macular degeneration, macular, diagnosis The Science Stuff – My Macular Degeneration Journey/Journal

Category: The Science Stuff

Sue – ‘Super Lab Rat’ – Fulfills a Pledge. March 2023

Hi, it’s Sue! Back in 2018 or so, I was celebrating getting into a clinical trial. I vowed I would do whatever I could to become the best, damn “lab rat” that Wills Eye Hospital had ever seen. I was going to be a super lab rat with all sorts of great accomplishments to my credit. [Lin/Linda here: it was actually June 2019 when she wrote about being accepted into the APL-2 clinical trial: Finally a Lab Rat. Considering how active her life is, I’m not at all surprised she can’t keep the dates straight! ::grin::]

Spokes Rat

Well, I don’t know if I have actually been good enough to be considered a super lab rat but today I fulfilled one of my pledges. Today I became a ‘spokes rat’ for the medication they have been shooting into my eye, Syfovre. Yes! If your mind can conceive it, you can achieve it. Positive thinking, folks, positive thinking. [At the end, I’ve listed the pages she’s written about her experience in this clinical trial.]

My friend took me to Wills Eye Hospital in Philadelphia today for my very first – and possibly last! – television interview! How do you like that for a kick in the pants? I was interviewed by the local CBS affiliate and I suspect the anchor person and the cameraman were really sorry they had caught this assignment. I talked their ears off…for about 45 minutes… or more. [It will be uploaded to YouTube. When it is, of course I’ll share it.]

I was anxious; yes. By the time they pare my 45 minute ramble to about 45 second, I will not have much exposure but it was still my FIRST TV APPEARANCE. There are over 1.5 million people in Philly. What if somebody sees me? Gulp.

But more important is this: I wanted to get out the right message. I did not want to talk about what it was like to lose my sight. That was over 7 years ago. People who look to the past with sadness and regret get depressed. I have no time for such things. I wanted to talk about now and the future. I wanted to talk about hope.

When I thanked Dr. Garg for recommending me for this assignment he said he wanted someone with energy and enthusiasm. How can I NOT be enthusiastic? In seven years i have gone from the hopelessness of being told there is no treatment and no cure to the approval of the first treatment for geographic atrophy. And I helped. Sort of.

Syfovre can buy us time. Time to ultimately find the cure for dry age-related degeneration, a disease that some say is of epidemic proportion. Lot of people losing their sight out there but at least they now have hope.

Of course, there are still some hurdles to jump over. One does not manufacture millions of doses of a new drug overnight. Apellis is gearing up even as I type. Also, this is not an inexpensive proposition. It was mentioned that the research staff is thinking about injecting both eyes of us ‘lab rats,’ but they are not sure how to cover the cost. How much will Medicare and other insurance companies cover? These are questions for which the answers are still being formulated.

And future treatments? I am still lobbying hard for stem cells but today I heard gene therapy is looking very promising.

The word is promising. It is related to hope. It is related to a brighter future, if your mind can conceive it, you can achieve it. If I can give a TV interview, just about anything can happen!

Sue’s Series on Syfovre

Lin/Linda: Her first aspiration to be a ‘super lab rat’ was not long after she considers the start of her status as legally blind: February 2016. You can read about that here: In the Beginning.

It was June 2019 she was Finally a Lab Rat. In July of that year, she wrote about her first injection: The Beginning of My Clinical Trial.

In August 2022, before the FDA approved Syfovre and after she was accepted into the long-term follow-up study, she wrote about her ‘Diabolical Plan’ to be accepted into a stem cell clinical trial while she’s still alive: My Diabolical Plan: Stem Cell Transplant for Dry AMD.

She also wrote about the discussions of the studies: Pegcetacoplan Study Cliffhanger.

After the drug was approved, she revised her article from her perspective of being halfway through the 3-year follow-up study:  My Diabolical Plan Revisited March 2023.

She’s also written What Does Syfovre Mean for You?

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

Since there’s not a simple answer to that, I recommend that you choose this where I’ve provided an answer.

 

 

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 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?

Wolf Pack and the Letters B & L

Lin/Linda here: in her previous page, Sue wrote about a wolf pack: “I would like to think we are the pack. I know we are hungry for treatments for AMD. I would like to think we are cunning enough to pick good targets in our hunt for these treatments. I want to believe our hunger will not lead us to be deluded by some “quacker” offering empty promises …and a quick buck for himself.” She continues.

The last page I wrote started to share information about dry AMD treatments from research done in the UK at the request of the government. So far I have gotten to A….this might be a long series!

In the article by Waugh et al., B is for blue light. The blue light idea comes from knowledge that the macular pigments lutein and zeaxanthin absorb blue light as a protective action. Blue light appears to be a factor in AMD progression. The question for research became this: would reduction of blue light slow damage caused by AMD? There were four literature reviews found. Unfortunately, these reviews came to different conclusions. There was no definite proof that replacing the natural lens with a blue-light filter lens in cataract surgery gave a great deal of protection against AMD. Likewise, there was no evidence using a blue-light filtering lens in cataract surgery did any harm.

While there is a long-term study being done in Japan, right now it appears the decision to get a blue-light filtering lens during cataract surgery is a matter for you and your doctor to decide on an individual basis. It may be more a matter of preference than a matter decided by science.

The conclusion on blue-light filtering lenses and AMD seems to be “might not help, but probably won’t hurt either.”

