Some anti-depressant drugs are associated with an increased chance of developing cataracts, according to a new statistical study by researchers at the University of British Columbia, Vancouver Coastal Health Research Institute and McGill University.

The study, based on a database of more than 200,000 Quebec residents aged 65 and older, showed statistical relationships between a diagnosis of cataracts or cataract surgery and the class of drugs called selective serotonin reuptake inhibitors (SSRIs), as well as between cataracts and specific drugs within that class.

Published online in the journal Ophthalmology, the study does not prove causation but only reveals an association between the use of SSRIs and the development of cataracts. The study could not account for the possibility of smoking – which is a risk factor for cataracts – and additional population-based studies are needed to confirm these findings, the researchers say.

This study of statistical relationships is the first to establish a link between this class of drugs and cataracts in humans. Previous studies in animal models had demonstrated that SSRIs could increase the likelihood of developing the condition.

“When you look at the trade-offs of these drugs, the benefits of treating depression – which can be life-threatening – still outweigh the risk of developing cataracts, which are treatable and relatively benign,” says Dr. Mahyar Etminan, lead author of the article, a scientist and clinical pharmacist at the Centre for Clinical Epidemiology at Vancouver Coastal Health Research Institute and an assistant professor in the Dept. of Medicine at UBC.

Researchers found patients taking SSRIs were overall 15 per cent more likely to be diagnosed with cataracts or to have cataract surgery.

The degree of risk among specific and different types of SSRIs varied considerably. Taking fluvoxamine (Luvox) led to a 51 per cent higher chance of having cataract surgery, and venlafaxine (Effexor) carried a 34 per cent higher risk. No connection could be made between fluoxetine (Prozac), citalopram (Celexa), and sertraline (Zoloft) and having cataract surgery.

Co-author Dr. Frederick S. Mikelberg, professor and head of the Dept. of Ophthalmology and Visual Sciences at UBC and head of the Dept. of Ophthalmology at Vancouver General Hospital, notes that the average time to develop cataracts while taking SSRIs was almost two years.

“While these results are surprising, and might inform the choices of psychiatrists when prescribing SSRIs for their patients, they should not be cause for alarm among people taking these medications,” Mikelberg says.

Age-related macular degeneration (AMD) is a leading cause of severe vision loss among Americans ages 65 and over. Knowing your risk factors, being aware of your family history, and keeping regular appointments with your Eye M.D. can help reduce your risks for vision loss from macular degeneration. In its most severe form, known as wet AMD, the disease can lead to permanent loss of central vision which is essential for driving, reading, and recognizing faces.

March is AMD Awareness Month, and the American Academy of Ophthalmology, through its EyeSmart™ Campaign, encourages Americans to know their risks for AMD.

“The past few years have been marked by significant improvement in understanding the causes and the treatment of AMD,” says George Williams, MD, an AMD expert and Academy clinical correspondent. “New research and clinical advances are helping us to better treat both the “dry” AMD and “wet” forms of AMD. One strong risk factor that people may not be aware of is family history. It’s important to find out whether your relatives have had AMD, and to tell your Eye M.D., if you have a history of AMD in your family. Knowing your risks can save your sight.”

Here are the top 5 risk factors for AMD:

- Being over the age of 60
- Having a family history of AMD
- Cigarette smoking
- Obesity
- Hypertension

If you have any two of these risk factors, you should schedule an appointment with your Eye M.D for a complete evaluation. Your Eye M.D. may recommend certain preventive measures which can reduce your risk of vision loss from this disorder.

People who are at risk should know the symptoms of wet AMD, the form most likely to cause rapid and serious vision loss. These include sudden, noticeable loss or distortion of vision, such as seeing “wavy” lines. See an Eye M.D. right away if these symptoms occur. Current treatments for wet AMD provide an excellent chance of stopping vision loss and may actually restore some vision when macular degeneration develops. Earlier diagnosis of wet AMD gives a better chance of successful treatment.

