Several cross-sectional studies have detected an association between glucose intolerance (1,2) and type 2 diabetes (36) with diminutiveness particularly in women. Recently, a longitudinal study confirmed these data (7) but without explanations for the relationship.

Insulin is a hormone that participates actively in protein anabolism (8) during the growth phase, and insulin resistance (of genetic [9,10] or environmental [11] etiology) could be accompanied by a decrease in skeletal development resulting in a diminution of the final height attained. Hence, we tested the hypothesis that hyperinsulinemia or family history of type 2 diabetes is related to decreased stature.

Women attending the Outpatient Clinic of the Department of Internal Medicine of the Hospital Riotinto in Huelva, Spain were interviewed for recruitment into the study. Of the 3,024 women assessed, 230 fulfilled the following selection criteria: premenopausal, aged >17 years, nonusers of oral contraceptives, normoglycemic, and with normality of endocrine, metabolic, renal, and hepatic function. For statistical assessment of biometric and biochemical variables, the subjects were grouped, a posteriori, with respect to diminutive stature (<152 cm; 10th percentile of the overall study group). In the first phase, the values of basal insulin were assessed with respect to the presence or absence of normal height attainment. In the second phase, multivariate logistic and multiple linear regression analyses were used to test for associations between height and the anthropometric and biochemical variables measured. The following eight variables were introduced into the logistic multivariate analysis: age, basal insulinemia, basal glycemia, BMI (kg/m2) and waist circumference as continuous variables, tobacco and alcohol use, and the family history of type 2 diabetes as dichotomous variables. The dependent variable was the presence or absence of height diminution. Multiple linear regression analyses were performed with these variables but with height entered as a continuous variable. Relative to the rest of the study group, the subjects of short stature were older (P < 0.01), had higher BMI (P < 0.01) and greater waist measurements (P < 0.01), and had higher baseline insulin levels (P < 0.01) as well as a family history of type 2 diabetes (P < 0.01). In a multivariate analysis, fasting insulin levels (odds ratio [OR] = 1.03; 95% CI = 1.01–1.05; P < 0.02) and a family history of type 2 diabetes (OR = 3.72; 95% CI = 1.40–9.96; P < 0.01) were the only variables associated with diminutive stature. These variables also correlated significantly with height (as a continuous variable) in the multiple linear regression analysis (regression coefficient of family history of type 2 diabetes = −3.040 [95% CI = −2.98 to −3.10], P < 0.01]; basal insulinemia = −0.05 [95% CI = −0.01 to −0.09], P < 0.01), irrespective of age, BMI, waist circumference, or basal glycemia.

Our principal findings indicated that women of diminutive stature have a higher prevalence of obesity and hyperinsulinemia and a higher percentage of family members affected with type 2 diabetes. As such, we propose that family history of type 2 diabetes and hyperinsulinemia are associated with short stature in normoglycemic premenopausal women and could explain the perceived association of decreased height and increased risk of type 2 diabetes.

1
Williams DR, Wareham NJ, Brown DC, Byrne CD, Clark PM, Cox BD, Cox LJ, Day NE, Hales CN, Palmer CR: Undiagnosed glucose intolerance in the community: the Isle of Ely Diabetes Project.
Diabet Med
12
:
30
–35,
1995
2
Brown DC, Byrne CD, Clark PM, Cox BD, Day NE, Hales CN, Shackleton JR, Wang TW, Williams DR: Height and glucose tolerance in adult subjects.
Diabetologia
34
:
531
–533,
1991
3
Bayo J, Latorre PM, García F, Vázquez JA: Factores de riesgo asociados a la prevalencia de diabetes mellitus no insulinodependiente en Lejona (Vizcaya).
Med Clin (Barc)
107
:
572
–577,
1996
4
Sayeed MA, Hussain MZ, Banu A, Rumi MA, Azad Khan AK: Prevalence of diabetes in a suburban population of Bangladesh.
Diabetes Res Clin Pract
34
:
149
–155,
1997
5
Han TS, Feskens EJ, Lean ME, Seidell JC: Associations of body composition with type 2 diabetes mellitus.
Diabet Med
15
:
129
–135,
1998
6
Jang HC, Min HK, Lee HK, Cho NH, Metzger BE: Short stature in Korean women: a contribution to the multifactorial predisposition to gestational diabetes mellitus.
Diabetologia
41
:
778
–783,
1998
7
Njolstad I, Arnesen E, Lund-Larsen PG: Sex differences in risk factors for clinical diabetes mellitus in a general population: a 12-year follow-up of the Finnmark Study.
Am J Epidemiol
147
:
49
–58,
1998
8
Conover CA, Hintz RL, Rosenfeld RG: Comparative effects of somatomedin C and insulin on the metabolism and growth of cultured human fibroblasts.
J Cell Physiol
122
:
133
–141,
1985
9
Ho LT, Chang ZY, Wang JT, Li-SH, Liu YF, Chen-YD, Reaven GM: Insulin insensitivity in offspring of parents with type 2 diabetes mellitus.
Diabet Med
7
:
31
–34,
1990
10
Haffner SM, Stern MP, Hazuda HP, Mitchell BD, Patterson JK: Increased insulin concentrations in nondiabetic offspring of diabetic parents.
N Engl J Med
319
:
1297
–1301,
1988
11
Mo-Suwan L, Lebel L: Risk factors for cardiovascular disease in obese and normal school children: association of insulin with other cardiovascular risk factors.
Biomed Environ Sci
9
:
269
–275,
1996

Address correspondence to F.J. Guerrero-Igea, MD, C/Huelva 1, 2A, 21660 Minas de Riotinto (Huelva), Spain. E-mail: fguerreroi@meditex.es.