Lucky for you, we get to skip the letters C though K and go on to the letter L. In our alphabet here, L is for laser. That is specifically laser photocoagulation treatment of early age-related macular degeneration. The idea behind laser photocoagulation is to blast drusen before they get too big and prolific and start robbing us of our sight. While the process is not yet well understood and is definitely more involved than playing Blaster Master, there is evidence that laser photocoagulation enhances the clearance of debris (affectionately known on this site as “eye poop”) as well as doing a few other, beneficial things I did not understand.

Like all things that are being investigated, laser photocoagulation therapy has a few kinks that need to be straightened out. There are questions about the types and intensities of the lasers used. For example, in early work a too hot laser appeared to cause a more rapid progression to wet AMD. While they are now using “cooler” lasers and firing them for only milliseconds, there are still things to work out before lasers can be considered a bonafide treatment by most.

The take home message for laser photocoagulation is it is a definite maybe. There were several high quality studies either in process or about to launch when my reference article was published in 2018. They may help determine whether laser photocoagulation therapy has an effect on the development of age-related macular degeneration.

Just a caveat here: at the risk of being a killjoy, I need to remind you that none of the treatments reviewed here are able to restore lost photoreceptors. That means there would not be a significant improvement in vision. What they are hoping to do is to reduce the progression of the disease.

Considering that is where the state of science is presently and, considering I am a very willing lab rat in a clinical trial trying to reduce the rate of progression, that is good enough for me. Hope it is good enough for you as well.

And with that said, the hunt is on! I do believe our next target for consideration is an M word.

NEXT: WOLF PACK LETTERS M & N

 

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’s Visual Acuity?

The topic for today is visual acuity. A reader/member was in contact with someone who read one of my posts in another forum. That someone wanted to know what my visual acuity is that I could still ride my bike. The answer to that was “I don’t know. Let me get back to you.”

Why don’t I know? My vision is measured monthly when I go for the clinical trial. They are tracking it. I am not. Frankly, watching the numbers worsen would be too depressing and anxiety-provoking.

Ignorance can be bliss and I would rather concentrate on my abilities rather than my disabilities. No use rubbing my nose in it every month.

Also, while, yes, my vision keeps getting worse, the measurements fluctuate a bit. Some days I am “on”. Either I am able to hold the letters in my sweet spot for an extra half second or I am guessing well. Some days I am “off”. Visual acuity is a psychophysiological process and some days the “psycho” part takes more of the load than others.

So, that said, my visual acuity in my better eye is 71 and in my worse eye it is 52. Huh? Not the usual scores we see. That is because those are letter counts or simply visual acuity scores. Letter counts are used in research.

As I pointed out in a page on why I did not get into the stem cell study, my score reflected a moderate loss. My good eye is at the top of the range and my bad eye is at the bottom of the range. How I know this is I found a nifty little chart entitled Visual Acuity Ranges and Visual Acuity Notations published by Precision-Vision.com.

This chart compares several different ways to measure visual acuity. One is, of course, the Snellen chart. In the States that notation is 20/ xxx. The 20 is 20 feet and the xxx is the distance related to your acuity scores. Using my chart, my good eye is between 20/63 and 20/80 meaning I see at 20 feet what “good” eyes see at 63 feet. My bad eye has an acuity score between 20/160 and 20/200.

There is the decimal scale included on the chart as well. If you have been perplexed when somebody said her vision was 0.4 for example, the translation to Snellen is 20/50. According to Michael Bach and his Visual Acuity Cheatsheet, decimal acuity and Snellen numbers are identical. All you have to do is calculate the fraction. In other words, for my worse eye I have a Snellen score of 20/ 160. 20 divided by 160 is 0.125.

Looks to me like they just wanted to confuse the issue, but what do I know? Well, for one thing, I know the definition of MAR sounds very confusing to someone who is not a hard science person. Damien Gatineau gives the definition of minimal angle of resolution (MAR) as “the visual angle that must under tender two point sources to be resolved on the retina.” Alrightee then. In layman’s terms it sounds as if it means something like how much “space” has to be between two points for the person to see them as two separate points. Interesting but I don’t think we need to worry about those. They are also generally expressed as decimals.

So that is what I have learned about acuity measures. In my case 20/63 and 20/200 still leave “room” for my doing many things, including riding my bike. Maybe in your case, too?

Written August 14,2019

Next: SHOPPING

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

 

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

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Sue on Assignment: Non-genetic Causes of Macular Degeneration – Page 2

Back to the Patient article on Inflammatory eye diseases that can sometimes cause atrophy and scotomata. Our next broad topic after parasites – yuck- and viruses is fungal infections.

Histoplasma capsulatum can “cause vision problem related to exudative maculopathy.” Translation? Oozing, diseased macula. This page is just one happy thought after another!

Then there are mycobacterial infections. A quick search revealed (using the Merck Manual) that certain forms of mycobacteria cause tuberculosis. Another one causes leprosy. As most of us know, these two diseases are now rare in developed countries. However rare, though, don’t count them out yet. Yours truly tests positive for TB.

Then we get to the spirochaetal infections. Syphilis can affect various parts of the eye, including the retina. Ocular syphilis is rare.

How about Lyme disease? Reading this article I discovered that is a spirochaetal infection as well.

Personal observation of people and animals with Lyme disease has led me to believe it can attack any of the body systems. When it attacks the eye it can cause a number of issues including retinal vasculitis and exudative retinal detachment.

