Skip to main content
Download PDF

Inadequate care and excessive overprotection during childhood are associated with the presence of diabetes mellitus in adulthood in a general Japanese population: a cross-sectional analysis from the Hisayama Study

BMC Endocrine Disorders volume 23, Article number: 222 (2023) Cite this article

A Correction to this article was published on 21 November 2023

This article has been updated

Abstract

Objective

To investigate associations between parenting styles during childhood and diabetes in adulthood in a Japanese community.

Methods

In 2011, 710 community-dwelling Japanese residents aged ≥ 40 years were assessed for the presence of diabetes and for their perceptions of the parenting style of their parents, as measured using the “care” and “overprotection” scales of the Parental Bonding Instrument. Care and overprotection scores for each parent were dichotomized by age-specific median values. Diabetes mellitus was defined as a fasting plasma glucose level of ≥ 7.0 mmol/L, a 2-h post-loaded glucose level of ≥ 11.1 mmol/L, HbA1c ≥ 6.5%, and/or the current use of insulin or oral glucose-lowering agents. The odds ratios (ORs) for prevalent diabetes were calculated using a logistic regression model.

Results

The prevalence of diabetes was 14.9%. Subjects with a high paternal overprotection score had a significantly greater likelihood of prevalent diabetes than those with a low paternal overprotection score after adjusting for confounders (OR 1.71, 95% confidence interval [CI] 1.06–2.77), while there was no significant association between paternal care and diabetes. Additionally, the multivariable-adjusted ORs for the presence of diabetes were significantly higher in subjects with a low maternal care score (OR 1.61, 95%CI 1.00–2.60) or in subjects with a high maternal overprotection score (OR 1.73, 95%CI 1.08–2.80). Moreover, the subjects with a low care score and high overprotection score for both their father and mother had a significantly higher multivariable-adjusted OR of diabetes than those with a high care score and low overprotection score for both parents (OR 2,12, 95%CI 1.14–3.95).

Conclusions

This study suggests that inadequate care and excessive overprotection during childhood may contribute to the development of diabetes in adulthood.

Peer Review reports

Background

Diabetes has emerged as a major health problem. In 2019 the World Health Organization listed diabetes as one of the top 10 leading causes of both death and disability-adjusted life years globally [1], and in 2017 about 500 million people were estimated to be suffering from diabetes worldwide [2]. Therefore, prevention of diabetes is regarded as a public health priority.

Childhood is widely acknowledged to play an important role in the formation of lifestyles and eating behaviors in adulthood [3]. Previous studies have reported that parenting styles affect obesity and food consumption in children [4, 5]. Accumulating evidence indicates that perceived parental attitudes and behaviors, especially “affectionless control,” a style characterized by the combination of insufficient care and excessive overprotection as measured by the Parental Bonding Instrument (PBI) [6], are associated with an increased risk of obesity and eating disorders [7, 8]. Affectionless control has been proposed to be a maladaptive form of parenting that results in a particular vulnerability to the occurrence of psychopathology [9, 10]. Additionally, childhood has been considered to be a critical period for the development of hormonal reactions related to stress resistance and blood glucose homeostasis [11]. Therefore, it could be assumed that parenting styles affect the future onset of diabetes. However, there are no community-based studies addressing the relation between parenting styles in childhood and the prevalence of diabetes in adulthood.

The aim of the present study was to examine the association between parenting styles, particularly perception of insufficient care and overprotection during childhood, and diabetes in adulthood in a general Japanese population.

Methods

Study participants

The Hisayama Study is an ongoing, long-term cohort study conducted to examine cardiovascular disease and its risk factors in Hisayama, a suburban town adjoining the metropolitan area of Fukuoka City in southwestern Japan. Health check-up surveys have been performed annually in Hisayama since 1961 [12, 13]. The present study was conducted as a cross-sectional sub-study of the Hisayama Study. Participants for the sub-study were recruited in 2011. Among the 2,250 residents aged 40 years or older who participated in the health check-up in 2011, a total of 793 subjects consented to participate in the present study. After excluding 78 residents without available data for both parents on the parenting questionnaire and 5 residents without a fasting blood test, the remaining 710 subjects (270 men and 440 women) were enrolled.

