For adults in developed countries, the prevalence of overweight and obesity is higher for men, with obese men faring worse on most health indexes, compared with women (1,2). Being an overweight or obese father versus being an overweight mother increases the risk for weight gain or obesity in the child (3–5). Although not all of the studies agree (6), father's weight status has been shown to be strongly related to his child's (4). The specific inclusion of fathers in interventions targeting the management of child overweight has been noted as a research gap (7). Most interventions to date engage mothers primarily (8), and a systematic review has highlighted that it is unclear as to which parent should be targeted (8).
Fathers have rarely been the sole agent of change in family-based lifestyle interventions, with their contribution to improving child eating behaviours overlooked (8). The effect of paternal role models on child dietary habits and the extent to which these can be improved by targeting fathers exclusively remain unknown. We have previously reported the primary outcomes of the Healthy Dads Healthy Kids (HDHK) family lifestyle intervention (9) but only the baseline associations between father–child intakes of fruit, selected energy-dense, nutrient-poor foods, and some nutrients (10).
The aim of the present study is to evaluate the effect of HDHK on the dietary intakes of fathers and their children, and secondly whether changes in the father's intake are related to change in child dietary intake.
The full methodological details have been published elsewhere (9). In brief, HDHK was designed to help overweight and obese fathers lose weight while role modelling healthy diet and physical activity behaviours to their primary school-age children.
Participants and Recruitment
Fathers were recruited from the Hunter region, New South Wales, Australia, in August/September 2008. Inclusion criteria were male, BMI 25 to 40 kg/m2, age 21 to 65 years, with a child 5 to 12 years, access to internet and email, and available to attend assessments.
Father–child(ren) dyads were randomised to a 3-month HDHK programme or a 6-month wait-list control group. Both groups were assessed at baseline, 3, and 6 months by blinded trained assessors. The human research ethics committee of the University of Newcastle, Australia, approved the study with fathers providing informed written consent, and child assent before participation.
HDHK consisted of 8 × 1.5 hour weekly face-to-face sessions for 3 months. Five sessions were for fathers only, and 3 physical activity sessions involved fathers and children. Each session involved information, group discussion, and practical activities to reinforce programme aims and promote behaviour change. HDHK used social cognitive theory to facilitate behaviour change related to diet and lifestyle behaviours (11). Improvements in dietary patterns were targeted in 2 sessions with fathers only, using food-based guidelines successfully (12,13) (see supplemental Table 1, http://links.lww.com/MPG/A113). The dietary component encouraged fathers to covertly facilitate improved child dietary intakes (14). Children were actively encouraged in the practical sessions to support their fathers’ attempts at adopting healthy lifestyles by role modelling healthy eating to their fathers and ensuring their fathers were adhering to dietary recommendations.
Father's dietary intake was assessed using the 74-item Dietary Questionnaire for Epidemiological Studies version 2 and food frequency questionnaire (FFQ) developed and validated by the Cancer Council of Victoria as described in detail elsewhere (15–17) to assess usual eating habits during the last 12 months.
The Dietary Questionnaire for Epidemiological Studies (15) includes assessment of a portion size factor (PSF) (18) derived from responses to 4 sets of photos depicting 3 different serving sizes for potatoes, vegetables, steak, and casserole. Each photograph depicts the interquartile range (25th–75th percentile) of serving size distributions of adults from a range of ethnicities (19). Participants indicate whether they usually consume one of these 3 sizes on a 7-point Likert scale from 0.25 for a response of <25th percentile (PSF = 0.25), the median serving size (PSF = 1), up to >75th percentile (PSF = 1.75). The portion size responses are then averaged to give a single PSF used to generate a portion size calibrator for the FFQ.
Nutrient intakes were computed from the food composition database of Australian foods, NUTTAB 1995 (Australian Government Publishing Service, 1995, Canberra, Australia), using software developed by the Cancer Council of Victoria.
To reduce potential reporting bias for fathers reporting their child's intake, each child's mother completed the Australian Child and Adolescent Eating Survey (ACAES) FFQ to estimate usual child intake. ACAES is a 135-item semiquantitative FFQ developed and objectively validated for use with Australian children (20–22) to measure usual food intake during the previous 6 months (20). Data from the ACAES FFQ were scanned and nutrient intakes were computed in FoodWorks (version 3.02.581 Xyris Software [Australia] Pty Ltd, FoodWorks Professional version 3.02.581. 2004: Brisbane, Australia) using the databases Australian AusNut 1999 database (All Foods) revision 14 and AusFoods (Brands) revision 5 1999 (Food Standards Australia New Zealand, Canberra, Australia).
Complete dietary intake data were available for 53 father–child dyads at baseline and 35 at 6 months. Descriptive statistics were calculated and linear mixed models were used to determine differences in intakes over time. Analysis was conducted separately for fathers and children. Mixed models were fitted using unstructured covariance and results are presented as the difference of means (95% confidence interval). Statistical significance was set at P < 0.05. Change scores were calculated as 6-month posttest minus baseline. Pearson correlation was used to investigate the relation between father–child changes for nutrient and food group intakes. Statistical analysis was completed in SPSS version 17 (SPSS Inc, Chicago, IL).
