LASIK Eye Surgery
RealAge.com, October 18, 2010, by Mehmet Oz MD, Michael Roizen MD — At certain points in your life, it’s important to have your eyes examined by an eye care professional — even if your eyes feel fine and there doesn’t seem to be a cause for concern. Some eye diseases are virtually symptomless until you start to lose vision. So regular vision screening can help you address problems before they become major issues.
Here’s what the American Academy of Ophthalmology (AAO) recommends for each stage of life:
Baby and Toddler Time: It’s easy for vision problems to go undetected in very young children, so their eyes should be examined by a pediatrician during regular checkups. Once a child turns 3 years old, she can have her vision tested, too. And always alert the doctor if you notice any abnormalities, like droopy eyelids, crossed eyes, or a lazy eye.
Childhood and Teenage Years: Kids and teenagers between the ages of 3 and 19 should have their eyes checked by the family doctor at least once every 2 years during regular checkups. (Learn more about kids’ vision and eye health.)
Young Adult Era: Aim to get at least one complete eye exam between the ages of 20 and 29, and at least two complete screenings between the ages of 30 and 39.
Forty-Plus Period: All adults should get a baseline screening for eye disease by age 40, regardless of whether any symptoms or risk factors for eye problems are present. The AAO chose this age because it represents the time when age-related changes in vision and the earliest signs of eye diseases can be detected. Super important because catching and treating problems like glaucoma, cataracts, and diabetic retinopathy early can help minimize vision loss. And because the eyes can be a window into overall health, a thorough eye exam may also unearth other problems that can rear up at this age, such as diabetes and high blood pressure. How often you get follow-up screenings will depend on your test results, medical conditions, and other factors, such as your eye-health history.
Seniors and Beyond: Seniors 65 and older should have their eyes examined every 1 to 2 years to screen for common later-in-life vision problems like cataracts, glaucoma, diabetic retinopathy, and age-related macular degeneration. Regardless of when your next scheduled appointment is, always promptly see your eye doctor if you experience any eye pain or changes in your vision, see spots or flashes of light, or suffer from chronically dry or irritated eyes.
What Works for You?
These screening intervals won’t apply to everyone. If you’ve had any eye problems in the past, your doctor will probably want to check you more frequently. And certain risk factors for eye disease — such as high blood pressure, diabetes, or a family history of eye problems — typically mean more frequent screening as well. So work with your eye care professional to determine the screening schedule that’s right for you.
And if you wear glasses or contacts, you’ll need your vision tested at regular intervals, too.
Visian ICL: High Definition Intraocular Contact Lens
AMD: Illuminating a Blinding Mystery
You get old, and it may get you. “It” is age-related macular degeneration (AMD), a strange disease that’s the leading cause of blindness among those 60 and older. Macular degeneration destroys the macula, the site of fine-grained central vision. Patients with a bad case of AMD cannot recognize faces. They cannot read the Why Files or drive.
Signs of this common and essentially untreatable disease appear among 30 percent of Americans over 70 — about 14 million people. Up to 5 percent of these people will get the more severe, “wet, or exudative” version of AMD – which causes blindness in the center of vision.
Both forms of the disease will only grow more prevalent as the population grays. By 2025, AMD could be blinding 900,000 to 3 million Americans — unless someone can unravel the cause and learn to prevent or treat it.
Right now, only a charlatan can claim to fully understand AMD. Despite considerable progress in recent years, the views of cause, prevention or treatment are rather primitive. About the only “medicine” for the early stage is a vitamin cocktail that seem associated with reduced symptoms. Recently, a large multi-centered clinical trial sponsored by the National Eye Institute did show that vitamins can reduce the risk of severe vision loss by 25 percent in some patients with AMD. They are, in other words, slightly better than a shot in the dark.
Treatment for the blinding “wet” variety of AMD — where new blood vessels grow under the retina and leak fluid that kills light-sensitive cells — has been, until recently, even less promising.
