Visceral adiposity index is associated with silent brain infarct in a healthy population
The association between Visceral adiposity index (VAI) with various cardio-metabolic diseases has been well established; however, there is limited knowledge about its association with cerebrovascular diseases. Nam and colleagues published a study titled “Visceral adiposity index is associated with silent brain infarct in a healthy population” in The Nature Metabolism journal. The summary of the study is given below:
Objectives:
To study the association between VAI and silent brain infarct (SBI) in a neurologically healthy population to acquire insight into underlying pathological mechanisms.
Method:
2596 healthy volunteers over the age of 40 years were evaluated in the study between January 2006 and December 2013. SBI was explained as an asymptomatic, well-defined lesion having a diameter of ≥3 mm and the same features as the cerebrospinal fluid. VAI was calculated using sex-specific equations as described in previous studies: VAI= [WC/ (39.68 +1.88×BMI)] ×(TG/1.03) × (1.31/HDL cholesterol) for males and VAI=[WC/(36.58+1.89×BMI)] × (TG/0.8 1) x (1.52/HDL cholesterol) for females.
Findings:
The study concludes that high VAI levels are associated with both SBI prevalence as well as a burden in a neurologically healthy population, whereas VAT area was not. This may indicate that functional activity is more essential than the amount of visceral fat. Additionally, the study suggests that VAI which encompasses metabolic susceptibility caused by visceral adiposity is a more relevant predictor for SBI than simple VAT quantity. A mechanism to associate the relationship between VAI and SBI is unknown yet the following rationales can be considered:
1) Combination of risk factors included in the VAI calculation formula can be strongly associated with SBI than for each risk factor.
2) Metabolic comorbidities cannot be ignored as they are associated with VAI and are a major risk factor for SBI.
3) VAT tends to secrete more pro-inflammatory adipokines than subcutaneous adipose tissue (SAT). This can lead to endothelial dysfunction due to subclinical inflammation which can result in SBI development.
4) High VAI might suggest an underlying higher atherosclerosis burden. Advanced atherosclerotic lesions can progress to SBI with chronic diffuse hypoperfusion and extravasation of toxic metabolites into neural tissues.
Even after adjusting for sex differences to create VAI, it was found to be meaningful only in females. Authors have put forward the following reasons to support this finding:
1) The association between age and VAI could affect these sexual differences. In female patients, anthropometric indicators (e.g., waist circumference, VAT, and total adipose tissue) increases with age, and hence, VAI increases. On the other hand, VAI is negatively associated with age in male patients with decreasing SAT. Hence, as VAI also serves as an indicator for age, the results might be more pronounced in females.
2) Females had a lower prevalence of the metabolic disease, on the other hand, the association between metabolic disease and VAI was greater than in males. This might be due to visceral obesity which can be a risk factor for many confounders that can influence VAI’s impact on SBI.
Limitation:
The authors acknowledge that It is a retrospective observational study that included a relatively homogeneous and large population but the possibility of selection bias continues. Additionally, due to the limitations of the cross-sectional analysis, investigators could only prove the association, not causality. The results can’t be generalized to clinical fields as participants were included from a healthy population, the prevalence of SBI and cardiovascular risk factors were relatively small. Investigators acknowledge future studies to confirm these findings.
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