This is the first study that reports changes in dietary intakes for fathers and their children from a randomised controlled trial designed specifically using overweight and obese fathers as the agents of dietary change within families. The intervention resulted in a significant reduction in father's usual portion size and child's energy intake.
Baseline anthropometrics and dietary intakes of fathers and children are reported by intervention group in Table 1(23,24) (for detailed results, see supplemental Tables 2A and 2B, http://links.lww.com/MPG/A113). Briefly, 39 of 50 fathers were considered obese (BMI >30) at baseline. Using intention-to-treat analysis, there was a significant group-by-time interaction at 6 months for weight loss, with intervention group fathers losing significantly more weight (−7.6 kg; 95% CI −9.2 to −6.0 kg) than the control group (0.0; −1.4 to 1.6) (9).
The mean (SD) reported portion size for fathers at baseline was 1.5 (0.1) with 35% of energy derived from fat and >14% from saturated fat, which exceeds national intake targets (23). The mean percentage of energy from alcohol was 4% and was within the recommended maximum of 5% of total energy intake (23). Nutrient intakes, including calcium, iron, and zinc, were above estimated average requirements for both fathers and children at both time points. Fathers had lower fruits and vegetables intakes compared with their children at baseline and/or 6 months.
Changes in food, energy, and nutrient intakes for fathers and children from baseline to 6 months are reported in Table 1. Although intervention fathers significantly reduced daily energy intakes, the between-group changes were not significant (P > 0.05), (intervention −2895 kJ/day [−5161 to −629], control group −947 kJ/day [−3231 to 1336 kJ/day]). There was a significant group-by-time reduction in PSF, which decreased from 1.6 ± 0.1 at baseline to 1.3 ± 0.1 (P = 0.03) at 6 months for the intervention group compared with no change in the controls (1.5 ± 0.1 baseline, 1.4 ± 0.1 6 months). This suggests that reducing portion size is a key energy intake reduction strategy that fathers implemented as a result of HDHK. No significant reductions were reported in mean daily servings of specific foods in either the intervention or control groups (Table 1); however, small nonsignificant reductions in some items were noted. If these small changes in addition to a decrease in PSF are implemented on a regular basis, they will contribute to an overall reduction in total energy intake and facilitate gradual weight reduction (9), in line with the goal of HDHK. The degree of dietary change within the intervention group, although small, may have been sufficient to induce weight loss compared with the control group who did not change. The present study suggests that although the weight loss was variable, as evidenced by the wide confidence intervals and large SD, changes in diet do not have to be large to translate into significant weight loss. Future research with a larger sample size and sufficient power to detect these small improvements as statistically significant is required. Although we previously reported that men in the intervention group increased their physical activity by approximately 2000 steps per day, using objective pedometer data (1), this is not a sufficient energy deficit to induce a mean weight loss of 6.7 kg for 6 months.
Results from the present study are similar to that previously reported (25,26). Fathers’ sodium intakes decreased, which could be attributed to a reduction in intake of processed meats and takeout foods, which are commonly high in sodium.
At baseline, excess energy was contributed by energy-dense, nutrient-poor foods, including sweetened drinks (334 ± 287 mL/day), baked snacks (42 ± 33 g/day), and takeout foods (50 ± 33 g/day). Children consumed enough servings of fruit per day, but not enough vegetables at either baseline or follow-up.
For children, there was a statistically significant group-by-time reduction in mean total daily energy intake, when expressed both as total kilojoules per day and when adjusted for child body weight (kJ/kg) for the intervention group (−1809 kJ/day [−3000, −619] from baseline to 6 months compared with −600 kJ/day [−589, 1788] in the control group, [P = 0.02]). There was no change in children's weight status at 6 months (9); however, the majority of children were in the healthy weight range at baseline (73% healthy weight, 17% overweight, and 9% obese as determined by BMI z score (27)) and so this was expected. Small nonsignificant decreases in other food groups included sweetened beverages (soft drink, fruit juice, cordial), processed meat (devon, bacon, salami, sausages), and take-out foods.
These results support that father role modelling of healthy eating can influence child intake. The use of home-based tasks, for example in which fathers and children cooked together and spent time interacting, may have positively contributed to changes in dietary intakes and dietary behaviours, as has previously been suggested (28). Significant correlations were found between changes in father–child intakes for daily intakes of grains (g/day) (r = 0.56, P = 0.005), but no other significant correlations were detected.
The results of the present study support the targeting of fathers as agents of change within family dietary modification/lifestyle interventions; however, more research is required using a sample size powered to detect changes in food intake, to substantiate these findings.
Limitations include that dietary intakes for fathers and children were evaluated using an FFQ and are, at best, approximations of usual intake and known to be associated with overreporting and based on self-report. FFQ responses are categorical contributing to increased standard error of the mean for dietary variables and therefore increased chance of type II errors, and an inability to detect between-group differences as statistically significant. Mothers were used as a proxy for children's intake to try and minimise the reporting bias if the fathers had reported children's intake and to allow comparison with the literature, as fathers have rarely been used to report child dietary intakes (29). There were large SD for dietary variables and this may have contributed to nonsignificant findings.