AMD is a mysterious disease, and even its name is misleading, since the cell death can spread beyond the macula at the center of the retina. New studies indicate that the rods, which see in black-and-white toward the periphery, start to decline early in the disease, damaging night vision.
The good news is that in the past few years, researchers have uncovered major new clues that could, with luck, lead to real understanding and real treatments for AMD. The Why Files explored the subject at a September conference sponsored by the non-profit Research to Prevent Blindness.
A glance at the basics
AMD comes in two varieties:
Dry AMD starts with the appearance of drusen (fat deposits) under the retina. Cell deaths occur in the retinal pigment epithelium, an essential support structure for the retina, and in the rods and cones, which detect light. While dry AMD may only blur the vision, each year a few percent of cases convert to the dreaded “wet” form.
Wet AMD starts when new blood vessels rapidly appear in the back of the eye, under the retina. These immature blood vessels release toxic molecules. Scar tissue tears the retina from its supports, and blindness results where rods and cones die. Each year, a person blinded with wet AMD in one eye has a 15 percent chance of going blind in the other eye.
We’ve described a general picture of damage inside the eye, but today, prevention and treatment are hobbled by a wobbly understanding of what’s really taking place. Beyond vitamin cocktails, the best an ophthalmologist can recommend for dry AMD is watching and waiting. If your vision seems to be slipping away, that’s less than satisfactory.
The options for wet AMD – which may destroy vision in just weeks — are even less comforting. Doctors can zap the new blood vessels with a hot laser, hoping to cook them and block the flow of blood. A new and improved option is “photo-dynamic therapy,” in which a laser activates a light-sensitive dye in the blood, causing a toxic reaction that closes new blood vessels.
Needed – some understanding
Most eye doctors would agree that treatments for wet AMD are desperate measures. Hot lasers burn blind spots in the retina, causing black holes in the critical central vision. Hot lasers and photo-dynamic therapy may only temporarily close the actual leak. And in a few weeks, a regrowth of blood vessels may require more treatments, more cost, and, worst of all, the possibility of more retinal damage.
“For the majority of patients, what we have right now is better than nothing,” says AMD researcher Karl Csaky of the National Eye Institute, “but it’s not much better.”
After years of floundering in the dark, however, scientists have begun using new scientific techniques to gain a sharper picture of the disease process. The new theories about why and where the blood vessel form could lead to major advances in treatment, and perhaps more important, in preventing this blinding disease.
“If you look at what’s in clinical trials, and in phase I [early-stage] trials, and in the lab, there is a lot coming down the road” in potential AMD treatments, says Csaky.
For example, a study announced as we go to press indicates that the drug RhuFab V2 restored significant vision to wet AMD patients, in a 64-patient trial (see “New Drugs Show…” in the bibliography). After the three-month trial, the average patient could see two lines further down on a vision test, while the untreated controls lost one line. The genetically engineered drug, made by Genentech, must pass further tests before approval.
A major fringe benefit of improved treatment for AMD would be a better understanding of diabetic retinopathy, the leading cause of blindness among the middle-aged. Although it’s caused by the excess blood sugar of diabetes, this blinding illness also features the growth of leaky blood vessels.
But let’s return to our starting point. With any luck, before you get old, research doctors will have painted a better picture of why macular degeneration starts, and how it can be stopped. This is not something most retina specialists would have predicted 10 or even five years ago.
Inflammatory words? What’s the immune system got to do with AMD?
Meet the savage macrophage
Why do things go so tragically awry in age-related macular degeneration? Could the light-sensitive neurons be destroyed as a result of an immune system run amok? Five years ago, AMD was not considered an inflammatory disease. The illness did not, for example, start with an immune response, unlike such inflammatory diseases as rheumatoid arthritis and juvenile diabetes.