Assessment of diabetes mellitus

Blood samples were collected from an antecubital vein after overnight fasting. Diabetes mellitus was determined by a 75 g oral glucose tolerance test in 450 subjects (63%) and by only a fasting blood sample in 260 subjects. Blood glucose was measured by the hexokinase method. Hemoglobin A1c (HbA1c) was measured by high performance liquid chromatography. A self-administered questionnaire including items on the use of oral glucose-lowering agents and insulin was completed by each participant and was checked by trained interviewers at the screening [12]. Diabetes mellitus was defined as a fasting plasma glucose level of ≥ 7.0 mmol/L (126 mg/dL), a 2-h post-loaded glucose level of ≥ 11.1 mmol/L (200 mg/dL), HbA1c (NGSP) ≥ 6.5% (48 mmol/mol IFCC), and/or the current use of insulin or oral glucose-lowering agents, according to the American Diabetes Association criteria in 2010 [14].

Assessment of parental bonding

Perceived parenting styles were measured using the Parental Bonding Instrument (PBI), a self-report questionnaire with 25 items that measures parenting styles in the first 16 years of life, as recalled by the respondents [6]. The PBI is scored separately for the father and mother to evaluate the relationship between the respondent and each parent, as they are subjectively perceived. The respondents are asked to score their parents’ attitudes and behaviors separately, using a 4-point Likert scale. Two subscales of parenting style are measured by the PBI: care and overprotection. The “care” subscale reflects perceived parental emotional warmth, empathy, and closeness contrasted with coldness and rejection. The “overprotection” subscale reflects perceived parental over-control and intrusion contrasted with allowance of independence and autonomy. Each score of care and overprotection for each parent was dichotomized by the age-specific median values of each score, as shown in Supplemental Table S1. In addition, the parenting styles were also divided into four categories (PBI quadrants) by combining the dichotomized care and overprotection scores: “optimal bonding” (high care, low overprotection), “neglectful parenting” (low care, low overprotection), “affectionate constraint” (high care, high overprotection), and “affectionless control” (low care, high overprotection). The PBI score reflects the actual parenting attitude and is based on studies using corroborative witnesses and independent observers [15, 16]. The PBI has long-term stability [17] and its subscales have a high level of test–retest reliability and internal consistency [18]. The Japanese version of the PBI has been shown to have adequate validity [19].

Measurement of potential confounding factors

A self-administered questionnaire concerning marital status, education, subjective economic status, habitual smoking, habitual drinking, habitual exercise, the use of medications (i.e., antihypertensive agents, oral glucose-lowering agents and insulin), and paternal and maternal history of diabetes was completed by each participant and was checked by trained interviewers at the screening [12]. Subjective economic status was assessed by a question asking, “How difficult or easy is your current financial status?” [20]. Response options for this question were “Very hard”, “Hard”, “Normal”, “Easy” and “Very easy”. Based on the participant's response, the subjective economic status was divided into low (very hard or hard) and high (normal, easy or very easy). Body height and weight were measured in light clothing without shoes, and the body mass index (kg/m2) was calculated. Blood pressure was measured three times after the subject had rested for at least five minutes in the sitting position. The mean of the three measurements was used for the present analysis. Hypertension was defined as a systolic blood pressure ≥ 140 mmHg, diastolic blood pressure ≥ 90 mmHg, and/or current use of antihypertensive agents [21]. Serum total cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride levels and cortisol were measured enzymatically.

