When dryness of the surface of the eye persists well after environmental, chemical, or other irritants have gone, you may be diagnosed with some form of dry eye disease (DED).<\/p>\n\n\n\n
We say \u201csome form\u201d because dry eye disease is an umbrella term encompassing several separate pathologies that can produce similar symptoms beyond the cardinal symptom of dryness. <\/p>\n\n\n\n
Even when dryness, irritation, and other potential symptoms of dry eye disease subside after the irritant is removed, that doesn\u2019t mean solutions aren\u2019t available – especially if the irritant is attached to the person\u2019s work and\/or environment.<\/p>\n\n\n\n
To better navigate the clinical (e.g., medicated eye drops and\/or other conditions involved) as well as the sub-clinical sides of this oversimplified eye health issue, it\u2019s best to start with a closer look at the science.<\/p>\n\n\n\n
With that foundation in place – as well as some prevalence statistics to show just how common dry eye disease is – we can better appreciate the causes, symptoms, and treatments of dry eye disease. <\/p>\n\n\n\n
As detailed by this academic article<\/a> published on StatPearls, dry eye disease is often classified as either \u201caqueous deficient\u201d (insufficient tear production) or \u201cevaporative\u201d (tears evaporate too rapidly), though many cases blur the lines between these two classifications.<\/p>\n\n\n\n Before we explore those terms in-depth, it\u2019s important to have a basic understanding of how the tear film of the eye works.<\/p>\n\n\n\n Like any other fluid matrix in the body, the thin film of fluid that covers the surface of the eye requires its \u201clayers\u201d (an oily lipid layer, the aqueous water layer, and mucin, a protein component of mucus) to stay in certain proportions with each other for proper lubrication of the eye to occur.<\/p>\n\n\n\n If, for reasons explored below, production of any of the layers falls outside of the norm required for a healthy balance – aka, homeostasis – then dry eye disease can occur.<\/p>\n\n\n\n This is a bit of an oversimplification, as outside elements introduced into an otherwise healthy tear film can also produce DED symptoms, but the point is to think of the tear film as a proprietary \u201cformula\u201d that needs to keep everything in proper ratios to function normally.<\/p>\n\n\n\n The StatPearls article referenced above describes a number of ways in which homeostasis of the tear film can be affected.<\/p>\n\n\n\n Keeping within the context of the well-established \u201caqueous deficient vs evaporative\u201d paradigm, the former often involves a lack of tear production as a result of damage or dysfunction of the lacrimal gland.<\/p>\n\n\n\n The lacrimal gland is what produces the aqueous layer of tears, which is the most substantial layer in terms of volume.<\/p>\n\n\n\n Physical obstruction of the gland, disease and drugs\/medications can all affect lacrimal gland function in this manner.<\/p>\n\n\n\n In the case of evaporative DED, tears are evaporating too quickly, which is most commonly associated with meibomian gland dysfunction. <\/p>\n\n\n\n The meibomian glands produce the oily lipid component of tears, which helps prevent their evaporation in normal circumstances.<\/p>\n\n\n\n Like the lacrimal gland, physical obstruction of the meibomian gland can impair its function, as well as atrophy (shrinking) and a few other causes to be discussed later. <\/p>\n\n\n\n Evaporative DED can also be caused by not blinking frequently enough and environmental irritants.<\/p>\n\n\n\n Finally, it\u2019s important to note that both of these cases are associated with an excess of sodium and glucose in the tear film, which is often referred to as hyperosmolarity.<\/p>\n\n\n\n Hyperosmolarity leeches fluid from surrounding tissues while prompting the immune system to respond (the redness, irritation components), both of which do not bode well for eye lubrication and overall health when this occurs in the tear film.<\/p>\n\n\n\n Factoring in the high potential for misdiagnosis as well as the proportion of DED sufferers who do not seek (official) treatment, most global estimates on DED incidence are extremely broad.<\/p>\n\n\n\n This finding<\/a> in Ophthalmic and Physiological Optics<\/em>, a journal of the British College of Ophthalmic Opticians, estimates the global prevalence of DED at 11.59% with a standard deviation of 0.04, bringing several illuminating trends out in the data.<\/p>\n\n\n\n For example, the prevalence was lowest in North America and highest in Africa, and DED symptoms are least reported during the fifth decade of life, \u201cincreasing linearly thereafter.\u201d <\/p>\n\n\n\n Using DED diagnostic criteria from TFOS DEWS II, a very large database compiled over two years by more than 150 clinical research experts, the authors of this study produced an estimate as high as 29.5% of the world\u2019s population. <\/p>\n\n\n\n Reiterating, when the same study produces estimates as drastically different as these, it\u2019s hard to even hazard a guess, but even speculating into the 20-30% range suggests that billions of people are experiencing some form of DED. <\/p>\n\n\n\nMechanisms of Tear Film Damage<\/h3>\n\n\n\n
DED Prevalence and Known Risk Factors <\/h2>\n\n\n\n
Global DED Prevalence<\/h3>\n\n\n\n