macular degeneration, macular, diagnosis Dry AMD – My Macular Degeneration Journey/Journal

Questions and Answers – FDA Approved Treatment for Advanced Dry AMD/Geographic Atrophy/GA

Questions and Answers – FDA Approved Treatment for Advanced Dry AMD/Geographic Atrophy/GA

You may find a lot of the answers to your questions in this article ‘SYFOVRE for geographic atrophy in macular degeneration’ https://clearsightcorner.com/articles/syfovre-first-treatment-approved-geographic-atrophy-amd

Many of your questions will have to be answered by your eye specialist. A retinal specialist, a specially trained ophthalmologist, will administer the treatments.

Syfovre is pronounced “si-FOV-ree.” Where DO they get these names?

Patient Brochure

This is the patient brochure with some of the answers to your questions. https://syfovre.com/wordpress/wp-content/themes/apellis/pdf/SYFOVRE-Patient-Brochure.pdf

What is ‘geographic atrophy’ that I’m hearing so much about now?

A recent CBS News article and interview has been widely shared alerting many to this new treatment (approved on Feb. 17) so we’re getting a lot of questions. Here is the article and video. You may have heard me talk about my friend Sue who just happens to be the person interviewed in this because she’s been in the phase 3 clinical trial and is currently in the long-term follow-up study.  https://www.cbsnews.com/philadelphia/news/first-and-only-fda-approved-drug-to-treat-advanced-macular-degeneration/

AMD has 3 basic stages: early dry, intermediate dry, and advanced or late AMD. There are 2 types of advanced AMD: wet AMD and geographic atrophy which is the advanced stage of the dry form. There are 2 basic types of GA: outside the fovea (the center of the macula) and inside the fovea. For more information, here’s a good site. https://eyesonga.com/what-is-ga

How do I know if I have it?

It can only be diagnosed by testing done by an eye professional. Ask your eye specialist to tell you whether it is inside or outside of the fovea. In the early stages of GA, you might not be able to see any changes especially if it is outside the fovea.

Who is it NOT for?

It’s not for those with dry AMD at the early or intermediate stages. It’s not for those with other forms of macular degeneration such as Stargardt’s Disease or Myopic Macular Degeneration.

What if I have wet and GA?

In the clinical trials, they did not use the treatment for anyone with both GA and wet AMD in the eye they treated. For that reason, retinal specialists are discussing its use in this case and will make decisions for each individual.

What if I have GA and glaucoma?

If you have glaucoma and are considering Syfovre eye injections, it’s important to let your retinal specialist know about your condition. While it’s possible for people with glaucoma to receive these injections, they need to be monitored closely or have pre-treatment eye drops before their injections.

Eye injections can sometimes cause a temporary increase in eye pressure, which can be harmful to people with advanced glaucoma. This is why it’s important to take steps to prevent any increases in eye pressure before giving the injections. Your doctor may use anti-glaucoma eye drops to lower the pressure in your eyes before giving you the injection to help minimize any risk. Your condition will also be monitored more closely.

Is it only available in the US?

As of February 17, 2023, Syfovre received approval in the United States, according to the company’s press release. The European Medicines Agency is currently reviewing a marketing authorization application for Syfovre, with a decision expected in early 2024. Additionally, a marketing application for Syfovre has been submitted to Health Canada. If you live outside of the United States, Europe, or Canada, please check with your doctor to find out if Syfovre is available in your local market.https://investors.apellis.com/news-releases/news-release-details/fda-approves-syfovretm-pegcetacoplan-injection-first-and-only

What does it do? What does it not do?

It slows the progression of the disease which is measured by the size and rate of growth of what’s called a lesion which is an area of damage of the retina. The word ‘geographic’ comes from how the macula appears when an eye doctor looks at it: it’s like looking at a map where there are islands of damaged retinal cells – the lesion – in a sea of healthy ones.

The lesion starts outside the fovea – the center of the macula. The lesion causes you to have blind or blurry spots outside the very center of your vision. The lesions can progress to inside the fovea where you you will have one or more blind or blurry spots sometimes called scotomas.

It does not improve vision or restore any lost vision.

How well does it work?

Syfovre has been shown in studies to reduce the growth of geographic atrophy lesions more effectively than a sham injection. The treatment’s effects also increased over time.

A sham injection is a procedure used in clinical trials where everyone receives an injection, but some do not receive the drug being tested. The growth rate of the lesion in the treatment group is then compared to that in the sham group to evaluate the effectiveness of the drug.

For the actual results in numbers, you can find them here. You can ask your retinal specialist to help you understand them. https://syfovre.com/about-syfovre/what-is-syfovre/ and https://syfovreecp.com/oaks-and-derby-efficacy

How is it administered?

It is injected into the eye much like the treatments for wet AMD. The eye is disinfected, then a numbing agent is administered, then the injection is given with a very small needle. The eye is rinsed out, and you’d be given instructions about taking care of the eye at home.

It can be given every 25 to 60 days depending on the advice of your retinal specialist. The research showed that monthly treatments worked better than every two months. Also, the longer the treatment, the better the results.

To get the best results, you have to keep getting the treatments as your retinal specialist advises.

What are the possible side effects or risks?

You can find them all at https://syfovre.com/faqs/ and the patient brochure https://syfovre.com/wordpress/wp-content/themes/apellis/pdf/SYFOVRE-Patient-Brochure.pdf

Most common: floaters, eye discomfort, infection (can be treated), blood in the white of the eye (resolves over a period of time), wet AMD (can be treated)

Other possible side effects: eye infection, retinal detachment, temporary increased eye pressure after the injection

I keep hearing that it may cause my GA to become wet AMD. What’s the chance of that and what would happen if it did convert to wet AMD?

First, it’s your retinal specialist who can tell you more about the chance of this for you. Everyone is different so everyone’s risk of this will be different. For example, if you have wet in one eye but not the other, that non-wet eye has a higher risk of becoming wet than if you didn’t have wet AMD at all – even if you don’t have this treatment. In that case, your retinal specialist may not want to treat an eye with GA if you have wet in the other one. Everyone will be monitored closely for signs of this change and treatment for wet AMD will be started.

For the actual numbers, my friend Sue who was in the phase 3 clinical trial, is in the long-term follow-up study, and who was in the CBS News piece, wrote about that in this article ‘Pegcetacoplan Side Effect Hunting.’ https://maculardegeneration.net/living/pegcetacoplan-study and https://syfovreecp.com/safety/

She talks about the risk for those who have a higher risk of developing wet to begin with (above) vs those who do not. Remember, it’s your retinal specialist who is the only one who can evaluate YOUR risk. She talks about how she made her decision to get the treatment by evaluating the risks vs the benefits to her.

How do I decide if it’s worth it for me?

There are risks with anything. It comes down to evaluating the benefits vs the risks for you. It’s your retinal specialist who can best help you with this. Sue wrote ‘What Does Syfovre Mean For You?’ https://maculardegeneration.net/living/thoughts-on-syfovre

What will it cost? Will my insurance pay for it?

Please don’t freak out if you see the ‘cost’ of Syfovre as over $2000. That is the cash price and we don’t think anyone is going to pay that! But for some people, getting the cost covered or getting financial help will take time. This is how the process goes with all new drugs such as the newest treatment for wet AMD Vabysmo. All the cash prices for the wet AMD treatments are about this, except Avastin, but no one that we know of pays it because of insurance and financial programs.

Medicare has been the first insurance to pay with Medicare Advantage plans requiring pre-approval. Commercial insurances are working on it, but it takes time, just as it did with the new treatments for wet AMD. You can appeal to your insurance company which might speed things up.

What if my insurance does NOT pay for it, or I don’t have insurance?

There are several sources of financial help. Your retinal specialist should have someone to help you navigate this.

Apellis Pharmaceuticals, the company who makes it, has a program called Apellis Assist. They’ll help you work with your insurance company if necessary and if eligible, provide financial assistance. This might be the best first source.  https://syfovre.com/resources-for-you/apellisassist/

There’s another program called Good Days which has helped with costs for wet AMD treatments and is expected to help with this. You can check it our here. https://www.mygooddays.org

So this is the only treatment for geographic atrophy – my only option?

It is currently, but there’s a second treatment that completed the 3 phases of clinical trials and is waiting for FDA approval from Iveric Bio called Zimura. Approval is expected in August 2023. You can find out more about that here. https://investors.ivericbio.com/news-releases/news-release-details/iveric-bio-announces-fda-accepts-new-drug-application-and-grants

How do these 2 treatments (Syfovre and Zimura) compare? Should I wait?

You can find that here. You and  your retinal specialist can discuss whether it might be best for you to wait for this treatment.  https://clearsightcorner.com/articles/syfovre-first-treatment-approved-geographic-atrophy-amd

There are MORE treatments at various stages in the pipeline. This recent article (Feb 14 2023) is titled ‘2023: The year of geographic atrophy: A comprehensive look at 87 clinical programs for investigative treatments in retina.’ https://www.retina-specialist.com/article/2023-the-year-of-geographic-atrophy

Why is my retinal specialist not using it?

Some retinal specialists are conservative and are waiting for more information from the long-term study going on and the ‘real world’ data which means how well is working now with patients that it’s been approved.  Sometimes treatments go through clinical trials and are approved, but when they used with a winder population, problems can arise.

That’s a great question to ask your retinal specialist. You might find this article written by an authority in the field interesting as Charles Wykoff, MD, PhD, Director of Clinical Research, Retina Consultants of Texas, talks about how he is approaching it with his patients. https://www.hcplive.com/view/charles-wykoff-md-significance-pegcetacoplan-approval-geographic-atrophy?

Why aren’t researchers trying to stop the disease before it gets to an advanced stage?

That’s a great question especially since -85-90% of those with AMD have early or intermediate AMD. AMD is a complicated disease with many factors and no one cause. Therefore, researchers are working in many areas including the prevention of it and stopping or slowing it at the early and intermediate stages. In many complicated diseases, we see research in the advanced stages because that’s where there can be the most damage. That’s why we have had so many treatments for wet AMD for 20 years: most of the damage to central vision is from untreated wet AMD. It’s the same with advanced dry AMD: the disease process needs to be slowed to prevent central vision loss.

Here’s an article with 87 research studies for various stages and types of retinal disease. https://www.retina-specialist.com/article/2023-the-year-of-geographic-atrophy

Many of your questions will have to be answered by your eye specialist. It is a retinal specialist, a specially trained ophthalmologist, who would be giving the treatments.

This is the patient brochure with some of the answers to your questions. https://syfovre.com/wordpress/wp-content/themes/apellis/pdf/SYFOVRE-Patient-Brochure.pdf

Created April 20th, 2023 Linda Chernek Moore, light2sight5153@gmail.com

 

 

My Diabolical Plan – Revisited March 2023 – by Sue LaBar Yohey

Some of you may know I can be persistent -very ! -and even manipulative. I get a plan in my head and make the moves to follow it through.

Ever since I was diagnosed as legally blind with geographic atrophy, advanced age-related macular degeneration, in February 2016, I have had a master plan, a DIABOLICAL plan, for recovering my eye sight sometime before I die [Linda here: curious how old she is? At the time of this article, she is 69. She’s determined to live a LONG time. ::smile::]. This plan started with presenting myself as a patient to the esteemed retinologist Dr. Carl Regillo  from Wills Eye Hospital in Philadelphia. I then expressed interest in being in a study. I wanted a clinical trial hopefully involving stem cells.

After what seemed like dozens of trips to Bethlehem, Pennsylvania, my persistence paid off. I was offered a place in phase 3 of a study using a complement factor inhibiter that had been considered to have promise. While initially it seemed as if being offered this study was one step to the left of where I wanted to be, I decided to take it. It was my “in” and I was not guaranteed another opportunity.

As it turned out, I had the honor of being part of the trials that brought forth the first, FDA-approved treatment for geographic atrophy. This is Syfovre from Apellis.

How do I feel about this? While my contribution was small, it is still kind of cool to have been involved in the making of medical history. I feel like the water boy for the Super Bowl or maybe like the ball boy/girl at Wimbledon. Helping to make it happen gives me pride.

So here I am, two steps in the Diabolical Plan successfully behind me. I manipulated getting to see Regillo, I wanted him as a doctor and took steps to make that happen. Regillo almost guaranteed I would be in a study. Funny, although I had no way to determine the outcome of the study, I never doubted the treatment would be approved. Forgive my arrogance, but without its approval, my plan could not progress, and, as far as I am concerned, it IS happening. If my plan was going to work, the treatment had to work first. I never doubted.

Right now, I am half way through a 3-year study in which they are searching for side effects. For me, this study is a place holder in three ways. First of all, it keeps me in front of the doctors running the show. While I cannot go into just any old study, I could go into another study involving Syfovre. When one of those comes along, I will be bouncing up and down on the sidelines. “Put me in, coach. I want to play!”

The other reasons this study is a place holder are these: medical science is not there yet.
Also, Syfovre is not the best we can do.

Second one first: while the Benz Motorwagen was a great innovation in 1886, it was also not at the front of the pack for long. And yes, that really was the first car. I looked it up.) Just like the Benz Motorwagen was replaced by more efficient cars, there will be other, better treatments for GA. My believe is the ultimate “treatment” will be “replacement parts”. Enter stem cells.

