Abstract:Objective To investigate the risk factors for attention deficit hyperactivity disorder (ADHD) and to provide a basis for future prevention and treatment of this disease. Methods Following a systematic search for casecontrol studies on the risk factors for ADHD in China between 2000 and 2014, relevant family risk factors were extracted accordingly. The quality of selected studies was evaluated according to the NOS scale. A Meta analysis on the selected studies was conducted using Stata 12.0 software. Results A total of 16 studies were selected, involving 2 167 children with ADHD and 2 148 normal controls. Results of Meta analysis showed that good parenting (OR=0.32, 95% CI: 0.26-0.40), nuclear family (OR=0.56, 95% CI: 0.41-0.76), high education level of father (OR=0.56, 95% CI: 0.41-0.76), high education level of mother (OR=0.65, 95% CI: 0.47-0.89), and extroversion of mother (OR=0.33, 95% CI: 0.18-0.61) are favorable factors for ADHD. Poor parental relationship (OR=1.90, 95% CI: 1.17-3.06) and family history of ADHD (OR=5.86, 95% CI: 3.67-9.35) are risk factors for ADHD. Conclusions Good parenting, nuclear family, high education level of parents, and mother with extroversion are protective factors for ADHD, whereas poor parental relationship and family history of ADHD are associated with an increased risk for ADHD.
Stuart CA, Pietrzyk RA, Peters EJ, et al. Autophosphorylation of cultured skin fibroblast insulin-receptors from patients with severe insulin resistance and acanthosis nigricans[J]. Diabetes, 1989, 38(3): 328-332.
[23]
Shah PJ, Morton MJ. Adults with attention-deficit hyperactivity disorder-diagnosis or normality[J]. Br J Psychiatry, 2013, 5(4): 317-319.
Vanwesr D, Claes S. Deboutte D. Difference in hypothalamicpituitary-adrenal axis functioning among children with ADHD predominantly in attentive and combined types[J]. Eur Child Adolesc Psychiatry, 2009, 18(9): 543-553.
Stuart CA, Wen G, Williamson ME, et al. Altered GLUT1 and GLUT3 gene expression and subcellular redistribution of GLUT4: protein in muscle from patients with acanthosis nigricans and severe insulin resistance[J]. Metabolism, 2001, 50(7): 771-777.
Sprich S, Biederman J, Crawford MH, et a1. Adoptive and biological families of children and adolescents with ADHD [J]. J Am Acad Child Adolesc Psychiatry, 2000, 39(11): 1432-1437.
Kudo-Watanuki S, Kurihara E, Yamamoto K, et al. Coexistence of insulin-derived amyloidosis and an overlying acanthosis nigricans-like lesion at the site of insulin injection[J]. Clin Exp Dermatol, 2013, 38(1): 25-29.
[31]
Jiang S, Xin R, Lin S, et al. Linkage studies between attention deficit hyperactivity disorder and the monoamine oxidase genes[J]. Am J Med Genet, 2001, 105(8): 783-788.
[25]
Buzasi K, Sapi Z, Jermendy G. Acanthosis nigricans as a local cutaneous side effect of repeated human insulin injections[J]. Diabetes Res Clin Pr, 2011, 94(2): E34-E36.
[32]
Risch NJ. Searching for genetic determinants in the new millennium[J]. Nature, 2000, 405(6788): 847-856.
Ghosh S, Roychowdhury B, Mukhopadhyay S, et al. Clearance of acanthosis nigricans associated with insulinoma following surgical resection[J]. QJM-AN Int J Med, 2008, 101(11): 899-900.