Statistical analysis

We divided the participants into high or low care and overprotection groups based on the age-specific median values of the care and overprotection scores in order to control for the confounding caused by the difference in the scores among generations. Comparisons of characteristics between the high and low parenting subscales (care and overprotection) were performed by an analysis of covariance (ANCOVA) for continuous variables or a logistic regression analysis for dichotomous variables with adjustment for age and sex. Odds ratios (ORs) and the confidence interval (CI) of the parenting styles on the presence of diabetes were estimated by logistic regression analysis. In the multivariable-adjusted analyses, the risk estimates were adjusted for age (continuous), sex (men or women), paternal and maternal history of diabetes (yes or no), marital status (with or without a partner), educational level (≤ 9 years or > 9 years), subjective economic level (low or high), lifestyle factors (i.e., hypertension [yes or no], serum total cholesterol [continuous], serum HDL cholesterol [continuous], serum triglycerides [log-transformed, continuous], BMI [continuous], current smoker [yes or no], current drinker [yes or no] and habitual exercise [yes or no]) and serum cortisol (continuous). To account for the interaction between the care and overprotection subscales, paternal and maternal bonding were classified into four quadrants: “high care, low overprotection” (optimal bonding) as a reference, “low care, low overprotection” (neglectful parenting), “high care, high overprotection” (affectionate constraint), and “low care, high overprotection” (affectionless control). Additionally, in order to assess the combined influence of the “affectionless control” parenting style by the father and mother on the presence of diabetes, parents’ parenting styles were classified into four quadrants as shown in Supplemental Table S2: “optimal bonding (high care and low overprotection) for both father and mother” as a reference, “affectionless control (low care and high overprotection) for either father or mother”, “affectionless control for both father and mother” and “other combinations of paternal and maternal parenting styles”. We also performed a sensitivity analysis on the association between the parenting styles and the presence of diabetes after including the 19 participants with a single mother and 3 participants with a single father. Finally, we performed an analysis to compare the characteristics between included and excluded subjects (n = 1539) by a Student’s t-test for parametric continuous variables, a Mann–Whitney U test for non-parametric ordinal variables, or a Chi-square test for dichotomous variables. All statistical analyses were performed using SAS software (version 9.4; SAS Institute, Cary, NC, USA). Statistical significance was defined as a two-tailed P-value of < 0.05.

Results

Table 1 summarizes the age- and sex- adjusted characteristics of all participants according to the level of each parental care and overprotection score for the father and mother. Compared to women, men were more frequently distributed in the lower care group and higher overprotection group for both their father and mother. Subjects with a low level of care or high level of overprotection from their father and mother were significantly more likely to have low subjective economic level than those who received the opposite level of each parenting style. Additionally, subjects with a low level of care from their mother were significantly more likely to have a low educational level than those with a high level of care.

Table 1 Age- and sex-adjusted characteristics of participants according to the level of parental care and overprotection of the parent
Full size table

The median (IQR) fasting plasma glucose levels, prevalence of individuals with high blood glucose levels, and prevalence of the current use of insulin or oral glucose-lowering agents were 5.4 (4.6–6) mmol/L, 12.4% and 8.0%, respectively. The crude prevalence of diabetes was 15% (= 106/710) among all participants. The crude prevalence of diabetes was significantly higher in subjects with a high level of paternal overprotection, a low level of maternal care or a high level of maternal overprotection than in subjects with the opposite levels of each scale (Fig. 1). Table 2 shows the ORs for the presence of diabetes according to the level of care and overprotection for each parent. Subjects with a high level of paternal overprotection had a significantly greater likelihood of prevalent diabetes than those with a low level after adjustment for age and sex, sociodemographic factors, family history of diabetes, lifestyle factors, and serum cortisol (OR 1.71, 95% confidence interval [CI] 1.06–2.77), while there was no significant association between paternal care and diabetes. Additionally, the multivariable-adjusted ORs for the presence of diabetes were significantly higher in the subjects with a low level of maternal care (OR 1.61, 95%CI 1.00–2.60) or high level of maternal overprotection (OR 1.73, 95%CI 1.08–2.80) than in those with the opposite level of each scale. In a sensitivity analysis conducted after including the participants with a single parent, the findings were not changed substantially (Supplemental Table S3).

Fig. 1
figure 1

Crude prevalence of diabetes according to the level of parental care and overprotection. *P < 0.05 vs. optimal parenting

Full size image
Table 2 Association of the score of parental care and overprotection with the presence of diabetes
Full size table

Next, we examined the combined effects of low care and high overprotection on the presence of diabetes for each parent (Fig. 2). The multivariable-adjusted ORs for prevalent diabetes were significantly higher in subjects with both a maternal low care score and high overprotection score (affectionless control) than in those with both a high care score and low overprotection score (optimal bonding) (OR 1.94, 95%CI 1.12–3.35). A similar association was also observed for the paternal parenting style, but this association did not reach the level of statistical significance (OR 1.68, 95%CI 0.96–2.95).

