Asthma is a global health disease whose prevalence has increased significantly over the years . It has been postulated that this increase is due to changes in Western diet with reduction in saturated fat consumption and increased consumption of margarine and vegetable oils (omega-6 fatty acids) with an accompanying decrease in fish (omega-3 fatty acid) consumption [1, 2].
This chapter reviews the risk factors for asthma; its prevalence and geographical distribution; presents a brief summary of its development; health and economic costs; gives a brief description of dietary fatty acids; food sources of fatty acids; metabolism of fatty acids and the biologically plausible mechanism for an association between dietary fatty acids and asthma.
Asthma : a major global health burden
Asthma definition and risk factors
Asthma is a chronic inflammatory airway disorder characterised by varying episodes of airway obstruction, wheezing, chest tightness, cough, and shortness of breath which resolve spontaneously or in response to treatment .
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Several risk factors are implicated in the development of or in the worsening of asthma symptoms (Table 1.1). A recent focus of epidemiological research is on the role of diet as a risk factor for asthma [4-10].
Table 1.1 Risk factors for asthma
Prenatal risk factors
Maternal smoking in pregnancy
Prenatal maternal stress
Route of delivery(C-section)
Risk factors in childhood
Atopy and allergic sensitisation
Viral respiratory infections in infancy
Exposure to allergens(house dust mite , pet dander)
Risk factors for adult-onset asthma
Exposure to chemical irritants at workplace
Certain drug treatment (e.g. hormonal replacement therapy in women, use of non-steroidal anti-inflammatory drugs, beta-blockers)
Other triggers/exacerbating factors
Exposure to cold air
Maternal diet in pregnancy
Antibiotic use in pregnancy
Exposure to passive smoke
Low birth weight
Strenuous physical exercise
Extreme emotional arousal
Sources: references [3, 11-15]
Prevalence and geographical distribution
Over the past few decades, there has been a dramatic rise in the prevalence of asthma (Figure 1.1) and allergic diseases [13, 16, 17], though it seems that figures are now stabilising or showing a reversing trend in some countries [18, 19].
No single figure accurately describes overall prevalence as results of surveys differ by year and the specific population studied. However, it is estimated that about 300 million people worldwide are currently living with asthma . In the United Kingdom, about 5.4 million people are living with asthma . In 2005, the prevalence of asthma recorded in the Gedling primary care trust (now Nottinghamshire County PCT) was 6.8 % . Furthermore, there is a marked geographical variation in asthma distribution in adults and children (Figure 1.2) .
Figure 1.1 Changes in the prevalence of asthma over time
Changes in the prevalence of doctor-diagnosed asthma (A) and asthma symptoms (B) in adults and children over time.
Source: The Asthma Epidemic. New England Journal of Medicine 2006
Figure 1.2 Worldwide prevalence of clinical asthma
Source: The global burden of asthma: the executive summary of the GINA Dissemination Committee Report.
Overview of the immunopathogenesis of asthma
The commonest type of asthma is atopic asthma which develops in people with a family history of atopy . The basic pathogenic mechanism is a type-1 hypersensitivity reaction . Briefly, an initial sensitisation to environmental allergens leads to stimulation of type 2 helper (Th2) cells to produce chemical substances called interleukins (IL) ââ‚¬" mainly IL-4, IL-5, and IL-13 (Figure1.3). Interleukin 4 promotes the production of immunoglobulin E (IgE) by B-lymphocytes in blood. The Immunoglobulin E produced binds to mast cells and subsequently exposure of these IgE-coated mast cells to allergic particles generates chemical mediators (Table 1.2) within minutes to produce an immediate response characterised by narrowing of the airways, fluid in the lungs(from increased permeability of the blood vessels) and mucus production which are the foundation of asthma symptoms.
Figure 1.3 Summary of asthma pathogenesis
Source : Mechanisms of asthma 
Table 1.2 Effects of chemical mediators generated in response to an allergic trigger
IL-4 stimulates the production of IgE from B-cells
Always on Time
Marked to Standard
IL-5 leads to the activation of eosinophils
IL-13 stimulates the production of mucus which is reflected symptomatically by cough and phlegm production
Growth factors produce by mast cells stimulate the proliferation of smooth muscle in the small airways of the lung which narrows the airways(airway obstruction)
Leukotrienes C4,D4 and E4 cause constriction of the bronchi, increased vascular permeability and mucus production
Histamine causes spasm of the airway smooth muscle
Source: adapted from Mechanisms of asthma
Health and economic burden of asthma
There has been an increase hospital admissions for asthma in England over the past years with a 6% increase in the 1998-2008 period . Asthma is said to affect one individual in one in five households in the United Kingdom . In addition, over half of the people living with asthma in the UK have severe symptoms .In a primary care organisation seeing 330,000 people , it was estimated that 45,000 people will be treated for asthma, with 439 emergency hospital admissions and 8 deaths resulting from asthma yearly .
