To our knowledge, this is the first study to examine directly the association of %BF as measured by DEXA with allergic sensitization. We found %BF was associated with allergic sensitization in males but not females. Also, this study demonstrated an inverse association between HDL and allergic sensitization in both genders while LDL was associated with higher risk of allergic sensitization in males, even after adjusting for %BF. These associations can be partially explained by shared common genetic factors which may be involved in both the development of allergic sensitization and the regulation of %BF and serum lipid levels.
Prior epidemiologic studies of BMI and allergic sensitization in adults have yielded equivocal findings. 8, 10, 12
This may be in part due to the use of BMI, a surrogate measure of adiposity, as opposed to a direct measure of adiposity. For example, no association was found between BMI and allergic sensitization in rural Australia, 12
while BMI > 24.8 was found to be associated with about 1.5-fold higher risk of allergic sensitization in a Finnish study.10
Consistent with prior studies, we found unstable associations between BMI and allergic sensitization. However, when we evaluated FMI (fat mass index) instead of BMI, a positive FMI-sensitization association was observed in males, after controlling for LMI. In keeping with this finding, our study also demonstrated a persistent positive association between %BF and allergic sensitization in males but not in females. Our BMI data, as well as findings of previous studies may, in part, be a consequence of the limitation of BMI as a general adiposity measure. This underscores the importance of direct adiposity measures in evaluating the relationship between adiposity and allergic sensitization.
The gender differences in the effects of adiposity and serum lipid profiles on allergic sensitization were pronounced in this study. There are a number of potential explanations for this finding. From a biologic standpoint, previous studies have found gender differences in the production of IgE,3
T cell polarization20
and also in lipid profiles.18
Estrogen increases HDL concentration in females and testosterone decreases HDL in both genders.18
However, the exact mechanism underlying the gender differences of these associations cannot be fully explained by the current literature. From a methodologic standpoint, it is also possible that the limited variation of %BF in the females did not allow for detection of associations seen in the males. The coefficient of variation (CV) was 51.1% in males, and 20.8% in females.
In this study, we found an inverse association between HDL and allergic sensitization. In previous studies, both positive and negative associations between HDL and sensitization have been reported.14, 15
HDL was found to be associated with a lower risk of allergic sensitization in children but not in adults in NHANES III.14
In contrast, higher HDL was associated with greater risk of allergic sensitization in adults in a German study, but the association disappeared after controlling for age and gender.15
There are similar issues in prior studies of the association between LDL and allergic sensitization.14, 15
Higher LDL levels were associated with a lower prevalence of allergic sensitization in the German study15
but no association was found in NHANES III.14
In our study, a positive association of LDL quartiles and allergic sensitization was observed in males but not females. No associations were observed between TG and sensitization in either gender, which was consistent with results of previous studies.14
Differences in the association between lipid levels and allergic sensitization between studies may be partly due to differences between genders and how each of the studies accounted for this difference. We feel, given the marked gender differences, that stratification by gender is the most prudent approach.
Using our unique twin study design, we showed that common genetic factors may contribute to the observed associations between %BF, HDL, LDL and allergic sensitization. Shared genetic influences between two traits may result in a concomitant rise of both phenomena in response to environmental changes. Notably, shared- and non-shared environmental correlations between HDL, LDL and allergic sensitization were not statistically significant. It is possible that this might due to the limited number of twin pairs (n=238) with data available on zygosity in addition to the variables of interest (SPT, adiposity and serum lipid levels). In ACE models, we have limited power to determine relative importance of genetic (A) and common environmental (C) effects on low HDL and high LDL. The A+C component explained about 80-90% of the variance of low HDL and high LDL, while the individual environmental component (E) explained 9% (95%CI: 2-28%) of the variance of low HDL and 21% (95%CI: 11-36%) of the variance of high LDL. Taken together, it appears that both genetic and environmental factors may have also played a role in determining the magnitude of the observed associations.
Our findings may have important public health implications. These results provide a potential explanation for the phenomenon of increasing prevalence of allergic sensitization or allergic diseases in Asian immigrants commensurate with length of stay in westernized countries regardless of age at arrival.30
This increase might be due in part to that transition to a westernized nutrition and lifestyle from an original Asian lifestyle and environment increases the prevalence of obesity, and increases the risk of low HDL, high LDL and allergic sensitization in Asian immigrants,31
especially those genetically susceptible to both low HDL (or high LDL) and allergic sensitization.
Previous studies have suggested that adiposity predisposes to asthma, an atopic disease, but not vice versa.5
However, the associations between asthma and adiposity may not be the same as those between sensitization and adiposity. In this cross-sectional study, body fat was measured in adulthood while sensitization might have occurred in childhood. Another possible explanation of our findings is that allergic sensitization increases the risk of adiposity or abnormalities in lipid profiles. Further longitudinal studies are needed to evaluate the temporal relationship of these phenotypes.
This study has several strengths. First, body composition (such as %BF) was measured by DEXA, a technique that can accurately assess total BF.13
This community-based sample with a relatively low prevalence of obesity and high LDL and TG allowed us to investigate the relation between adiposity, lipids and sensitization among mostly healthy subjects. This may allow for the elucidation of relationships which may be obscured in predominantly obese populations. Since these are clinically asymptomatic subjects our findings were less likely confounded by lipid lowering medication use. Finally, our twin design offers the opportunity to examine whether genetic influences contribute to the associations between %BF, lipids and allergic sensitization. Such an analysis would not be possible in a general population.
The study also has limitations. (1) Our findings may not be generalizable to affluent urban populations or populations with a higher level of obesity. (2) This is a cross-sectional analysis which precludes any temporal or cause-effect conclusions. (3) This quantitative genetic study only provides estimates of the degree to which genes influence variation in each trait between subjects. This design does not identify specific genes or address associated mechanisms. Further studies are needed to determine which specific genes, environmental factors, or gene-environmental interactions contribute to the correlation of allergic sensitization, serum lipid levels, and adiposity.
In summary, in this lean Chinese population, higher %BF, lower HDL and higher LDL were associated with increased risk of allergic sensitization in males. We also found evidence for a common genetic element in this association. With the exception of HDL, no significant associations were found in females. These findings suggest a gender-specific link between adiposity, serum lipids and allergic sensitization. Continued follow-up of this cohort may help determine the temporal relationships between adiposity, serum lipids and allergic sensitization. These findngs may have relevance in understanding novel factors related to the etiology of allergic diseases, and may have implications for disease prevention.