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Letter to the Editor

Free Access

Synergistic Effect of Neuroticism and Body Mass Index on Glucose Metabolism in Nondiabetic Adults

Tsenkova V.K.a · Carr D.d · Coe C.L.b · Ryff C.D.c

Author affiliations

aCenter for Women’s Health and Health Disparities Research, bDepartment of Psychology and cInstitute on Aging and Department of Psychology, University of Wisconsin-Madison, Madison, Wisc., and dDepartment of Sociology and Institute for Health, Health Care Policy and Aging Research, Rutgers University, New Brunswick, N.J., USA

Corresponding Author

Vera K. Tsenkova, PhD

Center for Women’s and Health Disparities Research

University of Wisconsin-Madison, 310 N. Midvale Blvd.

Madison, WI 53706 (USA)

Tel. +1 608 698 8822, E-Mail tsenkova@wisc.edu

Related Articles for ""

Psychother Psychosom 2012;81:327–328

Obesity has an important influence on glucoregulation and is among the most prominent risk factors for developing type 2 diabetes [1,2,3]. While more than 80% of people with type 2 diabetes are obese, most obese people never develop diabetes [4], suggesting that other factors are involved, possibly in combination with body mass index (BMI), to influence the preclinical progression to type 2 diabetes. Increasing evidence shows that psychosocial vulnerability factors, such as stress-induced catecholamine release, perceived discrimination, and work stress, moderate the effects of BMI and central adiposity on glucose metabolism [5,6,7].

Neuroticism is a personality trait that reflects nervousness, moodiness, and temperamental style [8] and refers to a relatively stable tendency to respond with negative emotions to threat, frustration, and loss [9,10]. Neuroticism has been reliably linked to adverse mental health outcomes such as depression [11,12,13] and anxiety [14], as well as to physical health outcomes such as metabolic syndrome [15,16], cardiovascular disease [17], diabetes [18], and mortality [19,20].

The two specific questions addressed by the following analysis were: (1) whether neuroticism was associated with poor glucoregulation, and (2) whether it amplified the relationship between BMI and clinical indicators of glucose metabolism – fasting glucose, insulin, an index of insulin resistance (HOMA-IR), and glycosylated hemoglobin (HbA1c). We included only nondiabetic people, allowing us to focus on preclinical pathways leading up to type 2 diabetes. We expected that the most marked signs of dysregulation, as evidenced by high glucose, insulin, HOMA-IR, and HbA1c, would be found among people who had the highest BMI and highest neuroticism scores in our sample.

We used data from 952 nondiabetic participants of the biological subsample of the MIDUS II study [21,22]. We excluded participants with likely diabetes, including those with HbA1c >6.5%, fasting glucose >126 mg/dl, or taking anti-diabetic medications (e.g. metformin). Hierarchical multiple regression was used and all models included neuroticism (M = 2, SD = 0.6) and BMI (M = 29, SD = 6) as predictors and a comprehensive set of relevant covariates: age (M = 56.6, SD = 11.5), race (85% white, 15% black), gender (43% male), waist-to-hip ratio (M = 0.89, SD = 0.1), current depressive symptoms (M = 8.4, SD = 8.2) [23], lifetime depression diagnosis (23% yes), and years of education (M = 15, SD = 5). The outcomes included fasting glucose (M = 95, SD = 9.6), insulin (M = 11.9, SD = 9.8), HOMA-IR (M = 2.9, SD = 2.6), and HbA1c (M = 5.7, SD = 3.6). All continuous predictor variables were mean-centered and outliers were top-coded. Glucose, insulin, and HOMA-IR were log-transformed to achieve normal distributions.

Bivariate correlations showed that BMI was positively associated with all markers of glucose metabolism (r values ranged from 0.17 to 0.46, p < 0.01). Neuroticism was not significantly associated with BMI or glucose levels, but was positively associated with insulin (r = 0.08, p = 0.01) and HOMA-IR (r = 0.08, p = 0.01) and negatively associated with HbA1c (r = 0.07, p = 0.03). Multivariate-adjusted moderating analyses, in turn, showed that neuroticism interacted with BMI to predict insulin (R2 = 0.34, B = 0.05, p < 0.05) and HOMA-IR (R2 = 0.34, B = 0.05, p < 0.05). For both interactions, the highest levels of insulin and HOMA-IR were evident among people who had both higher BMI and higher neuroticism (fig. 1). In both models, the only statistically significant associations observed among covariates and glucoregulation were positive relationship between waist-to-hip ratio (p < 0.001) and insulin and HOMA-IR, and negative relationships between gender and insulin and HOMA-IR (p < 0.01). The interaction between neuroticism and BMI was not significantly associated with glucose or HbA1c.

