
- Parental lifestyle habits (smoking, alcohol consumption and physical activity) and
- Parental CVD risk factors,
with CVD risk factors in their children that could contribute to accumulation of CVD risk that tracks into adulthood.
The Uppsala Family Study
The Uppsala Family Study was initiated in 2000-2001 and comprises 602 families (parents and their two biological children; aged 5-14 years)5.
Parental SEP (measured by occupational class and educational level of both parents), and lifestyle habits [smoking, physical activity, and alcohol consumption] were obtained from questionnaires. CVD risk factors (serum cholesterol, ApoB/ApoA1 ratio, leptin, adiponectin, blood pressure, BMI and overweight/obesity combined) in parents and their children were measured by routine methods.
Overweight and obesity in children were calculated using the age and sex-specific cut-offs as described by the International Obesity Task force, whereas that in parents were calculated according to WHO criteria. Associations between parental exposures and CVD risk factors in their children were analysed using multivariable linear regression. Only associations with the binary outcome of normal BMI and overweight or obesity combined in children were analysed using multivariate logistic regression. All analyses were adjusted for child’s age, gender, pubertal stage and family clustering. Analyses of associations between parental lifestyle habits and children’s outcomes were additionally adjusted for parental SEP, and analyses of associations between parental and children’s CVD risk factors were additionally adjusted for parental SEP and parental lifestyle habits.
We found consistent associations between parental lifestyle habits and CVD risk factors in their children
However, associations between parental SEP and children’s CVD risk factors were few and inconsistent6. Children of least educated parents (≤9 years of compulsory schooling) had higher mean BMI and increased odds for being overweight or obese compared to children of university educated parents (adjusted Odds Ratio, OR 2.07, 95% CI 1.21-3.55 and OR 1.75, 1.00-3.13 for children of least educated fathers and mothers respectively).
We found stronger and more consistent associations between parental lifestyle habits and CVD risk factors in their children that were independent of parental SEP6. For example, children of both smoking fathers and mothers had higher mean BMI (equivalent to an adjusted increase of 4%, 95% CI 1-7% and 3%, 1-7% respectively). In addition, children of smoking fathers also had higher mean leptin levels (27%, 1.00-61.60%). There were few associations between parental alcohol consumption and CVD risk factors in their children6. Children of fathers that consumed alcohol once per week or more than once per week had higher mean cholesterol levels compared to children of fathers that did not drink, whereas children of mothers that reported alcohol consumption had both higher mean BMI and cholesterol levels.
Children of mothers reporting vigorous physical activity had lower mean BMI, cholesterol, and decreased odds for being overweight or obese with a possible dose effect. Compared with mothers reporting no vigorous physical activity, mothers with ≤75minutes and 76-150minutes/week vigorous physical activity had 43% (OR 0.57, 95%CI 0.22-0.89) and 72% (0.28, 0.14-0.60) lower risk of having an overweight or obese child respectively, after adjustment for confounders. Similarly, all fathers that reported vigorous physical activity (≥90min/week) had children with lower mean BMI compared to those that reported no vigorous physical activity6. We found independent, consistently stronger and statistically significant associations between all studied parents’ and children’s CVD risk factors6.
In this study sample of Swedish families, indicators of parental socioeconomic position were less likely to predict CVD risk factors in children. On the other hand, parental lifestyle habits such as smoking, alcohol consumption, and low levels of physical activity were associated with higher levels of CVD risk factors (BMI, being overweight or obese, cholesterol) in children. Strong correlations in CVD risk factors within families which are not related to either parental SEP or lifestyle suggest a role of genetics in influencing children's CVD risk factors. Both parental lifestyle habits and genetics influence CVD risk factors in their children.
- Berenson GS, Wattigney WA, Bao W, Srinivasan SR, Radhakrishnamurthy B (1995) Rationale to study the early natural history of heart disease: the Bogalusa Heart Study. Am J Med Sci 310 Suppl 1: S22-28
- Boulton TJ, Cockington RA, Hamilton-Craig I, Magarey AM, Mazumdar J (1995) A profile of heart disease risk factors and their relation to parents’ education, fathers’ occupation and family history of heart disease in 843 South Australian families: the Adelaide Children’s WHO Collaborative Study. J Paediatr Child Health 31: 200-206
- Garn SM, LaVelle M (1985) Two-decade follow-up of fatness in early childhood. Am J Dis Child 139: 181-185
- Kemper HC, Snel J, Verschuur R, Storm-van Essen L (1990) Tracking of health and risk indicators of cardiovascular diseases from teenager to adult: Amsterdam Growth and Health Study. Prev Med 19: 642-655
- Leon DA, Koupil I, Mann V, et al. (2005) Fetal, developmental, and parental influences on childhood systolic blood pressure in 600 sib pairs: the Uppsala Family study. Circulation 112: 3478-3485
- Khanolkar AR, Byberg L, Koupil I (2012) Parental influences on cardiovascular risk factors in Swedish children aged 5-14 years. European journal of public health 22: 840-847