Jule Klotter
Dry Eye Disease
Dry eye disease (DED), affecting up to 30% of the population, entails more than discomfort that can be relieved with eye drops. If untreated, DED can become a chronic, progressive condition that damages the cornea and leads to visual impairment and, possibly, blindness. Several factors can contribute to dry eye, including LASIK surgery, contact lens use, cosmetics, prescribed medications, and autoimmune disease. “Severe dry eye can be precipitated by several common autoimmune conditions [Sjögren’s syndrome, lupus, rheumatoid arthritis, and thyroid diseases] in which inflammation plays a key role,” explain Cynthia Matossian, MD, and colleagues. Women have a higher risk of DED (and autoimmune disease) than men.
The protective fluid that lubricates the eye’s cornea and creates a smooth, refractive surface, enhancing vision, consists of more than the salty solution that we call tears. The outermost layer contains lipids, secreted by Meibomian glands (MGs) that line the upper and lower eyelids. These lipids act as a seal that inhibits evaporation of the watery-mucin tears, produced by the lacrimal glands. Beneath the tears and directly covering the cornea is a mucous layer, produced by Goblet cells and conjunctival epithelial cells. DED symptoms occur with insufficient tear production from the lacrimal glands and/or with increased tear evaporation, due to MG dysfunction and insufficient production of the protective lipid layer. As damage occurs to the eye’s surface, inflammation ensues—leading to more damage.
Several prescribed medications can cause or aggravate dry eye, according to Matossian et al, including several antidepressants, antihistamines, antipsychotics, anxiolytics, and hormonal drugs. In addition, some topical eye medications contain active ingredients or preservatives that can destabilize the tear film, irritate the eye, and cause or aggravate DED. “The most widely used ocular administration preservative, BAK, has been shown to have cytotoxic and proinflammatory effects on the eye, and its detergent properties disrupt the tear film,” they write.
Prolonged digital screen use is another factor in DED. Regular, daily use of visual digital terminals has been associated with Meibomian gland dysfunction and goblet cell dysfunction. Moreover, in vitro studies indicate that some wavelengths of light emitted from the screens may cause corneal damage. Numerous studies have also shown that blinking frequency is significantly less during digital screen use (7±7 blinks per minute), compared to reading print (10±6; p = 0.001), and relaxed conditions (22±9; p<0.0001). People also have more incomplete blinks when using a computer screen (median 13.5%) compared to reading a book (median 5%). Blinking less and incomplete blinking means less of the protective lipid layer, more tear evaporation, and more symptoms.
Limiting screen time and using blinking exercises can help reduce DED symptoms. For every two hours of computer use, the American Academy of Ophthalmology and the American Optometric Association recommend taking a 15-minute break. Another suggestion is to focus on an object 20 feet away for 20 seconds after every 20 minutes of digital screen use. Performing a quick blinking exercise every 20 minutes during waking hours (gently close eyes for 2 seconds, open eyes, again gently close eyes for two seconds, followed by squeezing eyes closed for 2 seconds) reduced symptoms in 41 people with DED. Computer users have also reported some relief of DED symptoms by using a desk humidifier; dry air can exacerbate symptoms.
Nutrition, of course, also plays a role in tear film homeostasis—although advice regarding DED seems limited at this point. Matossian et al report that vitamin A and “sufficient intake of protein” are important. A 2016 by S.H. Bae and colleagues reported that vitamin D reduced eye surface inflammation, promoted tear secretion, and reduced tear instability in people with DED (Sci Rep. 2016;6:33083). Omega-3 fatty acids have also shown benefits in some studies. However, the 12-month Dry Eye Assessment and Management (DREAM) study and the follow-up extension study showed no significant difference in conjunctival staining, corneal staining, tear break-up time, or Schirmer test (for tear production) between the omega-3 group and control.
In addition to modifying digital screen use and nutrition, other suggestions for mitigating DED symptoms include warm eye compresses to improve Meibomian gland secretion, ophthalmic gels, used at night to maintain moisture, and twice-daily use of artificial tear replacement (while avoiding products with ingredients that can further irritate the eye).
Hussain M, et al. The Dry Eye Assessment and Management (DREAM) extension study – A randomized clinical trial of withdrawal of supplementation with omega-3 fatty acid in patients with dry eye disease (abstract). The Ocular Surface. January 2020; 18(1):47-55.
Matossian C, et al. Dry Eye Disease: Consideration for Women’s Health. J Women’s Health. 2019;28(4).
Mehra D, Galor A. Digital Screen Use and Dry Eye: A Review. Asia Pac J Ophthalmol (Phila). 2020;9:491-497.
