Stress has been linked to accelerated ageing and increased risk of disease. What does this mean for the health of your eyes, and could it stress floaters? We take a look at the science on stress and its implications on eye health.
Table of Contents
Introduction
Humans, being highly intelligent and social creatures, are particularly susceptible to feeling stressed. Some level of constant background stress has become the norm for many of us, with 7% of people in the UK saying they feel stressed every day.
A multitude of different challenges and pressures can cause psychological stress, with work and personal finances - universally experienced - have been identified as the major causes of stress..
While it is well known that stress can harm your physical wellbeing, the impact of stress on eye health is less commonly understood.
Some people who experience eye floaters - dark shapes that float around in your field of vision - have wondered whether stress contributes to floaters. This article aims to answer those questions and advise on how to reduce stress and eye damage - all backed by science.
What Happens to Your Body When You're Stressed?
Stress is an evolved response to danger intended to make you perform better when outmatched or out of your depth. The stress response prepares you for that danger, whether that be a sabretooth cat ready to pounce on your family, or your boss after you made a big mistake at work.
When the brain senses stressful situations like these, your brain activates the sympathetic nervous system (responsible for the ‘fight-or-flight’ response) and secretes the hormones adrenaline and cortisol, which increase breathing rate, pulse, and blood glucose.
Cortisol is longer-lasting than adrenaline and is responsible for prolonged stress. Cortisol redirects blood glucose from muscle to the brain so that high alertness can be maintained. However, this can lead to oversensitivity, which can cause sensory discomfort and make you misinterpret and overthink situations.
As a threat passes, cortisol levels decrease and you calm down. Or at least, that’s what should happen, but many people experience chronic stress where life stresses maintain cortisol secretion. It’s when stress is prolonged that it starts to impact your health.
Stress and Health
Chronic stress is not only psychologically unpleasant, but can be dangerous to your physical health. Several studies have linked prolonged life stress and chronic stress disorders such as PTSD to accelerated ageing. As such, chronic stress can increase the risk of age-related diseases such as cancer, cardiovascular, neurodegenerative diseases, and autoimmune diseases.
Studies have shown that chronic psychological stress causes the shortening of telomeres, which are structures at the ends of chromosomes which protect DNA from degradation.
Telomeres naturally shorten as you grow older and your cells divide, but chronic stress accelerates this process. Once telomeres are gone, cell lines ‘senesce’ i.e. stop dividing, meaning tissue growth is halted.
Some of these studies have linked telomere shortening to an increased production of reactive oxygen species (ROS). When in excess, these highly reactive chemicals can damage cells by reacting with cellular structures and DNA, a process termed oxidative stress.
They’re produced largely as a byproduct of respiration in the mitochondria (the ‘powerhouse of the cell’) and are kept under control by antioxidants in your body - they only become dangerous when antioxidants are outnumbered by ROS.
When cells sense a dangerous level of ROS, they undergo apoptosis i.e. they self-destruct. The cells of the eye are no exception, meaning ROS lead to tissue degradation and inflammation of the eye.
It’s unclear how psychological stress induces oxidative stress, but a correlation has been demonstrated by several studies. Cortisol increases global metabolic rate and provides fuel for respiration in the form of raised blood glucose, meaning your mitochondria are working overtime. It would make sense that this increases ROS production, but this link is yet to be demonstrated.
Some studies on socially isolated rats showed that psychological stress activates NOX proteins - enzymes which specifically catalyse the formation of ROS - and reduces levels of antioxidants produced by the rat’s body. A study on people with PTSD also found reduced antioxidants.
These studies suggest oxidative damage is an intentional part of the response to psychological stress that becomes harmful with chronic stress.
Does Stress Damage Your Eyes?
Short term stress is known to cause disturbances in your vision. Heightened senses and excess energy can make your eyes twitchy and eventually tired as the muscles become strained. Acute stress can even make your vision blurry. However, these symptoms are not permanent and should subside with your stress.
The oxidative damage caused by chronic stress, however, could cause long term problems. For example, oxidative stress to ocular surface tissues such as the cornea causes dry eye disease (DED), where the eye loses its moisture and becomes irritated.
Some studies have found a correlation between DED and psychological stress, although this doesn’t mean stress-induced ROS are the cause.
Behaviours associated with stress such as spending longer staring at screens or drinking and smoking can increase the likelihood of DED. Stress is associated with conditions such as depression and anxiety, the medication for which may increase the likelihood for DED. These explanations are more likely than stress-induced oxidative stress since DED correlates more strongly with pollutant, light and UV exposure, which themselves can induce oxidative stress.
