Category: Research

Chocolate!

Hi, looking back into some of old eye news I have gotten. My inbox is way too full. Gotta clean it out.

Last November Healio ran an article on the HULK experiment. I am ignoring the fact that this study is being done with people with diabetic macular edema and not age-related macular degeneration. Why? Because I get a kick out of the name! We love Marvel comics.

In addition to the association with the big, green guy I also liked two other things about this study. First of all, they developed a microneedle for the trials. I know next to nothing about microneedles as a delivery system but the smaller the needle you use on me, the smaller the ouchy. This is a good thing, especially when it comes to eyeballs.

The other thing is they are delivering the treatment through the suprachoroidal space. The suprachoroidal space is looking like it may become the preferred route for the delivery of all sorts of retinal treatments, including RPE replacement.

In short, advances in the treatment of their condition may lead to advances in the treatment of our condition. Science builds on itself. This is a good thing.

And in today’s Healio they are FINALLY talking about an ‘eye diet’ I can follow. Chocolate! According to Healthline, dark chocolate is chock full of antioxidants. It is crazy nutritious. It lowers blood pressure and helps brain function as well as doing several other wonderful things.

Now, as reported in JAMA Ophthalmology (2018) they have done this experiment comparing the vision of people who have eaten a milk chocolate bar and others who have eaten a dark chocolate bar. (And exactly WHY was I not informed about this study? I would have even been in the control group. After all, it is all about science.?)

The results should have us all running out for dark chocolate. Those who got the dark chocolate bar showed improvements in visual acuity and contrast sensitivity two hours later.

Of course, they are not sure about the duration of the improvement. They are also not sure of the real world influence of the improvement. Healio did not suggest any theories about the mechanism involved. In other words, there is a lot of research that still needs to be done. Want to be a lab rat for this study? The line forms behind me!?

And on that note, I think I will wrap this one up. Curl up with the puppygirls and watch some TV on my iPad. Maybe I can find some Marvel comics movies. Do you like Spidey? He’s probably my favorite. Of course, I might be able to talk my husband into going to see the new Avengers movie over the weekend. That has ALL of the heroes in it. Do you think they have dark chocolate bars at the refreshment stand?

Written April 25th, 2018

Next: News From Research

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Brighter Every Day

Greetings from what appears to be Pennsylvania’s version of monsoon season. Good grief. Tis wet out there!

This is going to be yet another hodge podge of unrelated ‘stuff’. Bear with me if you can.

First of all, I want to thank all of the kind people in the world and encourage you, if you are not going out because of fear of the stigma of vision loss or whatever, to get out there. Remember I told you I got left the other week? Strangers at the Y who saw that debacle are now checking on me. Do I have a ride? Be sure to say something if I get stuck again.

The clerk at a chain, sandwich restaurant gave me my change in $1s when I said I was visually impaired and needed singles for the van. 18 of them. Bless him.

Then there are my high school friends who drove 80 miles to have lunch and ‘catch up’ and the woman at Zumba who volunteered to give me a ride to Mom Prom and a dozen other people who look out for me and drive my sorry self around. Thank you!

Really. The more you get out there the better life will be. People are basically good and helpful. They will look out for you.

And in other news, I got lifetime dog licenses for the puppygirls. They offer a cut rate to the elderly and/or disabled. It should be about half of what I would have paid if I had bought licenses for the next 13 years. Saving money is a good thing. If you have younger dogs check it out.

NFB Newsline is expanding their offerings. They are now offering a children’s magazine, Stone Soup, as well as Sports Illustrated Online. These are in addition to Sporting News, Globe’s Israel and Science X, not to forget Medical Xpress and the newspaper Concord Monitor.

Remember Newsline comes to you through your phone, including landlines for people who don’t like their electronics to be ‘smart’. They offer a wide variety of local newspapers and you just may find some local news to listen to with your morning cup of coffee.