There are some AMD risk factors that a person can change such as smoking and diet to reduce the risk of vision loss from AMD. Other risk factors such as genetic factors cannot be changed. However, knowing your family medical history is one way to learn whether you may be genetically predisposed to a disease. One way to reduce AMD risk is to quit smoking or never start. For patients at high risk for developing late-stage AMD, taking a dietary supplement of vitamin C, vitamin E and beta carotene, along with zinc, has been shown to lower the risk of AMD advancing to advanced stages by 25 percent. Patients should check with their Eye M.D. before starting any dietary supplement.

About AMD

The disease takes two forms, termed “dry” and “wet.”

- Early-stage AMD: Yellow deposits called “drusen” develop under the retina, the light-sensitive tissue at the back of the eye that focuses images and relays them to the optic nerve. At this stage, most people would do not have reduced vision.

- Intermediate AMD: Patients have more and larger drusen and more pigment changes in the macula (the part of the retina responsible for central vision); they are at higher risk for both advanced dry and wet AMD. The majority of those with intermediate AMD do not progress to an advanced stage, but should be followed by an Eye M.D. so they can be treated if needed.

- Advanced “dry” AMD: Patients with more advance dry AMD may have a blind spot in their central vision. Currently there is no proven therapy to restore vision lost from advanced dry AMD. Low-vision technologies, including improved lighting and magnification, help maintain their quality of life.

- Advanced “wet” AMD: In this stage, abnormal blood vessel form under the retina. These blood vessels can leak fluid or bleed and cause sudden and drastic loss of central vision.

Although only about 10 percent of the 10 to 15 million Americans with AMD have the “wet” form, it is responsible for most severe vision loss. New, highly effective treatments such as the injectable medications ranibizumab and bevacizumab are dramatically reducing damage from “wet” AMD and can stabilize vision in more than 90 percent of patients and actually improve vision in up to 30 to 40 percent of patients.

Surgeons from UC Davis Medical Center have demonstrated that artificial muscles can restore the ability of patients with facial paralysis to blink, a development that could benefit the thousands of people each year who no longer are able to close their eyelids due to combat-related injuries, stroke, nerve injury or facial surgery.

In addition, the technique, which uses a combination of electrode leads and silicon polymers, could be used to develop synthetic muscles to control other parts of the body. The new procedure is described in an article in the January-February issue of the Archives of Facial Plastic Surgery.

“This is the first-wave use of artificial muscle in any biological system,” said Travis Tollefson, a facial plastic surgeon in the UC Davis Department of Otolaryngology – Head and Neck Surgery. “But there are many ideas and concepts where this technology may play a role.”

In their study, Tollefson and his colleagues were seeking to develop the protocol and device design for human implantation of electroactive polymer artificial muscle (EPAM) to reproducibly create a long-lasting eyelid blink that will protect the eye and improve facial appearance. EPAM is an emerging technology that has the potential for use in rehabilitating facial movement in patients with paralysis. Electroactive polymers act like human muscles by expanding and contracting, based on variable voltage input levels.

For people with other types of paralysis, the use of artificial muscles could someday mean regaining the ability to smile or control the bladder. Reanimating faces is a natural first step in developing synthetic muscles to control other parts of the body, said UC Davis otolaryngologist Craig Senders.

“Facial muscles require relatively low forces, much less than required to move the fingers or flex an arm,” said Senders.

Blinking is an essential part of maintaining a healthy eye. The lid wipes the surface of the eye clean and spreads tears across the cornea. Without this lubrication, the eye is soon at risk of developing corneal ulcers that eventually can cause blindness.

Involuntary eye blinking is controlled by a cranial nerve. In most patients with permanent eyelid paralysis, this nerve has been injured due to an accident, stroke, or surgery to remove a facial tumor. Many have no other functioning nerves nearby that can be rerouted to close the eyelid. Others were born with Mobius syndrome, characterized by underdeveloped facial nerves. These patients are expressionless and can neither blink nor smile.

Eyelid paralysis currently is treated by one of two approaches. One is to transfer a muscle from the leg into face. However, this option requires six to10 hours of surgery, creates a second wound, and is not always suitable for elderly or medically fragile patients.

The other treatment involves suturing a small gold weight inside the eyelid. The weight closes the eye with the help of gravity. Though successful in more than 90 percent of patients, the resulting eye blink is slower than normal and cannot be synchronized with the opposite eye. Some patients also have difficulty keeping the weighted lid closed when lying down to sleep. In the United States, an estimated 3,000 to 5,000 patients undergo this surgery every year and therefore might benefit from an alternative treatment.

