with an IOP spike after exercise (such as seeing halos around lights), then check the IOP soon after the patient engages in a simulated activity that seems to induce ocular symptoms.

31.2.2  Smoking

Acutely after smoking cigarettes, IOP does not increase appreciably [32]. Glaucoma patients who smoke have been reported to have only slightly higher IOP than glaucoma patients who do not smoke [33]. Crosssectional and prospective studies on the relation between cigarette smoking and POAG are mixed but in the aggregate taken, these studies do not suggest that smoking increases the risk of glaucoma [34–37]. Nonetheless, there may be an indirect deleterious relation between cigarette smoking and glaucoma. One study found that cigarette smoking was associated with a reduced chance that people who are earmarked as glaucoma suspects during glaucoma screenings actually present for a free follow-up confirmatory exam [38]. The CIGTS found that among OAG patients randomized to the trabeculectomy first arm of the study, smokers had a higher IOP than their nonsmoking counterparts after 9 years of follow-up [39].

Apart from the fact that cigarette smoking clearly increases the risk of lung cancer, it is also linked to cataract [40] and age-related macular degeneration [41]. Overall, cigarette smoking increases the risk of loss of vision so all physicians should encourage people to quit smoking. Primary care providers are aware that there is strong evidence that engaging patients in smoking cessation programs generally improves health outcomes [42, 43].

31.2.3  Alcohol Consumption

Alcohol consumption causes a dose related reduction in IOP that can last several hours [25, 44–47]. The mechanism is not clear but may involve a temporary osmotic effect [45, 48]. Nonetheless, some studies suggest that regular consumers of alcohol have higher IOP than those who abstain from alcohol use [49–51]. Several observational studies of the relation between alcohol consumption and POAG have been performed with one

study finding an inverse relation [52], others finding no association [34, 35, 53, 54], while another supported the notion that alcohol consumption is positively associated with POAG [55]. Consuming one alcoholic drink per day may have some cardiovascular benefits [56, 57] but gastroenterologists recommend abstinence to prevent digestive diseases related to alcohol consumption [58]. Thus, it is important to dissuade the notion that drinking alcohol will reduce the risk of glaucoma as the preponderance of existing evidence suggests that drinking alcohol does not have any major relation to glaucoma.

31.2.4  Diet

Very little data on the relation between diet and glaucoma exists. Theoretically, diet could influence the glaucomatous process by altering IOP, changing optic nerve blood flow, or by effecting retinal ganglion cell apoptosis. There is considerable interest in dietary antioxidants because oxidative stress may induce damage to the outflow channel as well as the optic nerve (reviewed by Kumar and Agarwal [59]). In a large observational study of predominately Caucasian health professionals located throughout the United States, dietary intake was assessed using validated food frequency questionnaires in order to study the relation between antioxidant intake and POAG [60]. No strong relations were detected between dietary antioxidant intake and the development of POAG, although protective effects from novel antioxidants cannot be ruled out. For example, in another study involving the same health professional group, a statistically significant trend for a protective effect of tea consumption (which is high in bioflavonoid content) was noted [21]. Certainly more study is needed regarding antioxidant intake and glaucoma, as the discovery of novel antioxidants that may favorably alter the course of POAG would be most welcome. Nevertheless, at this time one cannot promote antioxidant intake as a strategy to prevent the development of POAG or slow its progression.

Kang et al. [61] proposed that dietary fats might influence IOP by altering the availability of endogenous n-6 polyunsaturated fatty acids, which serves as a precursor for prostaglandin F2a. Prostaglandin F2a lowers IOP by increasing uveoscleral outflow. Figure 31.2 depicts how the essential fatty acids (linoleic acid and linolenic acid) compete as substrate for ocular enzymes