Now, however, it seems that early in AMD, an activation of the immune system sets the stage for a self-destructive process that eventually kills the photoreceptor (light-sensitive) cells. The apparent role for the immune system in AMD follows closely the realization that inflammation plays a key role in such other age-related woes as Alzheimer’s disease and atherosclerosis.
Under the old view of atherosclerosis, fat simply accumulated in the arteries until it broke off and formed a clot. The new view involves inflammation. “We now know that the lipid [fat] sticks to the vessel wall, but it’s not toxic until a macrophage [a kind of immune cell] ingests it and becomes activated and releases growth factors,” says Scott Cousins, who researches AMD at the Bascom Palmer Eye Institute at the University of Miami. “Atherosclerosis is now considered an inflammatory disease, it’s not simply a result of cholesterol.”
Meet the macrophages
Macrophages (loosely speaking, the name means “big-mouth”) are large white-blood cells that are central to many immune processes. Macrophages may come in several flavors, depending on what genetic program they happen to be running.
Scavenging macrophage simply eat up cellular debris. They’re as necessary as a vacuum cleaner, but considerably less obnoxious.
Reparative macrophages are partly activated. They release growth hormones and factors that cause blood vessel growth, but are implicated in athersclerosis and rheumatoid arthritis.
Activated macrophages release a mess of growth factors and nasties like tumor necrosis factor, a cell-whacking molecule that we’d liken to Arnold Schwarzenegger — a useful ally, perhaps — but dangerous in the wrong circumstances.
Drusen and other retinal changes signify the presence of dry AMD. Courtesy New England Eye Center, Boston, MA
A second component of AMD is the drusen, an abnormal deposit found under the retina at the start of the disease. Each morning, the bottom 10 percent of each rod and cone drops away, having become exhausted from converting photons of light into nerve signals.
See the trash strike
Each day, a typical RPE cell (that’s the retinal pigment epithelium – jargon we would love to avoid…) gobbles about 20,000 chunks of rods and cones. But if RPE cells tire with age (sound familiar?), trash removal breaks down, leaving drusen — the dregs of unprocessed rods and cones. As Martin Friedlander, chief of the retina service at the Scripps Research Institute, puts it, “When the garbage system quits, the city starts smelling.”
Cousins says this accumulation of garbage — the drusen — are probably the first stimulus of the inflammatory response in AMD.
Cousins, who says some scientists have been pointing to a role for macrophages in AMD for 15 years, says new images of eyes with AMD show macrophages linking to drusen. They may be trying to digest the drusen, or stimulating an inflammation, or both. (Kinda reminds us of dumpster-diving immune cells gobbling sub-retinal trash).
By the time wet AMD appears, Cousins adds, the inflammation is obvious, since lab studies show “abundant macrophages, releasing scarring factor and other chemicals.” Furthermore, when Cousins experimentally damages the eye of a research animal with a laser, he can watch new blood vessels being created, and macrophages “crawling into the retina.”
A classic example of the inflammation conflagration. When normal tissue is damaged or injured, a cascade of immune cells come to the rescue. National Institute of General Medical Sciences.
“Macrophages are an important contributor to neovascular formation,” he says, using jargon for the formation of new blood vessels. In other words, macrophages seem to be releasing chemicals that stimulate growth of new blood vessels, a process (forgive yet more jargon) that’s called angiogenesis.
But macrophages aren’t always harmful – they also play that essential “sanitation-worker” role in removing cellular trash. Why don’t these macrophage simply eat and run, without releasing a nasty chemical soup? Why, in other words, are they so excited? There are many possibilities, including genetic predisposition or the after-effects of a long-ago infection. When the Cousins lab checked for antibodies to various infective agents, they found that more people with wet AMD had been exposed to cytomegalovirus, which infects the young and lingers, dormant, for decades.
These data are preliminary.
Foreseeing a treatment?