Oxidative damage can cause other more serious eye conditions, such as glaucoma. Glaucoma is caused by damage to the optic nerve resulting from a build-up of pressure in the eye and can lead to irreversible blindness if left untreated. Oxidative damage to the trabecular meshwork can inhibit its role in draining fluid from the eye, resulting in pressure build-up which damages the optic nerve.
This is exacerbated by elevated ROS causing apoptosis of optic nerve cells. Increased oxidative stress as a result of chronic psychological stress might contribute to the development of glaucoma, although this is speculative and no direct correlation has been found.
However, the cortisol-induced increase in blood pressure does increase pressure inside the eye and sustained high blood pressure is a risk factor for glaucoma. There is even a correlation between anxiety and the progression rate of glaucoma. The risk of glaucoma also increases with age, meaning chronic stress could potentially increase glaucoma risk by accelerating ageing.
Age is a risk factor for several other eye conditions including macular degeneration and cataracts but there is currently no evidence linking stress to these conditions. Age-associated oxidative damage is not only caused by ROS produced by cells (endogenous); it can accumulate from constant exposure to light, UV radiation and pollutants over a lifetime (exogenous).
Exogenous ROS are not necessarily comparable to those related to endogenous ROS both in terms of quantity and target location. This means the endogenous ROS resulting from stress does not necessarily lead to increased risk of all age-associated eye conditions.
What Are Eye Floaters and Could They Relate to Stress?
A common eye condition associated with oxidative stress are floaters. Floaters are dark specky, stringy or cobweb-like shadows in your vision that move with your eyes. They are particularly visible when against a bright background such as the sky or a phone or laptop screen. Floaters are very common, with one study on phone users reporting around 76% of people experiencing floaters.
The main cause of floaters lies in the vitreous, a transparent gel that fills the eye. The vitreous is formed of a matrix of collagen (a protein) and hyaluronan (a carbohydrate). If collagen dissociates from hyaluronan, collagen fibres clump together, causing regions of the vitreous to liquify. Floaters arise when those collagen clumps pass our line of vision in the eye.
Floaters can be particularly noticeable when the vitreous separates from the retina at the back of the eye, a slow process which only becomes noticeable late into separation. The rear portion of the vitreous has a particularly dense collagen network that can suddenly become a distraction. Vitreo-retinal separation is associated with ageing and is not indicative of poor eye health.
However, studies on people suffering from floaters have demonstrated their negative impact on quality of life - one study found on average people would rather live 8.9 years without floaters than 10 years with. Correlations were found between vitreous degeneration and decreased contrast sensitivity (sensitivity to difference in brightness), as well as poorer quality of life.
When stressed, heightened sensitivity means floaters will become more visible in the short term. More importantly, there is a correlation between ageing, oxidative damage and the degeneration of the vitreous. The ROS resulting from elevated cortisol could potentially react with collagen fibres, causing them to dissociate from hyaluronan and crosslink with each other, producing floaters, although there are currently no attempts to study this link directly. Behaviours associated with stress, such as spending long hours working in front of a screen or a lack of sleep, can also lead to oxidative damage to the vitreous.
Because cortisol also raises blood glucose levels but inhibits its use by most of the body, stress can increase the risk of eye conditions for diabetics, such as diabetic retinopathy - diabetics should be more wary of blood sugar levels when stressed.
It’s important to remember that mild daily stresses are unlikely to produce any noticeable effect on your vision. The links described in this article between chronic stress and eye floaters are speculative, whilst connections between stress and risk of more serious diseases are well documented. Nevertheless, stress can be managed and it’s good to take measures to look after your eyes.
How to Manage Stress
1. Talking to people
Cortisol makes your brain hyperactive, and in isolation this can snowball into greater fears and worries. Social interaction helps vent and rationalise your thoughts, and releases neurotransmitters such as dopamine and oxytocin, which contribute to satisfaction and relaxation.
2. Exercise
When you’re stressed you have a lot of excess energy which can be expended more productively by exercising, which causes the release of endorphins - chemicals which uplift mood and calm you down.
3. Meditation and breathing exercises
Some people find meditation enables them to take control of their body when it is stressed, overriding that primitive instinct that would otherwise causing them to worry. Meditation also releases endorphins.
4. Stop taking stimulant drugs
Stop taking stimulant drugs. Drugs such as caffeine, nicotine and cocaine all share physiological effects with adrenaline and cortisol. Their effects compound with existing stress to make it more intense and harder to manage.
