Apr 6, 2012

Let us analyze the risk factors that could help to explain these phenomena:

Sex
In childhood, male sex has been considered to be a risk factor for having atopic diseases and asthma. Some years ago, this predominance was partially explained by an increased sensitivity to inhalant allergens.
However, we mentioned earlier that the increasing prevalence among girls equalized the male to female ratio
recently, even being more prevalent when considering eczema.
By the age of 11, male sex is still stronger when considering current wheezing. As the age of the sample evaluated increases, the predominance reverses. In a cohort evaluation, male in childhood declined by adolescence and early adulthood, considering female sex as one of the major risk factors for having asthma. It was also a predictive factor for persistence of asthma symptoms from childhood, but this conclusion needs to be reinforced in larger populations because the odds obtained revealed evidence of a wide confidence
interval.
Not only the former but also allergic rhinitis shows similar transition from male in childhood to female in adolescence. Having those repeated observations reinforced by evaluations in large population samples, the fact that estrogen has pro-inflammatory and testosterone anti-inflammatory effects could explain this trend.

Diet
Recently, Garcia-Marcos  evaluated the relationship of the Mediterranean diet (vegetables, pulses, cereals, potatoes, pasta, and rice) with asthma and rhinoconjunctivitis in more than 20,000 children, adjusting for exercise and obesity, finding its protective effect against current severe asthma in girls. Also, seafood and
fruit were protective against having rhinoconjunctivitis.
In the same direction, Wickens  corroborated that fast food intake was related with asthma symptoms in a frequency-dependent manner. Takeaway consumption greater than once a week showed an increased (although not significant) bronchial hyper-responsiveness, but had no effect on atopy.

Not only animal fat consumption was implicated as a risk factor for atopic diseases expressions. Vegetable oils contain linoleic acid, an Omega 6 polyunsaturated fatty acid (PUFA) precursor of arachidonic acid and consequently of eicosanoid metabolites, promoting the Th2 imbalance while decreasing interferong (IFNg); omega 3 PUFA found in fish oil inhibits PGE2 formation, modulating the production of immunoglobulin E (IgE) indirectly. However, the clinical relevance of adding fish oil in pregnancy diet demonstrated just a decrease in the severity of eczema in infants at high risk of atopy.
Feeding habits in the UK over the last decades, where atopic expressions grew, evidenced diminished saturated fat consumption. This growing could then be attributed to a reduction of antioxidants in the diet, since only the fatty acids deregulations could oversimplify the frame. Anyway, more studies are needed in
this field as interventional strategies have been disappointing as of date.

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