What else? Well, I found a healio.com article that talked about using immunosuppressants more frequently in Ophthalmology. This April 14, 2018 article did not mention AMD as a target condition, but given that AMD is thought to be related to immune system problems, they may want to look at the utility of immunosuppressants sometime down the line. My point in mentioning it was to show research in Ophthalmology is branching out in many different ways.

And case in point, remember the gene therapy for Leber congenital amaurosis that was developed in Philly and approved by the FDA? The really expensive one, Luxterna? The doctors at Bascom Palmer just injected Luxterna into the eye of a nine year old. His family is starting to see improved functional vision in this child. [Lin/Linda: actually, this March 23rd article says that there were 2 boys who were injected with Luxterna.]

And one more before I go: retinitis pigmentosa is a retina degeneration disease that leads eventually to total blindness. GenSight has gotten MHPRA approval to run clinical trials of gene therapy for RP in the UK. (Alphabet soup, anyone??) Why get excited about that in an AMD blog? To quote the GenSight CEO “If proven safe and effective, this therapy could be transferable from retinitis pigmentosa to dry AMD.”  [MHPRA stands for Medicines and Healthcare Regulatory Agency and is the UK’s equivalent to the US’s FDA.]

Oh! That’s a good reason! Things are looking brighter every day!

Next:  I Got This

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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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Different Paths

Good morning! I promised myself I would be productive today. Bedding stripped and in the washer, dishes in the dishwasher, a good pancake breakfast in my tummy, now if this webinar would load I might be able to DO something!

Speaking of pancakes, I was taught to flip the pancake when the bubbles are coming up in the middle. Visual cue. I burnt a couple today because I did not catch the little bubbles.

Short of singeing my nose on the griddle, how do I know when my pancake is ready to turn? Any low vision cooking suggestions? Inquiring minds want to know.

Moving right along, I happened upon a 2015 article in Drug Discovery and Development (DD&D) magazine. The article is a bit dated which actually goes to prove the point: research is advancing incredibly fast. Besides remarking that a Nobel laureate, Sir John Gurdon, called RPE replacement one of the most successful stem cell treatments in existence at that time, the article also talked about how regulatory agencies such as the Food and Drug Administration in the States and the Medicine and Health Care Products Regulatory Agency (MHRA) in the UK needed to get up to speed in the area of stem cells.

The article tells a cautionary tale about how the company Geron tried to get the first ES-cell clinical trial approved back in 1998. Their request and justification document ended up being 22,500 pages long and the approval came in – ready for this? – 2009! Good grief. The point is not that the FDA is an obstructionist organization. The point is stem cell science was an ostrich and they were used to dealing with elephants. Nothing fit their paradigms and they had no knowledge about it all.

Pete Coffey of the London Project to Cure Blindness told his own, mini horror story. He had two regulatory agencies to deal with. His wait was one year. Once again his ‘ostrich’ did not fit a system set up to deal with elephants. But kudos to the MHRA. They were not so hidebound that they could not adapt and modify.

The recent, controversial study published by Coffey, et al., was also discussed a bit in the DD&D article. After battling with the regulatory agencies and having his sponsor bail because of no fault of his own, Coffey expressed optimism that, essentially, the worst was over and his research would be moving on. In fact, there are rumors coming out of the UK that they may already be preparing for the next leg of this research. (Remember Lin has spies and secret agents everywhere.)

The article goes on to compare some of the different paths that stem cell treatment of AMD is following. Coffey used stem cells in people with wet AMD early in their disease progression. Work in the States is using stem cells in patients with geographic atrophy. In other words here we are treating after major damage has been done. Coffey and several others have started to be critical of the approach being taken in the US. Are we not at a point now we can pretty much trust the stem cell treatment? Must we wait until so late in disease progression? [Lin/Linda: click here for an article that talks about both the UK stem cell and the US stem cell trials results.]

The other comparison Coffey made was between simple injection of stem cells into the appropriate place and the use of a membrane to give structure to the cells. Coffey supports the latter approach….but that is the topic of an article Lin just sent me. Later!