The research focus on angiogenesis and immune responses have been transformed into a frantic search for a treatment. If the immune system is freaking out, it’s tempting to put it out of business. But it may be dangerous “to start mucking around with the immune system,” says ophthalmologist Martin Friedlander. While some studies indicate that steroid hormones treatment may slow wet AMD, “If I take someone with [new blood vessels under the retina] and bash them with prednisone [a steroid with major side effects], we can get the blood vessels to shrink.”
But the side effects of long-term prednisone treatment, he says, are often unacceptable. We don’t need to stress that the immune system also protects against trivialities like cancer and infection – key risks after heart transplants, when strong immune-regulating drugs are used to protect the new heart from the immune system.
The inflammatory hypothesis, previously discussed, remains a hypothesis: AMD may also result from damage by free radicals or ultraviolet radiation, or a shortage of blood flow. Still, inflammation is a key possibility, says Friedlander. “It’s easy to imagine that, due to aging changes, you begin to accumulate debris” under the retina. Whatever the trigger, he adds, “the end result is that you get atrophy of the RPE [retinal pigment epithelium], dysfunction of associated photoreceptors … and abnormal angiogenesis [new blood vessels]. That’s when the disaster happens.”
However, while it’s nice to try to interfere with the start of a disease, for diseases that have many separate triggers, it may be better to block the “final common pathway” that actually destroys tissue. In AMD (and diabetic retinopathy), that would mean blocking angiogenesis.
Not wanted: New blood vessels
Drug companies, which think the market for anti-angiogenic drugs in eye care alone could total $4-billion to $6-billion, are rapidly putting today’s improved understanding of the formation of blood vessels into clinical trials. Here are some examples.
New blood vessels form from endothelial cells, which use adhesion (sticky) molecules to move around. Blocking an integrin (one type of adhesion molecule) causes endothelial cells to commit suicide. In an animal experiment, the blocking agent interfered with angiogenesis in the retina, Friedlander says.
Endothelial-cell movement also needs protein-dissolving enzymes. Several drug companies are trying to block the protein-dissolving (jargon red alert!) matrix metalloproteinases (some experiments, however, have been stopped by side effects).
It may be possible to stop angiogenesis with smart, targeted drugs like anecortave acetate, which slowed the decline of vision in a 6-month test. “It has no side effects, is administered locally, and is devoid of the glucocorticoid activity,” says Friedlander, “where you retain water, get heavy, maybe get psychotic, all the things you don’t want to do with an 80- or 90-year-old” who is a typical AMD patient.
Another tactic would be to force the leaky, immature blood vessels to grow up. Friedlander says that experiments have shown that adult stem cells, derived from bone marrow, can be incorporated into retinal vasculature, where they apparently cause it to stop leaking.
Drug companies are testing vascular endothelial growth factor (VEGF), which plays a key role in the formation of sub-retinal blood vessels. At least two VEGF inhibitors are now being tested in clinics.
It all looks so promising that we almost forgot to mention that many promising medical developments are skewered by too little effect, or too many side effects. For example, Jayakrishna Ambati, an assistant professor of ophthalmology at the University of Kentucky, says that while the idea of blocking growth factors seems more sophisticated than zapping blood vessel with a laser, it’s “very simplistic to say, ‘Let’s block VEGF.'” For one thing, because normal blood vessels need the growth factor to keep calm, “It’s not going to be a magic bullet that will target only bad vessels.”
Far better, says Ambati, to “affect upstream events.” Rather than try to plug Niagara Falls, he’d rather block the tributaries to the Niagara River before it reaches the Falls.
Still, as ophthalmologists debate the best strategy to prevent, block or reverse AMD, one fact is clear. For the first time in history, it’s a good time to be an AMD specialist. For the first time, it’s possible to hold out hope for patients. “There’s optimism in the field, yes,” says Friedlander. “There’s excitement. Now we have our chance in the clinic.”
About the Authors
Michael F. Roizen, MD, is cofounder of RealAge, chief wellness officer at the Cleveland Clinic, and chairman of the RealAge Scientific Advisory Board.