Fig. 2
figure 2

Multivariable-adjusted odds ratios of diabetes according to combined categories of parenting factors for each parent. Values are shown as odds ratios (95% confidence interval). *P < 0.05 vs. optimal parenting. The risk estimates were adjusted for age, sex, paternal and maternal history of diabetes, marital status, educational level, subjective economic level, hypertension, serum total cholesterol, serum HDL cholesterol, serum triglycerides, BMI, current smoker, current drinker, habitual exercise, and serum cortisol

Full size image

Finally, we assessed the combined influence of an “affectionless control” parenting style by the father and mother on the presence of diabetes. The combinations of paternal and maternal parenting styles were classified into 4 categories (Supplemental Table S2). Consequently, the subjects with affectionless control by their father and mother had a significantly higher multivariable-adjusted OR of prevalent diabetes than those with the optimal bonding by both parents (OR 2.12, 95%CI 1.14–3.95). On the other hand, the ORs of diabetes for participants with affectionless control by either parent or with other combinations of bonding did not reach significance (Table 3).

Table 3 Combined influence of an “affectionless control” parenting style by the father and/or mother on diabetes
Full size table

In the analysis comparing the characteristics between included and excluded subjects, we found that the excluded subjects were older, and showed higher frequencies of hypertension and current smoking, higher serum total cholesterol and BMI, and lower serum HDL cholesterol than the included subjects, whereas there was no clear difference in the prevalence of diabetes (Supplementary Table S4).

Discussion

The present study demonstrated that paternal high overprotection, maternal low care and maternal high overprotection in childhood were associated with higher likelihood of the presence of diabetes in adulthood after adjusting for sociodemographic factors, family history, lifestyle factors and biological factors. Additionally, the parenting pattern of affectionless control by both parents significantly increased the risk of presence of diabetes compared to optimal bonding by both parents. These findings suggest that parenting styles during childhood, especially insufficient care and excessive overprotection (affectionless control), are related to diabetes in adulthood. On the other hand, the risk of the presence of diabetes was not increased in subjects with affectionless control by only one parent in the present study. This result suggests that a child’s future risk of diabetes could be decreased if at least one parent avoids the “affectionless control” parenting style.

As far as we know, there are no population-based epidemiological studies showing a significant association between parenting style and diabetes in adults. On the other hand, several hospital-based and population-based studies have shown a relationship between inadequate parenting, especially the “affectionless control” parenting style (i.e., low care and high overprotection), and the risk of eating disorders, obesity, and coronary heart disease [7, 8, 22, 23]. Since eating disorders and obesity are likely to be involved in the onset of diabetes, these previous findings may support ours. In the present study, moreover, low maternal care and parental overprotection were associated with diabetes, but there was no association between low paternal care and diabetes. Intriguingly, a previous study examining the association between parenting style and obesity found that only paternal care was not significantly associated with obesity [7]. In addition, previous studies examining mammalian childcare reported that mothers are significantly more likely to relate to their children than fathers during the breastfeeding stage [24]. The authors of that study stated that mothers have more frequent contact with their children at an early age compared to fathers. Therefore, this difference may impact the magnitude of the different results between fathers and mothers in regard to the association between care and diabetes. On the flip side, it is probable that high maternal care may have a protective effect against diabetes, as shown by the ORs of diabetes in participants parented with a high overprotection pattern (Fig. 2).