They have now learned how to “reverse engineer” blood and skin cells to become induced pluripotent stem cells. Once you have these, they can be “coaxed” and “massaged” into becoming retinal pigment epithelial cells. Remember RPEs are the “servant cells” that keep the photoreceptors alive. Without RPEs there are no photoreceptors and no sight.

According to a panel member on the March 2nd, 2023, webinar ‘Towards a Stem Cell Cure for Blindness,’ lab-grown RPE cells might be available to the general public in about six years. They are moving fast but they are still in phase 1 trials. In other words medical science is not ready for me yet.

Moving on with my thinking, Syfovre will be a way for me, and perhaps millions of others, to buy time. Syfovre slows the deterioration. Current wisdom is that stem cell therapy and RPE replacement stops deterioration. If Apellis wants to sell their drug, they have to prove it will not keep people from eventually benefitting from the superior treatment. Voila! There is my – yet imaginary – next step in my Diabolical Plan. Put me in, coach!

And just a reminder, replacing RPEs will not restore vision. As I have said before, dead is dead and a number of my photoreceptors are dead. However, replacement RPEs will stop my vision from getting worse. They may also improve it slightly, not much, by resuscitating photoreceptors on their last legs.

What about photoreceptor replacement? After all, I do need those replaced to restore my vision. That technology is much further down the road but still getting closer every day. It will get here in time. After all, I have a Diabolic Plan to complete!

Who is Sue and Why Should You Get to Know Her?

The Facebook Group

First, it weren’t for Sue, the Facebook group wouldn’t exist! We’ve been close friends since college which is now a LONG time ago. In June 2015 she was driving, got something in one eye and closed it, and the car in front of her disappeared! You can read about that and how her journey with AMD began here: In the Beginning. In February 2016 when she was told that she was legally blind, she asked me to create a site for her so that she could process what was going on and to hopefully help others. In May 2016 after months of not being able to easily have conversations with followers, I started the Facebook group. The rest, as they say, is history.

Her Journey

After less than a year of learning how to deal with her visual impairment both physically and emotionally, Sue created a ‘normal for her’ life. What is it like? It’s like her life ‘before’ except she does not drive. What she does is travel domestically (sometimes even by herself) and aboard, works as a psychologist, walks her 2 active Labrador Retrievers, attends multiple exercise classes every week, rides her bike safely, takes photographs (some of which have won awards locally), skis in the Winter and rafts in the Summer, goes to social events with her friends and co-workers. She’s also taught courses in the psychological therapy called DBT (Dialectical Behavioral Therapy) that she uses with her clients and used herself in the beginning of her journey.

What she does NOT do is let her geographic atrophy stop her from doing what she wants to do. As she said herself she is persistent and determined.

For quite a few years, she wrote for this site, but it’s now more an archive. She writes for Health Union’s maculardegeneration.net site where you can read her more recent articles. As she wrote, she was in the phase 3 Apellis Pharmaceuticals clinical trial for what was called APL-2 then, was invited to be in the long-term follow-up study where it was called pegcetacoplan which is called Syfovre since it’s approval by the FDA on February 17th. 2023.

When asked what her visual acuity is, she says it’s 20/63 to 20/80 in one eye & between 20/160 and 20/200 in the other. Yes, she has a blind spot in the middle of each eye but has taught herself how to use her ‘sweet spot’ also called a Preferred Retinal Location.

 

 

 

 

AMD: The Disease Process by Amanda Legge, OD

Dr. Amanda Legge (pronounced Leg-ee) is a member of our Facebook group. She’s an Optometrist at the Wyomissing Optometric Center in Eastern Pennsylvania.

I want to summarize AMD as a disease process. I explained this during my Facebook Live talk with Linda on 12/12/2021. I also recommend looking in Guide 2 for “what tests does my eye doctor do to diagnose and manage macular degeneration”. In that post I show what normal retina health and normal OCT looks like in comparison to this post about AMD.

Click on image for larger version.

AMD is a disease of the transport process of nutrients in and waste products out of the macula. Oxidative stress and other factors damages the bottom layer of the retina called the RPE (retina pigment epithelium). The RPE has several jobs, but one of its main responsibilities is to help transport waste OUT of the retina, through the RPE, and into the blood vessels below so that the waste is eliminated then with the rest of the waste our bodies produce. It is also responsible for carrying nutrients from the blood vessels under the macula, through the RPE, and INTO the macula where it nourishes the photoreceptors that are responsible for our vision.

The disease of AMD is a fault of this transport system as a whole. Studies show AMD starts 3-5 years before eye doctors can view this clinically in the macula as drusen. An entire wash of waste deposition already builds between the blood vessels and macula as very early AMD starts (shown in electron biomicroscopy of donor eyes, we cannot visualize this yet clinically). As that waste product builds more and more, eventually eye doctors can see the iceberg peaks of that waste deposition that we call drusen. Drusen look like yellow bumps/deposits in the macula during a dilated eye exam.

Drusen can be present for a very, very long time (decades even) in the macula before vision deteriorates. But if the disease progresses, not only is waste not able to escape the retina (and builds up as drusen), it also creates a thicker and thicker barrier for nutrients to get through in order to feed the retina.

Advanced AMD

That is what is at the heart of vision loss in AMD, the photoreceptors are not getting enough nourishment so over time either AMD can progress to advanced dry AMD or turns to wet.

Advanced Dry AMD (often called geographic atrophy) occurs when the photoreceptors don’t get enough nourishment and slowly die off (atrophy) over time until there are no photoreceptors left in large areas of the macula. No photoreceptors = no vision in that area.

Wet AMD occurs also because of lack of nourishment and oxygen to the retina. 15-20% of the time the body decides it’s a good idea to grow NEW blood vessels from the vasculature underneath the retina, through the RPE, and into the retina itself. In theory this sounds good, right? New blood vessels = new route for more nutrients and oxygen to get to the photoreceptors. It is a good idea……but unfortunately it’s only good in theory.

These new blood vessels, known as neovascularization, do not have the same structure as the blood vessels we are born with. They are much more fragile. Because of this they very easily leak and bleed causing fluid and blood to accumulate in the center of our vision which can quickly cause vision distortion or vision loss. So, it makes absolute sense why diet, exercise, control of diseases that affect our vasculature (diabetes, high blood pressure, high cholesterol, obesity, cardiovascular disease as the most common) and supplementation helps to protect the retina.

We can control oxidative stress by providing the retina with the fighting power of antioxidants to protect the RPE from further deterioration and thus less waste deposition.

Exercise helps increase the “push” through that thicker barrier, AMD diet helps feed the retina more nutrients when not enough gets through on its own. Control of vascular systemic conditions helps the blood vessels stay healthy so they can do their job easier of giving nutrients and taking waste. And as AMD progresses, AREDS2 and extra nutraceuticals [medicinal foods supplements, fortified foods, etc] help further boost the amount of good nutrients our macula craves to stay healthy (carotenoids and antioxidants).

It can be hard to change and maintain a healthy lifestyle for the long term. But hopefully understanding this process makes that a little easier when it all makes sense in the end. Have a great weekend everyone!. ~Dr Legge

Written December 7th, 2021.

Images with Dr. Legge’s Notes

Click on each image. To go to the next one, look for the arrow pointing to the right. To go back to the previous one, look for the arrow pointing left.

 

Personal Message December 11th, 2021 Our Genetic Guns: Part 5 and Final

Continued from part 4

Comment 10: Should The Moores Take a LMZ Supplement?

Looks like it would be of benefit to us since:

  1. We are not confident that our diets give us enough LMZ.

  2. We don’t know if our macular pigment and level of carotenoids in the brain are sufficient, which is what this research has shown to be important in reducing our risks of both AMD and Alzheimer’s

Can’t We Just “Pop a Pill”?

Taking a supplement is NOT a substitute for eye- and brain-healthy eating. We will still be eating our leafy green vegetables and colorful fruits and vegetables and other eye-healthy foods to get the other nutrients we need such as Vitamins A, B, C, and E (we were found to be deficient in D so we each take a Vitamin D supplements) and the other essential nutrients. We eat healthy plant-based foods and wild-caught salmon 2 or 3 times a week to get our Omega-3 fatty acids.

First Things First

There are always 2 concerns when considering any supplement:

• Are the ingredients generally safe to take & specifically safe based on one’s medical history & use of medications?
• If they are, which product is the best one as verified by one or more respected, independent testing labs?

Are the Ingredients Safe for Each of Us?

You should ALWAYS talk to your medical doctor before starting a supplement, especially if you have other diseases and take medications. We have different GPs, and we’ve been in touch with them. No problem.

Here are the 2 things I always look for:

  • Are there interactions with the medications we take and the diseases we have? I checked rxlist.com and drugs.com. I checked each of the 3 carotenoids. No interactions for either of us. There are very few issues for anyone, but check it out for yourself.

The 20 years of this research has shown these 3 carotenoids are very safe. There is research to back that up, but it’s beyond the scope of this post.

Comment 11. Which Brand?

I came to this stage in my research feeling confident that taking LMZ was safe for both my husband and me. I had also, to the best of my ability, gone through the research done by Dr. Nolan and his colleagues and felt confident that it met my criteria for solid, scientific research (according to the criteria I listed in Comment 4.)

The next step was to confirm which product was used in Dr. Nolan’s research. It’s what’s currently in the products MacuHealth (available in the US & Canada) and MacuPrime (UK & Europe).

If you watched the ‘Preventing Macular Degeneration Through Science’ video I posted last week (you did, right? ::smile::) you heard Dr. Kerry Gelb say he takes the MacuHealth product when he interviewed Dr. Nolan. Dr. Nolan said he takes it, his wife takes it, and his young daughter sometimes does as well. He and his family have since switched to MacuPrime.

Confusion

If you read the 2014 scientific paper from the CREST trials (you did, didn’t you? ::smile::), you’ll see the product listed as MacuShield. There’s a LOT of confusion about that! I reached out to Dr. Nolan who apologized for it (though it certainly was not his fault). At that time, the company that commercialized the formulation available to Dr. Nolan in the UK was MacuVision Europe, and they branded it as MacuShield. The company was then sold to Alliance Pharma who did not continue with the same formula that was tested. The company in the US that had the world rights to the formulation at the time of the study was MacuHealth (founded in 2006) and the product was then and still is MacuHealth.

Any research after this change in companies was with MacuHealth.

Clarification

Currently, MacuShield is a product only licensed in the UK and Europe. It is a TOTALLY different product than MacuHealth. I confirmed that in an email to the MacuShield company. They were very good and replied clearly & quickly. To be clear (again), MacuShield is NOT the product recommended here.

Bottom Line

MacuHealth products in the US and Canada and MacuPrime products in the UK and Europe are the products that contain the formulation used in Dr. Nolan’s research.

For those who are good candidates for an AREDS2-based formulation, there’s MacuHealth Plus and MacuPrime Plus. For everyone else, it’s just MacuHealth and MacuPrime.

For those who want an AREDS2-based formulation with 0 zinc, you can take MacuHealth/MacuPrime with LMZ and add 500 Vitamin C and 400 IUs Vitamin E separately. That’s the whole AREDS2 formulation.

Please remember my cautions for some of you who are or will be taking an AREDS2-based supplement – those of you with other diseases and who take medications. Please talk to your medical doctor before you start because the doses of Vitamin C and E in the AREDS2 formulation may be too high for you.

Comment 12: More Validation

I could have stopped there, but I wanted to make sure that I did everything for this product that I do for all supplements I choose to take.

Independent Testing

Of course, knowing that others take a product, especially if it’s the researchers themselves, is important, but so is independent analysis of a product.

Consumer Reports

Consumer Reports, a U.S. independent, non-profit organization recommends that since the FDA does not regulate food supplements in the US, it’s important to look for independent labs that test the products to make sure that what is on the label is in it. https://www.consumerreports.org/supplements/how-to-choose-supplements-wisely-a2238386100/

Consumerlab.com

My ‘go to’ independent lab, one recommended by Consumer Reports, is Consumerlab.com of which I’m a member. THEY are confused, too! Even though they are a U.S. company, they tested MacuShield, but not MacuHealth! I emailed them, and they replied that they DO know of the confusion and are working to resolve and report in it. I’m watching for their update.

NSF International

Another source of independent testing referred to by Consumer Reports is NSF International (it was originally the National Sanitation Foundation). The NSF has tested and certified  MacuHealth products (you can see what that means in the Consumer Reports Article above).
https://www.nsf.org/consumer-resources/articles/supplement-vitamin-certification

Supplement Certified

Another certification they have is ‘Supplement Certified,’ another independent lab that I referred to earlier. It’s a new project from Dr. Nolan’s Nutrition Research Centre Ireland (NRCI).
https://supplementcertified.ie/

Company Responsibility

If you listened to the podcast I referred to in Comment 3 (you did, didn’t you? ::smile::), you heard the story of how in one of Dr. Nolan’s clinical trials, when they used an early formulation with just lutein, they unexpectedly found meso-zeaxanthin in it. The trial was stopped, and the company stopped production and sales of the product for over a year. They did produce the new product and the trial continued.

Why Does It Matter?

So if a product has all 3 carotenoids (there are a few), what difference does it make which product you buy?