For their study, Senders and Tollefson used a novel alternative method for eyelid rehabilitation in permanent facial paralysis. They used an eyelid sling mechanism to create an eyelid blink when actuated by an artificial muscle. Using cadavers, the surgeons inserted a sling made of muscle fascia or implantable fabric around the eye. Small titanium screws secured the eyelid sling to the small bones of the eye. The sling was attached to a battery-operated artificial muscle. The artificial muscle device and battery were into a natural hollow or fossa at the temple to disguise its presence.

Senders and Tollefson found that the force and stroke required to close the eyelid with the sling were well within the attainable range of the artificial muscle. This capability may allow the creation of a realistic and functional eyelid blink that is symmetric and synchronous with the normal, functioning blink. A similar system also could give children born with facial paralysis a smile.

The three-layered artificial muscle was developed by engineers at SRI International of Palo Alto, Calif., in the 1990s. Inside is a piece of soft acrylic or silicon layered with carbon grease. When a current is applied, electrostatic attractions causes the outer layers to pull together and squash the soft center. This motion expands the artificial muscle. The muscle contracts when the charge is removed and flattens the shape of the sling, blinking the eye. When the charge is reactivated, the muscle relaxes and the soft center reverts back to its original shape.

“The amount of force and movement the artificial muscle generates is very similar to natural muscle,” Tollefson said. An implanted battery source similar to those used in cochlear implants would power the artificial muscle.

For patients who have one functioning eyelid, a sensor wire threaded over the normal eyelid could detect the natural blink impulse and fire the artificial muscle at the same time. Among patients lacking control of either eyelid, an electronic pacemaker similar to those used to regulate heartbeats could blink the eye at a steady rate, and be deactivated by a magnetic switch.

With Avatar now heading into its fifth week as a box office hit, many people are headed to movie theaters to see what the excitement over 3-D is all about. Unfortunately, many of them may be disappointed because they didn’t know they can’t see 3-D.

While the concept of being “3-D ready” means that the new 3-D TVs, showcased at the Consumer Electronics Show last week, will be able to provide 3-D viewing, the College of Optometrists in Vision Development state that our eyes need to be “3-D ready” to be able to fully enjoy Avatar. In other words, you need to be able to see 3-D for the entire 2 hours and 40 minutes of riveting 3-D action.

The 3-D version of Avatar has two images projected on the screen, each image seen by one eye. The images are then merged into one by your brain. If the images aren’t perceived correctly, it will be very difficult to merge or fuse the images into 3-D. The technology behind the Avatar 3-D effects is based on the premise that the viewer has the ability to see 3-D.

“There are a variety of vision problems which may cause intermittent problems, where you will see 3-D part of the time. This can definitely cause headaches or at the least make viewing very uncomfortable,” explained Dr. Bradley Habermehl, President of the College of Optometrists in Vision Development.

Research has shown that up to 56% of those 18 to 38 years of age have one or more problems with binocular vision and therefore could have difficulty seeing 3-D. In addition, about five percent of the population have amblyopia (lazy eye) and/or strabismus (eye turn) which makes 3-D viewing impossible.

But there is hope. Thanks to optometric vision therapy, thousands of people who previously could not see 3-D are enjoying every special effect Avatar has to offer. Dr. Susan R. Barry, professor of neurobiology in the Department of Biological Sciences at Mount Holyoke College, who lived most of her life stereoblind until she went through an optometric vision therapy program at the age of 48, shares, “I am happy to say I am no longer stereoblind. I can enjoy the 3-D effects in Avatar as well or more than anyone else. The scenes of the forest receding way into the distance and the seeds from the Tree of Life floating in front of the screen were fantastic.”

In fact, Barry’s life changed so dramatically by gaining 3-D vision that she wrote Fixing My Gaze (June, 2009), to share her experience with the world. In an interview published in Scientific American, From 2-D to 3-D Sight: How One Scientist Learned to See, Barry shares, “Seeing in 3-D provides a fundamentally different way of seeing and interpreting the world than seeing with one eye. When I began to see in stereo, it came as an enormous surprise and a great gift.”

