Aim: To describe and analyse the epidemiology and management of asthma, atopy and related morbidity in a Scottish Primary Care population by exploiting the Continuous Morbidity Recording database. Methods: The patient information used in this thesis was extracted from the computerised data of general practices contributing to the Continuous Morbidity Recording project. Results: A significant increase in the prescribing of short-acting beta2 (p<0.005) and adjunct therapy prescribing (p<0.001) occurred over the four study years. There was a significant shift to treatment steps 3 and 4 of the British Asthma Guidelines (p<0.002) in asthma patients followed up over the four study years. Significant declines in the incidence of asthma were observed in children (p<0.001), with no apparent compensatory diagnostic shift. There was a significant increase in the risk of presenting with a Th1 mediated autoimmune condition in patients with a history of allergic disease. There was a particularly strong association between current psoriasis and current eczema. Conclusions: The concurrence of morbidity and prescribing epidemiology with external sources of data such as surveys suggest high quality of data stored by the Continuous Morbidity Recording database. General practitioners prescribed higher doses of inhaled corticosteroids and more new adjunct therapies during the study period, possibly due to the impact of new British Asthma Guidelines completed in 1995 and published in 1997. The decrease in asthma prevalence suggests that the burden of this disease on general practitioner workload is in decline. The decrease of the incidence of asthma gives the first indication of either a permanent or temporary decline of this disease in Scotland after reported increasing prevalences over several decades. The new finding that Th1 and Th2 mediated diseases are significantly associated in a large general practice population supports the proposal that these diseases share risk factors that increase the propensity of the immune system to generate both Th1 and Th2-mediated inappropriate responses to non-pathological antigens.