The lutein in ANY a product probably comes from marigolds. Where the marigolds are grown, what farming methods are used, and how it is processed is important. The processing creates the lutein, zeaxanthin, and meso-zeaxanthin that goes into the tablet or capsule that a person takes. The marigolds used for MacuHealth come from the same fields in Mexico and are tightly managed for specific best-farming methods.

In 2020, Dr. Nolan and colleagues did research (COAST study) to validate a new production method called Micro-Micelle(tm) that MacuHealth uses to make sure the LMZ has the highest possible bioavailability which means how well a substance is able to get into our circulation, to get to the target area, and to do what it’s intended to do. They confirmed that when they take the carotenoids in their ‘free’ form as in the original MacuHealth products, and enhance their stability plus use an oil base because carotenoids are oil solvable, this new technology gives you the best absorption of LMZ.

Read Reviews Online? Misinformation & Testimonials

I rarely do that (they are testimonials, after all), but out of curiosity I went to the Amazon listing for MacuHealth or MacuShield – can’t remember which, and found inaccurate information. Someone asked about MacuHealth and MacuShield: (paraphrasing) “are they the same?” and someone said “yes, they are. It’s the same company, but it’s called MacuHealth in the US and MacuShield in the UK.” WRONG! Yes, I told them that. ::smile::

Here’s another source of confusion. You CAN go to the Amazon US site and buy MacuShield. I emailed the MacuShield company about that since they’d told me they only have a license to distribute their product in the UK and Europe. The seller on Amazon US is a 3rd party distributor. If you purchase MacuShield through Amazon US, you will not get it right away because the 3rd party seller has to get it from the UK!

Got it?

Comment 13: A Beginning and The End

Whew!! Are you thinking, “All this to just pop a supplement? They’re ‘vitamins’ and as such, they can’t hurt!!”

If you’ve been with me long enough, you know how I react to that often-repeated opinion. They CAN and DO hurt SOME people.

However, having gone through this ENTIRE procedure which included talking to the researcher Dr. Nolan and others:

I CAN say that the research shows that taking LMZ in the MacuHealth and MacuPrime supplement is safe!

The Beginning

Change takes time. Making sure we’re getting the proper foods is work and a long-term commitment. We’ve only been taking MacuHealth for 2 months. We’ll be taking it for the rest of our lives.

As for us, I don’t expect to see quick improvements in our vision, but I certainly will be happy to have it be the best it can be as time goes on.

We both have issues with cognitive processing and memory (most likely due to medication), especially word retrieval which is a source of frequent ‘Charades’ (“You know, the thingie that you use for…whatever!”). Maybe someday we won’t have to spend so much time doing that! ::smile::

Not Pulling The Trigger

I started this with the sentence, “Genetics loads the gun, lifestyle pulls the trigger!”

What I HOPE and PRAY I can do is come back in 10 years to say that neither of us have AMD or Alzheimer’s Disease!

The End!

If you’ve read this far, thanks so much! Please let me know if you have any questions.

Personal Message December 11th, 2021 Our Genetic Guns: Part 2

Continued from Part 1

Comment 3. Three (3) Carotenoids, Not Just 2!

I knew that antioxidants are important in battling oxidative stress, so I decided that I should go back to one area that doesn’t get much attention despite its 20-year history of solid research. You probably have heard about 2 of them: lutein and zeaxanthin. There’s a third antioxidant called meso-zeaxanthin.

About abbreviations: Meso-zeaxanthin is often abbreviated as M or Mz, lutein as L, zeaxanthin as Z. Sometimes you’ll see LMZ or LMZ3.

Carotenoids

Lutein, zeaxanthin, and meso-zeaxanthin are called carotenoids. There are MANY others, including beta-carotene. They are pigments that give plants their yellow or orange color. When we eat plant foods, these pigments benefit the body in essential ways.

Macular Pigment

At the back of the eye, at the very center which is known as the macula, LMZ collectively join and concentrate to form a yellow pigment that is called macular pigment (MP). Macular pigment protects the macula from harmful blue light (because it is yellow and can filter out the blue) and provides antioxidants to keep the photoreceptors nourished & healthy to fight oxidative stress.

We Need All 3

The short story is that research has shown that even though there are about 700 carotenoids, only these 3 are found in our macula: LMZ. They have a synergistic effect on each other, which means we need all 3 of them, so they work at optimal levels. Pretty amazing that of all the carotenoids available from nature, the eye ‘chose’ these 3!

Eating Plant Foods

The important thing to know is that if we don’t eat plant foods, we won’t have macular pigment. A researcher quit eating plant foods for 21 days & had virtually no macular pigment at the end of that period. When he resumed a diet which included plants, his macular pigment recovered. https://profjohnnolan.com/wp-content/uploads/2018/05/loughman2012a-bjn-letter.pdf

It also means that if we don’t eat a sufficient amount of plant foods, we don’t have sufficient macular pigment.

It also means that if we don’t eat the plants that contain these 3 carotenoids, we may not have sufficient macular pigment.

Healthy macular pigment, which protects, nourishes the photoreceptors and fights oxidative stress, comes from getting enough of these 3 carotenoids.

With me so far? I hope so!

Comment 4. What Is Meso-zeaxanthin? Why Is It Important? Show Me the Research!

So what is meso-zeaxanthin, and why is it important? To be honest, it depends on who you talk & listen to and what you read. Research frequently comes down to the stories of the people who conduct it. That’s certainly the case with my journey.

The path I followed began when I listened to a September 3rd, 2021, podcast interview with Dr. John Nolan who has been doing research into the 3 carotenoids for the last 20 years (I’ll give you the link in Comment 5). Since then, I have watched countless hours of video, listened to hours of podcasts, and read (or tried to read) LOTS of scientific papers. I have enough of a background, education, and confidence in the scientific method that I felt I was able to understand and assimilate what I needed to be able to follow the research.

Little did I know how MUCH there was, but I was determined to dig through as much of it as I could. That’s why it took so long!

I found that there are many others who were involved and are still involved – quite a multidisciplinary collection of people. I’ll be introducing you to some. These are professionals who have dedicated their careers to the study of macular pigment in the macula which is only about 5.5 mm in the size!

Dr. Nolan (often referred to as Professor Nolan) is not only a scientist & researcher but also a compelling speaker and effective educator. He makes it clear that he’s only one part of this multidisciplinary team that has evolved over his 20-year career. During that time, he became the author or one of the authors of over 100 articles in peer-reviewed journals. You can find all his articles at https://profjohnnolan.com.

In the Beginning

In 2005 in Ireland, John Nolan defended his PhD in Biochemistry on a Wednesday and left for the US on a Friday. He’d applied for and was awarded a prestigious Fulbright Scholarship to study at the Medical College of Georgia. There he worked with researchers who were studying how lutein affects our eyes. [Personal note: My husband got his Occupational Therapy degree at Medical College of Georgia, although he wasn’t there at the same time. I’m always amazed at what a small world it is!]

When he returned to Ireland, he set up the Macular Pigment Research group at the Waterford Institute of Technology. There they began to collect a body of evidence that pointed to the macular pigment as critical to the health of our eyes and as an indication of the level of carotenoids in our brain.

In 2016, he set up the Nutrition Research Centre Ireland (NRCI) where he is the Director. They’re involved in numerous project including the new Supplement Certified program where they are testing supplements to certify that what is on the label is in the product. In 2021, they analyzed 47 nutritional supplements containing carotenoids and found that 64% did not meet the content described on their labels. They are also working with supplement companies, so they make sure that what’s on the label is indeed in the product. Since supplements aren’t regulated, this is welcome news! For more, go to. https://www.supplementcertified.ie

Continuing Down the Path

There’s MUCH more to Dr. Nolan’s biography. I hope you’ve read what I wrote in the Events post (Facebook page) which is more complete.

Here are the reasons I chose to continue:

⁃ Dr. Nolan’s research is based on recognized scientific methodology, where the results are published in peer-reviewed journals. In the world of scientific research, there’s something called the ‘Hierarchy of Evidence.’ Although the details vary from country to country, Level 1 scientific evidence means it was obtained through randomized, controlled clinical trials. Dr. Nolan’s research has been Level 1. https://en.wikipedia.org/wiki/Hierarchy_of_evidence

⁃ He does not work alone. He repeats this over and over in his articles and interviews. He frequently refers to people he’s worked with over the years. This isn’t a ‘one man show.’

⁃ His research depends on objective measures of the levels of the carotenoids in blood, the macula, and the brain. He uses state-of-the-art equipment, equipment that has improved significantly over the years.

⁃ He does not work for any company exclusively. He has tested many supplement products. The main funding for his research comes mostly from government sources, including that of Ireland and the EU.

⁃ When he first started using an LMZ formulation from a specific company, it was with the agreement that he would publish the results no matter what they were. And he did!

NEXT: PART 3 –COMMENT 5. DR. NOLAN’S RESEARCH: HIS QUESTIONS AND ANSWERS

Personal Message December 11th, 2021 Our Genetic Guns: Part 1

A Personal Message from Me, the Founder and Administrator of This Group. December 11th, 2021.

This began as a project for my Facebook Group founded in May 2016 to be an extension of this site. The day before I posted it, I decided that it should be here, too, for anyone who can benefit. I apologize about the ‘comment’ format. I hope it’s not too distracting.  – Linda Chernek Moore.

Who should read this?

Everyone who is concerned about eye and brain health:

• those with and without macular degeneration,
• those with and without cognitive problems, including Alzheimer’s Disease.

In my opinion, that means everyone here.

My Journey Story

I will – for the first time in over 5 years here – tell you what supplement my husband and I take and why. I will take you step-by-step through the process of how I came to select it for us.

This isn’t a sales pitch because I’m not actually promoting a product, I’m actually promoting good scientific research.

Why am I sharing it in what seems to be a ‘big way’? It’s because I think it is important. You probably know how cautious I am about supplements. I do not promote the “It’s a supplement/vitamin, it can’t hurt!” They CAN hurt some people. I have many examples of that.

This is one of the FEW times I’ll be able to say, “It can’t hurt! It’s safe!”

Our Genetic Guns

My dad had advanced dry AMD/geographic atrophy. My husband’s mother had AMD, but we’re not sure of the type. Neither of us have AMD – yet – but research has shown that we each have a higher risk of it than someone with no family history. We each have additional risk factors as well.

There’s another disease for which we both have an inherited risk factor: Alzheimer’s Disease. My mother had it. We think my husband’s mother had it as well, although it may have been another form of dementia.

In memory of Harry & Genevieve Chernek and Elizabeth & Jacob Moore

I’ve shared this quote that’s often used for discussions of genetics:

genetics loads the gun, lifestyle pulls the trigger.

What does that mean? It means that a person may have a specific genetic makeup that predisposes them to a disease, but lifestyle factors DO matter. They can prevent the expression of the genes or can lessen the impact of them.

With family histories of AMD -and- Alzheimer’s, our guns are loaded!

We are COUNTING on those lifestyle factors! I’m 68 and my husband is 70. There’s a third risk factor: age. They’re both age-related diseases, so our guns are REALLY loaded!

Comments

I’ve been working on this in ‘fits and starts’ since early October, so it’s been almost 2 months. I hope I’ve managed to put together a coherent description of this long process. Because there’s been so much to it, I’ve put the details in the comments (on the Facebook page, that is). Here is an outline, so you can go to what you’re interested in if you don’t want to read the whole story.

Outline

1 The Eyes and the Brain: Same Lifestyle Factors
2 Oxidative Stress and Antioxidants
3 Three (3) Carotenoids, Not Just 2!
4 What Is Meso-zeaxanthin? Why Is It Important? Show Me the Research!
5 Dr. Nolan’s Research: His Questions and Answers
6 Where Do People Get LMZ? My Questions and Answers
7 Time to Get Personal: Are The Moores Getting Enough LMZ?
8 Can The Moores Improve Their Diet?
9 Those of You With AMD: Your Benefit
10 Should The Moores Take a LMZ Supplement?
11 Which Brand?
12 More Validation
13 The Beginning and The End

Comment 1. The Eyes and The Brain: Same Lifestyle Factors

The eyes are actually part of the brain, so it’s not surprising that what benefits the eyes, benefits the brain. If you’re not familiar with the connection between the eyes and the brain, here’s a brief explanation. https://youtu.be/4Na0Mj0b_6A

Lifestyle Factors for the Eyes and the Brain

The same lifestyle factors affect them both. Nutrition and smoking are the main ones. I never smoked, but my husband did but quit 40 years ago.

I started my investigation with nutrition because of our continued struggles with the Mediterranean way of eating, which is recommended for both diseases. We try our best to eat healthy but found that we were falling short of the very specific nutrition advice given frequently.

Not Just Healthy Eating

Years ago I found out that ‘eating healthy’ does not necessarily mean ‘eating healthy enough for the eyes’ and now discovered the same thing applied to eating healthy for the brain! Much more to it!

Comment 2. Oxidative Stress & Antioxidants

In both diseases, oxidative stress is a major factor because research has shown that it leads to inflammation, which leads to diseases such as AMD and Alzheimer’s. I wanted to make sure I understood the terms oxidative stress, free radicals, and antioxidants.

What Exactly IS Oxidative Stress?

Think about an apple that you cut and is exposed to the air. It changes & spoils the apple, doesn’t it? Also, think about what rust is. Both processes are from oxidation, which means something is exposed to oxygen and is changed.