Retinal vasculitis is, according to Wiki, inflammation of the branches of the retinal arteries. This condition can cause blurred vision, floaters, scotomata and decreased ability to distinguish colors. Sounds like someone I know.

Wikipedia lists several, other reasons for scotomata. High blood pressure can damage the retina. Ingestion of wood alcohol is another thing. Ethambutol is an anti-tuberculosis drug that has been found to have the potential for damaging the retina. Quinine is another. Quinine is, of course, for malaria as well as some other things of which I am not aware. Nutritional deficits can also cause retina damage. In short, there are probably a couple of dozen different ways to have retina damage without a genetic cause.

So that is what I found for my first, member-requested assignment. Macular atrophy does not necessarily have to come from a genetically-based condition such as AMD or diabetes. There are a large number of diseases and even poisonous substances that can cause damage. I have mentioned a number of them in this page as well as the previous page.

I know Lin has a few things she wants me to look into, but that does not mean I won’t do requests from YOU. Keep those cards and letters coming. What else do we want to learn about?

Written September 29th, 2018

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Sue on Assignment: Non-genetic Causes of Macular Degeneration – Page 1

Good evening! Hope everyone is well.

I have my first assignment from a reader/ member! She asked about non-genetic causes of macular degeneration.

When I started to research, I thought I was going to fail my first assignment! I found a list of over 50 causes of blindness, and the great majority of them had a genetic basis. According to the Cleveland Clinic, 60% of cases of blindness in infants are genetic. Add such things are glaucoma, basic refraction errors and AMD and a good portion of vision problems are, indeed, genetic. It does appear we are made with some planned obsolescence in the design!

Then I looked again (and yes, Lin gave me a nudge in the right direction), and I realized the reader had asked more specifically about viral or other disease causes. That search yielded much better results.

Here goes…

Retinas can be affected by a wide variety of diseases. There are all sorts of articles on ocular infections. Things such as ocular toxoplasmosis can cause retinal infections particularly in individuals who are immunocompromised. Toxoplasmosis is a parasite frequently found in cats. The endpoint of ocular toxoplasmosis is scarring. Depending upon where on the retina the scarring is located, vision may or may not be compromised.

The Patient (March 12, 2014) article on Inflammatory Retina Diseases went on to mention several other diseases that can cause severe visual impairment. Keeping to parasites, dog and/or cat roundworm can cause ocular toxocariasis. The larvae can migrate to the back of the eye and die. Lovely thought. Apparently dead roundworms in your eye can cause retinal fibrosis (read scarring) and even retinal detachment. Yuck.?

And continuing in that vein, diffuse unilateral subacute neuroretinitis (DUSN) is caused by, not dead larvae, but larvae poop! This disease can cause scotomata (blind spots) and floaters. Depending upon where the larvae poop is, it could potentially affect the macula, but wherever they go, DUSN is sight-threatening. Another yuck.

Moving on to infectious disease, The Patient reviewed the effects of herpes on eyes. Not necessarily talking “social disease” here. Herpes simplex causes cold sores. Varicella zoster is a herpes virus. It causes chickenpox and shingles.

When left untreated in eyes the herpes virus can wreak havoc. It causes scar tissue and once again depending upon where that scarring is, there can be significant vision loss. Also, without treatment herpes in one eye will spread in the other eye in a whopping 65% of cases. Herpes eye infections can also cause retinal detachment and optic nerve damage.

I am starting to think I would rather the parasites. Yuck.

Cytomegalovirus (CMV) is, according to the Wiki people, another member of the herpes family. The CDC reports CMV is in half of all adults over 40. While it generally does not cause problems in its host, CMV can reactivate. In the eyes, CMV can cause hemorrhages and necrosis of the retina. Necrosis is a fancy name for death.

And I haven’t even gotten to the fungi yet! I guess that means I write a follow-up page on this.

Yuck.

Written September 28th, 2018

Next: Sue on Assignment: Non-genetic Causes of Macular Degeneration – Page 2

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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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Stem Cell Study Part 1

Happy Saturday! Even though I am pretty convinced I will not be invited to be a part of this study – my vision is not bad enough – I did get the patient informed consent packet and I can browse through that with you. I want to look at it and see what’s happening.

The formal title is very long. What it says is it is a two-part study. One part is a phase one, safety and tolerability study, and the second part is a phase two, proof of concept study. Both studies are being run in several different locations (multicentered), and they are unmasked. Unmasked means that everyone knows what he or she is being given. For example, if they were testing to see if aspirin is better than Tylenol, all the participants would know which drug they had been given.

The independent variable in each is the size of the dose of stem cells. The independent variable is what the researchers are manipulating. The protocol is dose escalation meaning there are different groups of subjects, and they will be receiving increasingly larger numbers of stem cells, one group to the next.

And I am still working through the title, guys!

Two more terms and the title is done: parallel groups and randomized groups. In parallel design, research subjects are assigned to different treatment groups – in this case, size of dose – so that the effects of the different treatments can be compared. Randomized assignment is done pretty much by chance and is hoped to yield groups that have no real differences between them. It is hoped that any differences found after the research is run will be because of differences in treatment and not due to some other factors.

Ok. THAT was the title! Moving on.

The study uses human embryonic-stem-cell-derived retinal pigment epithelial cells (RPEs). Remember these cells come from blastocysts. Blastocysts are balls of between 200 and 300 cells and are about 0.1 to 0.2 mm in diameter according to Wikipedia. A sheet of paper is 0.1 mm thick to give you a point of reference. Blastocysts, at 5 to 6 days after fertilization, have not yet implanted in the uterus.