Written April 7th, 2018

Next: The Patch

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Disappearing Fingerprints

I am back. Yes, we have snow. About three inches. Shirt sleeves and sandals back to ski jackets and mukluks in less than 18 hours.

I am trying to get back into the webinar. When I lose the connection it kicks me right back to the beginning of the session and I have to fight with the scroll bar again. Thinking it may be the friction ridges on my fingers. They are barely there.

This is a real tangential subject – and I promise to get back on topic soon – but many of us are ‘of a certain age’ and might be interested in this. The simple fact is, as we age, our fingerprints disappear. If you ever wanted a life of crime, now may be the time!

No, seriously. They disappear. A few years back I had to renew my clearances and I had to go back to be fingerprinted at least three times. We finally just gave up and declared me safe to work with kids. It was crazy frustrating.

Another Aging Puzzle: The Case of the Disappearing Fingerprints has all sorts of neat info on this topic. You might want to look at it. Especially if you need to be fingerprinted for volunteer work or something. Get you prepared for having to go back and back and….

Back on subject: the article on nine things to think about when considering a stem cell trial. I am still looking at the bullets under the first point so this review might take a while.

Expense was another thing to consider that they mentioned. The last I looked the pay for the trial I want was $75 a day. Holiday Inn Express was giving discounts on rooms if you needed to stay. So basically, we might be able to stay for ‘free’ but meals, gas and wear and tear are going to be all ours.

Knew that. Actually, it is part of the reason I am retiring. Retired I have a pension, a guaranteed income even if I need to spend days in Philly. If you are still working and looking at clinical trials of any type, you will need to consider the possibility of lost wages. Nasty thought but it may need to happen.

Oh, and we have said this before but it is worth repeating:

We do NOT pay to be in stem cell trials or to get any other experimental treatment.

If some ‘doctor’ says he has a great, experimental treatment but you need to pay? Get out of there as quickly and graciously as possible and call your local medical ethics board. There is something wrong and it needs to be looked into.

Second bullet is covered. Yes, we know there are different types of stem cells. There is a whole bunch of science involved here but they have done all these manipulations to be sure the stem cells in my chosen trial are appropriate.

The caveat here is know your provider. Wills Eye Hospital has been ranked the second best in the nation. (What’s first? Bascom-Palmer in Miami.)

Carl Regillo, my retinologist, has credits as long as your leg. Open a page covering an ophthalmology convention and the boy’s picture is there. Too legit to quit…or to do shoddy research.

OK. That covers points 1 and 2. Bye!

Written April 2nd, 2018 Continue reading “Disappearing Fingerprints”

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”

Behold the Turtle

Two days down on a three-day weekend. I am doing reasonably well with my ‘to do’ list. Progress through those is a good thing. It makes me feel a bit more accomplished.

I sent an Easter greeting to the researchers who will be conducting the clinical trial I have been trying to get into.  The answer I got was the trial that was slated to launch in March (never believe those predictions!) is now in startup phase and should be ready this Summer. Maybe.

Of course, I was hoping – still AM hoping! – to be a first draft pick lab rat and for the research to actually begin this Summer.  It will work out better for my schedule.

Not that the world revolves around moi…although it would make things a lot easier. You know what I am saying?

Of course, the treatment I have been wishin’ and’ hopin’ and thinkin’ and prayin’ (with apologies to Dionne Warwick way back in 1958) for is a stem cell treatment. Regenerative medicine. Therefore it was with interest that I read the article Nine Things You Should Know About Stem Cells that was shared in the Facebook group.

The article says there are complications that may occur with any treatment. The trial I am signed up for involves a vitrectomy.  Vitrectomies almost inevitably lead to cataracts. The stem cells themselves may trigger an innate, immune response that could cause more damage. Then there is the possibility the stem cells could be contaminated and cause infection. Or they might migrate and cause a growth.  There are dozens of potential SNAFUs. Most of us are old enough and wise enough to know there is no such thing as a sure thing.