Some people say that since we depend so much on oxygen, aging is just rusting! Lovely image, huh? Soon I’ll be introducing you to Dr. John Nolan who says this is “the cost of doing business with life.”

In the body, oxidation is a chemical reaction in a cell when it is exposed to oxygen. Our retinas use the most oxygen of any cells, so that’s a LOT of oxidation!

In these cells, there can be an imbalance of what are called free radicals (the ‘bad guys’) and anti-oxidants (the ‘good guys’).

Oxidative stress is when the ‘bad guys’ are getting control, which is NOT good! Here’s a short video that explains this.
https://m.youtube.com/watch?fbclid=IwAR2pV_Z35dnfoWxdzx9IXdmQSm9t6MfMR1VAkHCsAkFCQHNlB9b3ks69XS8&v=9OgCjhAFCC0&feature=youtu.be

Oxidative Stress and Inflammation

Oxidative stress can trigger inflammation which is thought to cause dis-eases (yes, I purposefully put in the -) like AMD and Alzheimer’s, or at least it’s thought to be a major factor. For more information about the effects of oxidative stress on the body—> https://www.medicalnewstoday.com/articles/324863#summary

Anti-oxidants

So to battle oxidative stress, we need a good and consistent supply of anti-oxidants (that is ‘anti’ for ‘against’ & ‘oxidants’ referring to oxidation and oxidative stress; I’ll leave out that ‘-‘ from now on).

This 15-minute video is the first part of a Continuing Medical Education course which gives a GREAT explanation of the process and introduces the role of the 3 powerful antioxidants that are critical to protecting and nourishing our photoreceptors, which are the cells that convert light to sight. ‘Macular Pigment Supplementation: A Prescription for Vision and Cognitive Health.’
https://youtu.be/-8n9rz2AmXE

I highly recommend part 2 as well.

Next: PART 2 – THREE (3) CAROTENOIDS, NOT JUST 2!

Personal Message December 11th, 2021 Our Genetic Guns: Part 3

Continued from Part 2

Comment 5. Dr. Nolan’s Research: His Questions and Answers

Perhaps the best way to understand how this research evolved over time is to listen to Dr. Nolan describe it in detail before he joins us on Tuesday, December 14th (see the Events section on the Facebook group’s page). It was this podcast from September 3rd, 2021, that helped me to understand how the researchers started by looking at lutein and then measuring and testing all 3 carotenoids.
‘Age-related Macular Degeneration, Supplementation, and Key Research Findings in the Field of Ocular Nutrition.’
http://broadeye.org/nolan/?fbclid=IwAR29J6lcBxCYHkAGuV8wTfsxD7t6cbnNieWFC8U1wLihlVrcStYcR_0DC0g

The Questions

What’s clear from the podcast is that he approaches all his research as you should – with questions. The basic ones were:

  • Can we prevent eye diseases like AMD by enhancing the macular pigment?
  • By optimizing all 3 carotenoids in the macular pigment, can we improve contrast sensitivity (ability to detect differences in shading and patterns), reduce glare issues, improve photostress recovery (ability of vision to come back to normal after exposure to bright light) and other measures of vision in everyone with or without AMD?
  • Does the measurement of the macular pigment give us an indication of the levels of the carotenoids in the brain?
  • Does enhancing the level of carotenoids in the body prevent a disease like Alzheimer’s?
  • Does enhancing the level of carotenoids in the brain help improve memory and cognition?
The Answers

The answers after 20 years of doing study after study were yes, yes, yes, yes, and yes!

He and his colleagues were able to move beyond subjective measures to objective measures that could be validated and reproduced.

Summary

As far as the research about our eyes, they not only looked at the ‘traditional’ measure of vision which is visual acuity, but objectively measured contrast sensitivity, glare sensitivity, and other aspects of vision. Having sufficient levels of LMZ meant significant improvements in these measures.

As far as research about Alzheimer’s, they not only looked at preventing the disease but at improving memory and cognition.

Understand My Excitement?

I hope you understand why I was so interested in the work he and his colleagues did and continue to do 20 years later!

Onward!

After digging through all the research I could and talking to Dr. Nolan personally to fill in the gaps, it was now time to apply the findings from the research to my life and my husband’s.

Comment 6 Where Do People Get LMZ? My Questions and Answers

So MY big question at this point was:

If we need all 3 carotenoids, can we get them from our diet by eating plant-based foods?

Although we can get enough lutein from plant-based foods, it’s harder to get zeaxanthin and almost impossible to get meso-zeaxanthin because it’s found only in the skin of some fish like trout and shellfish. We don’t eat trout or shellfish.

Somewhere along the line before this project, I’d read that zeaxanthin & meso-zeaxanthin are made from lutein in the body.

There are researchers who believe that the body metabolizes lutein and produces meso-zeaxanthin so as long as we’re getting enough lutein, we are fine.

Dr. Nolan says that he believes that SOME people do produce meso-zeaxanthin from plant foods, but not everyone. He’s done extensive testing of people’s macular pigment over the years and estimates that 15% of the population don’t have optimal macular pigment for whatever reason.

What reasons? Not getting enough lutein? Getting enough lutein, but their body isn’t converting it to meso-zeaxanthin? The ‘jury is still out’ on this, but it may be because of a lack of certain enzymes.

Next: PART 4 – TIME TO GET PERSONAL: ARE THE MOORES GETTING ENOUGH LMZ?

Personal Message December 11th, 2021 Our Genetic Guns: Part 4

Continued from Part 3

Comment 7: Time to Get Personal: Are The Moores Getting Enough LMZ?

How do WE know if we are among those who get enough lutein from our food and make enough meso-zeaxanthin from it? We don’t.

What I understood at this point from the research:

This is big!

This is the key to stopping that genetic gun from firing!

Since we cannot get a measure of our macular pigment, we have to assume it’s not as healthy as it needs to be to prevent both diseases.

Comment 8: Can The Moores Improve Their Diet?

My husband and I have had general concerns about our nutrition for some time:

  • We have trouble finding produce that we’re convinced is nutritious because there are well-documented problems with farming, distribution, and availability.

  • We often don’t get the vegetables cooked properly. Sometimes they are in the refrigerator for too long. Our health issues mean that some days we just don’t have the energy to prepare a healthy meal, even though we have the food.

  • We both have diseases for which we take medications, so we know we don’t absorb nutrients from food as well as someone with no other diseases and who do not take medications.

  • Because of our age, we don’t absorb nutrients as well as someone younger.

Even if we were to try to follow the Anti-AMD Diet that I refer to frequently (see Guide 11), the daily recommendation is to eat 6-7 servings of fruit and vegetables a day: 2.5 cups of vegetables & 2 cups of fruit). A serving is ½ cup cooked, 1 cup raw. The vegetables should include leafy greens, but I’ve not seen any recommendations of the ratio of leafy greens to other vegetables.

That’s a LOT! Do YOU eat this every day? We certainly don’t!!

Comment 9: Those of You With AMD

So far, I’ve shared research that says that having the optimal amount of LMZ in the macula is linked to the PREVENTION of AMD which applies to me, my husband, your kids, your grandkids – those of us with a family history – and your friends and neighbors who do not have AMD or a family history of it.

Want Me To Fast Forward? Sure!

You’d like me to fast-forward, right, to the part where I tell those of you who already have the disease what, if anything, LMZ will do for you?

Relief From the Symptoms

Full disclosure: this is not about slowing the disease – at least we don’t yet know/haven’t proven if having optimal macular pigment reduces the risk of AMD progressing to an advanced stage such as wet AMD or Advanced Dry AMD/Geographic Atrophy. Those types of clinical trials take a LONG time.

We DO know it is about:

  • protecting the photoreceptors from further assault and damage from oxidative stress;

  • improving the symptoms that make vision with AMD problematic: problems with glare and contrast, slow recovery from bright light, slow dark adaptation;

  • protecting the photoreceptors from damaging blue light. Here’s a great video where Dr. Nolan talks to Dr. Kerry Gelb about it. https://youtu.be/wpV4dWd3_80

AREDS2 Formulation Plus Meso-zeaxanthin for Some

What HAS been shown is that for those who are good candidates for an AREDS2-based formulation – those with intermediate dry AMD or with wet AMD in one eye but not the other – adding meso-zeaxanthin DOES improve vision while providing that same reduced risk of progressing to wet AMD found in the AREDS & AREDS2 research.

Dr. Nolan’s CREST Trials

In 2011, Dr. Nolan received funding from the European Research Council to do 2 trials called ‘Central Retinal Enrichment Supplementation Trials (CREST).

Their research question was: if we enrich a person’s macular pigment by giving them LMZ as a supplement, can we improve visual function as measured by contrast sensitivity as the primary endpoint and visual acuity, glare disability, and other measures of vision as secondary endpoints.

CREST AMD (sometimes referred to as CREST 2)

There were 2 CREST trials, but I’m leaving out the details, including those for Trial 1. Dr. Nolan can fill us in about it (and a lot of his OTHER research that I’ve not discussed – there’s just been SO much!).

Trial 2 is called CREST AMD, so they studied people with early AMD. Their primary measure was contrast sensitivity. There were 32 tests in all!

There were 2 treatment groups who both got a supplement with the ingredients from the AREDS2 formulation: Vitamin C and E and 25 mg of zinc, lutein and zeaxanthin.

Group 1 also got meso-zeaxanthin.

You’ll find a good graph in this article that shows the results. The article says, “Patients with AMD would have usually been expected to experience a continued deterioration in their vision throughout the 2 years of the clinical trial. Instead, those receiving carotenoid supplementation showed a significant improvement across 24 out of 32 tests of vision. Improvements in vision were particularly marked among those patients receiving all three carotenoids (group 1) compared with those receiving only Z and L (group 2). Of note, 34.8% of trial participants who received all three carotenoids had what is deemed to be a clinically meaningful improvement in their vision after 24 months, compared with 19.6% of patients on the AREDS2-like formulation (see Figure 1).”

‘CREST AMD Trial: Vision Improvement Among Patients with AMD Who Consume Xanthophyll Carotenoids’ https://www.optometricmanagement.com/newsletters/nutritional-insights-for-clinical-practice/may-2018

What If Your AMD Is Beyond the Early Stage?

It’s not been studied, I’m sorry. However, since we know that LMZ protects the macula from further damage from oxidative stress and from further damage from blue light and has proven to reduce symptoms of glare and contrast sensitivity, improves dark adaptation, and improves photostress recovery, I think it’s safe to assume it will have a positive effect for you, too!

It’s Also About Alzheimer’s

No matter what stage AMD you have, LMZ also reduces your risk of developing Alzheimer’s Disease. Every time there’s an article about the link between AMD and Alzheimer’s Disease, it causes quite a stir.

The connection isn’t between AMD and Alzheimer’s: it’s the connection between the eyes and the brain!

Next: PART 5 AND FINAL-COMMENT 10: SHOULD THE MOORES TAKE A LMZ SUPPLEMENT?

Daydreams About Driving – Part 1

I gave up driving over five years ago, but that does not mean I don’t miss it. In the past few days I have been daydreaming about going to visit a friend on a small Caribbean island. When I inquired about how I could get around when she is working, she said I could rent a golf cart. Could I actually drive a golf cart around the island?

Pitiful to say, but I got all excited with the idea of being independently mobile. I got almost giddy with thoughts of driving myself to the store and to the beach. How fast can a golf cart possibly go? I certainly could drive a golf cart!

The next thought was wondering if I had given up driving too soon. Maybe I could have gotten another year behind the wheel.

Although dry age-related macular degeneration is not supposed to act this way, it seemed as if I lost my second eye overnight. Would I have decided to give up driving so quickly if my vision loss had been more gradual? When and how do we know to stop driving?

I found an article from Caring Home entitled Seniors and Driving : A Guide. The statistics quoted in the article are a few years old (2015) and they are scary. In 2015, 14 million Americans were in an auto accident caused by an elderly driver and 19 elderly drivers were dying in an accident every day. This does not assume every one of those elderly folks was visually impaired but certainly some were.

We slightly older folks all have good ideas of what factors make it harder for us to drive. In addition to our vision loss there are things like chronic health problems, hearing problems, and drug effects and drug interactions that can limit our ability to drive safely.

But since this is a blog on AMD, let me focus on vision for just a second. The article quotes Elizabeth Dugan, author of The Driving Dilemma, who says 90% of the information that is needed to drive safely comes to us through our eyes.

And what happens when we are not getting that information? How do we know when it is no longer safe to drive?

The article suggests the police and the insurance company may notice before we do. Are you getting traffic tickets when you never had any before? Have those “little” fender benders resulted in a jump in your insurance premiums?

And even if you have not had any fender benders, how about scratches and dings to the car? In the months before my mother and her siblings took my grandfather’s keys, there were multiple “mystery” scrapes and dents on his car that my grandfather always insisted had just appeared out of thin air.

About that time I was a teen with a job but without my own car. I was reluctant to have my grandfather drive me to work and white knuckled it all the way. The man was scary behind the wheel, and I was always grateful to get there alive.

And speaking of reluctance, have you been recently reluctant to do the driving? Quite frankly, have you scared even yourself a few times?

Lastly, the article talks about your tension when you are driving. Do you lean forward and strain to see? Do you feel overly tense and come home exhausted? Does driving seem like a chore?