5. Seek a mental health professional
Conditions such as PTSD and anxiety can be managed with the help of a medical professional such as a therapist. Even if you don’t consider your stress extreme, if it at all prevents you from going about your day then it’s worth seeking a professional
How to Protect Your Eyes
Oxidative damage is a serious threat to your eyes and can be caused by more than just stress. Light and UV exposure throughout your lifetime produce ROS so oxidative damage accumulates over time. As you age, there is also a diminished presence of antioxidants in your eyes.
By incorporating naturally-occurring antioxidants into your diet you can counteract this process. The antioxidant lutein is found in leafy vegetables such as spinach, and anthocyanin can be found in berries and currants. Supplements containing antioxidants, such as TheiaBio Clearer, can be a convenient way of getting antioxidants into your body. For more information on natural sources of antioxidants, take a look at our blog on the topic.
Conclusion
Psychological stress has become an all-too familiar part of life in the modern world. We can easily become overwhelmed, fixed on minor issues or stretched too thin across many, feeling unable to shake that stressed feeling.
Experiencing stress over a prolonged period causes accelerated ageing through oxidative damage. This increases the risk of developing age-related diseases. Organs including the eye will deteriorate more rapidly. Stress might therefore increase the risk of developing eye floaters, although these pose comparatively less danger to your health than other age-related diseases.
It’s important to remember that studies examining chronic stress often observed individuals who had suffered for very extended periods of time. Psychological stress experienced from PTSD can last for several years. Stress more commonly experienced is manageable and less likely to cause disease. In any case, you certainly shouldn’t let the fear of stress-induced ageing stress you out further.
Academic References
Ramanathan R, Desrouleaux R. “Introduction: The Science of Stress.” The Yale Journal of Biology and Medicine 2022, 95,1 1–2.
Lightman SL, Birnie MT, Conway-Campbell BL: Dynamics of ACTH and Cortisol Secretion and Implications for Disease. Endocr Rev 2020, 41.
Yegorov YE, Poznyak AV, Nikiforov NG, Sobenin IA, Orekhov AN: The Link between Chronic Stress and Accelerated Aging. Biomedicines 2020, 8.
Schulz R, Beach SR: Caregiving as a risk factor for mortality: the Caregiver Health Effects Study. Jama 1999, 282:2215-2219.
Ohlin B, Nilsson PM, Nilsson JA, Berglund G: Chronic psychosocial stress predicts long-term cardiovascular morbidity and mortality in middle-aged men. Eur Heart J 2004, 25:867-873.
Dube SR, Fairweather D, Pearson WS, Felitti VJ, Anda RF, Croft JB: Cumulative childhood stress and autoimmune diseases in adults. Psychosom Med 2009, 71:243-250.
O'Donovan A, Tomiyama AJ, Lin J, Puterman E, Adler NE, Kemeny M, Wolkowitz OM, Blackburn EH, Epel ES: Stress appraisals and cellular aging: a key role for anticipatory threat in the relationship between psychological stress and telomere length. Brain Behav Immun 2012, 26:573-579.
Hayflick L, Moorhead PS: The serial cultivation of human diploid cell strains. Exp Cell Res 1961, 25:585-621.
Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, Cawthon RM: Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci U S A 2004, 101:17312-17315.
Salpea KD, Talmud PJ, Cooper JA, Maubaret CG, Stephens JW, Abelak K, Humphries SE: Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation. Atherosclerosis 2010, 209:42-50.
Hewitt G, Jurk D, Marques FD, Correia-Melo C, Hardy T, Gackowska A, Anderson R, Taschuk M, Mann J, Passos JF: Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nat Commun 2012, 3:708.
Wiseman H, Halliwell B: Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer. Biochem J 1996, 313 ( Pt 1):17-29.
Schiavone S, Jaquet V, Trabace L, Krause KH: Severe life stress and oxidative stress in the brain: from animal models to human pathology. Antioxid Redox Signal 2013, 18:1475-1490.
Schiavone S, Sorce S, Dubois-Dauphin M, Jaquet V, Colaianna M, Zotti M, Cuomo V, Trabace L, Krause KH: Involvement of NOX2 in the development of behavioral and pathologic alterations in isolated rats. Biol Psychiatry 2009, 66:384-392.
Djordjevic J, Djordjevic A, Adzic M, Radojcic MB: Chronic social isolation compromises the activity of both glutathione peroxidase and catalase in hippocampus of male wistar rats. Cell Mol Neurobiol 2010, 30:693-700.