Some people may have 3-D vision but feel nauseous or dizzy when watching Avatar. This can be caused by something known as visual motion hypersensitivity.

“People who have visual motion hypersensitivity, will find Avatar quite challenging to view,” according to Kenneth J. Ciuffreda, O.D., FCOVD-A, Ph.D., a professor at SUNY, State College of Optometry, Department of Vision Sciences in New York City, and leading research expert in binocular vision. Ciuffreda recently co-authored a paper on the topic of visual motion hypersensitivity (VMH) and one of the signs of VMH is feeling dizzy when watching a movie in the movie theater. And, this isn’t even a 3-D movie! Adding the third dimension can make viewing stressful for someone with VMH. (The reference for the paper is: Winkler Pa, Ciuffreda KJ. Ocular fixation, vestibular dysfunction, and visual motion hypersensitivity. Optometry 2009;80(9):502-512.)

As technology quickly advances to provide us with 3-D ready TVs so we can watch movies, like Avatar, in the comfort of our own home, there are still millions of people whose eyes are not 3-D ready. “It is our mission to educate the public on the fact that you can become 3-D ready. Optometric vision therapy has helped thousands of people across the world to be able to see 3-D; even those who have had multiple eye surgeries, such as Dr. Barry,” Habermehl states.

There’s more to the eye makeup that gave Queen Nefertiti and other ancient Egyptian royals those stupendous gazes and legendary beauty than meets the eye. Scientists in France are reporting that the alluring eye makeup also may have been used to help prevent or treat eye disease by doubling as an infection-fighter. Their findings are scheduled for the next (Jan. 15, 2010) issue of the American Chemical Society (ACS) semi-monthly journal, Analytical Chemistry.

Christian Amatore, Philippe Walter, and colleagues note that thousands of years ago the ancient Egyptians used lead-based substances as cosmetics, including an ingredient in black eye makeup. Some Egyptians believed that this makeup also had a “magical” role in which the ancient gods Horus and Ra would protect wearers against several illnesses. Until now, however, modern scientists largely dismissed that possibility, knowing that lead-based substances can be quite toxic.

In earlier research, the scientists analyzed 52 samples from ancient Egyptian makeup containers preserved in the Louvre museum in Paris. They identified four different lead-based substances in the makeup. In the new study, they found that the substances boosted production of nitric oxide by up to 240 per cent in cultured human skin cells. Modern scientists recognize nitric oxide as a key signalling agent in the body. Its roles include revving-up the immune system to help fight disease. Eye infections caused by bacteria can be a serious problem in tropical marshy areas such as the Nile area during floods, the scientists note. Therefore, the ancient Egyptians may have deliberately used these lead-based cosmetics to help prevent or treat eye disease, the researchers suggest, noting that two of the compounds do not occur naturally and must have been synthesized by ancient Egyptian “chemists.”

The full text of their paper is available here. An excerpt follows:

“The present data thus establish that the eyes of Egyptians bearing the black makeup were presumably prone to immediately resist a sudden bacterial contamination with extreme efficiency through the spontaneous action of their own immune cells. Indeed, it is well recognized today that in most tropical marshy areas, such as was the Nile area during floods, several bacterial infections are transmitted to humans following any accidental projection of contaminated water drops into one’s eye. These data fully support that Horus’ and Ra’s protection that ancient Egyptians associated with this makeup and particularly with its laurionite component was real and effective, despite the fact that its “magic” implications seemed a priori totally irreconcilable with our modern scientific views and contrast with our present understanding of the toxicity of lead ions. One cannot evidently go as far as to propose that laurionite was purposely introduced into the composition of the makeup because of any recognized antibacterial properties. Yet, one can presume that ancient Egyptian “chemists” recognized empirically that whenever this “white precipitate” was present in the makeup paste, their bearers were enjoying better health and thus decided to amplify this empirical protective function by specifically manufacturing laurionite. Many examples of such subtle observations and medical conclusions that would have a priori been surprising can be found even in our recent history. It is sufficient, for example, to think about the historical origin of penicillin, aspirin, or quinine. . . Anyway, whether or not the manufacture of these lead chlorides was deliberately connected to preventive health care by Egyptians, it is clear that such intentional production remains the first known example of a large scale chemical process. It is no wonder that “kemej,” the Egyptian word that referred to the Egyptian land and to the black earth of the Nile valley, was handed to us via the Greeks and then the Arabs to eventually coin our present ‘chemistry’.”