The exact mechanisms underlying the association between parenting styles and diabetes are not clear at present. However, we considered several possible mechanisms. First, there is the possibility that long-term stress from childhood affects diabetes. The “affectionless control” parenting style has been reported to be associated with the stress reaction, mental distress, lack of stress-coping skills, and interpersonal sensitivity [25,26,27]. The cumulative physiologic toll exacted on the body over time by efforts to adapt to life experiences, the so-called allostatic load, has been reported to result in prolonged responses to stress due to delayed shutdown of physiological reactivity [28, 29]. Long-term allostatic load from childhood to adulthood may lead to diabetes through activation of the hypothalamic–pituitary–adrenal (HPA) axis and/or sympathetic–adrenal–medullary (SAM) axis as stress responses [30, 31]. In the present study, however, the adjustment for serum cortisol, as an indicator of activity of the HPA-axis, did not attenuate the association between parenting style and diabetes. Therefore, another mechanism such as the activation of the SAM axis might underlie the association. Second, it is possible that eating behavior may have mediated the association between parenting style and diabetes. In the present study, the associations between parenting styles and diabetes were not altered substantially even after adjusting for lifestyle factors (e.g., smoking, drinking, habitual exercise and BMI) and family history of diabetes. However, some residual factors such as eating behavior and dietary pattern may mediate the association. Previous studies have reported that parental low care and parental low overprotection were associated with eating disorders such as bulimia nervosa and binge eating disorder [31, 32]. Maternal low care has been reported to be associated with emotional eating (i.e., eating driven by an emotional state) [31]. Chronic life stress has been reported to be associated with a greater preference for energy- and nutrient-dense foods, particularly those that are high in sugar and fat [33, 34]. An “affectionless control” parenting style might affect diabetes through those eating behaviors that cause increased blood glucose levels [35].

Parental low care refers to a parenting style where parents provide minimal emotional, physical, or financial support to their children. Parents who practice low care parenting may be emotionally distant or absent, neglectful, or indifferent to their children's well-being. Children who grow up with low care parents may struggle with issues such as low self-esteem, poor social skills, and difficulty forming healthy relationships [6, 36]. Overprotection refers to a parenting style in which a parent is excessively cautious and protective, to the point of limiting their child’s opportunities for growth, learning, and independence. Overprotection can manifest in different ways, such as preventing a child from taking risks or making decisions, shielding them from negative experiences, or not allowing them to engage in age-appropriate activities. Parental overprotection can have a range of effects on children, both in the short-term and long-term. These include lack of independence, anxiety and fear, low self-esteem, poor social skills and difficulty coping with adversity [6, 37]. There are many factors that can contribute to poor parental care and overprotection, including parental anxiety, parental history of abuse or neglect, cultural and societal expectations, unrealistic expectations of child development and lack of parenting skills and knowledge [38]. To avoid poor outcomes from parenting conducted under these limitations, it is important that parents be given support and appropriate resources to help them provide the best possible care and support for their children.

This study has several limitations. First, the ability to infer causality between the parenting style and diabetes was limited, because this study is a cross-sectional study. In this study, parenting styles in childhood were used as an exposure factor, but we could not deny the possibility that having diabetes might have an unfavorable impact on the scoring of past parenting styles. Prospective longitudinal studies are needed to clarify the contribution of inadequate parenting styles to the development of diabetes. Second, there is a possibility of selection bias, because only approximately one-third of individuals who attended the health check-ups consented to participate in the present study. In the analysis comparing the characteristics between included and excluded subjects, we found that the excluded subjects were older, and showed higher frequencies of potential confounding factors, whereas there was no clear difference in the prevalence of diabetes (Supplementary Table S4). Therefore, the results of the present study may have underestimated the association between parenting and diabetes. Third, the influence of residual confounders (e.g., lack of social support, serious life events, economic status in childhood, eating behavior, and dietary patterns) may still be present, although we did account for a wide range of confounders. In addition, the involvement of stress-related factors in adulthood in the association between parenting style and diabetes could not be examined because, with the exception of serum cortisol levels, the requisite data were not available. Lastly, we urge caution in generalizing our findings to populations with different backgrounds, since participants were recruited from a single town in Japan.

Conclusions

The findings of the present suggest that inadequate care and excessive overprotection during childhood are related to diabetes in adulthood and that the association is much more significant when the inadequate parenting is received from both parents. Mass-education and social support for optimal parenting would thus be potential initiatives for the prevention of diabetes. Further prospective and interventional studies will be needed to clarify the mechanisms underlying the relation of parenting style to diabetes.

Availability of data and materials

The datasets used in the current study are not publicly available because they contain confidential clinical data on the study participants. However, the data are available on reasonable request and with the permission of the Principal Investigator of the Hisayama Study, Toshiharu Ninomiya (Department of Epidemiology and Public Health, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan).