If clinical trials were sure things they would not be called experiments. They would be called certainties. Who said “Behold the turtle. He only makes progress when he sticks his neck out”? (Found it. James Bryant Conant). Sometimes you have got to stick your neck out. You do it with thought. You do it with your eyes wide open but you do it.

Doing this trial will automatically make me ineligible for any other trials. That is just the way it works.  It is important the researchers know the results they got are a result of THEIR treatment. Not the result of a treatment you had somewhere else.

It is for that reason you chose a clinical trial with a treatment you have researched and believe in. We have a Facebook group member whom Lin told me was offered a trial with a treatment he was not sold on. He turned it down. You get one trial. You get one shot at this. Pick something you know about and believe in. [Lin/Linda: you can read about Facebook group member Bob O’Connell’s decision making process on page 2 of his Guest Author’s pages]

Those were just two points under the first of the nine reasons; believe it or not. I will look at the rest and may just write a follow-up page. Maybe not.  Right now, it is bedtime for this ‘turtle’.  Catch ya later!

Written April 1st, 2018 Continue reading “Behold the Turtle”

No Respect

Anybody remember Rodney Dangerfield?   His catchphrase was “I get no respect”.

Although I have at times thought that dry AMD was being treated as the proverbial red-headed stepchild, I have always tried to talk myself out of that attitude. The people with wet have real problems. They are one bleed away from blindness. It makes sense they would work for a cure for them first.

However, I finally found someone who at least in part shares my concern. Philip Rosenfeld  down at Bascom-Palmer feels the same way. He doesn’t think dry AMD gets any respect either!

Rosenfeld talked about how all of the clinical research seems to have been focused on wet AMD. However, the truth of the matter is good responders to Anti-VEGF and dry AMD folks alike just keep getting blinder. Rosenfeld remarked how atrophy after ‘eye shots’ and dry AMD has become the most common causes of vision loss from AMD.

Rosenfeld – bless him! – goes on to say the effects of dry AMD are  ‘underappreciated’. Go, Philip! You tell ’em, buddy!

The functional vision loss associated with macular atrophy can be devastating. Okay, so we don’t have these dramatic crises like the wet people but that doesn’t mean we are not suffering. Dry AMD folks have feelings, too.

In addition Rosenfeld goes on to say the proof that dry AMD – and I quote – “never got the respect it deserved” can be found in the International Classification of Disease codes. Dry AMD was seen as so unimportant that there were  no subclassifications.  That is sort of like saying cancer without assigning a type or a stage.  Does the patient have stage 1 skin cancer and we remove the offending spot in the dermatology office or is it stage 4 bone cancer?  Doesn’t matter. It is just cancer.

Once again Rosenfeld notes the societal impact slowing macular atrophy will have. He remarked that vision loss has real impact on quality of life and it is much more than reading letters on an eye chart.

For example, I could not read the forms given to me at the veterinarian’s yesterday. I asked for help. (In case you did not notice, I am trying to be a good role model here. Do ask for help!) Multiple the three minutes the clerk took to help me by 1,000. How about 10,000? That is 500 man hours the people who are helping us could be doing other things!  Good grief.

Rosenfeld then went on to talk about how it has finally dawned on some researchers that we really may be having – and causing – some real problems.  Enter the studies they are now trying to slow the progress of dry AMD.

Lampalizumab looked promising but died in the stretch. Horse racing idiom there.

APL2 is getting a lot of hype. Just the same, there are concerns. As we saw, some people who saw the PowerPoint presentation on the drug  decided “this horse is lame”. (Coming from my heritage, I prefer “that dog don’t hunt” but the idea is the same and I really did not want to mix my references ?) [Sue wrote about this in her page Another $64,000 Question.]

Rosenfeld opined that failure of APL2 to produce any substantive functional vision differences may lead to the question of when to intervene with dry AMD. Rosenfeld seemed to suggest early intervention may be better than late.

Me? I am with Rosenfeld. We know where this stuff leads. There is no question of the potential endpoint. I say nip it in the bud! Treat early!