That last paragraph is information someone might need to make an informed decision on whether or not they want a treatment with human embryonic stem cells. If you think life begins at conception, this might not be a treatment for you.

If you decided to participate in a stem cell study, at least one using embryonic stem cells, you will need immunosuppressants. Getting these cells is actually a transplant. It is related to getting a new kidney (related but NOT the same). Even though the eye has immune privilege, the study will do 13 weeks of immunosuppressants. I imagine it is the immune privilege of the eye that limits this to 13 weeks rather than a lifetime of immunosuppressants as happens with major organ transplants.

Immune privilege? Oh yeah. According to the Wiki people, immune privilege basically means the organ can tolerate the introduction of antigens without eliciting the inflammation response, part of the body’s defenses; remember? The big immune-privileged organ is the brain. Since the eyes are actually just extensions of your brain, they have great immune privilege also.

I am officially way over my 500 words for this so I am quitting now. Back to it later!

Written July 7th, 2018

Next: Stem Cell Study Part 2

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Glad They’re On Our Side

Thank God it’s Friday, Friday, Friday! I would ‘sing’ the lyrics to you but I just looked them up and they are really rather uninspired. Good memories with the music, though. In 1978, I was a disco queen! Anyone else who had a totally enjoyable, misspent youth in the clubs? Those were the salad days.

Anyway, I am really packing tight three days a week at the counseling office. Still not enough clients for four. That means I will drive Lin crazy with many, many pages. Pray I get more work so she gets a break! [Lin/Linda: Please pray she gets more work! Pleasssseeee!]

Derek Daniel has Leber Hereditary Optic Neuropathy (LHON) and, true to form, when I learned about something, suddenly it is like Underdog. It’s everywhere. It’s everywhere!

Healio reported GenSight just announced more information on their REVERSE phase 3 clinical trial results. It turns out this clinical trial assessing the efficacy of a treatment for LHON did not meet primary endpoint goals but did meet several secondary endpoint goals.

What does that mean? eSearch tells us primary endpoints are results that will answer our most important questions for the research. Secondary endpoints are about other questions. They are not necessarily what we were trying to find out but the answers are generally kinda cool and good to know.

For example, contrast sensitivity almost doubled after treatment… Hey! We have problems with that! Maybe this treatment for LHON will have some crossover potential. Their secondary outcome measure may prove to be a boon for us.

LHON is a mitochondrial disorder with a maternal inheritance. In other words, it is a disorder of the powerhouse of the cells. (Mitochondria turn energy from food into a form that cells can use). Since the mitochondrial DNA comes to us through the maternal line only, it stands to reason the inheritance for LHON is through the maternal line.

Doesn’t sound like us; right? Stay with me. I do have something in mind.

The Healio page sent me to a 2012 journal article on Leber hereditary optic neuropathy and oxidative stress. After several paragraphs about how they produced mutant, transgender, blind mice (don’t ask me) to study the disorder, they got to what is, for me, the crux of the matter. Specifically, they are thinking miscoding in the mitochondria leads to this-then-that and then to super oxidation and then all hell breaks loose. In other words, they are thinking oxidative stress is a huge causative factor in yet one more eye condition! There is a pattern forming here.

They are reported to be experimenting with ways of reducing oxidative stress in those with LHON. There is evidence that should slow the progress of their condition.

Of course, as of 2012, they were still talking leafy greens and AREDS2, but that does not mean there will not be other ways of doing this the researchers will discover something. They have to be pretty clever; right? After all, a bunch of folks who say “Hey, let’s make a mutant, transgender, blind mouse!” and then actually do it have to be pretty smart.

Just glad they are on our side.

Written June 17th, 2018

Next: Priorities

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Pushing the Envelope

Happy Monday! Trying to “earn my keep” on my first “non-school” day. The recycling has been taken to the center and the extra fridge has been cleaned.

The ‘extra’ fridge is actually our old one. After we bought the new one, we found out it was only a $50 repair. Voila! Two refrigerators.

I also took delivery of my loaner CCTV. Transporting this thing should be interesting but there is something about not looking a gift horse in the mouth. People do not have to be as kind to me as they are. Gratitude is in order. Thank you!

Found an interesting thing when I was looking at the Brightfocus spring newsletter. They have this eyechat thing. They have eyechats the last Wednesday of the month. It is 1:00 pm. Eastern standard time, I think. I forgot to ask. [Lin/Linda: their eyechat feature is a free telephone conference that is done live where you can listen and ask questions of the guest.  And yes, it is 1:00 pm Eastern Time.]

Anyway, the number to sign up for the live chat is 800-437-2423. If that does not work for you, you can call 800-250-7274 and listen to past chats. Want that on your iPad? Try brightfocus.org/pastchats.

Umm, maybe not that easy. That address took me to their chat page. I had to scroll down to the bottom of the page and click on “listen to previous chats”. THAT gave me the chat menu. You might want to try that. [It’s a little easier on my laptop. Also, you can sign up for their newsletter on many, if not all, of their webpages.]

They have audio and PDF file with the transcript. Audio is taking forever to download. Might be my system. Might not. [Again, faster and easier with my laptop.]

