Many studies have linked indoor mold exposure with increased risk of asthma. The Quansah et al meta-analysis of 16 published studies on asthma and mold (11 cohort and 5 incident case-control) reported significantly higher rates of asthma which were related to dampness (EE 1.33, 95% CI 1.12-1.56), visible mold (EE 1.29, 1.04-1.60), mold odor 1.73 (1.19-2.50), and any mold or dampness exposure (EE 1.50, 95 CI 1.25-1.80) (Quansah R 2012).
Allergy to mold is also a major risk factor for serious asthma. (Note: fungal allergy can be measured by either testing skin prick allergy to various fungal allergens or by measuring levels of the immunoglobins = antibodies IgE and IgG in the blood.) A Texas study of 307 asthmatics with serum IgE testing for molds and other allergens reported that patients with fungal IgE sensitization had significantly higher levels of total IgE as compared to patients with no sensitization or non fungal sensitization (such as sensitivity to pollen or dust mites) only (median 825, 42, and 203 IU/ml, p<0.001) (Medrek, Kao et al. 2016). Compared to the non-sensitized and non-fungal sensitized patients, the fungal sensitized patients (as measured by levels of mold IgE in the blood) were also significantly more likely to require intensive care unit (ICU) care (13.2%, 3.7%, and 3.4% respectively, p=0.02) and mechanical ventilation (11.3%, 1.5%, and 0.9%, p<0.001) (Medrek, Kao et al. 2016).
Severe asthma with fungal sensitization (SAFS) is an increasingly common diagnosis which is seen in about 4-8% of adult asthmatics with a potential worldwide total among children and adults of over 6.5 million (Denning 2015, Overton, Simpson et al. 2017).
SAFS seems to have a strong genetic component, with one UK study of 47 SAFS patients, 279 healthy controls, and 152 atopic asthmatic subjects reporting that SAFS is significantly associated with a number of genes compared with atopic asthma including Toll-like receptor 3 (TLR3)(p=.009),TLR9 (p=.025), C-type lectin domain family seven member A (dectin-1) (p=.043), interleukin-10 (IL-10) (p=.0010), mannose-binding lectin (MBL2)(p=.007), CC-chemokin ligand 2 (CCL2)(p =.025), CCL (p=.002), plasminogen (p=.049) and adenosine A2a receptor (p=.024) (Overton, Simpson et al. 2017
Asthma-scratching the surface is so profitable!
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Doug Kaufmann developed his diet after years studying the clinical effects of pathogenic fungi on the body. Fungi and yeasts can become parasitic organisms on and inside our body, causing health problems that can be difficult to diagnose. Learn more about the Kaufmann Diet, change your life and know the cause.
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