Fig. 1

Neuroticism amplifies the effect of BMI on insulin (p < 0.05). Note that high neuroticism is plotted at 1 SD above the mean for neuroticism and low neuroticism is plotted at 1 SD below the mean. Very high neuroticism is plotted at 2 SD above the mean for neuroticism and very low neuroticism is plotted at 2 SD below the mean. Absolute values of insulin are plotted for ease of interpretation.

http://www.karger.com/WebMaterial/ShowPic/208476

High BMI is among the most prominent risk factors for type 2 diabetes, yet the variability in the association between BMI and disease suggests other factors are required to more fully understand the progression from preclinical risk to diabetes. We investigated the relationships among BMI, neuroticism, and glucoregulation in a sample of nondiabetic people and found support for the hypothesis that neuroticism acts synergistically with BMI to promote insulin resistance and higher circulating levels of insulin, which constitute the first stage of progression to diabetes [24]. Our study suggests that neuroticism is an instigating factor that works interactively with BMI to initiate the progression to disease.

While previous studies by our research group and others [5,6,7] have shown that the combined influences of obesity and psychosocial variables are associated with higher glucose and HbA1c, no relationships were detected for glucose or HbA1c in the present study. The overall pattern of findings underscores the fact that these four clinical indicators of glucose regulation track different steps in the progression from normoglycemia to disease [24]. Future studies need to investigate the relationships among psychosocial factors, obesity, and multiple indicators of glucose regulation longitudinally to more clearly delineate the causal antecedents and mediating pathways.

Our findings extend previous work showing that other psychosocial vulnerability factors such as stress-induced catecholamine release, perceived discrimination, and work stress interact with BMI and central adiposity to predict different clinical indicators of glucose metabolism [5,6,7]. Taken together, these lines of inquiry suggest that overweight and obese people, who are already at a higher risk for disease due to increased production of free fatty acids and pro-inflammatory cytokines by adipose tissue [25], may be more susceptible to the effects of psychosocial vulnerabilities on clinical indicators of glucose metabolism. While the underlying mechanisms are still unclear, a primary hormone candidate is glucocorticoid activity and its daily secretion pattern of cortisol. Previous analyses have shown that the slope of the diurnal cortisol decrease is flatter among obese people and that a flatter decrement is positively associated with neuroticism [26]. Moreover, once obesity is present, adrenomedullary activity has been implicated in the development of glucose dysregulation [5].

Although we found support for the hypothesis that neuroticism compounds the effect of BMI on glucose regulation, our study was constrained by its cross-sectional design that does not allow for determination of causal directionality. However, it seems less plausible that poor glucose regulation contributes to obesity or neuroticism than vice versa. Nevertheless, our analyses point to neuroticism as one specific personality trait that acts together with BMI to influence the progression to disease. Overall, the findings suggest that neuroticism deserves further attention as a psychological vulnerability factor which may aggravate the morbidity associated with hyperinsulinemia and insulin resistance.

Acknowledgements

This research was supported by a grant from the National Institute on Aging (P01-AG020166; Carol D. Ryff, Principal Investigator) to conduct a longitudinal follow-up of the MIDUS (Midlife in the US) investigation. The original study was supported by the John D. and Catherine T. MacArthur Foundation Research Network on Successful Midlife Development. We thank the staff of the Clinical Research Center at the University of Wisconsin-Madison, at the University of California, Los Angeles, and at Georgetown University for their support in conducting this study. Data collection was supported by the following grants M01-RR023942 (Georgetown), M01-RR00865 (UCLA) from the General Clinical Research Centers Program, and 1UL1RR025011 (UW) from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources, National Institutes of Health. The first author of this study was also supported, in part, by award number T32HD049302 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Eunice Kennedy Shriver National Institute of Child Health and Human Development or the National Institutes of Health.