Also in that edition was a follow-up on gut microbes. It has been said our guts are our second brains. It has also been said the state of your gut determines the state of your health. According to Exploring gut microbes in human health and disease: pushing the envelope, there is a good chance such disorders as irritable bowel disease, cancer, diabetes, autism, asthma, and obesity (I am not fat. My gut microbes just don’t like me!??) may be due to imbalances in the gut.

Apparently, we might have to add AMD to that list. Remember we talked about this last fall? Rowan at Tufts is looking at how gut microbes interact with our high sugar and starch diets. He has now added an extra wrinkle. He is killing off gut microbes in mice and switching samples between mice fed high and low sugar diets. Trying to figure out if the culprit is the sugary diet or the microbes.

And speaking of pushing the envelope, how they get new gut microbes into people is definitely pushing things to the limit! Before I said I wanted them to change my microbes so I would not have to change my diet. Rethinking that.

I changed my mind after watching a Nova program, Wonders: what is living in you? This woman had a serious digestive problem after a course of antibiotics. The only way they could solve it was giving her poop pills! There are these people with great gut microbes who come in almost daily. They get paid for making a ‘deposit’ which is turned into poop pills! Yuck.

Could be worse. Supposedly in fourth-century China they made “yellow soup” out of poop. I don’t want to think about it but, you know, those leafy, green vegetables are looking better and better.

Later! ?

Written June 11th, 2019

Next: Lookout

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Shine a Light Under the Bed

Happy Memorial Day! Even though the summer solstice does not come for a few weeks yet, temperature-wise and culturally, it is summer! Hot time in the summertime! (Sly and the Family Stone, 1969).

We opened the pool yesterday. My husband wrenched his back in the process so the puppygirls and I are hanging at home together. No chauffeur. Such is life when you cannot drive any more.

The girls are ‘helping’ with pool maintenance. I am vacuuming and they are getting in my way. We need to get Etta water wings. I think we have the only Labrador Retriever in the world who is a bad swimmer!

Last time I reached in to fish her out, she clawed me all up. It would be nice if ‘maturity’ did not bring such thin skin!

So, moving right along, I hope you all saw Lin’s post about Dan Roberts yearly summary. I loved what Dan said about knowledge. Dan said, “Knowledge is the best way I know of to keep the fear of the unknown at bay, making living with low vision less stressful, and acceptance a little easier.” So glad that great minds think alike!? When you shine a light under the bed the monsters disappear.

Looking at what Dan has covered, I see we have some overlap, much stuff that is exclusively his. One thing he reviews is a very recently published research study that may ‘coax’ (my word) Muller glia cells into becoming photoreceptors without doing all the stem cell production stuff.

So, inquiring minds…sometimes bite off more than they can chew! Researchgate has an abstract about Muller Cells in the Healthy and Diseased Retina. The article says Muller cells ensheath all retina neurons and there is a “multitude of functional interactions” between Muller cells and retina neurons. In other words, they are work buddies and they are tight! It appears to my social scientist little mind that Muller cells help to maintain a good working environment for retinal neurons. (Please read and interpret yourself as the girl has been known to be wrong before!) There is some evidence they have a role in angiogenesis. That is you, you wet folks. Angiogenesis is the creation of new blood vessels.

Now all is not perfect with this bromance. The abstract also says “virtually every disease of the retina is associated with a reactive Muller cell gliosis”. According to Wikipedia gliosis is a nonspecific reactive change of glial cells to damage to the central nervous system. The rest of the explanation is a lot of sciencey stuff that made my eyes cross but it sort of sounded like damage to you causes damage to me and then I return the favor. Oh, and the macrophages get into the act, too. Social scientist here…would you like to talk learning theories? I am pretty good at that. ? This, not so much.

Bottom line here is our Muller glia cells and retina neurons really need one another. They share a lot and it may be possible to ‘retrain’ a Muller glia cell to do the job of a retinal neurons and actually even ‘become’ a retinal neuron. Very cool.

And now back to zen and the art of pool maintenance…with apologies to Edward Abbey. Have a good weekend!?

Written May 26th, 2018

Next: Catch-Up Days

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Picturing AMD

Morning! A week past Easter already! Wow, time does seem to fly! Maybe I will research time perception one of these years.

This page is going to be odds and ends again. A couple of things have come past me. First of all, my March Macular Degeneration Partnership newsletter has been sitting in my email for a while. When I looked at it, the first article was on a very small ‘n’ study (6 people) concerning the accuracy of the AMD example photo published by NIH. I would suspect you have seen the photo of the two little boys and the balls. When modified to be what we are ‘supposed’ to be seeing, the photo had a big, gray blob in the center and blurry periphery.

It would appear NIH never asked any of us what we actually see. The arrogance of expertise, perhaps? (Did I say that? So judgmental! Ouch.)

It turns out when six of us were asked, they got six different versions of what AMD folks see. The pictures are in the article. There is only one, apparently a person who had quite the catastrophic bleed, who had a big, black spot. No gray spots with blurs outside of that.

So, I propose a little experiment: let’s take a poll and see which one of those photos is closest to what each of us sees. I am closest to G.

If we get more than six people I will write it up. I suspect the Macular Degeneration Partnership would publish for us. We might be able to be published researchers!

And in other news, when I was reading that article on using a membrane to support stem cell-derived RPEs, I came upon this line: The ELM is a structure present in the normal retina and absent in the area of disease in patients with geographic atrophy.

Oh, hell! Something I am supposed to have, have apparently lost and I don’t even know what it is! ELM?