Mehmet C. Oz, MD, is a member of the RealAge Scientific Advisory Board and vice chairman of cardiovascular services, Department of Surgery, Columbia University Medical Center.
An old prescription for revving up your immunity, an apple a day, really can help you.
Studies have revealed that pectin, a special kind of fiber found in apples, may help boost levels of immune-supportive proteins. So crunching one a day could very well help keep the doctor away this cold season.
Apples aren’t the only source of pectin. You’ll find it in pears, citrus, and other fruit, too. And in a recent animal study, this soluble fiber helped increase levels of interleukin-4, a compound that stimulates production of infection-fighting mast cells. And as a result, munching on pectin weakened illness severity and duration in the test subjects.
Sweet, Creamy, Steamy, Crunchy
Oranges, yogurt, tea, and pumpkin seeds are the order of the day when it comes to giving your immune system a treat, according to RealAge experts Michael Roizen, MD, and Mehmet Oz, MD, authors of the best-selling (and now newly expanded and updated) YOU: The Owner’s Manual. Here’s how these four superfoods help:
- Oranges are chock-full of vitamin C, an antioxidant vitamin that helps your immune system fend off disease-causing invaders. Other good C options: bell peppers, strawberries, cantaloupe, and broccoli. Or take 400 milligrams of vitamin C three times daily.
- Yogurt (unpasteurized) contains Lactobacillus acidophilus — a healthy bacterium that helps thwart fungus-related infections. Or take a 20-milligram acidophilus supplement twice daily.
- Tea is full of flavonoids, powerful vitamin-like substances that reduce immune-system aging. You’ll also find them in oats, onions, broccoli, tomatoes, apples, and berries.
- Pumpkin seeds are great year round, not just at Halloween, because they contain zinc — a nutrient that’s been shown to help reduce the average length of the common cold.
A Good Support System
One catch, though: Soluble fiber wasn’t a quick fix. It took about 6 weeks of daily soluble fiber doses to get results. The authors of the study suggest that aiming for 25 to 38 grams of total fiber per day — both soluble and insoluble — would be a good immune-supportive goal. So have an apple a day, but add some whole-grain oatmeal, oranges, and beans to your day, too. Plus exercise
Q & A: What’s Best: Fish Oil or Flaxseed Benefits?
Q – Can I get the same heart-health benefits from flaxseeds as I do from fish oil?
— Cynthia, Port Jervis, NY
A – Nope. Fish oil has got it all over flaxseeds in terms of DHA and EPA omega-3s, the ones that studies have shown make blood platelets less sticky, reducing the risk of blood clots that can cause a heart attack or stroke, and also help lower your blood pressure and triglyceride level. That’s because flaxseeds, unlike fish oil, are indirect sources of omega-3s. Flaxseeds are packed with ALA (alpha-linolenic acid), of which your body converts about 2% to EPA omega-3s, and 2% of EPA gets converted to the really effective DHA. At 2% of 2%, though, your body’s about as skilled at doing this as a 2-year-old is at getting spaghetti into his mouth.
Flaxseeds do have other great things on their resume: They contain fiber, which helps reduce cholesterol, and lignans, which fight cancer. Plus, some of their ALA is converted to omega-3s, and some is better than none. But little ALA makes it all the way to our favorite omega-3: DHA (docosahexaenoic acid), which is essential to keeping your brain sharp and your heart healthy. Those are benefits that ALA can’t touch. So eat flaxseeds; just don’t rely on them for your DHA and EPA omega-3s.
But here’s the surprise ending: Don’t rely on fish oil, either. We YOU Docs recommend taking capsules of algae-based omega-3s, which are high in DHA (aim for 900 milligrams a day). Algae is where fish get their DHA, so you’re going directly to the source. Plus, you’ll get all of DHA’s perks without the fishy burps fish oil capsules may cause.