Researchers in the US believe they have discovered why light can make the pain of migraine worse, even in some blind people: they found photoreceptors in a part of the brain called the thalamus appear to process both light and pain, revealing for the first time that it is possible for neural pathways for pain and non-image-forming light sensitivity to converge.

The study was the work of senior author Dr Rami Burstein, an associate professor of anesthesia and neuroscience at Beth Israel Deaconess Medical Center and Harvard Medical School in Boston, Massachusetts, and colleagues, and appeared online in advance on 10 January in Nature Neuroscience.

Burstein told the media that up to 90 per cent of migraine sufferers experience photophobia, where light makes the migrane hurt more.

“We had no clue in the world where in the world light and pain talk to each other in the brain,” he said. “They have completely different pathways in the brain.”

But for light to make pain worse, the pathways have to converge somewhere, thought the researchers.

So first they studied 20 blind migraine sufferers, 6 of whom had no light perception at all, no functioning optic nerve, and experienced no photophobia.

The remaining 14 blind migraine sufferers could sense light and dark and also had photophobia. Burstein and colleagues wrote:

“We found that exacerbation of migraine headache by light is prevalent among blind individuals who maintain non-image-forming photoregulation in the face of massive rod/cone degeneration.”

Burstein said this suggested that the optic nerve is critical to photophobia, ie for the light to exarcebate the headache.

In the next stage of the study, the researchers studied neural pathways in rats.

With “single-unit recording and neural tract tracing” they found “dura-sensitive neurons in the posterior thalamus whose activity was distinctly modulated by light”.

The thalamus is the brain’s sensory switching center: it receives sensory signals from different parts of the body and redirects them to various sensory, motor and cognitive areas of the brain’s cortex.

The researchers wrote that the cell bodies and dendrites (filamentous fingers through which cells link up and pulse electrical signals to each other) of these “dura/light-sensitive neurons were apposed by axons originating from retinal ganglion cells (RGCs), predominantly from intrinsically photosensitive RGCs, the principal conduit of non-image-forming photoregulation”.

Burstein and colleagues proposed that these findings suggest:

“Photoregulation of migraine headache is exerted by a non-image-forming retinal pathway that modulates the activity of dura-sensitive thalamocortical neurons.”

Essentially, as they explained to the media, they had discovered a group of photoreceptors (known as melanopsin, a light sensitive pigment) projects onto neurons on the thalamus that also process pain signals.

Burstein said:

“We identified a new pathway in the brain that originates in the eye and goes to the brain areas where neurons are found that are active during migraine attacks.”

“The light can increase the electrical activity in neurons that are active to begin with,” he explained.

One expert said these findings should put to rest any suggestion that patients exaggerate their sensitivity to light; they are not whining or imagining their symptoms.

Dr Richard Lipton, director of the Montefiore Headache Center and professor of neurology and epidemiology at Albert Einstein College of Medicine in New York City, commented that:

“This provides an anatomic and physiological basis for a common experience — that light makes pain worse, not because you’re a whiner, but because there is an anatomic pathway that links the visual system to the pathway that produces head pain.” .

“”That odd bit of clinical symptomatology has a firm basis in brain science,” added Lipton, who was not an author of the study.

However, while the findings help us understand more about migraine and photophobia, they are unlikely to help migraine patients in the near future, said Dr Michael Palm, an assistant professor of neuroscience and experimental therapeutics and internal medicine at Texas A&M Health Science Center College of Medicine, College Station, and director of the Parkinson’s and Headache programs at Texas Brain and Spine Institute in Bryan.

“This gives us a little better insight as to the theory and mechanism behind migraine,” said Palm, who was also not an author of the study.

“We are making progress in understanding this phenomenon,” he added.

US researchers found that even after the age of 80, smoking increased a person’s risk of developing AMD, age-related macular degeneration, the leading cause of blindness among Americans aged 65 and over, suggesting it is never too late to give up the habit.