Verjee, MA, Brissette AR, Starr CE. Dry Eye Disease: Early Recognition with Guidance on Management and Treatment for Primary Care Family Physicians. Ophthalmol Ther. 2020;9:877-888.
Tinnitus and Oxidative Stress
Oxidative stress is a major factor underlying the ringing, roaring, or other annoying (even debilitating) sounds that characterize tinnitus. Those sounds can cause sleep disorders, depression, and impair social cohesion and quality of life. Cochlear degeneration is the main cause of tinnitus. Oxidative stress is known to produce cochlear degeneration and changes in auditory hair cells and nerve fibers. As Celik and Koyuncu explain in their 2018 article, “The sensorineural epithelial tissues of the cochlea are more susceptible to deleterious effects caused by free radicals than other tissues of the body.”
Because of the known relationship between oxidative stress and tinnitus and because tinnitus patients have “higher plasma concentrations of oxidative stress biomarkers and lower antioxidant activity” than healthy people, a group of Greek researchers, led by Anna I. Petridou, decided to test the effects of supplementation on people with tinnitus. Their 2019 randomized, double-blind, placebo-controlled trial enrolled 70 people, between 25 and 75 years old. All participants had tinnitus in one or both ears for at least six months; the noise required at least 5 decibels of competing sound to mask it. Inclusion criteria also included a score of 4 or above on the Tinnitus Handicap Inventory (THI) questionnaire, which assesses the emotional and functional impacts of having tinnitus. Participants needed to have normal hearing or only moderate hearing loss. Exclusion criteria included Meniere’s disease, otosclerosis, several chronic conditions and use of tinnitus-inducing medication (e.g., aminoglycosides, chemotherapeutics, loop diuretics, high doses of aspirin or quinine).
Three participants (2 placebo group; 1 antioxidant group) discontinued the trial, due to unscheduled surgery; and four in the placebo group were lost to follow-up. Participants underwent a baseline assessment that included anthropometric, audiometric, and tinnitus psychoacoustic measures; tinnitus discomfort; psychological symptoms; physical activity; and dietary assessment as well as blood sample collection. Participants were re-assessed three months later, at study’s end.
The treatment group took a commercially available multivitamin-multimineral supplement (Lamberts), which included 500 mg of standardized grape seed extract once a day with a meal. Grape seed extract is a rich source of phenolic compounds, such as epicatechin, resveratrol and procyanidin oligomers; “many experimental studies have proven the protective effect of polyphenols against cisplatin-induced ototoxicity and cochlear hair cell damage after intense noise exposure.”
Participants in the treatment group also took one tablet of alpha-lipoic acid (300 mg) twice a day on an empty stomach. Animal and human studies show that alpha-lipoic acid protects against noise-induced hearing loss. The placebo group took three placebo pills with similar shape and color to the supplements, made by a local manufacturing pharmacy. An investigator, uninvolved in the study, packaged the supplements and the placebos in identical containers and bags and labeled each with a participant’s number.
At study’s end, only participants in the supplement group had a significant reduction in tinnitus loudness from baseline, reflected in lower minimum masking levels (p<0.001). The supplement group also had a mean reduction in the Tinnitus Handicap Inventory of 6 points (“considered clinically relevant”). Also, the supplement group, unlike the placebo group, displayed “a significant decrease in the auditory threshold at the frequencies of 250 Hz, 500 Hz, 1000 Hz, 2000 Hz and 6000 Hz”—that is, their hearing improved. Blood serum changes in total antioxidant capacity, superoxide dismutase, and oxidized LDL were insignificant.
The authors note that the commercial multivitamin and mineral supplement used in this study contained only 150 mg of vitamin C and only 100 mg (150 iu) of vitamin E (dl-alpha tocopherol acetate), but they did not want to use isolated nutrients: “…our hypothesis was that an antioxidant combination might be more effective compared with single nutrients, since various antioxidants have a synergistic/complementary activity.” Although the combination of vitamins, minerals, phytochemicals, and alpha lipoic acid reduced tinnitus intensity and patient discomfort, they would like to see further investigation on its possible effect on oxidative stress biomarkers.
Celik M, Koyuncu I. A Comprehensive Study of Oxidative Stress in Tinnitus Patients. Indian J Otolaryngol Head Neck Surg. Oct-Dec 2018;70(4):521-526.
Petridou Ai, et al. The Effect of Antioxidant Supplementation in Patients with Tinnitus and Normal Hearing or Hearing Loss: A Randomized, Double-Blind, Placebo Controlled Trial. Nutrients. December 12, 2019.