Tylee DS, Chandler SD, Nievergelt CM, Liu X, Pazol J, Woelk CH, Lohr JB, Kremen WS, Baker DG, Glatt SJ, et al.: Blood-based gene-expression biomarkers of post-traumatic stress disorder among deployed marines: A pilot study. Psychoneuroendocrinology 2015, 51:472-494.
Seen S, Tong L: Dry eye disease and oxidative stress. Acta Ophthalmologica 2018, 96:e412-e420.
Yilmaz U, Gokler ME, Unsal A: Dry eye disease and depression-anxiety-stress: A hospital-based case control study in Turkey. Pak J Med Sci 2015, 31:626-631.
Na KS, Han K, Park YG, Na C, Joo CK: Depression, Stress, Quality of Life, and Dry Eye Disease in Korean Women: A Population-Based Study. Cornea 2015, 34:733-738.
Galor A, Feuer W, Lee DJ, Florez H, Faler AL, Zann KL, Perez VL: Depression, post-traumatic stress disorder, and dry eye syndrome: a study utilizing the national United States Veterans Affairs administrative database. Am J Ophthalmol 2012, 154:340-346.e342.
Li M, Gong L, Sun X, Chapin WJ: Anxiety and depression in patients with dry eye syndrome. Curr Eye Res 2011, 36:1-7.
Wang TJ, Wang IJ, Hu CC, Lin HC: Comorbidities of dry eye disease: a nationwide population-based study. Acta Ophthalmol 2012, 90:663-668.
Izzotti A, Bagnis A, Saccà SC: The role of oxidative stress in glaucoma. Mutat Res 2006, 612:105-114.
Abe RY, Silva TC, Dantas I, Curado SX, Madeira MS, de Sousa LB, Costa VP: Can Psychologic Stress Elevate Intraocular Pressure in Healthy Individuals? Ophthalmology Glaucoma 2020, 3:426-433.
Coleman AL, Miglior S: Risk factors for glaucoma onset and progression. Surv Ophthalmol 2008, 53 Suppl1:S3-10.
Shin DY, Jung KI, Park HYL, Park CK: The effect of anxiety and depression on progression of glaucoma. Sci Rep 2021, 11:1769.
Webb BF, Webb JR, Schroeder MC, North CS: Prevalence of vitreous floaters in a community sample of smartphone users. Int J Ophthalmol 2013, 6:402-405.
Milston R, Madigan MC, Sebag J: Vitreous floaters: Etiology, diagnostics, and management. Surv Ophthalmol 2016, 61:211-227.
Wagle AM, Lim W-Y, Yap T-P, Neelam K, Au Eong K-G: Utility Values Associated With Vitreous Floaters. American Journal of Ophthalmology 2011, 152:60-65.e61.
Mamou J, Wa CA, Yee KMP, Silverman RH, Ketterling JA, Sadun AA, Sebag J: Ultrasound-Based Quantification of Vitreous Floaters Correlates with Contrast Sensitivity and Quality of Life. Investigative Ophthalmology & Visual Science 2015, 56:1611-1617.
Nuzzi R, Marchese A, Gulino GR, Versino E, Ghigo D: Influence of posterior vitreous detachment and type of intraocular lens on lipid peroxidation in the human vitreous. Mol Vis 2015, 21:1106-1112.
Akiba J, Ueno N, Chakrabarti B: Mechanisms of photo-induced vitreous liquefaction. Curr Eye Res 1994, 13:505-512.
Bishop PN, Holmes DF, Kadler KE, McLeod D, Bos KJ: Age-related changes on the surface of vitreous collagen fibrils. Invest Ophthalmol Vis Sci 2004, 45:1041-1046.
Krach S, Paulus FM, Bodden M, Kircher T: The rewarding nature of social interactions. Front Behav Neurosci 2010, 4:22.
Harte JL, Eifert GH, Smith R: The effects of running and meditation on beta-endorphin, corticotropin-releasing hormone and cortisol in plasma, and on mood. Biol Psychol 1995, 40:251-265.
Sasaki M, Yuki K, Kurihara T, Miyake S, Noda K, Kobayashi S, Ishida S, Tsubota K, Ozawa Y: Biological role of lutein in the light-induced retinal degeneration. The Journal of Nutritional Biochemistry 2012, 23:423-429.
Khoo HE, Azlan A, Tang ST, Lim SM: Anthocyanidins and anthocyanins: colored pigments as food, pharmaceutical ingredients, and the potential health benefits. Food & Nutrition Research 2017, 61.