Is height an independent marker of metabolic syndrome in a developing society?
A cross-sectional study of 22,180 Chilean adults.
1
Koch ,
2
Romero ,
1
Sandoval ,
1
Romero ,
1
Bravo ,
1
Henríquez ,
E.
T.
D.
CX.
M.
O.
L. Urrutia.
1 Department of Family Medicine, Faculty of Medicine, University of Chile (Santiago, CL) - 2 School of Medicine, University of California (San Diego, US)
Background: A paucity of information exists in reference to the independent influence of
height, a marker of adverse early life exposures, and cardiovascular risk in developing societies.
The purpose of this study was to investigate the relationship between height and metabolic
syndrome (MS) in a Chilean adult population.
Methods: A cross-sectional study of 22,180 individuals (ages 20 to 64 years) in 27 primary care
centres of Chile. Blood pressure, fasting blood glucose, total cholesterol and waist-to-height
ratio (WHtR) were obtained from an adult preventive screening survey. Height was
categorized according to 50th and 75th percentiles by sex. Men <50th percentile of height
(shortest) measured <168 cm; betwen percentiles 50-75 (medium) were between 169-173 cm;
and >75th percentile (tallest) were >174 cm. Women of short stature measured <156 cm; those
of medium were between 157-160 cm; and the tallest were >161 cm. The association with MS
was assessed using a logistic regression.
Results: The mean age of participants was 40.4 ± 11.4 years (men 41.4±11.8; women
39.9±11.2; p< 0.001). From the total sample, 25.5% and 16.8% had high systolic and diastolic
blood pressure, respectively; 27.2% were with high fasting blood glucose, 41.5% with high total
cholesterol, and 56.8% were abdominally obese (WHtR >0.55). In general, the prevalence of
cardiovascular risk factors was greater in shortest individuals regarding tallest individuals,
especially for abdominal obesity. Using a linear ordinal term for height, an inverse doseresponse gradient between height and the risk of MS was observed (Table). This relationship
was partially explained by a lower risk for abdominal obesity in the taller individuals (OR 0.71;
p for trend 0.001).
Conclusion: In this cross-sectional study, increasing height had a protective effect for MS.
This relationship may be partially explained by the increased abdominal obesity observed in
shorter individuals. A plausible explanation is the "thrifty phenotype" hypothesis. Low height
is partially a marker of early adverse life exposure during critical stages of growth including in
utero development (Figure). An adverse environment (e.g. socioeconomic stress, poor
nutrition, infectious diseases, etc) would act programming a phenotype characterized by low
height and greater predisposition to abdominal adiposity, insulin resistance and cardiovascular
risk factors in adult life.
Table. Prevalence of metabolic risk factors according to Height.
Prevalence (%)
Shortest
Medium
Odds Ratio
(95% Confidence Interval)
Tall
Crude Risk
Age - and Sex Adjusted Risk
High Systolic Blood Pressure
(≥140 mmHg)
11.8
9.9
8.6
0.83 (0.79-0.88)
0.99 (0.94-1.05)
High Diastolic Blood Pressure
(≥90 mmHg)
14.1
12.8
12.0
0.91 (0.86-0.95)
1.05 (0.99-1.10)
High Fasting Blood Glucose (≥100
mg/dL)
27.3
26.8
24.8
0.94 (0.90-0.98)
1.01 (0.96-1.03)
High Total Cholesterol (≥200 mg/
dL)
42.9
37.2
33.6
0,82 (0.78-0.86)
0.95 (0.91-1.00)
Abdominal Obesity (WtHR >
0,55)
61.8
49.5
41.6
0.65 (0.62-0.68)
0.71 (0.69-0.75)
Presence of two or more
metabolic risk factors
53.3
45.6
39.9
0.75 (0.73-0.78)
0.86 (0.83-0.89)
Figure. Causal model of the thrifty phenotype hypothesis to explain the
inverse relationship between height and metabolic syndrome.
Early life adverse exposures
In utero exposures
Exposures during childhood
Thrifty Phenotype
Low Height
Other unknown mediators
Abdominal Adiposity
Insulin Resistance and
Cardiovascular risk factors
Cardiovascular
Outcomes