The genetic basis of asthma heritability has been extensively studied and the studies are yielding some understanding. There is, as yet, no set genetic pattern that predicts presence of asthma or defines it severity. There are usually reasons or risk of asthma factors that makes someone susceptible to asthma and respiratory allergy problems. Asthma doesn’t just happen randomly to anyone without asthma gene factors risk factors.

Let’s consider some asthma risk factors and see how they increase the chance that a individual will have the asthma signs or symptoms of cough, wheezing, as well as shortness of breathing associated with the disease. After determining your personal risk factors for asthma, decide on the ones you can control as well as try to make some lifestyle changes. Avoidance of the risk factors you can control is important in preventing asthma symptoms. While you cannot change your own gender to family history, you can avoid smoking with asthma, breathing polluted air, and obesity. Take control of your asthma by controlling the asthma risk factors. By understanding all of the risk factors, you are able to prevent to control your asthma.

Genetic factors cannot explain the rise in asthma prevalence, morbidity, or mortality. However, a small change in the prevalence of relevant environmental exposures could explain a significant rise in disease prevalence among genetically susceptible individuals. Gene-environment interaction, defined as the co-participation of genetic and environmental factors, is particularly relevant to the etiology of asthma morbidity, especially in individuals who experience a disproportionate burden of environmental exposures. Relevant exposures include smoking, stress, nutritional factors, infections, allergens, and occupational asthma exposures. In addition, racial/ethnic variability in the distribution of genetic polymorphisms can potentially modify the response to pharmacotherapeutic agents, such as the ß 2 -adrenergic receptor. A genetic polymorphism in the ß 2 -adrenergic receptor gene has been associated with asthma severity, as well as with the susceptibility to develop asthma among individuals who smoked.

Childhood asthma happens more frequently in boys than in girls. It is still not known precisely why this occurs even though some experts find a young male’s airway size is small compared to the female’s airway, that may contribute to increased risk of wheezing after a cold or perhaps other viral infection. Around age 20, the ratio of asthma between people is the same. At age 40, more females than men have adult asthma.

The inherited genetic makeup predisposes you to having asthma. In fact, it’s thought that three-fifths of all asthma cases are hereditary. Based on CDC report, if a person has a parent with asthma, there is 3 to 6 times more probably to develop asthma than someone who does definitely not have a parent with asthma.

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A general pattern of factors influencing development of asthma seems to be emerging, including family allergy history/ asthma genetics, smoking, diet, obesity, and inactivity, all of which seem to influence the development of asthma and disease outcomes (Table bellow).

Many clinical or area studies have reported substantially higher rates of asthma prevalence, hospitalization, and mortality among racial and ethnic minorities. However, asthma is also most common among low socioeconomic groups, regardless of race. While black children have higher rates of asthma than white children, most studies have found that black race is not a significant correlate of asthma after controlling for location of residence and socioeconomic status (SES). The basis for the effects of poverty and urban residence on asthma prevalence is not known. One potential asthma factor is allergen exposure and allergen sensitization are common in urban environments. Black children in inner city Atlanta are exposed to high levels of dust mites and cockroach allergen, and a high proportion of the children with asthma were sensitized to these allergens. Litonjua and colleagues also concluded that a large proportion of racial/ethnic differences in asthma prevalence can be explained by factors related to income, area of residence, and level of education.

Asthma Factors that Influence Disease Development and Severity

Income is a determinant of access to health care, and frequently, the quantity and quality of health care available. Persons who have low income, regardless of race or ethnicity, are more likely to be uninsured, to encounter delays or be denied care, to rely on hospital clinics in emergency departments for health services, and to receive substandard care. The usual socioeconomic indicators, education and personal or household income, serve only as surrogates for more complicated correlates of individuals within populations and multiple asthma factors that can impact both on prevalence of asthma and adverse outcomes from the disease.

Studies from Germany comparing the populations of East and West Germany have shown the prevalence of hay fever and asthma as significantly higher in West German children, suggesting that asthma environmental factors explain the difference in prevalence in these ethnically similar populations. Early exposure to infections (as with being in a day-care environment early in life) or exposure to endotoxin (as with growing up on a farm with close exposure to the farm animals) are associated with a decreased prevalence of asthma. In contrast, growing up in an urban environment or generally with an increased standard of living are associated with an increased prevalence of asthma. Such correlates are also present for atopic disorders other than asthma. In fact, Strachan, who noted that prevalence of hay fever was inversely related to family size, was the first to recognize the importance of early exposures on atopic disease. In the USA, asthma is more prevalent in African-Americans and Puerto Ricans. These findings are not explained by the observations on the role of social class in European studies. Given the ethnic differences between African-Americans and whites, these studies may represent gene-by-environment interaction producing varied phenotypic outcomes.