If these things are happening, it might be time to think about giving up driving. But don’t want to give up driving? There might be a reprieve for a little while. Next, I will review some of the driving rehabilitation services that may be available to you.

Next: Daydreams About Driving – Part 2

Retinal Repair Using Stem Cells: Part 2 – Current Status 2020

There have been stem cell trials for retinal repair going on in various locations around the world since the FDA approved their use for retinal repair research in 2010.

Warning: there are no FDA-approved stem cell trials outside of research. Why is that important? Check out the first article in this series for the details.

The Problems in Early Research

The goals of the continued clinical trials are to solve these problems:

  • There have been ethical issues with using embryonic stem cells related to religious and political disputes about when life begins.
  • Early research using embryonic stem cells found that these cells were often rejected.  That means that if they are used, the participant takes immunosuppressant drugs exposing them to other diseases. Also, early research found that sometimes these cells migrated and caused tumor growth outside the eye.
  • Stem-cell-induced RPEs injected in a suspension under the retina didn’t stay in that area to integrate with the person’s RPE cells.
  • The method of getting these stem-cell-induced RPEs into the retina through a  surgery called a vitrectomy adds to the risk of adverse effects such as retinal detachments.

I am greatly simplifying this topic because it IS complicated! If you would like a detailed review of this period of time, check out Retinal stem cell transplantation: Balancing safety and potential. It’s written using highly-technical language, but I think the conclusion is clear:

“The promise of stem cell therapy to preserve or restore vision in retinal degenerative diseases is finally taking shape. Whereas a decade ago, such ideas were confined to basic and translational laboratories, in the current era, stem cell transplantation into the retina is finally in human clinical trials in the setting of well-run registered clinical trials with the oversight of the FDA and appropriate ethical and safety review infrastructure built in. These aspects promote the protection of study subjects from undue harm, and facilitate the dissemination of the results to the scientific community and the peer review process.”

Status as of 2018

If I counted correctly, there are 18 clinical trials listed in a chart in the article Stem Cell Therapy in Retinal Disease. Sometimes they are called ‘RPE transplantation.’ They vary in:

  • location of the research: US, UK, Japan, China, and others.
  • source of the stem cells: embryonic, autologous cells which are cells taken from the participant (bone marrow, blood, skin).
  • how the stem-cell-induced RPEs are organized:
    • loose in a suspension which is a fluid or
    • on a single layer of some kind of material (monolayer) that connects them to keep them together. This simulates how normal RPEs are positioned on Bruch’s membrane. The designs and composition vary, but some other terms for this approach are patch, scaffold, layer, implant, or sheet.
  • type of delivery method: injected into the vitreous fluid or inserted below the retina using various procedures.
  • type of retinal disease: AMD both wet and dry, Stargardt’s Disease, Myopic Macular Degeneration and Glaucoma.

Status in 2020

There are 3 stem cell clinical trials that have been making headlines in late May and early June 2020.

London Project to Cure Blindness

In 2015 in a phase 1 UK clinical trial, stem-cell-derived RPEs on a patch were inserted into the retinas of 2 people who had vision loss from wet AMD. In 2018, it was reported that they had gone from not being able to read at all, even with glasses, to reading 50-80 words per minute with normal reading glasses.

A recent update said that 5 years later, these 2 people have retained this improvement. There are other people enrolled in this clinical trial. When the COVID-19 lockdown has lifted, they will be treated.

Lineage Cell Therapeutics OpRegen Clinical Trial

For those who have advanced dry AMD called geographic atrophy (GA), there are 2 issues:

  • There are areas of no vision from dead photoreceptors which are called scotomas or blind spots.
  • These scotomas continue to grow and vision loss gets worse.

In 2015, the company Lineage Cell Therapeutics started a phase 1/2a clinical trial in locations in the US and Israel using their biologic product OpRegen. OpRegen is a suspension containing human embryonic stem cells. There were 4 cohorts (groups) where the treatment varied by the severity of the GA of the participant, 1 of 2 forms of the suspension, the delivery system used, and the number of cells use. For some of the participants they used a delivery system they developed called Orbit Subretinal Delivery System which delivers the stem cells into the retina without the need for a vitrectomy.

The FDA ‘fast tracked’ the clinical trial because “the drug fills an unmet medical need in a serious condition.” That means it will get faster communication and review with the FDA (more details in ‘BioTime’s Subsidiary Cell Cure Neurosciences Ltd. Receives FDA Fast-Track Designation For OpRegen® For The Treatment Of The Dry Form Of Age-Related Macular Degeneration.’

Preliminary data for the 5 participants in cohort was presented in 2020. The findings were:

  • The stem cell product and new delivery system were safe and well tolerated in all 17 participants.
  • For 5 people, there was an average of a 10 line increased in visual acuity over the 15-month followup period.
  • Testing showed improvement of the RPE area with a reduction of the amount of drusen and a decrease in the size of the scotomas of some participants.

National Eye Institute

After positive results using animals, the National Eye Institute announced a Phase 1/2a clinical trial in which a person’s own blood will be used to create stem-cell-induced RPEs that will be transplanted into the retinas of 12 participants who have geographic atrophy. There are two important aspects of this clinical trial:

  • By using a person’s own cells, it reduces the chance that the body will reject them. That reduces the need for Immunosuppressant drugs.
  • The stem-cell-derived RPEs are put onto a single-cell (monolayer) biodegradable scaffold or patch. It’s the first clinical trial in the US to do this.

As a phase 1/2 trial, the participants will be monitored for a year for adverse events to make sure that the stem cell patch and procedure to insert it are safe. Based on the promising results of past stem cell clinical trials, they also hope to see improvements in visual acuity.

Hope for Those With Vision Loss

Vision loss from the advanced stages of any type of macular degeneration is devastating. This line of research has advanced greatly in 10 years. There have been promising results so far. Current and future research is building on those results to give HOPE that vision loss can be stopped and even reversed!!

 

Retinal Repair Using Stem Cells: Part 1 – Background

Research into macular degeneration is aimed at:

  • stopping the disease from developing
  • treating it so that the disease process stops
  • reversing damage that has been done
  • curing it

I’ve shared many examples of each of these areas. You’ll find links at the end to 4 of my articles about research for wet AMD, for dry AMD, for gene therapy research, and for a cure.

In this article, we’ll look at what’s being done in clinical trials to reversing damage and to restore vision that has been lost.

Reversing Damage That Has Been Done

What about those who have an advanced form of macular degeneration and have suffered vision loss? This can occur in any form of macular degeneration including AMD, Stargardt’s Disease, and Myopic Macular Degeneration. The stem cell research applies to all of these.

Vision loss occurs when the photoreceptors die. These cells transmit signals to the brain which is where we get our sight. They convert ‘light to sight.’ They die because the cells that keep them alive called RPEs (Retinal Pigment Epithelium) falter and die. These RPE cells are critical to the retina’s ability to dispose of waste and to make sure the photoreceptors are nourished. We know that retinal cells don’t regenerate, so researchers have been asking the questions:

Can we keep the RPE cells healthy? Can we replace RPE cells that have died? If we do that, can we restore vision that is lost?

There is research into replacing photoreceptors, but it’s more difficult to do. It is currently being explored in the lab and with animals which is called pre-clinical research. 

Restoring RPE Cells – Restoring Sight?

The answer to those questions about RPE cells have been found in the area of stem cell research. What are stem cells? They are specialized cells in our body that can make other types of cells. No other cells can do that. The stem cells used in research come from different sources. You can learn more about them in National Institute of Health’s Stem Cell Basics and A Closer Look at Stem Cells.

Here’s a very simplistic explanation as to why stem cells are of interest in retinal repair:

  • If they can make other types of cells, can they make RPE cells? The answer is yes! These new RPEs are called stem-cell-derived RPEs, and they’re created by the ‘magic’ of science (it’s complicated!) in the lab.
  • If we could take those stem-cell-induced RPEs and get them into the retina, could they replace failing or dead RPEs and keep the photoreceptors alive?

That’s exactly what researchers are working on.

Warning

The topic of using stem cells is one that has been discussed in MANY areas of healthcare. For retinal repair, there is NO proven safe and effective use of stem cells as a treatment for macular degeneration outside clinical trials which follow procedures that are rigorous and based on the scientific method. The first step is to establish the safety of the proposed treatment – that’s Phase 1. Only if the treatment is proven to be safe do the clinical trials progress to find the right dosage needed to be effective and to monitor any side effects. FDA approval comes at the end of a series of phases. You can learn more about clinical trials and why they are important by reading Treatments and Cures: Too Good to Be True? You can also find out what the FDA does and does not do related to macular degeneration.

Beware Unproven So-Called Treatments

Some people and clinics sell these unproven, not-FDA-approved stem cell treatments for macular degeneration. These costly procedures have blinded people & have not been effective for others. For more information about that, you can read FDA Warns About Stem Cell Therapies – Some patients may be vulnerable to stem cell treatments that are illegal and potentially harmful. The FDA has been working to shut down the sellers – that’s what they are – of these possibly dangerous procedures.

Unreliable Resource

The NIH National Library of Medicine has an online resource available called clinicaltrials.gov. It’s where researchers can list their studies which can be accessed by patients, their family members, health care professionals, and the public. Unfortunately, the site has no oversight, no vetting of the entries to make sure they are legitimate studies. Just because you find something that sounds interesting to you or someone you love, it doesn’t mean it is something to seriously pursue. You need to do much more research. I recommend the article Nine Things to Know About Stem Cell Treatments.

Stem Cell Research for Retinal Repair

The FDA approved their use for retinal repair in 2010. You can read about the early research in the 2018 article Stem Cell Treatment in Retinal Diseases: Recent Developments.  Also, you can watch a great 2018 video Retinal repair: Bringing stem cells into focus.

The study of using stem cells is called regenerative medicine.

The Basics

Since retinal repair research started in 2010, the studies have varied primarily in two aspects:

    1. The source of the stem cells. The options used so far are embryonic stem cells and induced pluripotent stem cells which are adult cells that are reprogrammed to look and act like embryonic stem cells. You can read about these in What Are Stem Cells and How Do They Work.  The more recent research has moved to using the induced pluripotent stem cells for several reasons: use of embryonic stem cells has raised ethical issues, they are hard for researchers to get, have a higher risk of rejection, and they can migrate to other places with a possibility of creating tumor cells.
    2. The method of transplanting the stem-cell derived RPEs. The purpose is to get these new cells in the area of the RPEs so they can be integrated with them. Initially, the cells were put into a suspension (a fluid) and injected into the retina. Unfortunately, those stem cells didn’t stay where they were placed. With the help of engineering experts, more recent research has put these cells on a monolayer (single layer) of a material to keep them together so that when they are implanted in the retina, they will stay in that area. The designs vary. Some other terms for this approach are patch, scaffold, layer, implant, or sheet.

Summary of the Concept

The basic way stem cell research is conducted is that ‘new’ RPE cells are created in the lab from stem cells and injected into the retina. Hopefully, these stem-cell-derived RPEs should then integrate with the person’s own RPE cells so that they can do what RPE cells do: nourish and clean up after photoreceptors. Sounds simple, yes? It isn’t. There are issues regarding rejection of these new cells and the safety of using immunosuppressive drugs, their possible migration to other places in the body where they may create tumors, safety of the method that delivers the stem-cell-derived RPEs, and more. That’s why the clinical trial process is so important!

The History

As I wrote above, the FDA approved the use of stem cells for retinal repair in research in 2010. Phase 1 clinical trials started that year. The purpose of phase 1 clinical trials is to make sure the treatments are safe. Since stem cell research for retinal repair was so new, researchers were very careful. These early studies used embryonic stem cells with their possible complications. One early trial was stopped out of concern for the participants

Since then, many clinical trials have been done.

When doing your own research on this topic, make sure to check the dates of the resources since much has changed since 2010.

Two early Phase 1 studies were started in 2010 by Advanced Cell Technology (then called Ocata which became Ocata Therapeutics; it’s Astrellas currently). Professor Steven Schwartz, MD, and colleagues reported that 4 months after the first patients had the procedure they found no safety issues of tumor growth or rejection from using embryonic stem cells and no loss of vision. In 2015, they reported that of the 18 patients treated, more than half had improvements in visual acuity. They found evidence that the new RPE cells were integrated in the retina. They also reported that although the treatment was safe, which meets the objective of a phase 1 clinical trial, more follow-up was needed. 

I could give you a LONG list of articles about the clinical trials that came after this one. A lot of progress was made, a lot was learned. I want to fast-forward to where we are today with this promising research.

Next: RETINAL REPAIR USING STEM CELLS: PART 2 – CURRENT STATUS 2020

More Research

A Cure in Our Lifetime?

Have Dry AMD and Wonder When There Will Be a Treatment? 

Have Wet AMD and Hoping for Something Other Than Injections?

Gene Therapy Research for AMD. Stopping the Disease

What is geographic atrophy?

Question: What is Geographic Atrophy?

Answer: There are stages of AMD: early dry (everyone starts at that stage even if not diagnosed them), intermediate AMD, and advanced AMD which is either advanced dry which is geographic atrophy (GA) and/or wet AMD. A few things to clarify:

  • Although it is rare, a person can have both wet and GA in the same eye.
  • Not everyone progresses to an advanced stage. 85-90% of all people with AMD have the early or intermediate dry form.
  • Although they all have the word ‘dry’ in them, progression is not necessarily from early to intermediate to advanced dry AMD. The progression CAN be from early dry to intermediate dry. Not everyone progresses beyond that.
  • It’s called ‘geographic’ because when the eye doctor looks at the retina, there are often what looks like ‘islands’ of damaged macular cells.