The study was the work of lead author Dr Anne Coleman, professor of ophthalmology at the Jules Stein Eye Institute at University of California, Los Angeles (UCLA), and colleagues, and is published in the January issue of the American Journal of Ophthalmology.

AMD causes a darkening and/or blurring of central vision, and prevents you from being able to read, drive and recognize people you know. It is a progressive degeneration of the macula, the centre of the retina, the part of the membrane inside the back of the eye that allows us to see fine details.

Advanced AMD with loss of vision affects about 1.75 million Americans: this figure is expected to rise to just under 3 million by 2020.

Smoking is the second most common risk factor for AMD: age is the first. Coleman and colleagues wanted to find out whether age was linked to the effect of smoking on AMD risk.

Coleman told the press that age was the strongest predictor for AMD, yet most of the research done on the disease only looked at people aged 75 and under.

“Our population was considerably older than those previously studied,” said Coleman.

“This research provides the first accurate snapshot of how smoking affects AMD risk later in life,” she added.

For the study, Coleman and her team compared the retinal photographs of nearly 2,000 women taken at age 78 and 83, looked for signs of AMD and then did logistical regression statistical tests to find out whether smoking affected the women’s risk of developing the disease.

The women were already taking part in a study called the Study of Osteoporotic Fractures, where 45 degree stereoscopic fundus retinal photographs were part of the observations taken at clinic follow ups in year 10 and 15 of the study.

They found that:

* Overall, the smokers had 11 per cent higher rates of AMD than the non-smokers of the same age.

* But among the over 80s, the smokers were 5.5 times more likely to develop AMD than the non-smokers.

The authors concluded that:

“The magnitude of the greater-than-additive effect of smoking on the age-adjusted risk of AMD reinforces recommendations to quit smoking even for older individuals.”

“The take-home message is that it’s never too late to quit smoking,” said Coleman.

“We found that even older people’s eyes will benefit from kicking the habit,” she added.

Speculating on the underlying biological reasons for this link, the authors said there is a theory that smoking increases AMD risk by reducing levels of antioxidants in the blood, changing the blood flow to the eyes and reducing the amount of pigmentation in the retina.

Dr Paul Sieving, director of the National Eye Institute, which funded the research with the National Institute on Aging, said this study gives:

“Yet another compelling reason to stop smoking and suggests that it is never too late to quit.”

Infants as young as one-month-old are prescribed contact lenses at pediatric eye surgery centers so their visual system will develop correctly. Infants may be fitted for contacts if they have had cataract surgery, need extremely high-strength prescription glasses, or have very different prescriptions for the two eyes.

According to Dr. Natalia Uribe, who directs the Contact Lens Program in The Vision Center at Childrens Hospital Los Angeles, “The brain’s visual system is not fully mature until about age eight. It is critical that infants and very young children with eye problems have their sight corrected so the visual pathway develops properly. Otherwise it may not be possible for them to enjoy normal vision as an adult.”

Dr. Uribe, an optometrist, said her clinic is growing and will treat more than 700 young patients this year, making it one of the largest centers in the nation. She said more infants are being diagnosed with major eye problems due to better screening and to the higher rate of survival among extremely preterm infants.

Premature infants are at risk for retinopathy of prematurity (ROP), a disease affecting the blood vessels feeding the retina and for other eye problems. Medical studies have shown that approximately 20 percent of all premature babies will develop some form of strabismus (crossed eyes), amblyopia (lazy eye) or serious refractive error (require glasses) by the time they are 3 years of age.

According to Dr. Uribe, “Many of the children I see have a medical condition that affects only one eye. Wearing glasses with one thick lens and one clear lens will not work on very young children. A properly fitted contact lens can produce near-normal vision — the images are the same size, clear and focused, and input equally from both eyes–spurring proper brain development.”

For example, if an infant is born with a congenital cataract, the lens inside the eye, which is used for focusing, is cloudy. Vision development in that eye is blocked, leading to amblyopia as the child grows.

When a cataract is surgically removed in an adult, it is usually replaced with a lens implant. Lens implant surgery does not work for very young children because their eyes are growing so rapidly. Contact lenses are the preferred choice because they can be refitted frequently and they provide more natural vision than lop-sided cataract glasses.