References

  1. American Diabetes Association: Diagnosis and classification of diabetes mellitus. Diabetes Care 2010;33(suppl 1):S62–S69.
    External Resources
  2. Bloomgarden ZT: World Congress on Insulin Resistance, Diabetes, and Cardiovascular Disease: Part 2. Diabetes Care 2011;34:e126–e131.
    External Resources
  3. Bloomgarden ZT: World Congress on Insulin Resistance, Diabetes, and CARDIOVASCULAR disease: Part 1. Diabetes Care 2011;34:e115–e120.
    External Resources
  4. Attie AD: Genetic and genomic studies of type 2 diabetes in mice. Int Congr Ser 2004;1262:220–223.
    External Resources
  5. Surwit RS, Williams RB, Lane JD, Feinglos MN, Kuhn CM, Georgiades A: Plasma epinephrine predicts fasting glucose in centrally obese African-American women. Obesity (Silver Spring) 2010;18:1683–1687.
  6. Tsenkova V, Schoeller D, Carr D, Ryff C: Perceived weight discrimination amplifies the link between central adiposity and nondiabetic glycemic control (HbA1c). Ann Behav Med 2011;41:243–251.
    External Resources
  7. Heraclides AM, Chandola T, Witte DR, Brunner EJ: Work stress, obesity and the risk of type 2 diabetes: gender-specific bidirectional effect in the Whitehall II Study. Obesity (Silver Spring) 2011;20:428–433.
    External Resources
  8. Goldberg LR: The structure of phenotypic personality traits. Am Psychol 1993;48:26–34.
  9. Lahey BB: Public health significance of neuroticism. Am Psychol 2009;64:241–256.
    External Resources
  10. Costa PT, McCrae RR: Four ways five factors are basic. Pers Individ Dif 1992;13:653–665.
    External Resources
  11. Roberts SB, Kendler KS: Neuroticism and self-esteem as indices of the vulnerability to major depression in women. Psychol Med 1999;29:1101–1109.
  12. Fanous A, Gardner CO, Prescott CA, Cancro R, Kendler KS: Neuroticism, major depression and gender: a population-based twin study. Psychol Med 2002;32:719–728.
  13. Wouts L, Janzing JG, Lampe IK, Franke B, de Vegt F, Tendolkar I, van Iersel MB, Buitelaar JK, Oude Voshaar RC: The interaction between cerebrovascular disease and neuroticism in late-life depression: a cross-sectional study. Int J Geriatr Psychiatry 2011;26:702–710.
  14. Bienvenu OJ, Nestadt G, Samuels JF, Costa PT, Howard WT, Eaton WW: Phobic, panic, and major depressive disorders and the five-factor model of personality. J Nerv Ment Dis 2001;189:154–161.
  15. Phillips AC, Batty GD, Weiss A, Deary I, Gale CR, Thomas GN, Carroll D: Neuroticism, cognitive ability, and the metabolic syndrome: The Vietnam Experience Study. J Psychosom Res 2010;69:193–201.
    External Resources
  16. Sutin AR, Costa PT Jr, Uda M, Ferrucci L, Schlessinger D, Terracciano A: Personality and metabolic syndrome. Age (Dordr) 2010;32:513–519.
    External Resources
  17. Suls J, Bunde J: Anger, anxiety, and depression as risk factors for cardiovascular disease: the problems and implications of overlapping affective dispositions. Psychol Bull 2005;131:260–300.
  18. Goodwin RD, Cox BJ, Clara I: Neuroticism and physical disorders among adults in the community: results from the national comorbidity survey. J Behav Med 2006;29:229–238.
  19. Mroczek DK, Spiro A 3rd: Personality change influences mortality in older men. Psychol Sci 2007;18:371–376.
  20. Shipley BA, Weiss A, Der G, Taylor MD, Deary IJ: Neuroticism, extraversion, and mortality in the UK health and lifestyle survey: a 21-year prospective cohort study. Psychosom Med 2007;69:923–931.
  21. Love GD, Seeman TE, Weinstein M, Ryff CD: Bioindicators in the MIDUS national study: protocol, measures, sample, and comparative context. J Aging Health 2010;22:1059–1080.
    External Resources
  22. Radler BT, Ryff CD: Who participates? Accounting for longitudinal retention in the MIDUS national study of health and well-being. J Aging Health 2010;22:307–331.
    External Resources
  23. Radloff L: The CES-D scale: a self-report depression scale for research in the general population. Appl Psychol Meas 1977;1:385–401.
    External Resources
  24. Weir GC, Bonner-Weir S: Five stages of evolving β-cell dysfunction during progression to diabetes. Diabetes 2004;53(suppl 3):S16–S21.
  25. Kahn SE, Hull RL, Utzschneider KM: Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 2006;444:840–846.
  26. Nater UM, Hoppmann C, Klumb PL: Neuroticism and conscientiousness are associated with cortisol diurnal profiles in adults – role of positive and negative affect. Psychoneuroendocrinology 2010;35:1573–1577.

Author Contacts

Vera K. Tsenkova, PhD

Center for Women’s and Health Disparities Research

University of Wisconsin-Madison, 310 N. Midvale Blvd.