The Science of AMD

One of the best websites I’ve found is called The Science of AMD. 

If you scroll/move down the page, you’ll find a section about Geographic Atrophy. This site gives you the ability to hear the text (convert text to speech) if you select the speaker icon in the upper right of any section.

I recommend that you take the time to explore this site.

Other Resources

‘What is Geographic Atrophy?’

‘Geographic Atrophy’

Living With GA

Living With GA

My friend of 40+ years Sue has had geographic atrophy for over 6 years. That means she has a blind spot in each eye and is legally blind. She has always led an active life and that hasn’t changed any. At 69, she works as a psychologist, attends multiple exercise classes, kayaks, skis, rides her bike, walks her 2 boisterous dogs…you name it, she does it. The only thing that she does not do that she did ‘before’ is drive. That hasn’t stopped her from going places and doing things.

I’ll let her tell you about living with Geographic Atrophy: “I am not a victim. I have had geographic atrophy (dry age-related macular degeneration) for over 6 years but it has not destroyed my life. It has not destroyed me. Nothing is in ruins and I am not suffering.”

Her story continues at ‘Living With Geographic Atrophy.’

She was enrolled in the phase 3 clinical trial for a drug then called APL-2, now called Pegcetacoplan. At the end of that trial, she was enrolled in the long-term study of the drug which will show the safety and effectiveness of it over a 3 year period. You can read about that and also about her plan to find a stem cell clinical trial! ‘My Diabolical Plan: Stem Cell Transplant for Dry AMD.’

You can read about the early days of her journey on our site ‘My Macular Degeneration Journey/Journal.’ In 2019, she started to write for the site maculardegeneration.net where you can read her articles.


GO BACK TO FREQUENTLY ASKED QUESTIONS

I have dry AMD. Will It Turn to Wet? What is wet AMD?

QUESTION: I have dry AMD. Will it turn to wet?

ANSWER:

Not everyone with AMD progresses to wet AMD. There is another FAQ with details about the risk of vision loss from AMD. Briefly, if you have early or intermediate dry AMD, your risk of progressing to wet is 10-14 or 15 %. That means that 85-90% of all people with AMD have the dry kind, so that’s the majority. Wet AMD is in the minority and rare, but if left untreated it can quickly cause central vision loss.

Parts of the Retina

The parts of a healthy retina.
Click on image to see it larger.

Let’s review the parts of the retina that are involved in AMD. From top to bottom there are the Photoreceptors (rods & cones) that convert light to sight, RPEs that take care of the Photoreceptors, Bruch’s Membrane, and the blood supply in the Choroid.

How and Why The Process Starts

VEGF (Vascular Endothelial Growth Factor) is a protein produced from cells that causes new blood vessels to develop when needed, such as after an injury or lack of oxygen. In most places in the body, that’s a good thing. But not when it happens in the retina.

Photoreceptors, RPEs and Angiogenesis

All AMD starts as dry even if it’s not diagnosed until it’s wet. As the disease progresses, drusen (we call it ‘eye poop’) builds up and can weaken Bruch’s Membrane. This causes inflammation which signals the release of VEGF. This process is called angiogenesis (‘angio’ refers to blood, ‘genesis’ refers to development of something).

These unwanted blood vessels grow through the weakened Bruch’s Membrane into the area of Photoreceptors and the RPEs.

Wet AMD and CNV

This process is called wet AMD and CNV (Choroidal Neo-vascularization refers to the Choroid, ‘neo’ refers to new, and vascularization refers to blood vessels).

Wet AMD is Exudative Macular Degeneration

Those new blood vessels are fragile and can leak fluid, can rupture and leak blood, or both. That’s where the ‘wet’ descriptor came from. These fluids are ‘edudates’ which is why sometimes you’ll see wet AMD referred to as Exudative AMD and dry as Nonexudative AMD.  CNV can occur in any form of macular degeneration.

Symptoms from Wet AMD/CNV

For normal vision, the macula needs to be flat. The blood or fluid collects in something similar to a blister which distorts vision and causes a person to see wavy lines and have other distortions. Have you ever had a drop of water fall on a piece of paper with writing? It distorts what is under it, right?

Make sure if you have any changes in your vision that you contact your eye doctor as soon as possible. Research has shown that the sooner treatment is started, the better the prognosis.

Inflammation

This buildup of fluid or blood causes inflammation (edema) and can form scar tissue which cannot be removed. It can also cause damage to the RPEs, so they’re not able to keep the Photoreceptors working well. It can also kill the RPEs. If the RPE dies, the Photoreceptor dies, and central vision loss occurs. That’s why it is so important to get treatment as soon as possible!

The Injections

The medications that are injected into the eye are called anti-VEGF because they block the further release of VEGF. They are also called angiogenesis medications. That stops new blood vessels from growing. You might think of a VEGF protein as a lock. The anti-VEGF medication puts the key in the VEGF lock to stop it.

Current Anti-VEGF Medications

The current anti-VEGF medications are Lucentis, Eylea, Avastin, and Beovu. For some people, the disease is slowed down by repeated treatments. For some, vision improves. Everyone is different.

‘Dried Up’ is not Dry AMD

The blood and/or fluid is then reabsorbed by the body. That’s why you’ll hear the retinal specialist say that the eye is ‘dried up.’ That’s not the same as dry AMD. Wet AMD cannot go backwards, but sometimes it goes into something similar to remission and can remain stable. You always have to be diligent to check your vision and report any changes.

The anti-VEGF medications wear off quickly, so repeated injections are necessary.

New and Better Treatments on the Horizon

There is a lot of research related to wet AMD/CNV. New treatments will extend the time between them and replace injections with eye drops and oral medications. It’s the drops and pills that many people are looking forward to! You can find out more in the article ‘Have Wet AMD and Hoping for Something Other Than Injections?’

Even better, with gene therapy, a ‘one-and-done’ treatment may stop the disease entirely. There’s more about this in ‘Gene Therapy Research for AMD.’

Great Resource

One of the best sources of information about AMD is from the Angiogenesis Foundation’s site ‘Science of AMD.’  There you can find text explanations with audio available, colorful illustrations, videos, and brochures.  They are a not-for-profit site, so they don’t sell anything. That’s a good indication that their information is not biased.

There is an excellent infographic explaining the angiogenesis of AMD.


GO BACK TO FREQUENTLY ASKED QUESTIONS

 

Should I take eye vitamins? What’s AREDS2?

QUESTION: Should I take eye vitamins? What’s AREDS2?

(Updated October 2022)

This only applies to those with Age-related macular degeneration (AMD or ARMD) not any other form of macular degeneration (MD).

This is NOT medical advice. It is information for you to use:
– to do your own research
– to ask questions of your eye specialist
– to ask questions of your medical doctor.

The Basics

1. What is AREDS and AREDS2?

They are NOT brand names.

AREDS stands for Age-Related Eye Disease Study. There were 2 studies: AREDS results released in 2001; AREDS2 results released in 2013.

2. What was the purpose of the studies?

The purpose of these studies was to see if a specific combination of vitamins and minerals would slow the progression of AMD to the advanced forms of wet or advanced dry/geographic atrophy. They were both conducted by the US National Insititute of Health (NIH) National Eye Institute (NEI). The Bausch & Lomb company provided the formulations & financially supported both studies. Click here to read the information provided by the NIH NEI about AREDS and AREDS2.

3. What were the formulations?

Both studies used 500 mg of Vitamin C and 400 IUs of Vitamin E. In the first study (AREDS or AREDS1), they used 15 mg of beta carotene, a carotenoid. When research showed a connection between beta carotene and lung cancer in smokers and former smokers, beta carotene was removed in AREDS2 and replaced with 2 other carotenoids: 10 mg of lutein and 2 mg of zeaxanthin.

Both studies included zinc: AREDS used 80 mg of zinc. In AREDS2, there were 2 groups, one with 80 mg of zinc and a second with 25 mg of zinc. Both groups had the same posotive results, but because AREDS2 did not have a true placebo group, the NEI says that the ‘gold standard’ for the formulation includes 80 mg of zinc. Because zinc removes copper from the body, copper was included: 2 mg of copper with 80 mg of zinc, 1-1.2 mgs of copper with 25 mg of zinc.

Bausch & Lomb has the patent to both the AREDS & the AREDS2 formulations with 80 mg of zinc. Because of that, their PreserVision products are the only ones with 80 mg of zinc. After AREDS2 results were published in 2013, many companies marketed their ‘AREDS2-based’ products with the same formulation but with 25 mg of zinc.

4. Who in the studies did they help?

They were effective in slowing down the progression to wet AMD (but not geographic atrophy) for some people with:

a) intermediate dry AMD.
b) wet AMD in one eye but not the other.

5. What about the rest: those who do not have AMD, have early AMD, have wet AMD in both eyes or have another form of macular degeneration such as Myopic Macular Degeneration (MMD) or Stargardt’s Disease (SD).

a) They were NOT tested on those who do not have AMD or have wet in both eyes.

b) They were tested on those with early AMD in AREDS but not AREDS2 because they showed NO benefit in the 6+ years of the study.

c) They’ve NOT been tested on those with another form of macular degeneration.

6. What’s the harm taking them if they weren’t tested on people like me?

Some of the ingredients are high doses. There’s been no research on whether taking them if you don’t need them is safe or effective. Would you take a blood-pressure-lowering medication if you did not have high blood pressure?

7.  What is the controversy about zinc in AREDS and AREDS2?

A 2018 study using the genetic profiles of some of the participants of the AREDS study (the first one where 80 mg was used) found that for 15% of the people with a specific genetic makeup (I call it being ‘zinc sensitive’), their AMD progressed faster than those in the study with a different genetic makeup.

8. I’ve heard not everyone agrees with those findings. What’s up with that?

This finding has been disputed by the NIH NEI researchers involved in the AREDS and AREDS2 research. The NEI, some eye specialists, and the AAO (American Academy of Ophthalmologists) take that side and say that genetic testing is NOT necessary because there is no difference in effectiveness of the 80mg of zinc based on genetics.

The opposite view is taken by the researchers involved in the 2018 and prior research. The genetic testing they used in that study and previous studies is available through your retinal specialist by the ArcticDX company.

9. My stomach hurts when I take PreserVision. Why would that happen?

The National Institute of Health’s Office of Dietary Supplements says that the upper tolerable limit of zinc is 40 mg.  According to their page, some of the signs of too much zinc are “nausea, dizziness, headaches, upset stomach, vomiting, and loss of appetite. If you take too much zinc for a long time, you could have problems such as lower immunity, low levels of HDL (“good”) cholesterol, and low copper levels. Taking very high doses of supplemental zinc can reduce your body’s absorption of magnesium.”

References

AREDS Results. ‘A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss’ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1462955/

AREDS2 Results. ‘Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial.’ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5369607/

 


go back to frequently asked questions

Happy Anniversary to Us!

Hi! Happy Anniversary to us! It was February 2016 we started this crazy journey. For those of you who have been around since nearly the beginning, thank you for sticking around and putting up with us! For you who are newcomers, welcome! [Lin/Linda: To read Sue’s very first page, it’s In the Beginning.  At the bottom of the page, there’s a link to In the Beginning: Revisited where you can read about how her life has changed.]

I had a déjà vu experience at the beginning of the week. It was January 31, 2016, when I went skiing and came home to a drastic vision loss. It was January 29, 2019, I went back to the same ski slope, had the same sort of glorious day on the slopes and…came home to the same vision loss I had when I went. That was a bit of a relief! [To read about that day of skiing, it’s The Perfect Storm.]

I cannot tell you I am above engaging in a bit of superstitious thinking about such things. I was relieved when nothing happened.

Anyway. What does my vision look like now ? I have a fuzzy section pretty much in the middle of things. Anything I want to focus on is not all there. I recognize people across a room by body type or other clues. I can see faces well enough to identify them from about two feet.

If I am running the dogs at the dog park, they can disappear into my blind spot at maybe 20 yards or so. That is a guesstimate. I am definitely not able to drive. There were men working on the road the other day. I did not see them until we were maybe 30 yards away. Not enough distance to stop if I had been driving at the same speed.

Reading is done but is greatly curtailed as compared to my pre-AMD rates. I can read a couple of pages of standard font using eccentric viewing. I have a terrible time reading handwriting, especially handwriting of those I do not know. Heck, sometimes I have trouble reading my own handwriting! [To read Sue’s page describing how she uses eccentric viewing, it’s How She Sees What She Sees.]

I am typing this with a standard, 12 point font. I read it back to myself and find typos at a fair, not excellent, level. That is on my iPad. If I am writing reports on the standard laptop I use 28 point font. After the office staff puts it in standard form, I proof it using my CCTV.

I am able to do most of my life skills just fine…or as fine as I ever did. I have never been a housekeeper or a cook. If I don’t want to resort to using my toys, I sometimes have trouble reading directions. I have trouble plugging plugs into outlets and, at the beginning of the cold weather, zipping my jacket can be an event.

In other words, it is not awful. A few toys, a few tricks and a little help from my friends and I am making it. This is three years into being legally blind.