Contact lenses for young children run from $90 to $300 per lens depending on the prescription. Because of the huge changes that occur in the eye during a baby’s first year of life, children may require up to six different prescriptions. The lenses are considered medically necessary (vs. cosmetic use), so insurance generally covers at least some of the costs associated with them.

Dr. Uribe reports that parents are generally scared to insert the lenses at first, but quickly develop ways of coping. As the child grows, he/she often becomes responsible for his/her own lenses at age seven or eight.

“Although we often think of contact lenses as appropriate cosmetically for teenagers, they can also be a good alternative for school-age children who wear glasses and want to participate in sports or are subject to teasing,” said Dr. Uribe.

An estimated 3 million Americans have glaucoma, which can stealthily cause vision loss even before people realize they have the disease. People with diabetes face special risks from glaucoma. This January during Glaucoma Awareness Month, through its EyeSmart(TM) campaign, the American Academy of Ophthalmology in partnership with the American Glaucoma Society and the Glaucoma Research Foundation, remind Americans that knowing your glaucoma risks can save your sight and that people with diabetes need to be extra-vigilant.

“Only about half of the people who now have glaucoma are aware that they do,” said James Heltzer, MD, a glaucoma specialist in Bethesda, Maryland, and an Academy clinical correspondent. “To end blindness from glaucoma, we need millions more Americans to become aware of this disease and get eye exams in time. It’s even more important for people with diabetes.”

Both diabetes and glaucoma are leading causes of blindness. In their early stages these diseases often have few symptoms, so damage may occur before people know they need treatment. Several large studies suggest that people with diabetes are more likely to develop glaucoma, and other data shows that glaucoma patients who are diabetic are more likely to suffer vision damage. If caught early, diabetes and glaucoma can usually be managed and vision can be saved.

Luis Quinones, a painting contractor, learned he had diabetes when he was 46, about 10 years ago. He visits his Eye M.D. (ophthalmologist) regularly so any vision problems he might develop can be dealt with right away. A few years ago his doctor found that both of Luis’ eyes had high intraocular pressure (IOP), a key sign of glaucoma. A laser procedure followed by eye drop medications successfully reduced his IOP until last year, when Luis noticed blurry vision in his right eye and had painful headaches for the first time in his life.

“We tried different eye drops, but my problems didn’t get better,” Luis said. “My doctor sent me to Dr. Heltzer, a glaucoma expert, and he put in a small tube to help with fluid drainage. Now I can see well again, and the headaches are gone. I use one kind of eye drop in the morning and another in the evening.” Dr. Heltzer explained that Luis has neovascular glaucoma, a condition seen most often in people with diabetes. Fortunately it can now be treated with drainage implants, lasers and medications called VEFG inhibitors, so it is no longer necessarily a blinding condition.

An annual dilated eye exam can help prevent vision loss from glaucoma and other eye diseases in people with diabetes. To promote awareness the Academy, along with partners the American Society of Retina Specialists, the Macula Society and the Retina Society, has launched EyeSmart EyeCommitted, a social media campaign to encourage people with diabetes to pledge to get an eye exam every year. The EyeCommitted campaign includes an interactive application that:

* Encourages taking the EyeCommitted pledge to have an annual diabetic eye exam.

* Allows users to share the pledge and campaign information with friends and family.

* Features important diabetic eye disease information and a new video that tells the compelling stories of two patients with diabetic retinopathy.

* Allows users to post the application onto their preferred social media sites.

As the weather turns colder and the sunlight hours dwindle, more and more Americans flock to indoor tanning salons to get that much desired straight-from-the-beach bronze glow. In fact, nearly 30 million people in the United States tan in salons every year, most of them women between the ages of 16 and 49. But before you start baking under the lights, you might want to consider the numerous health risks associated with tanning bed use.