Madison, WI 53706 (USA)

Tel. +1 608 698 8822, E-Mail tsenkova@wisc.edu


Article / Publication Details

Received: August 16, 2011
Accepted: February 21, 2012
Published online: August 01, 2012
Issue release date: August 2012

Number of Print Pages: 2
Number of Figures: 1
Number of Tables: 0

ISSN: 0033-3190 (Print)
eISSN: 1423-0348 (Online)

For additional information: https://www.karger.com/PPS


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References

  1. American Diabetes Association: Diagnosis and classification of diabetes mellitus. Diabetes Care 2010;33(suppl 1):S62–S69.
    External Resources
  2. Bloomgarden ZT: World Congress on Insulin Resistance, Diabetes, and Cardiovascular Disease: Part 2. Diabetes Care 2011;34:e126–e131.
    External Resources
  3. Bloomgarden ZT: World Congress on Insulin Resistance, Diabetes, and CARDIOVASCULAR disease: Part 1. Diabetes Care 2011;34:e115–e120.
    External Resources
  4. Attie AD: Genetic and genomic studies of type 2 diabetes in mice. Int Congr Ser 2004;1262:220–223.
    External Resources
  5. Surwit RS, Williams RB, Lane JD, Feinglos MN, Kuhn CM, Georgiades A: Plasma epinephrine predicts fasting glucose in centrally obese African-American women. Obesity (Silver Spring) 2010;18:1683–1687.
  6. Tsenkova V, Schoeller D, Carr D, Ryff C: Perceived weight discrimination amplifies the link between central adiposity and nondiabetic glycemic control (HbA1c). Ann Behav Med 2011;41:243–251.
    External Resources
  7. Heraclides AM, Chandola T, Witte DR, Brunner EJ: Work stress, obesity and the risk of type 2 diabetes: gender-specific bidirectional effect in the Whitehall II Study. Obesity (Silver Spring) 2011;20:428–433.
    External Resources
  8. Goldberg LR: The structure of phenotypic personality traits. Am Psychol 1993;48:26–34.
  9. Lahey BB: Public health significance of neuroticism. Am Psychol 2009;64:241–256.
    External Resources
  10. Costa PT, McCrae RR: Four ways five factors are basic. Pers Individ Dif 1992;13:653–665.
    External Resources
  11. Roberts SB, Kendler KS: Neuroticism and self-esteem as indices of the vulnerability to major depression in women. Psychol Med 1999;29:1101–1109.
  12. Fanous A, Gardner CO, Prescott CA, Cancro R, Kendler KS: Neuroticism, major depression and gender: a population-based twin study. Psychol Med 2002;32:719–728.
  13. Wouts L, Janzing JG, Lampe IK, Franke B, de Vegt F, Tendolkar I, van Iersel MB, Buitelaar JK, Oude Voshaar RC: The interaction between cerebrovascular disease and neuroticism in late-life depression: a cross-sectional study. Int J Geriatr Psychiatry 2011;26:702–710.
  14. Bienvenu OJ, Nestadt G, Samuels JF, Costa PT, Howard WT, Eaton WW: Phobic, panic, and major depressive disorders and the five-factor model of personality. J Nerv Ment Dis 2001;189:154–161.
  15. Phillips AC, Batty GD, Weiss A, Deary I, Gale CR, Thomas GN, Carroll D: Neuroticism, cognitive ability, and the metabolic syndrome: The Vietnam Experience Study. J Psychosom Res 2010;69:193–201.
    External Resources
  16. Sutin AR, Costa PT Jr, Uda M, Ferrucci L, Schlessinger D, Terracciano A: Personality and metabolic syndrome. Age (Dordr) 2010;32:513–519.
    External Resources
  17. Suls J, Bunde J: Anger, anxiety, and depression as risk factors for cardiovascular disease: the problems and implications of overlapping affective dispositions. Psychol Bull 2005;131:260–300.
  18. Goodwin RD, Cox BJ, Clara I: Neuroticism and physical disorders among adults in the community: results from the national comorbidity survey. J Behav Med 2006;29:229–238.
  19. Mroczek DK, Spiro A 3rd: Personality change influences mortality in older men. Psychol Sci 2007;18:371–376.
  20. Shipley BA, Weiss A, Der G, Taylor MD, Deary IJ: Neuroticism, extraversion, and mortality in the UK health and lifestyle survey: a 21-year prospective cohort study. Psychosom Med 2007;69:923–931.
  21. Love GD, Seeman TE, Weinstein M, Ryff CD: Bioindicators in the MIDUS national study: protocol, measures, sample, and comparative context. J Aging Health 2010;22:1059–1080.
    External Resources
  22. Radler BT, Ryff CD: Who participates? Accounting for longitudinal retention in the MIDUS national study of health and well-being. J Aging Health 2010;22:307–331.
    External Resources
  23. Radloff L: The CES-D scale: a self-report depression scale for research in the general population. Appl Psychol Meas 1977;1:385–401.
    External Resources
  24. Weir GC, Bonner-Weir S: Five stages of evolving β-cell dysfunction during progression to diabetes. Diabetes 2004;53(suppl 3):S16–S21.
  25. Kahn SE, Hull RL, Utzschneider KM: Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 2006;444:840–846.
  26. Nater UM, Hoppmann C, Klumb PL: Neuroticism and conscientiousness are associated with cortisol diurnal profiles in adults – role of positive and negative affect. Psychoneuroendocrinology 2010;35:1573–1577.