Change history

Abbreviations

OR:

Odds ratio

CI:

Confidence interval

PBI:

Parental Bonding Instrument

HbA1c:

Hemoglobin A1c

HDL cholesterol:

High-density lipoprotein cholesterol

BMI:

Body mass index

HPA-axis:

Hypothalamic–pituitary–adrenal axis

SAM axis:

Sympathetic–adrenal–medullary axis

References

  1. World Health Organization. Global health estimates: life expectancy and leading causes of death and disability, 2019. Available from https://www.who.int/data/gho/data/themes/mortality-and-global-health-estimates. Accessed 28 May 2021.

  2. International Diabetes Federation. International diabetes federation. Vol. 9 th editi. 2017. Available from www.diabetesatlas.org. Accessed 28 May 2021.

  3. Kim J, Lim H. Nutritional management in childhood obesity. J Obes Metab Syndr. 2019;28:225–35.

    Article  PubMed  PubMed Central  Google Scholar 

  4. Vereecken C, Legiest E, De Bourdeaudhuij I, Maes L. Nutrition: associations between general parenting styles and specific food-related parenting practices and children’s food consumption. Am J Heal Promot. 2009;23:233–40.

    Article  Google Scholar 

  5. Larson NI, Wall MM, Story MT, Neumark-Sztainer DR. Home/family, peer, school, and neighborhood correlates of obesity in adolescents. Obesity. 2013;21:1858–69.

    Article  CAS  PubMed  Google Scholar 

  6. Parker G, Tupling H. A parental bonding instrument. Br J Med Psychol. 1979;52:1–10.

    Article  Google Scholar 

  7. Cooper MJ, Young E. Parental bonding and body mass index in a female community sample: the mediating role of eating disorder thoughts and core beliefs. Behav Cogn Psychother. 2016;4:123–7.

    Article  Google Scholar 

  8. Tetley A, Moghaddam NG, Dawson DL, Rennoldson M. Parental bonding and eating disorders: a systematic review. Eat Behav. 2014;15:49–59.

    Article  PubMed  Google Scholar 

  9. Parker G. Parental affectionless control as an antecedent to adult depression - a risk factor delineated. Arch Gen Psychiatry. 1983;40:956–60.

    Article  CAS  PubMed  Google Scholar 

  10. Sato T, Sakado K, Uehara T, Hirano S, Nishioka S, Kasahara Y. Dysfunctional parenting as a risk factor to lifetime depression in a sample of employed Japanese adults: evidence for the “affectionless control” hypothesis. Psychol Med. 1998;28:737–42.

    Article  CAS  PubMed  Google Scholar 

  11. Charmandari E, Kino T, Souvatzoglou E, Chrousos GP. Pediatric stress : hormonal mediators and human development. Horm Res. 2003;1583:161–79.

    Google Scholar 

  12. Ohmura T, Ueda K, Kiyohara Y, et al. Prevalence of type 2 (non-insulin-dependent) diabetes mellitus and impaired glucose tolerance in the Japanese general population: the Hisayama Study. Diabetologia. 1993;36:1198–203.

    Article  CAS  PubMed  Google Scholar 

  13. Ninomiya T. Japanese legacy cohort studies: the Hisayama Study. J Epidemiol. 2018;28:444–51.

    Article  PubMed  PubMed Central  Google Scholar 

  14. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2010;33:S62-69.

    Article  PubMed Central  Google Scholar 

  15. Parker G. Parental reports of depressives. J Affect Disord. 1981;3:131–40.

    Article  CAS  PubMed  Google Scholar 

  16. Parker G. Validating an experiential measure of parental style: the use of a twin sample. Acta Psychiatr Scand. 1986;73:22–7.

    Article  CAS  PubMed  Google Scholar 

  17. Kay W, Heather N, Gordon P, Dusan H-P. The stability of the parental bonding instrument over a 20-year period. Psychol Med. 2005;35:387–93.