Fathers significantly reduced their mean PSF, reflecting small changes across a range of foods, whereas children significantly reduced total daily energy intakes; however, there were few associations detected between changes in father–child intakes. Although further research is required, the present study suggests that fathers could be targeted to improve dietary intake within family interventions.
1. Arber S. J.G. Gender and inequlaities in health in later life. Soc Sci Med
2. Australian Government Department of Health and Ageing. National Male Health. http://www.health.gov.au/internet/main/publishing.nsf/content/male-policy
. Accessed August 17, 2012.
3. Burke V, Beilin L, Simmer K, et al. Predictors of body mass index and associations with cardiovascular risk factors in Australian children: a prospective cohort study. Int J Obes
4. Perez-Pastor E, Metcalf B, Hosking J, et al. Assortative weight gain in mother-daughter and father-son pairs: an emerging source of childhood obesity. Longitudinal study of trios (EarlyBird 43). International Journal of Obesity. Int J Obes
5. Freeman E, Fletcher R, Collins CE, et al. Preventing and treating childhood obesity: time to target fathers. Int J Obes (Lond)
6. Leary S, Smith G, Ness A. No evidence of large differences on mother daughter and father-son body mass index concordance in a large UK birth cohort. Int J Obes
7. Golan M. Parents as agents of change in childhood obesity-from research to practice. Int J Pediatr Obes
8. McLean N, Griffin S, Toney K, et al. Family involvement in weight control, weight maintenance and weight loss interventions: a systematic review of randomised trials. Int J Obes
9. Morgan P, Lubans D, Callister R, et al. The’ Healthy dads healthy kids’ randomised controlled trial: Efficacy of a healthy lifestyle program for overweight fathers and their children’. Int J Obes
10. Hall L, Burrows T, Collins C, et al. Fathers intake of fruit and non core foods but not vegetables is related to thier children's intake—the Healthy Dads Healthy Kids study. J Am Diet Assoc
11. Bandura A. Social Foundations of thought and action: A Social Cognitive Theory.
Englewood Cliffs, NJ: Prentice-Hall; 1986.
12. Burrows T, Warren JM, Baur LA, et al. Impact of a child obesity intervention on dietary intake and behaviors. Int J Obes
13. Burrows T, Warren J, Collins C. Long-term changes in food consumption trends in overweight children in the HIKCUPS intervention. J Pediatr Gastroenterol Nutr
14. Ogden J, Reynolds R, Smith A. Expanding the concept of parental control in childrens snacking behaviour. Appetite
15. Hodge A, Patterson AJ, Brown WJ, et al. The Anit Cancer Council of Victoira FFQ: relative validity of nutrient intakes compared with weighed food records in young to middle-aged women in a study of iron supplementation. Aus N Z J Public Health
16. Giles G, Irelan P. Dietary Questionniare for Epidemiological Studies.
Melbourne: The Cancer Council Victoria; 1996.
17. Ireland P, Jolley D, Giles Gea. Development of the Melbourne FFQ: a food frequency questionnaire for use in an Australian prospective study involving an ethnically diverse cohort. Asia Pac J Clin Nutr
18. Hunter D, Sampson L, Stampfer M, et al. Varaiblility in portion sizes of commonly consumed foods among a population of women in the United States. Am J Epidemiol
19. Cancer Council Victoria A. Dietary Questionnaire for Epidemiological Studies
, Version 2 (DQES v2), User Information Guide.
20. Watson J, Collins C, Sibbritt D, et al. Reproducibility and comparative validity of a food frequency questionnaire for Australian children and adolescents. Int J Behav Nutr Phy
21. Burrows TL, Warren JM, Colyvas K, et al. Validation of overweight children's fruit and vegetable intake using plasma carotenoids. Obesity
22. Burrows T, Berthton B, Garg M, et al. A comparative validation of child food frequency questionnaire using red blood cell membrane fatty acids. Eur J Clin Nutr
23. NHMRC. Nutrient Reference Values for Australia and New Zealand. Council NHaMR. Introduction. http://www.nrv.gov.au
. Accessed August 17, 2012.
24. NHMRC. Dietary Guidelines for Australian Adults.
Canberra: National Health and Medical Research Council; 2003.
25. Morgan P, Lubans D, Collins C, et al. 12-Month outcomes and process evaluation of the SHED-IT RCT: an Internet-based weight loss program targeting men. Obesity
26. Andersson I, Lennernas M, Rossner S. Meal Pattern and risk factor evaluation in one year completers of a weight reduction program for obese men—the ’Gustaf’ study. J Intern Med
27. Cole TJ, Bellizzi MC, Flegal KM, et al. Establishing a standard definition for child 252 overweight and obesity worldwide: international survey. BMJ
28. Swarr A. M. R. Longitundinal effects of adolescents girls pubertal development, perceptions and pubertal timing and parental relations on eating problems. Dev Psychol
29. Burrows T, Martin R, Collins C. A systematic review of the validity of dietary assessment methods in children when compared with the method of doubly labelled water. J Am Diet Assoc