Regulatory T cells Treg (picture above) is the existence of suppressor cells, which limit ongoing immune responses and prevent autoimmune disease, was postulated over 30 years ago. The recent phenotypic and functional characterization of these cells has led to a resurgence of interest in their therapeutic application in a number of immune-mediated diseases. Two broad subsets of CD3+CD4+ suppressive or Treg cells have been described: constitutive or naturally occurring versus adaptive or inducible Treg. (more…)

The Ras-dependent pathway can be triggered by a variety of cytokine receptors, as well as by certain adhesion molecules and by many other surface receptors when they contact appropriate ligands. Signaling in this pathway can be initiated by cytosolic proteins called Src-family kinases, so named because they bear regions of sequence homology to the oncoprotein Src. These Src-like kinases contain specialized protein domains, termed SH2 domains (for Src-homology region 2), that enable them to bind other proteins containing phosphorylated tyrosine residues. When a cytokine receptor binds ligand, subunits of the receptor become phosphorylated and can immediately be bound by a Src-family kinase. (more…)

Although it is commonly imagined that hematopoiesis takes place in a liquid environment resembling the blood, with progenitors responding mainly to soluble hormone-like cytokines, this is in fact not the case at all. It is much more accurate to think of the bone marrow as a solid tissue in which different types of hematopoietic cells develop in physically different locations. These microenvironments are visible in histologic sections of bone marrow, which reveal a patchwork of microscopic foci, each devoted to the production of a particular cell type (Figure bellow). The bone marrow microenvironment is set up and maintained by bone marrow stromal cells. Within each microenvironment, contact of cells with one another or with proteins and other substances that make up the extracellular matrix (ECM) greatly facilitates cell division and differentiation. (more…)

Normally present at very low levels in plasma, antibodies of the immunoglobulin E (IgE) isotype were first discovered in 1967, decades after the description of IgA, IgG, and IM. IgE antibodies are produced primarily by plasma cells in mucosal-associated lymphoid tissue and their levels are uniformly elevated in patients suffering from atopic conditions like allergic rhinitis, asthma and atopic dermatitis. Production of allergen-specific IgE in atopic individuals is driven both by a genetic predisposition to the synthesis of this isotype as well as by environmental factors, including chronic allergen exposure. (more…)

CD14 is part of the receptor complex for endotoxin, which is a component of tobacco smoke. The CD14 gene is located on chromosome 5q, a region previously demonstrated to be linked to asthma when stratified for smoke exposure. This study was designed to extend these findings by determining whether polymorphisms in the CD14 gene are related to this gene–environment interaction on asthma. Puerto Rican (n = 362 trios) and Mexican (n = 259 trios) families ascertained through a child with asthma were studied. (more…)

Asthma is characterized by Th2-dominant cytokine profiles. The risk of developing asthma is lower in children attending day care in the first year of life. Therefore, this study was conducted to assess the interaction between day-care attendance, T-cell cytokine profiles and atopic phenotypes in early childhood. Children (n = 208) in the Childhood Onset of Asthma (COAST) study were genotyped for 72 polymorphisms in 45 immune response genes. The COAST cohort was selected on the basis of a high risk of asthma. Measurements of IFN-y (Th1), IL-5 and IL-13 (Th2), and IL-10 (Treg) were made at birth and at age 1 year and the children were stratified by day-care attendance. Wheeze and atopic dermatitis phenotypes were documented in the first year. (more…)

This study sought to determine the influence of passive exposure to tobacco smoke during childhood on the results of genetic linkage analyses for asthma. A genome wide linkage screen for asthma and bronchial hyper responsiveness was performed in 200 families (containing 1183 individuals) from The Netherlands. A set of 266 polymorphic autosomal markers was used. Analyses were performed separately for the entire population and for the smoking exposed and non exposed families separately. (more…)

Asthma and allergic diseases are common in both children and adults. Their development depends on an interaction between asthma genetic and asthma environmental risk factors. Genetic manipulation in multi factorial diseases such as asthma is not feasible in the foreseeable future. However, theoretically, environmental exposures can be controlled in an attempt to stem the rising prevalence of these diseases (primary prevention). Environmental exposures may also influence the frequency of symptoms and the requirement for medication in those with established disease. (more…)