Let’s begin with infections. If the surface of the tanning bed isn’t cleaned properly or if the towels you use aren’t washed in hot water, you can get infections like pubic lice (crabs) and warts caused by the human papillomavirus, or HPV. Tanning beds and exposure to UV rays can have a detrimental effect on your immune system as well because it reduces the activity level of natural killer cells and T cells. UV exposure is also thought to promote the spread of skin-associated infections because the T cells are suppressed. Dr. Dawn Davis, a dermatologist at the Mayo Clinic, has seen plenty of infections from tanning beds. “It’s very dangerous,” she said. “I’ve seen people come to my office who’ve gotten severe burns and scarring from tanning beds and lots of infections.” The federal Centers for Disease Control and Prevention in Atlanta reports an estimated 700 emergency room visits per year are related to tanning salon exposure.

When you don’t use goggles in the tanning bed, your eyes can be severely burned by the intense ultraviolet (UV) rays. You can develop arc eye or flash burns, a painful ocular condition sometimes experienced by welders who fail to use adequate eye protection. UV rays can also cause cataracts and damage the retina of the eye. And every time you expose your skin to UV rays, you increase your risk for developing melanoma; the most deadly form of skin cancer because it spreads easily to other organs and bones through the blood or the lymph system.

One of the biggest risk factors for melanoma is persistent exposure to UV rays, one part of the spectrum of light that reaches the Earth from the sun. The longer ultraviolet rays (UVA), which penetrate deep into the skin, are responsible for tanning and are often associated with allergic reactions, such as a rash. Shorter rays (UVB) penetrate the top layers of skin and are responsible for sunburn. Tanning salons use fluorescent bulbs that emit both UVA and UVB radiation. The amount of UVA radiation emitted in a tanning bed is up to three times more intense than the UVA in natural sunlight, and the UVB intensity in tanning beds approaches that of bright sunlight. So it makes perfect sense that tanning devices, like the sun, would increase skin cancer risk.
“Although some people think that a tan gives them a ‘healthy’ glow, any tan is a sign of skin damage,” says Sharon Miller, M.S.E.E., a Food and Drug Administration (FDA) scientist and international expert on UV radiation and tanning. “A tan is the skin’s reaction to exposure to UV rays,” says Miller. “Recognizing exposure to the rays as an ‘insult,’ the skin acts in self-defense by producing more melanin, a pigment that darkens the skin. Over time, this damage will lead to prematurely aged skin and, in some cases, skin cancer.”

In a recent report from the International Agency for Research on Cancer (IARC), the cancer division of the World Health Organization, classified tanning beds that emit UV radiation as “carcinogenic to humans”—the agency’s highest cancer-risk category, which also includes radon gas, plutonium, radium, tobacco and the hepatitis B virus. Since 1992, the beds had been deemed “probably carcinogenic to humans.”

IARC’s conclusions were based on an analysis of 19 studies conducted over 25 years on indoor tanning and the risk for melanoma. The review found that people who begin using tanning beds before age 35 increase their risk of developing skin cancer 75 percent. Overall, the melanoma risk for anyone who has ever used a tanning bed goes up by 20 percent. Because the development of cancer is a long process that may take decades, IARC recommends banning commercial indoor tanning for those younger than 18 years to protect them from the increased risk for melanoma and other skin cancers. “Young people may not think they are vulnerable to skin cancer,” says Dr. Ron Kaczmarek, and FDA epidemiologist who analyzed the report. “They have difficulty thinking about their own mortality.”

Since 2003, UV radiation from any source has been listed by the U.S. National Toxicology Program as a known carcinogen (cancer-causing substance). Currently, many government agencies caution against tanning. Yet of the more than 68,000 people in the United States who will learn they have melanoma this year and one out of eight will die from it, according to NCI estimates. In addition, the American Academy of Dermatology reports that melanoma is the second most common cancer in women 20 to 29 years old.

The bottom line is that long-term exposure to UV rays, whether from the sun or a tanning bed, increases the risk of developing skin cancer. However, there are alternatives. Instead of using a tanning bed, the American Cancer Society advises people to use sunless self-tanning creams, lotions or sprays along with regular skin checks by your doctor or dermatologist. Dr. Ellen Marmur, chief of the division of dermatologic and cosmetic surgery at Mount Sinai Medical Center suggests, “Go for a 10-minute walk three times a week or eat salmon or tuna or eggs or fortified cereal. You don’t need to use a dangerous habit like a tanning booth.” Marmur, like most other dermatologists, says the message of the IARC report is clear: “What I’m really hoping for is that people will opt out of using tanning beds.”