Again, a reminder: I have geographic atrophy. That is “the other” advanced age-related macular degeneration. Even though we dry folks make up something like 80% of the AMD population, we get short shrift.

Why? Well, we do not have the dramatic changes in vision or the severe damage the wet people can have. We also do not have any treatments. If any one knows the term AMD and he finds out I have it, he will almost always ask about “eye shots”. Afraid not, buddy. No treatment. No cure. This girl is dry.

I gotta go, but I refer you to some pages Lin is putting on the FB page. Not everyone gets wet AMD. Most of us actually have dry.

Do I think I will get wet AMD? Nope. None of my doctors think I will either. GA is my way.

Thanks again for being with us!

[By the way, February is also AMD and Low Vision Awareness Month. What are YOU doing to make more people aware of these two important topics?]

Written February 2nd, 2019

Next: READING AND WRITING

Sue on Assignment: Mitochondria – Part 3

In the interest of full disclosure, I would like to say this: I appear to have screwed up. I could have sworn I read Stealth has gotten FDA fast track status for a phase 1 clinical trial of its mitochondria treatment, elamipretide. Not exactly. It is a phase 2b trial and not a phase 1. Consider this to be my correction and my apology. Mea culpa. Mea culpa. [Lin/Linda: Sorry, Sue, I can’t let you take all the blame. I didn’t catch it, either. Sorry about that.]

According to a Medtran article on clinical trial phases, phase 2a trials are to evaluated the short-term safety of a drug. Sounds like phase 1 redux to me. The phase 2b trial is to start to check the efficacy of the treatment. It is also used to determine dosage range.

The press release Lin sent me appears to be where I initially saw the new drug is injected subcutaneous. That is under the skin. That is that mystery solved.

The dosage schedule is to be daily for 24 weeks. Read six months for that. Zounds. I don’t like the idea of having to go monthly!

I looked up elamipretide + age-related Macular Degeneration on clinicaltrials.gov and got one hit. It was the phase 1 study that was done with 40 people at Duke University in Durham, North Carolina. This study was listed as active, not recruiting. Either phase 1 is not totally finished yet or they have not let the clinical trials.gov people know it is finished.

Looking back on what Stealth published in 2016, I found they were looking for people with intermediate AMD in at least one eye but no geography atrophy or, for a second group, people with noncentral geographic atrophy. An exclusionary factor was having received “eye shots” to prevent blood vessel growth (anti-VEGF treatments.) This study appeared to be totally for those with dry AMD. I am assuming the experimental design and exclusionary criteria for phase 2 will be the same.

It appears information on all of this is rather sparse right now. We will keep our eyes open and see what else we can learn.

And my boo boo? Ahhh, really sorry about that.

Written December 22nd, 2018

Go back to the list of “On Assignment” pages

Sue on Assignment: Mitochondria – Part 1

Hi, again! I am not exactly on assignment for this piece. More responding to a couple of messages we received from a Facebook member. She was expressing excitement over new research on mitochondria. Lin and I knew little to nothing about this line of inquiry and I decided to look a little more closely.

Mitochondria. I have defined this word before and will do it again here. First of all, mitochondria contain their own DNA. This DNA is different from the rest of the DNA in your body. Why? Thank you for asking. The reason is this: the DNA in the nuclei of your cells comes from both parents. The mitochondrial DNA comes only from your mother and your grandmother and your great-grandmother and so on into the recesses of history. Sort of neat when you think about it. Anyway, the head of a sperm is 23 chromosomes packed into this itsy, little package. Nothing else in there. The egg, on the other hand, is relatively massive. The egg contains all of the parts cells have. This includes mitochondria. Ergo, your mitochondria is the same as every female in your mother’s direct female lineage. It can also be found in the male children of these women. In other words, when it comes to mitochondria, girls rule!

And mitochondria don’t have any old, little job. Every cell in your body, and by extension you, is alive because of the tireless work being done by the mitochondria. Mitochondria are described as the powerhouses of the cell. It is their job to mix oxygen with nutrients and produce ATP, adenosine triphosphate. ATP is the fuel for the cell. No, ATP, cells die. Cells die; you die. Thank mitochondria for your life.

Mitochondria also do other things. In Mitochondria and the Many Disorders That Compose Mitochondrial Disease they reported mitochondria have other duties tied to the specialized duties of the cell in which they are lodged and these duties change as we age. It is these other functions of the mitochondria that can lead to problems.

All of which is a rather long-winded way of saying it is looking more and more like some eye disorders are related to mitochondria malfunctions. Age-related Macular Degeneration might just be one of them.

Back in 2015 when the above mentioned piece was published in Mitochondrial Disease News, they cited work being done by a company named Stealth. Stealth was working on Ocuvia, this was a topical treatment for back-of-the-eye diseases such as AMD. Although only tried in non-clinical trials (read “rat lab”), Ocuvia was hoped to have a protective function for mitochondria. The medication was hoped to be able to deal with excessive oxidative stress and decreased energy supplies to the cells of the eye.

In the words of Artie Johnson (Laugh-in, 1968 to 1973), “very interesting.”

Lin gave me a couple of articles to look at concerning what Stealth is doing now. It would appear they are following this course of inquiry and looking for ways to treat mitochondria and AMD. Get back to you later on that. Bye!

Written December 12th, 2018

Next: Sue on Assignment: Mitochondria -Part 2

Go back to the list of “On Assignment” pages

Sue on Assignment: Mitochondria – Part 2

Like I said, it looks like they are now investigating the role of mitochondrial DNA in retinal diseases. Researcher Christine Kenney proposed damaged mitochondrial DNA sends signals that cause retinal cells to die at an increased rate.

Since a woman passes her mitochondrial DNA to every one of her offspring – unchanged except for possible mutations – and each of her female descendants passes the same mDNA to her offspring, it is possible to trace maternal lineage fairly easily. And you want to hear something wild? See Wikipedia for more data but suffice it to say here, researchers believe they have located the time and region of the most recent, common, female ancestor for us all. Or at least of whom we are aware. This woman lived in sub-Saharan Africa about 150, 000 years ago. How many greats Grammy would THAT be? Wow.

Now, since then mutations have happened and subgroups – referred to as haplogroups – have been produced. And that gets me back on track here. Kenney discovered our family members who are Jewish and originated in Central and Eastern Europe – you can think of them as Aunt Millie’s kids in Cleveland if that makes it easier for you – have much more AMD than Aunt Mary’s kids in Dallas. Those family members are black and came from Africa.  For all intents and purposes, the only  consistent difference between these two branches of Mom’s family is their haplogroups.

Hmmm, the plot thickens.

Nw, the problem becomes, this is just one more line of inquiry for AMD research. We thought we were looking for the needle in two haystacks – nucleus genes and environment – and now we are looking in three! We have to add mDNA to the list!

Kenney has decided to concentrate on the mDNA “haystack”. She has compared the Ashkenazi Jews (Aunt Millie’s kids in my little family saga) to Aunt Margaret’s kids. Aunt Margaret’s kids are white, Western European.  Aunt Millie’s kids have major differences in cholesterol and lipid metabolism, different inflammation and complementary genes and they have different sensitivities to amyloid, a toxin found in AMD and Alzheimer’s disease.

It would seem Kenney is on to something.

Fast forward to this week. Stealth Biotherapeutics has been granted FDA fast track status for elamipretide, a mitochondrial targeted treatment for dry AMD. This is a phase 1 study and is concerned with safety and tolerability only. This stuff is very early in the game. [Lin/Linda: both Sue and I missed the part of this press release that says, “In early 2019, Stealth plans to initiate a Phase 2b, randomized, double-masked, placebo-controlled clinical study to evaluate the safety and efficacy of subcutaneous injections of elamipretide in patients with dry AMD with geographic atrophy.” Sorry about that!  You’ll see that we’ve added a page to this series – see the link below.]

Elamipretide is hoped to restore the mitochondria’s ability to produce energy. It can be applied directly to the eye or injected. I thought I saw it could be a standard injection and not an eye shot, but now I cannot find where I saw that. Don’t hold me to it.

And there you have it. Here is another, possible line of inquiry for discovering what is happening to our retinas. And more importantly, in trying to stop and maybe even reverse it. Here’s hoping!

(And a special thanks to our cousins, those of  Ashkenazi descent, who are participating in this research. Their mDNA makes them like Baby Bear, “just right”,  for the research. Their willingness to help might take us to a cure.)

Written December 13th, 2018

Next: Sue on Assignment: Mitochondria -Part 3

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Sue on Assignment: AREDS2 Study & Geographic Atrophy – Page 2

Hi! Back with trying to understand the last, three pages of the article “Progression In Geographic Atrophy in Age-related Macular Degeneration”.

It would appear they are having trouble figuring out exactly how these suspect genes are causing the problems they seem to be causing. Like watching a magic show: you know the magician has something to do with what is happening but you cannot seem to figure out how he is doing it!

They have come up with theories, of course. Some people think ARM2 encodes for a mitochondrial protein. Remember the mitochondria are the powerhouses of the cells. Others believe the ARM2 gene has something to do with our old friendly nemesis, the complement immune system.

While in some cases they believe it makes more sense to believe one mechanism is responsible for several lesion characteristics, in other cases they believe there are separate mechanisms at work. And to make matters even more complex, they are thinking the whole thing may work on the “Goldilocks principle.” In other words, certain genes may not necessarily be bad or good. Like the chairs and the porridge, they may have times they are “just right” and highly beneficial for the cell. Other times? Not so much.

In short? Damned if I know and, more importantly, damned if the researchers know either. However, they are hot on the trail of…something.

Right now at this stage of the game, they are collecting knowledge. It may be quite a while until they connect the dots with all of this stuff, but connect the dots, they will. Then we shall see what the picture is.

So, what did I get out of this article? A lot of questions. Like good investigators, right now the researchers are gathering data. The AREDS2 study has made available to researchers thousands of people with AMD. These people are being poked, prodded and scanned in the name of trying to understand the nature of the beast. No clue what they may find but the hypotheses being generated are intriguing. Which one do you think may prove to be right?

Written September 20th, 2018

Next: coming soon!

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Sue on Assignment: AREDS2 Study & Geographic Atrophy – Page 1

I am back on “special assignment”. Lin asked me to try to make heads or tails out of a very scientific article entitled “Progression of Geographic Atrophy in Age-Related Macular Degeneration.” It is report number 16 in the AREDS series.

Me thinks she has more confidence in me than I have, but let’s give it a shot. Just remember, social scientist here. My interpretations are always subject to errors.

The article starts with a description of Geographic Atrophy (GA). As many of us know, GA is defined as discrete areas of cell death (atrophy) that eventually grow and come together to form “continents” of damage in the macula. Part of the definition requires the damage to be such that someone examining the eye can see the blood vessels in the next layer (the choroid).

GA usually starts in the macula but generally does not immediately affect the fovea. The fovea is the “prime” area of the macula where the best seeing is actually done. However, as the disease progresses, the fovea is often also involved.

GA involves scotomata, Greek for darkness. Scotomata are those dark islands in our visual fields and result from the death of the cells in those locations.

I am going to skip the methods sections of this article and go right to results….believe me, it is better for everyone that way?.

Okay…because there is no treatment and no cure for GA, science is presently focusing on trying to slow this train down. Worry about actually stopping it once we buy some time. In order to slow it down, we need to know something about it.

The study first calculated how many of their early AMD subjects either went on to develop wet AMD or went on to develop GA. This gave them some idea what the progression of the disease looks like when nothing is done. Basically, they were learning about the natural history of the disease as well as establishing a baseline.

They did make some interesting, incidental discoveries. For example, noncentral lesions grow faster than central ones. Enlargement of lesions occurred more rapidly if the subject had GA in both eyes as opposed to one eye.

Those of us with certain genotypes may be in worse trouble than others. Those who have risk alleles (half a gene pair) on ARMS2, for example, are potentially destined for faster lesion growth. One CFI at-risk allele is another example. Unfortunately, there are several more.

So, on to discussion! What did they actually conclude? Vision loss from GA was steady over the five-year life of the study. Of those in whom there was no central involvement when they were first assessed, 60% developed central involvement within five years. Up to 30% of the eyes with GA developed neovascular AMD within those five years. This was especially true if the companion eye was “wet.” GA lesions may grow more slowly when they are small and when they are large and more rapidly when they are midsized.

There are some genotypes – once again the infamous ARMS2 – that seem to predict both the formation of lesions and their faster growth. If you don’t have those genes, take up smoking. Smoking continues to be found to be a risk factor for both GA presence and growth.

There are three, more pages to go on this thing but I am above my self-imposed word limit here. Also, it is just about nap time. Take this up again tomorrow!

Written September 20th, 2018

Next: Sue on Assignment: AREDS2 Study & Geographic Atrophy – Page 2

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No Train for Christmas

Hi! Server is down again. This does not bode well. I have two hours I could be working, but I guess I bother you folks again.