Asthma is not only common and sometimes severe condition , but is also expensive to treat . In 2004, the cost of asthma to the .By 2009, the cost of asthma to the NHS was estimated at about 1 billion pounds of which 6.1 million is spent on emergency hospital admissions .
1.2 Dietary fatty acids
1.2.1 Biochemistry of dietary fatty acids
Fatty acids are carboxylic acids (composed of methyl and carboxyl groups), which can be either saturated or unsaturated depending on the presence of double bonds. Fatty acids with a single double bond are termed monounsaturated fatty acids (MUFAs) while those with double bonds in their chains are termed polyunsaturated fatty acids (PUFAs). They can also be classified based on the length of their structural chain. In addition, different fatty acids exist within each group each with its own specific biochemical structure (Table 3).Two classes of essential fatty acids-omega 3 and omega-6 fatty acids- exist based on the location of their first double bond from the methyl end of the fatty acid chain .
Table 1.3 Common polyunsaturated fatty acids
Common name Short hand designation
Polyunsaturated fatty acids
Alpha linolenic acid 18:3n-3
Eicosapentaenoic acid 20:5n-3
Docosahexaenoic acid 22:6n-3
Linoleic acid 18:2n-6
Arachidonic acid 20:4n-6
Humans lack enzymes to synthesise these fatty acids and must obtain them from diet [31, 32].In addition, they lack the enzyme required to convert omega-6 to omega-3 (Figure 6) [31-33].
Figure 1.6 Conversion of n-6 fatty acids to n-3 fatty acids
Omega-6 FA CH3-CH2-CH2-CH2-CH2-CH=CH-...-COOH
Omega-3 FA CH3-CH2-CH=CH-CH2-CH=CH-...-COOH
*Omega-3 desaturase is absent in mammalian cells. It catalyses the introduction of a double bond into the third position from the methyl end of the chain to form omega-3 fatty acids.
1.2.2 Dietary sources of fatty acids
Dietary fatty acids are obtained from several food sources in varying amounts. The main sources of specific types of fatty acids in diet are oily fish such as tuna, salmon, sardines, and trout for omega-3 fatty acids ; corn , sunflower, safflower, and cottonseed oils for omega-6 fatty acids ; margarine for monounsaturated fatty acids , baked foods, snacks, partially hydrogenated vegetable oils and margarine for trans fatty acids ; and dairy products and meat for saturated fatty acids [34, 35].
In the National Diet and Nutrition Survey (NDNS) of British adults, the principal sources of total fats, trans fatty acids, saturated fatty acids, and cis-monounsaturated fatty acids in the diets of survey participants were cereals and related cereal products, milk& milk products, meat & meat products, fat spreads for bread or toast, and potatoes and savoury snacks (Figure 1.7) .
Figure 1.7 Sources of fat in the British diet
Source: British Nutrition Foundation: Healthy living-fats
1.2.3 Metabolism of omega-6 and omega-3 fatty acids
The metabolism of polyunsaturated fatty acids involves a series of desaturation and elongation reactions in which the same set of enzymes generate arachidonic acid from linoleic acid as well as eicosapentaenoic acid and docosahexaenoic acid from alpha-linolenic acid (Figure 1.7) .
Figure 1.7 Elongation and desaturation of omega-6 and omega-3 fatty acids
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Biological plausible mechanism of a relationship between dietary fatty acids and asthma
It is suggested that the mechanism by which fatty acids may lead to the development of allergic diseases is via eicosanoid production. Linoleic acid is a precursor of arachidonic acid; which itself is a major precursor of the eicosanoid family of chemical mediators (prostaglandins, leukotrienes, thromboxanes and related oxidised compounds) [40, 41]. Some of these substances stimulate the inflammatory processes in asthma and other allergic diseases. By contrast, omega-3 fatty acids compete with omega-6 fatty acids for enzymes required in their metabolic processes, and are converted into less inflammatory substances. More details of the experimental evidence on polyunsaturated fatty acids in allergic diseases have by extensively discussed by Simopoulos and Calder.