But who am I? Just somebody with a disease that gets no respect.

Written April 1st, 2018 Continue reading “No Respect”

Bedlam

Greetings from bedlam. If you are interested in the etymology of words you probably already know bedlam is a bastardization of Bethlehem as in St. Mary of Bethlehem in London. ‘Bedlam’ in the Middle Ages was where they housed the insane of the city.

Who said we are not educational here? To steal a motto from a huge assessment and publishing house: Always learning.

Bedlam is appropriate here because, well, for one thing, I am still crazy. Tomorrow we have to take the puppygirls to be spayed. Responsible pet parenthood is important.

Then over the weekend I have to apply for Medicare. Moving along swimming through all the red tape and nonsense that seems to be involved in dealing with the federal government.

I still have reports to write and webinar hours to listen to on top of client contact hours, exercise and puppy parenthood among other things. That means some less urgent things are going by the wayside. Like writing a web page for instance.

Thankfully Lin has been doing a lot of legwork for me. She has been sending me all sorts of interesting things.

First of all, back to Londontown. Lin sent me a link to a radio program called In Touch. I had never heard of it, but I am just a dumb Yank, so what do I know? Anyway, it seems like a great resource. It is produced by the visually impaired for the visually impaired on topics of interest to the visually impaired. Cool.

The segment I got was about, first of all, the death of their first producer, a woman by the name of Thena Heshel. Listening to some speeches she had made about the early years had me shaking my head. Heshel commented about how people were only supposed to get information from vision professionals and the professionals were telling them nothing! When she, a layperson, started sharing information, she was chastised by the powers that be!

While we have not gotten a good tongue-lashing (yet), I could identify with the no info part. It drives me crazy when people feel they have the right to withhold or to parcel out knowledge as if it were their own private property.

Knowledge only gains real value when it is given away.

So, in other words, if you are ever playing a trivia game and the question is about the etymology of bedlam, you now know the answer! Giving the information to you helped to give it value because you could use it. Same with knowledge of our eye disease. Please use it and pass it along. Sharing knowledge can only increase its value.

And jumping down from my soapbox ?, I want to say I was relieved to listen to the rest of the In Touch segment Lin sent. The rest of the segment dealt with Professor Pete Coffey and his recently published study. They spoke of the sensational way the study had been publicized and the problems associated with that.

Professor Coffey also spoke about the research being extremely promising especially for wet AMD patients who have not responded to Anti-VEGF shots and who have been gotten to quickly. He made the point the therapy is not currently available. Several more clinical trial phases must be navigated before it is available to the public.

Thank, goodness! Balanced reporting. In Touch, it was good to meet you!

Written March 30th, 2018 Continue reading “Bedlam”

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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Children Cannot See!

First of all I have a confession: I am cranky. Thursday, transportation left me stranded. Thank God for compassionate souls with cars. Yesterday,  I had a full schedule of clients and lunch was at 4 pm. Hungry! I have a 12-hour – count them, 12! – webinar to listen to and about six reports to write. I have gotten ridiculously behind and my days don’t have enough hours.

Now, I understand I generally do this to myself. I also understand I generally am able to pull my own proverbial fat out of the fire so most people don’t worry about (or even listen to!) me. [Sorry, did you say something Sue? ::grin::] But – and that is a big but – I feel like whining and Lin showed me something to whine about!

To wit: “Breakthrough treatment may cure 50% of all cases of blindness”! What the rinky dink is that all about? It turns out the article is all about the stem cell work just published. Huh?

Okay. Age-Related Macular Degeneration is our nemesis but on the radar of the world in general, it is pretty much a blip! One blip. A little blip at that.

VisionAware reminds us that 90% of all of the 39 million folks who are blind actually live in the low-income countries of the world. Looking at our demographics, for the most part, honey, that ain’t us. Yes, AMD is the leading cause of blindness in the developed world, but if you live in dozens of other places, you may not keep your sight long enough to even think about the possibility of developing AMD.