Like I said, Lin gives me stuff. This one she gave me with the warning I need to be good. Generally, that is advice that goes in and one ear and out the other. I am a brutally honest sort. One of my mother’s favorite questions for me growing up was “Can’t you lie?” I assume you get the point. [Lin/Linda: Sue is paraphrasing what I said. What I said to her didn’t include a ‘warning’.  Whatever advice I DID give her obviously went in one ear and out the other. ::grin::]

The last article Lin gave me was the results of a poll taken by general ophthalmologists, retinal specialists, and patients with AMD. The poll asked for the highest priorities in retinal research. Number 1 was “the development of choroidal neovascularization.”  Number 3 was “retinal hemorrhaging.” Both of these are, of course, related to wet AMD. The second one had to do with studying geographic atrophy, i.e. advanced dry AMD.  Number 4 was “gains in vision.” Number 5 was “slowing vision loss”, and 6 was “serious ocular events.”

Now all of these are fine and noble areas of endeavor. I don’t have a problem with any of them in theory. So, why did Lin suggest I try to behave myself and not stir up trouble? Emotionally I have some problems with it.

Imagine a kid at Christmas. Her brother gets a train. She gets told there was nothing available for her they could buy. She gets nothing.  The next year her brother gets a bigger and better train. It will run smoother and go faster. She gets nothing. Her parents tell her they thought there might have been something for her, but it didn’t work out. Maybe next year. Next year comes and brother gets all sorts of accessories plus an even better train. Nothing for our girl. Nothing available.

I am getting tired of being that girl. I go to the research and there are nine, different, exciting opportunities for advancements in Wet AMD research. The tenth one may be for dry AMD, but it is often something that has since “died” in clinical trials.  No joy again.

Very selfishly, I feel we need to be first on the list. I appreciate you wet folks go blind more severely and much faster. I appreciate eye shots can be pretty horrible. The thought of having someone put a needle in my eye might make me want to throw up.

On the other hand, I would also like you wet people to try to appreciate what it is like to come to the table time and time again (or to the Christmas tree. Sorry for mixing metaphors) and come up empty. Think of the frustration and the demoralization of religiously looking, reporting great news for other people …but finding nothing for you.

Eye shots are horrible, but if they could come up with an eye shot that would stop the progression of this disease, I would be fighting to be at the front of the line. At least it is something. Right now we have nothing. [Just to be clear, the injections for wet AMD do NOT stop the progression of AMD. They work to protect the vision a person has. Sometimes, that only works as long as one is having injections. Sometimes, sadly, they don’t work at all or for long. In either case, there is no way of knowing ahead of time – it’s an injection-to-injection battle.]

So, yes, I get snarky, and I can be offensive. Some people don’t like my snide comments about how the wet people have another, miraculous advance coming down the pipeline and we have…nothing. Please just remember how blessed you are and wish your dry brethren a little bit more than nothing under the tree…and spare me a charitable thought when I look with jealousy on what you have. It is not easy out here.

August 28th, 2018

Next: “Wrap Up” Blindness in our Lifetime!

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Our Cub Reporter: Notes from an Awareness Program – Page 1

by Joann Davis

Joann recently attended the seminar ‘Your Eye Sight Matters! 2018’, an awareness program organized by the Macular Degeneration Association. These seminars are held in various locations in the US.  She’s generously sharing what she learned.  For more information about the agenda for this program which was held in Skokie, IL, on July 28th, 2018, click here.  The agendas for all of them are similar.


As the My Macular Degeneration Journey/Journal cub reporter, I will first describe the overall conference agenda.

They held the conference in a hotel ballroom with a nice breakfast set up outside. Pre-registration was done over the phone. The conference is presented by the Macular Degeneration Association, which is a 501(c) (3) non-profit supporting research and education. The founder and chairman is Larry Hoffheimer, a former federal prosecutor with the US Dept of Justice and a practicing healthcare attorney. Larry kicked off the meeting and served as the MC. The executive director, Donna, was also in attendance.

The two main speakers were Rajiv Rathod, MD, MBA, a Retina Specialist with Orange County Retina in California and Greg Hines, President and CEO of ArcticDX. Greg is the former CEO of a pharmaceutical company and lives in Toronto, CA.

Regeneron Pharmaceuticals is the primary sponsor of the conferences. Other sponsors are providers of products and services for the low vision community. Locally, the Chicago Lighthouse was a sponsor and provided info on their many services including their Seniors Program for those over 55 with low vision or blindness.

I sat next to a cool lady with advanced wet AMD who runs a low vision group in Des Plaines, IL. Like Sue, she had to wait for the special bus to pick her up when we ended a bit early. I gave her info on our group, and she should be joining soon.

Rajiv presented two technical topics. The first was Diabetic Macular Edema (DME), which is the leading cause of blindness in working people in industrialized countries. DME is caused when high blood sugar damages the small blood vessels in the eyes and causes the leakage of fluid, swelling of the central retina and blurred vision.

Treatment includes laser, intravitreal injections, and surgery. They have stopped using lasers because the lasers burn the macula and create blind spots. Primary treatment is the same anti-VEGF injections that wet AMD patients receive. DME can also be treated by the injection of steroids. Vitrectomy Surgery is used to remove scar tissue and is only used in very severe cases.

Prevention includes controlling blood sugar and blood pressure and getting annual screening exams if you have diabetes.

Continued on page 2.


About Joann

Joann Davis is 70 and has recently been diagnosed with mild dry AMD in both eyes. Her mother and grandmother both had AMD and her son has the genes. Joann also has cataracts, floaters, and dry eyes. With glasses, her vision is 20/40. Joann spends most of the year in northern Illinois and the winters in Ft. Myers, Florida. Joann is retired but very busy with numerous board memberships. Joann exercises every day, beginning with yoga, crunches, planks, ‘boy’s pushups’, weights, and then a long walk. Joann wants to do as much traveling as she can while she can still see and is heading to Italy soon and plans to go to South Africa next year. Joann’s career was in technology and cybersecurity sales, and she still belongs to cybersecurity organizations where she gets to hang out with the FBI and Secret Service.

These are not her first pages.  Check out her series Rookie in Training.

Gold in Them There Eyeballs

Good morning! End of July. How amazing! My elders always told me time flies as you get older. One more month of summer and that will be that.

Anyway, I have been ignoring my inbox. I need to get back to that. With four full days of clients and my “free” class homework and….sorry. In the news today or whenever this came…

As I suspected, the retina specialists discovered what was causing the inflammation after Eylea shots. It turns out that four lots of Eylea were responsible for 62% of the problems. The syringes included in the kits appear to have been somehow contaminated. Maybe. At this point, it is all speculative.

Lot numbers were made available to doctors at the end of February. All of these kits should be out of circulation at this time.

The take-home message for the consumer is this: report negative side effects. It may not be “just me”. You could be saving dozens of people from problems.

That was one tidbit from Healio. Another from Healio is they have fast-tracked APL-2.

As many of you know but some may not, fast-tracking is basically just making something a priority, rush job in FDA parlance. The FDA talks about facilitating the development and expediting the review of drugs that treat serious conditions and try to meet unmet needs. What fast track means in practical terms is the drug has a visitor’s pass that allows it to skip the line and get on the ride pretty much first.

Don’t you hate it when you are at the amusement park in line for what seems like hours in the hot sun and some clown waltzes up to the front…? Anyway, that is fast-tracking.

APL-2 is another pretender to the throne for the first, truly effective treatment for dry AMD. It is currently in the spotlight just like lampalizumab was until it failed in phase 3 trials. Hopefully, this complement factor inhibitor will have more success than lamp stuff.

And in case you are losing hope and don’t think any of the drug companies are truly interested in finding treatments for us, Healio gave cynical little me some reason to believe. Last year Novartis earned $2 billion during the second quarter. This year they earned $7.8 billion the second quarter. Novartis makes Lucentis. Sound familiar? How about ranibizumab? Same thing. The drug seems to be an up and comer in the treatment of wet AMD. A good portion of Novartis’ growth was due to ophthalmological treatments such as Lucentis.

Then there is Johnson and Johnson. That company is no longer just the band-aid people. Johnson and Johnson saw over a 10% growth in profits from second quarter 2017 to second quarter 2018. Johnson and Johnson makes contact lenses and eye surgery devices.

In short, there is gold in them there eyeballs! Considering there are roughly ten dry AMD patients for every wet one, how could any red-blooded capitalist resist? Dreams of riches beyond imagination!

And here you thought they did not care!

Written July 29th, 2018

Next: Do I Rage or Go Gently?

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Denizens of the Dry Side

Hi. I will have you know I just finished shampooing the living room carpet.? Done is done, and I am done in. Just a little too much pushing and hauling for my taste. Even with coasters under all the legs, that furniture is heavy!??

The moral to this story? There is always tomorrow…and if tomorrow doesn’t come, a half-shampooed carpet is the least of our worries! Do as I say, not as I do, and take care of yourself.

And since I am just about totally worn out, I guess that means it is time for a page. Don’t you love I think about you when my eyes are crossing, and I can’t get out of my chair?

Medscape published an article by Laird Harrison (cool name, Mom Harrison. Good job!) It seems there have been some reactions to anti-VEGF shots. A LOT of reactions. There have been “clusters” of inflammatory responses and they have many retina specialists concerned. One retina specialist was really unnerved when he had six patients with bad responses in one day!

The problem has been significant enough they will be talking about it at the American Society of Retina Specialist upcoming meeting. Maybe they will be able to do a bit of detective work and figure out what is happening. Bad batch? Allergic reactions? I don’t know, Watson, but I would suspect the game will be afoot!

If you had a bad reaction to a shot, I would suggest you make sure your specialist passes on the information. If it were a bad batch or something similar, there may need to be a recall. Get that stuff off the shelves.

Also at the ASRS conference, they will be talking about the port delivery system for ranibizumab and the phase 3 SCORE findings. SCORE is the study that compares bevacizumab to aflibercept. So far they are finding bevacizumab to have comparable effects.

HAWK and HARRIER are not only fighter jets. They are also studies trying to find a way to predict which anti-VEGF may work for a given patient….hmm. British fighter jets. British studies? No se.

And coming to the dry side, it appears APL2 is being investigated as a prophylactic measure for dry AMD. Remember the information from the poster session suggested APL-2 slowed the progression of atrophy but did nothing for acuity. Not sure why that would happen but most people want to see acuity losses slow and people became skeptical. Not sure what this move to prevention is all about but it may bear watching.

As usual, wet AMD continues to be the favored child with the researchers. Scanning the Retina Specialist article about what is in the pipeline and expected to emerge in 2018, the great majority of potential new products are for the wet form. There were three for dry and one of these was “lamp stuff” which most of us know failed in phase 3 trials.

Frustrating as it may be, hang in there oh denizens of the dry side. Miracles have been known to happen. I shampooed my carpet!?

Next: Mailbox or child?

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Orphan Drugs

Waiting for the puppygirls to dry before we go in the house. Explain why some dogs will go for a swim and then roll in the dirt. That is one of Etta’s favorite tricks. When the “mudbug” finally dries and I brush her, the dirt flies like it is coming off of Pigpen!

So, on the list today was at least thinking about shampooing the carpet. At this point, I have found the detergent for the shampoo machine. …oh, c’mon! That IS thinking about it! ?

I was going to do it. I really was, but Maggie the Mouth (aka MaggieVox with apologies to the electronics company) decided to have a barking fit at 3 am. Consequently, hubby is napping…good excuse; right?

Good reason for a page!

Number 2 on the Healio list of five top stories for June was about diabetic macular edema so I am skipping number 2 to go to story 3. They have implanted the EyeMax Mono lenses in the first cataract/AMD patient in Argentina.

We talked about the EyeMax Mono in spring 2017. The EyeMax Mono will move the image away from damaged parts of the retina and move it to a healthy location on the peripheral retina. The concept is the same as prism glasses; I think.

Remember neither of the new lenses they are implanting in cataract/AMD patients does a thing to stop the progression of the disease. What they both do is make the effects of the disease be less for a while. Not bad, but not the best I can imagine.

EyeMax Mono has been granted a CE mark in 34 countries. It has been embedded in patients in 25 countries.

The last article with any relevance to us….or at least what I see as relevant to us…is one about a drug for Stargardt’s being granted orphan drug status in Europe. For those just joining us, Stargardt’s is macular degeneration for young people. It proceeds at least generally like dry AMD progresses.

The drug, LBS-008, prevents the build-up of toxins in the eyes. It was granted orphan drug status by the FDA in 2017.

Just to be thorough, let me review the US definition of an orphan drug. According to the FDA’s site Developing Products for Rare Diseases and Conditions, the government provides funding for approved products intended to treat diseases and conditions affecting less than 200,000 people in the USA. Because of the rarity of the conditions they are trying to treat, companies developing these products could not be expected to recover development costs, let alone make a profit. Many of these product lines are abandoned due to cost.

The FDA reported that since the inception of the program in 1983, They have brought over 600 treatments for rare diseases to market. Between 1973 and 1983 the public section brought ten products to market.

And since I am ridiculously curious, I also looked up LBS-008. According to the article Lipofuscin in Dry AMD, LBS-008 tries to reduce Lipofuscin. In my usage, that is eye poop. LBS-008 is supposed to reduce the retinol in circulation, reduce the production of eye poop and lead to a better visual outcome. Once again it sounds like those low bulk dog foods they sold so people would have to pooper-scooper less. However, if it works out, it could be a good thing.

As of 2017, LBS-008 was in phase 1 trials. Remember that is safety and tolerability so they have a long way to go.

I got a long way to go, too. I have not gotten a thing done today. Time to get busy!

Written July 14, 2018

Next: Denizens of the Dry Side

HOme