The External Limiting Membrane is also called the Outer Limiting Membrane (OLM). But whatever it is called, it appears those of us with GA “ain’t got it” any more. According to an article on the histology of the eye published by Researchgate, the retinal is divided into ten layers. With my limited knowledge – and remember we are not experts, not doctors. We are just curious people with access to WiFi – it would appear to me the first seven layer starting from the inside are nearly all some sort of neuron or piece of a neuron. The eighth layer is the ELM/OLM and creates a “junction between Muller cells and photoreceptors.” What else does it do? No clue. I looked at a dozen articles and not one said what the primary purpose is. What they all said was degradation of the ELM/OLM layer is predictive of vision loss.

So where we are knowledge-wise appears to be we with GA have lost our ELM/OLM layer which is somehow crucial for good vision. The article about using the polymer membrane to support the transplanted cells suggested their procedure promoted growth of something that resembled the external limiting membrane and that their procedure might “promote restoration of retinal architecture”. So maybe someday we could get it back???? Who knows.

Anybody know anything about this? Anybody have more questions? Still searching here.

“Trust those who seek the truth but doubt those who say they have found it.” – Andre Gide

Next: Brighter Every Day

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The Patch

8:00 pm and I am rewarding myself. I just had a piece of chocolate and I am playing dance music on my iPad. This was the second day in a row I have felt as if I have actually accomplished something. Hallelujah. The to do list is starting to dwindle!

It won’t stay that way. Of course not. I know me. Besides, it is not good to become redundant. Meaning and purpose are like air. We need them to survive. Stay busy!

And on that note, I guess I should stop waxing philosophical and get to work here.

Lin sent me another article. As I alluded to on the last page, this one was about the development of a membrane to support the stem cell-derived RPEs. The research just keeps moving along!

It turns out this new development is coming out of Southern California. Specifically, the University of Southern California, the California Institute of Technology and the University of California at Santa Barbara.

Stop there a minute. University of California at Santa Barbara (UCSB)? Pete Coffey is at UCSB! The good Professor Coffey is co-director of their Molecular, Cellular, and Developmental Biology department. Gee, do you think there could be a connection? ? [Lin/Linda here: Professor Coffey is one of the researchers at Moorfields Eye Hospital in London who conducted the clinical trial that recently made the news with positive results of a similar trial conducted with 2 participants with wet AMD.  He is also Director of the London Project to Cure Blindness.  I found out that he splits his time 50-50 between University College London (UCL) and University of California Santa Barbara (UCSB).  He isn’t directly involved in this study but does collaborate with the UCSB researchers.]

OK. Now it’s time to stop being a smart a** and tell you what they did; right? Right!

What they did was develop a “bioengineered implant consisting of stem cell-derived, mature, polarized retinal pigment epithelial cells in a single layer on an ultrathin synthetic parylene membrane”. Yikes. Let’s ‘unpack’ that as the saying goes.

Wikipedia gives an obscenely long and complicated explanation of bioengineering. You can look at it and figure it out if you wish. The definition in thefreedictionary.com was more simply “the application of engineering principles and technology to the field of biology, especially biomedicine, as in the development of prostheses, biomaterials, and medical devices and instruments.”

We have gone over stem cells quite extensively. We also mentioned that RPEs are polarized but I will go into that a little more deeply. In biology having polarity means the cell has distinct anterior and posterior parts. There is a ‘head’ and a ‘tail’. If they don’t line up right, they don’t work right.

Parylene is a polymer and is ‘green chemistry’. I refer you back to Wikipedia if you are interested in reading more. Social scientist here!

The purpose of putting the stem cell-derived RPEs on a membrane was to support them and and maintain their polarity. The patch was delivered to the back of the eye via the subretinal space (which we have talked about before) during an outpatient surgical procedure.

So how did they do? Apparently pretty well. Bear in mind it was only a phase 1/2a trial and there were only a few subjects, but the ‘patch’ seems to have integrated well and some of the people showed improvement in visual acuity.

For you on the west coast: they are enrolling subjects in six, different locations in California and Arizona. The clinical trial number is NCT02590692. If you are interested, get crackin’! Their numbers will be very small.

Next: Picturing AMD

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Dissemination of Ideas and Facts

I am distracting myself. Still fighting with the webinar. If I don’t step away the laptop is flying into the yard and it is not mine.

Looking at the next point in that article, I noticed they have “embryonic stem cells” in italics. Perhaps a subtle way to make people raise their eyebrows?

I double checked the source of the article after seeing that. It is the International Society for Stem Cell Research. Their purpose is to promote and foster the dissemination of ideas about stem cells.

Promote and foster the dissemination of ideas. Facts, too. Sounds like a plan.

I am aware there are folks reading this who are totally opposed to stem cell research. No problem. That is your prerogative. Depending upon religious views about such things as when does life start, etc., people may decide it is an immoral practice. I just want to put some facts out there for the people who may be making their decisions on half or incorrect information.

Scientific American in Getting It Right About Stem Cells quoted at that time (2010) there were 800 stem cell lines worldwide. A stem cell line is a family of constantly dividing cells produced from a group of parent cells harvested from a single embryo.

Now stop there for a minute. Embryo here does not mean a well delineated little person. Embryo in this case is a blastocyst four to five days after fertilization. According to Medicinenet.com a blastocyst is a thin-walled, hollow structure made up of two layers, the inner and the outer layers. Conception: How It Works tells us a fertilized egg does not attach until at least five to six days after fertilization. Conception also tells us 50% of all fertilized eggs are lost before the woman’s next cycle.