    Article  Google Scholar 

  18. Parker G. The parental bonding instrument: psychometric properties reviewed. Psychiatr Dev. 1989;7:317–35.

    CAS  PubMed  Google Scholar 

  19. Kitamura T, Suzuki T. A validation study of the Parental Bonding Instrument in a Japanese population. Jpn J Psychiatry Neurol. 1993;47:29–36.

    CAS  PubMed  Google Scholar 

  20. Cheng YH, Chi I, Boey KW, Ko LS, Chou KL. Self-rated economic condition and the health of elderly persons in Hong Kong. Soc Sci Med. 2002;55:1415–24.

    Article  CAS  PubMed  Google Scholar 

  21. Mancia G, De Backer G, Dominiczak A, et al. Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens. 2007;25:1105–87.

    Article  CAS  PubMed  Google Scholar 

  22. Almeida ND, Loucks EB, Kubzansky L, et al. Quality of parental emotional care and calculated risk for coronary heart disease. Psychosom Med. 2010;72:148–55.

    Article  PubMed  PubMed Central  Google Scholar 

  23. Turner HM, Rose KS, Cooper MJ. Schema and parental bonding in overweight and nonoverweight female adolescents. Int J Obes. 2005;29:381–7.

    Article  CAS  Google Scholar 

  24. Rogers FD, Bales KL. Mothers, fathers, and others: neural substrates of parental care. Trends Neurosci. 2019;42:552–62.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Otani K, Suzuki A, Matsumoto Y, Kamata M. Parental overprotection increases interpersonal sensitivity in healthy subjects. Compr Psychiatry. 2009;50:54–7.

    Article  PubMed  Google Scholar 

  26. Stenbæk DS, Jensen CG, Holst KK, Mortensen EL, Knudsen GM, Frokjaer VG. Does harm avoidance mediate effects of recollected parental bonding on mental distress in adulthood? Compr Psychiatry. 2014;55:1007–14.

    Article  PubMed  Google Scholar 

  27. Seeman TE, Singer BH, Rowe JW, Horwitz RI, Mcewen BS. Price of adaptation-Allostatic Load and its health consequences. Arch Intern Med. 1997;157:2259–68.

    Article  CAS  PubMed  Google Scholar 

  28. McEwen BS, Stellar E. Stress and the individual: mechanisms leading to disease. Arch Intern Med. 1993;153:2093–101.

    Article  CAS  PubMed  Google Scholar 

  29. Steptoe A, Hackett RA, Lazzarino AI, et al. Disruption of multisystem responses to stress in type 2 diabetes: investigating the dynamics of allostatic load. Proc Natl Acad Sci U S A. 2014;111:15693–8.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Shields GS, Slavich GM. Lifetime stress exposure and health: a review of contemporary assessment methods and biological mechanisms. Soc Personal Psychol Compass. 2017;11:1–18.

    Article  Google Scholar 

  31. Ergang BC, Molle RD, Reis RS, et al. Perceived maternal care is associated with emotional eating in young adults. Physiol Behav. 2019;201:91–4.

    Article  CAS  PubMed  Google Scholar 

  32. Fassino S, Amianto F, Rocca G, Abbate DG. Parental bonding and eating psychopathology in bulimia nervosa: personality traits as possible mediators. Epidemiol Psichiatr Soc. 2010;19:214–22.

    Article  PubMed  Google Scholar 

  33. Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition. 2007;23:887–94.

    Article  PubMed  Google Scholar 

  34. Dallman MF, Pecoraro NC, La Fleur SE. Chronic stress and comfort foods: self-medication and abdominal obesity. Brain Behav Immun. 2005;19:275–80.

    Article  PubMed  Google Scholar 

  35. Park M, Quinn L, Park C, Martyn-Nemeth P. Pathways of the relationships among eating behavior, stress, and coping in adults with type 2 diabetes: a cross-sectional study. Appetite. 2018;131:84–93.

    Article  PubMed  Google Scholar 

  36. Jones JD, Cassidy J, Shaver PR. Parents’ self-reported attachment styles: a review of links with parenting behaviors, emotions, and cognitions. Pers Soc Psychol Rev. 2015;19:44–76.