Coca’s Pulse Test for Allergens
Can the pulse rate be used to identify allergens? Arthur F. Coca, MD (1875-1960), found evidence that it did. Dr. Coca was the founder of the peer-reviewed Journal of Immunology and served as the journal’s first editor from 1916-1948.In addition to teaching at Cornell and Columbia University, he was medical director at Lederle Laboratories, a pharmaceutical company. Dr. Coca also held the title of Honorary President of the American Association of Immunologists from his retirement in 1949 until his death.
Coca first became aware of a connection between increased pulse rate and adverse reactions to foods and other allergens when his wife suffered a sudden attack of angina pectoris after receiving a morphine derivative. Instead of slowing down with the drug, her heart rate increased to over 180 beats a minute. Other episodes of tachycardia followed. She noticed that the attacks occurred after eating specific foods. Dr. Coca began using heart acceleration as a way to determine which foods were “injurious” and which were safe for her. As long as she refrained from eating the foods that caused heart rate acceleration, she remained pain free and was able to garden and do ordinary housework without becoming overtired. Moreover, conditions that had affected her for much of her life—migraines, colitis, attacks of dizziness and fainting, indigestion, and fatigue—disappeared.
Dr. Coca began investigating the use of pulse rate to identify and remove allergens from patients’ diets. He eventually wrote a book for medical colleagues, Familial Nonreaginic Food Allergy (1943). Some doctors, like Milo G. Meyer, followed his lead. Dr. Meyer, an internist, wrote an article about his experience with the pulse test, which was published in Annals of New York Academy of Sciences (December 1949). For the most part, however, Dr. Coca’s observations were censored and ignored. Patients urged him to write a book for nonmedical readers. The result, The Pulse Test (1956), is in public domain and available at www.soilandhealth.org. This 110-page manuscript explains how to conduct the pulse test and the benefits of avoiding foods that speed up the pulse, using patients’ experiences as examples.
The test consists of taking the pulse before rising (while in the recumbent position); just before each meal and three times, at 30-minute intervals after each meal (sitting or standing); and before retiring (sitting or standing). The same posture should be used for each count. Coca recommends that people begin the test while following their usual diet for five to seven days: “If the highest count is the same each day, and if it is not over 84, you are most likely not allergic, and the range of your pulse from the lowest count (usually before rising) to the highest will be not more than 16 beats—probably much less.”
Counts over 84 beats/minute indicate “food allergy.” Also, variation in the maximal count of more than two beats from day to day (ie, Monday 72, Tuesday 78, Wednesday 76, etc.) indicate an allergic reaction—if no infection is present. If the initial pulse test indicates an allergen is present, Coca explains how to identify the offender(s) by taking a day or two to test suspect allergens singly—eating a single food in small quantities at hourly intervals and taking the pulse at 30-minute intervals.
An array of conditions and symptoms disappeared in patients who refrained from consuming or using items that increased the pulse rate: gastrointestinal symptoms, such as constipation, indigestion, heartburn, abdominal and gallbladder pain, and colitis; recurrent headaches and migraines; hives; asthma; sinusitis; epilepsy; diabetes; heart pain (angina) and hypertension; fatigue; and emotional symptoms, such as nervousness, depression, and irritability. The symptoms returned when patients again consumed the offending foods.
I found Dr. Coca’s chapter on high blood pressure and allergens particularly interesting. As an example, he wrote about a 60-year-old woman whose blood pressure was 198/120. “Sixteen days after avoidance of her major food-allergens the pressure was 112/78.” When she resumed eating one of the allergens (wheat), the pressure gradually rose. She stopped eating wheat. Thirteen years later, her blood pressure was 124/70. He explained that part of the allergic reaction is a blockade of lymph vessels, producing internal pressure from edema. Compression of the kidneys was known to produce hypertension in animals. Coca postulated that “it is reasonable to surmise that allergy…produces [human hypertension] through the internal pressure of allergic edema affecting both kidneys.”
Like elimination diets, the pulse test, in Dr. Coca’s studies, found that wheat, cow’s milk, and egg are typical allergens. Cane sugar, coffee, orange, pineapple, banana, and white potato also are on Coca’s list. In addition, to foods, Coca found that some people were reacting to tobacco, aluminum cooking utensils, house dust, medicines, cosmetics, and paint fumes. The pulse test—for those with the ability and patience to follow Dr. Coca’s instructions—might provide quicker and more specific feedback about suspected foods than an elimination diet.
This column was first published in Townsend Letter (April 2021).
Published June 29, 2024
About the Author
Jule Klotter has a master’s in professional writing from the University of Southern California. She joined Townsend Letter’s staff in 1990. Over the years, she has written abstract articles for “Shorts” and many book reviews that provide information for busy practitioners. She became Townsend Letter’s editor near the end of 2016.