Next question: where do the blastocysts come from? According to Getting It Right again as of 2010 there were 400,000 fertilized eggs (blastocysts) in storage in the United States alone. The New York Times estimated that number had grown to 612,000 by 2011. By 2015 when the article was written? Estimates were around 1 million.

What to do with all those blastocysts? Implant them? The reason they are still in storage years later is often because the original donors (or parents if you prefer) have successfully delivered several children and want and can handle no more.

Give them away? To whom? There are tons of problems there.

Keep them in storage at the fertility clinic? The Times reported storage costs of up to $1200 a year. What if you cannot afford that? And what happens when you age and die?

That leaves destruction or donation to science. How many fertilized eggs are destroyed every year? I could not find a number for the States but the Telegraph claimed in 2012 there were 1.7 million fertilized eggs “thrown away” in the United Kingdom.

One more point before I sign off. Wikipedia reported in 2017 there were 378 approved stem cell lines in this country. However, only a handful of these lines are actually being used. The National Stem Cell Bank reported 77% of the requests they received were for only two of the lines they control.

And I lied, one more point. How long can a stem cell line last and be productive? We don’t know but some people have hypothesized they could be ‘immortal’.

There is precedence for that. Cancer cells taken from a woman in Baltimore in 1951 are still alive, multiplying and being used in research. Don’t believe me? Her name was Henrietta Lacks and the story is interesting. Look her up.

There you go. Change you mind? No? Your prerogative. I just wanted to share a few facts.

Written April 2nd, 2018 Continue reading “Dissemination of Ideas and Facts”

Do As I Say – Again

Do as I say. Do not do as I do.

In the interest of full disclosure I must make a confession. Moments before starting this page I ate a BLT with mayo. It was yummy. [Lin/Linda: don’t know what a BLT is?  It’s a Bacon Lettuce and Tomato sandwich, mayo is mayonnaise.]

Now, with that off my conscience, I guess I can move on…wait, do I need to tell you about the potato chips, too? Sigh. OK. I also had potato chips.

Now…before dessert, I want to go into the topic of prostaglandins. I imagine I have heard about them before, but at the seminar I was at last Friday the presenter referred to them several times. At this seminar on chronic pain the presenter mentioned how inflammation is a big part of chronic pain. He went a bit into how prostaglandins are a precursor to inflammation.

First point: what are prostaglandins ? According to You and Your Hormones – can you imagine naming a website You and Your Hormones? Go figure – prostaglandins are a group of lipids – read fats – made at the sites of tissue damage or infection. They control inflammation, blood flow, the formation of blood clots and labor.

Prostaglandins are being investigated for their role in autoimmune disorders. There is excellent evidence there is some role there because, for one thing, substances such as NSAID pain relievers are known to reduce prostaglandins levels. If they work on your arthritis, there should be some connection; yes? Yes.

According to another source, Omega-3 Fatty Acids in Inflammation and Autoimmune Disease authored by Artemis Simopoulos, omega-6 fatty acids are kinda bad for inflammation. Meats and vegetable oils – read BLTs with mayo – provide really wonderful building blocks for prostaglandins and therefore inflammation. Oh, fudge! (I really like that, too!) In other words, my usual diet is fertile ground for the development of prostaglandins and, by extension, inflammation.

So why do I mention this in a blog on Age-Related Macular Degeneration (as well as everything else that intrigues my devious, little mind)? There is what seems to be building evidence for the case that AMD is an autoimmune disorder. There is evidence AMD is caused by problems with the complement immune system. Those who have been following for some time recall the complement immune system is the one that deals with non specific threats. It fights disease with fever and inflammation Hmmmm, this is all starting to come together here.

As I write, it is becoming apparent my diet may not be the best for my eyes. What the literature suggests we should be eating includes omega-3 fatty acids such as those found in fish. Omega-3 fatty acids are also found in dark green vegetables. WikiHow suggests things such as mangoes, pomegranates and tomatoes. Tomatoes, yes! Finally, something I really love !

Anyhow, just thought I would mention this all actually makes a bit of sense. The foods we are told to eat for our eyes have been discovered to reduce prostaglandins. Prostaglandins fuel inflammation. Inflammation happens in autoimmune disease. AMD, it has been theorized, could very likely be an autoimmune disease. Voila! Neat little package.

Of course, for us whose diet consists mainly of carbs, fat and salt, this is sorrowful news. I imagine I should mend my ways. Tomorrow. Everyone should have at least one vice; right? ? After all, I did say do as I say!

Written March 28th, 2018

Next: Bedlam

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Eye Poop

Today was a “get your ‘stuff’ together” day. Every once in a while it gets so that if I don’t stop and take care of the business at hand, I will be having a screaming fit.

Like last evening for example! However, I have now gotten a haircut, gone grocery shopping and cleaned the living room, as well as having completed a few other tasks, like taking the recycling. Feeling a little more in control – I probably should not say that too loudly – and ready to tackle a page Lin suggested.

That page will be on – drum roll, please – eye poop! Okay, so that is not what they are really called. Most of the world call them drusen.

In a Harvard Health Publishing article that asks the questions: what are drusen and why do I have them, the author describes drusen as “deposits of extracellular waste”. You got it, eye poop.