In 2017 the World Health Organization (Who? The World Health Organization. WHO? That’s right. What? No, WHO…with apologies to Abbott and Costello.?) estimated there are 1.4 million children worldwide with irreversible blindness. There are 19 million children in this world with vision impairment. Of those, 12 million have refractive errors. In other words, we could cure 12 million cases of childhood visual impairment with glasses!

Un-operated cataracts are the major cause of blindness worldwide with a 35% share of the pie. Please note that word is un-operated not inoperable. These people could be made to see with a simple operation.

Uncorrected refractive errors come in in second place with a 21% share of the pie. Add 35% and 21% and you already have 56% of the causes of blindness, immediately putting to lie the 50% “cure” claim of that nutty headline.

So, worldwide, how much moderate-to-severe vision loss is due to age-related macular degeneration? About 8%. Please note the words did not say blindness. They said moderate-to-severe vision loss.  There is a big difference.

Do I like being visually impaired? Not by a long shot! Do I want a cure? Uhh, yeah. But do I want to feel sorry for myself and swallow every crazy headline that gets published. No!

The treatments and eventually the cures are coming, but they are not here yet. A little skepticism about some of the claims out there now is a good thing.

And, the truth of the matter is, most of us – yes, us with AMD – are pretty dang lucky. Our impairment has hit us late in life. I became myopic at age 12.  What would my life have been like if my parents could not have gotten me glasses?  How much human potential are we wasting because CHILDREN cannot see?

Think about it.

Written March 24th, 2018

Next: Overwhelmed – Again

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Another Cautionary Tale

Watching a ‘circus act’ out on the deck. The pups are now able to hit the top of the picnic table from a stand. Yesterday they got a bunch of bananas off the counter. Fought over them and rolled on them. On the living room rug. If nothing else they get points for unique and creative.

As with everything, the pups’ exploits bring mixed reactions. Some of you are laughing. Others are appalled.

The ‘big news’ of the week is making a lot of people pretty excited and happy. I imagine you heard Pete Coffey, of the London Project and University of California – Santa Barbara, is saying he will make stem cell treatments readily available to all comers in five years. He is reporting utterly amazing results for a phase 1 stem cell experiment.  [Lin/Linda here: to see the list of articles from various sources, click here.]

Whoa! Hold on for a minute! Unfortunate I must take the loyal opposition stance on this one! I am – to understate things – a tad skeptical. There are problems here.

Lin has her ways of getting things. She has a pretty good network of spies and other secret agents. One of her spies shared the published article with us. I have not read it all yet, as a matter of fact, I have barely started it – things are just not calming down around here – but some stuff I did see made me concerned.

Let us start with the timelines they lay out. This research was done in the summer of 2015 but we are just hearing about it now. Where have they been for the past two and a half years?!?!?! If this stuff is so hot, they should have been shouting it from the rooftops a lot earlier than now.

Even more suspicious? The submission date for publication was November, 2016 but the acceptance date was February, 2018! Anyone who has written a thesis or a dissertation knows what that year and a half lapse represents: a whole pot load of rewrites! What was wrong with the original work? Inquiring minds and all that.

There are other things that are wrong, wrong, wrong. Now, I applaud Douglas and the second person who wishes to remain anonymous. I really do and I will come back to why in a second. But seriously, how often can you be on a first name basis with half of a subject pool? There were two people in this study! The FDA suggests 20 to 100 people is the appropriate number of subjects for a phase 1 study. What happened to the other 18 people? This study sounds likes it is providing more anecdotal information than research findings.

And why do I applaud Douglas and the other person? They had enough guts to participate in phase 1 research. Phase 1 research is safety and tolerability, folks. They are looking for weird reactions like growing hair out of your eyeballs or having your head spin around. ( OK, so I am a little fanciful. You still get the idea.) This is not the proof of concept phase.

The Food and Drug Administration (FDA) gives an estimate of six to eleven years to get a medication or treatment through phases 1, 2 and 3. Coffey is saying he will have his treatment on the proverbial shelves in five years. Now granted, he is talking about availability in the United Kingdom, but I assume they also have a cautious regulatory agency working there. How does this get shelf ready in five years?