    Article  PubMed  Google Scholar 

  37. Ohtaki Y, Ohi Y, Suzuki S, Usami K, Sasahara S, Matsuzaki I. Parental bonding during childhood affects stress-coping ability and stress reaction. J Health Psychol. 2017;22:1004–11.

    Article  PubMed  Google Scholar 

  38. Jones LB, Hall BA, Kiel EJ. Systematic review of the link between maternal anxiety and overprotection. J Affect Disord. 2021;295:541–51.

    Article  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgements

The authors thank the residents of the town of Hisayama for their participation in the survey and the staff of the Division of Health and Welfare of Hisayama for their cooperation with this study. We thank Ryota Nakayama for technical support with the electronic processing of the data. The statistical analyses were carried out using the computer resources offered under the category of General Projects by the Research Institute for Information Technology, Kyushu University.

Funding

This study was supported in part by the Ministry of Education, Culture, Sports, Science and Technology of Japan (JSPS KAKENHI Grant Number JP19H03752, JP19H03752, JP21H03200, JP21K07522, JP21K11725, JP21K10448, JP22K07421, JP22K17396, JP23K09692, JP23K09717, JP23K16330, JP23K06787, and JP23K09060); by the Health and Labour Sciences Research Grants of the Ministry of Health, Labour and Welfare of Japan (JPMH23FA1006, and JPMH23FA1022); and by the Japan Agency for Medical Research and Development (JP23dk0207053, JP23km0405209); by JST Grant Number (JPMJPF2210).

Author information

Authors and Affiliations

  1. Department of Psychosomatic Medicine, Kyushu University Hospital, Fukuoka, Japan

    Mao Shibata, Masako Hosoi, Kozo Anno, Rie Iwaki & Nobuyuki Sudo

  2. Department of Epidemiology and Public Health, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan

    Mao Shibata, Naoki Hirabayashi, Yoichiro Hirakawa & Toshiharu Ninomiya

  3. Division of Research Management, Center for Cohort Studies, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

    Mao Shibata & Toshiharu Ninomiya

  4. Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

    Masako Hosoi, Naoki Hirabayashi, Hiroshi Kawata, Ryoko Sawamoto & Nobuyuki Sudo

  5. Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

    Yoichiro Hirakawa

Authors
  1. Mao Shibata
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Masako Hosoi
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Kozo Anno
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Naoki Hirabayashi
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Yoichiro Hirakawa
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Hiroshi Kawata
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Rie Iwaki
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Ryoko Sawamoto
    View author publications

    You can also search for this author in PubMed Google Scholar

  9. Nobuyuki Sudo
    View author publications

    You can also search for this author in PubMed Google Scholar

  10. Toshiharu Ninomiya
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

M.S. and T.N. contributed to the study design; conducted the data collection, analysis, and data interpretation; drafted the first report; and edited the report drafts. M.H. and K.A. contributed to the study design; conducted the data collection and data interpretation; and edited the report drafts. R.I., H.K., R.S. and Y.H. contributed to the data collection and edited the report drafts. N.H. and N.S. contributed to the data interpretation and edited the report drafts. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Mao Shibata.

Ethics declarations

Ethics approval and consent to participate

Research was conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from all participants. This study was conducted with the approval of the Kyushu University Institutional Review Board for Clinical Research.

Consent for publication

Not applicable.

Competing interests

No potential competing interests relevant to this article were reported.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

The original version of this article was revised: “Figure 2 has been revised after publication due to the author's request.”

Supplementary Information

Additional file 1:

Supplemental Table S1. Parental care and overprotection scores for all participants according to age group. Supplemental Table S2. Combination of paternal and maternal parenting styles. Supplemental Table S3. Association of the score of parental care and overprotection with the presence of diabetes after including the participants with a single parent. Supplemental Table S4. Characteristics of included and excluded subjects.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Shibata, M., Hosoi, M., Anno, K. et al. Inadequate care and excessive overprotection during childhood are associated with the presence of diabetes mellitus in adulthood in a general Japanese population: a cross-sectional analysis from the Hisayama Study. BMC Endocr Disord 23, 222 (2023). https://doi.org/10.1186/s12902-023-01474-4

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12902-023-01474-4

Keywords

BMC Endocrine Disorders

ISSN: 1472-6823

Contact us