In younger people, the sanitation department in eyes generally takes care of the eye poop. That ‘sanitation department’ is the retinal pigment epithelial cells aka RPEs. Yes, your RPEs are supposed to ingest eye poop. But you know what? Your RPEs are into recycling, too! They are discovering your eye is its own, little ecosystem. James Hurley at the University of Washington at Seattle and his team have discovered RPEs and the retinal cells are in this close relationship in which the wastes and byproducts of metabolism in one type of cell are the food another type of cell needs. Mess up in one part of the system and everything goes to Hades.

Why would the RPEs stop doing their recycling thing? No answers, just theories but one thing is for sure, age has something to do with it. Most people over 60 have at least a few piles of eye poop hanging around.

You know how it goes. Things don’t seem to work as well when we are older. Some messes pile up.

http://patient.info/health/age-related-macular-degeneration-leaflet

Eye poop becomes a problem when it starts wiggling in between the RPEs and the Bruch’s membrane. Bruch’s membrane is where the RPEs get the nutrients they need to feed the photoreceptors.

Think of it as a huge landslide standing between you and the grocery store. If you cannot get to the store, you go hungry and may die. If you die, those you are responsible for die too. Same with RPEs and photoreceptors.

Again, no one is exactly sure why some people get away with just a few, stray piles of eye poop and others have dozens. There is an underlying error or errors that have yet to be proven. The researchers are working on it.

The Harvard paper points out drusen aka eye poop do not cause AMD. They are just manifestations of the disease process.

Hope that was a help. Hope you understand things a little more thoroughly. Night!

Written March 18th, 2018

Next: Another Cautionary Tale

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What’s the Difference?

Hello. Spent a good part of yesterday working on getting my Wi-Fi connection back. My friend says she enlists the aid of the archangels and the saints. Supposedly Hilarion is the patron saint of technology. How a guy who, according to Wikipedia, spent his life wandering in the desert has anything to do with my Wi-Fi is beyond me. Of course, Hilarion sounds like hilarious and tech and I are a cosmic joke….

But before things went dark, Lin sent me a list of things the Facebook members thought would be of concern for those newly diagnosed. At the top of the list was the difference between dry and wet AMD.

I am going to tackle this sans references because, well, I think I got it. But, if I don’t, feel free to call me on it.

To begin with, both dry and wet AMD start out as dry. With the drusen accumulating between your retinal pigment epithelial cells and their food source, the RPEs start to die.

http://patient.info/health/age-related-macular-degeneration-leaflet

RPEs? Those are the servant cells to the photoreceptors. The photoreceptors are the cells that change light energy into chemical energy and then into electrical energy so your brain can see. Without their servant cells, photoreceptors died.

The death of cells and withering of a body part is called atrophy. In advanced dry AMD that is pretty much all that happens. RPEs die. Photoreceptors die and we loose part of our vision. Advanced dry AMD is called geographic atrophy (GA) because the pattern of living and dead retinal cells once looked to someone like oceans and continents on a map.

That is GA. It is generally a slow process. Vision loss is mild to moderate. In my inelegant terminology, your macula just sort of rots away. Yippee.

Now, that is not exactly what happens when you develop wet AMD. In wet AMD, the way I conceptualize it, your RPEs and photoreceptors send out messages begging for more supplies. Excuse me! We are dying here! The body responds by building more supply routes. These are blood vessels. However, these new vessels are substandard products and they leak. Those of us with wet AMD have eye bleeds.

Wet AMD is clinically called neovascular. Neo for new and vascular for blood vessels.

Bleeding in and about the retina causes cell death. You lose cells and vision quickly. One of the commandments of AMD is thou shalt not ignore an eye bleed! Wet AMD only happens in about 10% of us but it accounts for about 90% of the severe vision loss in AMD.

Now, treatments. The short answer for dry AMD is there are none. They are getting closer and I am hopefully but right now the answer is still none.

The AREDS/AREDS2 formula has been proven effective in reducing the rate of progression from dry to wet. Ask Lin. She is our expert. AREDS as a topic makes my head hurt. To my knowledge supplements do little to stop the slow progression of dry AMD. [Lin/Linda here: I’ve put some information about this at the end.]

The treatment for wet AMD is anti-VEG-F shots. VEG-F is the chemical messenger that calls for new blood vessels. Shut that guy up and there is less that can bleed. There are several different types of “eye shots”. Some work better for some people. Others work better for other people. Work with your doctors on that.

That is the difference between dry and wet AMD according to me. Hope it helped.

Written March 13th, 2018

For more information, here’s a good place to go: The Science of AMD.  I highly recommend the 2 videos on this page as well as the other information.

Lin/Linda: OK, more about AREDS/AREDS2.  The short answer is that they HAVE been shown to be effective in reducing the risk of wet AMD but only for those with intermediate dry AMD or advanced wet or dry AMD in one eye but not the other.  There is an issue about one’s genetic makeup in regard to taking the high dose of zinc in the original formulation (80mg).  For some people with a specific genetic marker, taking that much zinc can cause one’s AMD to progress FASTER to wet than those without that marker.  More about this at AREDS/AREDS2: A Guide where you can get more about the short answer, a link to a page where there’s “If you have…” which will tell you if the AREDS/AREDS2 supplements have been studied or not for the stage of your eyes & whether they’ve helped, and a link to 6 pages with details about the research that produced these supplements.]

Continue reading “What’s the Difference?”

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