And these are just questions I have off the top of my head!

My emotional self would love to believe this is happening. My rational self is very skeptical. My advice would be to stay hopeful but also remain skeptical. Like puppies mashing bananas into my carpet, this study may create some positive emotions but I think there is still something wrong with the picture.

Lin/Linda here: I’ve created a page with some other concerns that we have: Considerations in Evaluating Recent Stem Cell Clinical Trial in the UK

Written March 19th, 2018

Next: Furious and Proud

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Considerations in Evaluating Recent Stem Cell Clinical Trial in the UK

I hope that you know that I am NOT trying to say that the results of this study are not valid or not hopeful.  Not at all!  It’s a great first step but Sue and I and others believe that this treatment won’t be available in 5 years as is being claimed. There is still too much yet to do.

Here are some considerations that we’ve found:

1.  This is not a ‘cure’, the person’s vision was not restored to the before-AMD state and this will not help everyone.   If a person’s photoreceptors have been damaged, inserting RPEs will not restore vision which is what the photoreceptors do. RPE cells ‘help’ the photoreceptors function. This is for those people who have some functional photoreceptors with RPEs that can be restored or rejuvenated.

2.  The scientific article was received by the Nature Biotechnology publishers on November 6th, 2016 (yes, 2016!), accepted on February 28th 2018, and published online March 19th, 2018.  This journal is peer-reviewed so it’s highly likely that the delay was because they had questions, asked the authors to explain what they did and how they did something.

3.  There were 10 people enrolled and only 2 people got the treatment (stem cells).  They can say they have 100% success but what about the others? I read that they said they would be treating another participant but no mention of timeline.  Just this morning I saw a video that said that 8 more patients will undergo the procedure but there’s no timeline.

4.  The Pfizer company was the sole funding source when the clinical trial started.  When 2 of the 10 participants were enrolled, Pfizer suspended funding for ‘strategic commercial reasons’ not related to the trial.  We are not sure where the funding will be coming for future research.

5.  This is a really early phase of clinical trials.  Phase I is the first of the phases.  Its purpose is to make sure they’ve got the proper dose and to see if there is any ‘hint’ that it works.  Phase II is the preliminary safety, final dose finding and looking at the results according to ‘endpoints’ they set at the start.  Phase III is where they really prove if it worked and to make sure it is safe.

6.  Before this can be used on the public, it will have to pass through regulators.  Consider the phase & this aspect, it’s hard to believe that it could be available in 5 years.

7.  They’ve only observed these 2 people for 12 months.  They will be followed for 5 years. One thing that can happen with stem cells is that they can migrate to other locations and grow tumors or they can be rejected..  That’s why they give immunosuppresant drugs after surgery. It this case it was prednisone delivered directly to the eye. There’s no information about the long-term use of it. The woman who was treated is diabetic and the prednisone caused a change in her blood sugar (they were able to adjust it).

8.  The purpose is to insert a ‘patch’ of RPEs generated from stem cells.  It won’t replace all RPEs. It definitely won’t replace photoreceptors that give us sight.

9.  There is no sham surgery done so you can’t 100% say that it was the stem cells that improved their vision.  Sham surgery would be the researchers using the surgical technique exactly as the treatment technique but without the RPEs.

Yes, we will follow this and report anything we find to you.

Written 3/23/2018

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?”

Things Are Getting Better

Just about time to get ready for bed but I thought I would start this while I was thinking about it. Point one: Sunday I went in and activated the educator’s discount on my phone plan. I kept forgetting about it before, which was stupid. I will save 15%, which will be about $27 a month.

Lots of companies and professions have discounts for a variety of things. If your employer or former employer does not have discount arrangements, consider joining AARP or another such organization. AARP is about $12 a year, for which you get a list, as long as your arm, of business offering discounts. For example, Cirque du Soleil tickets in Vegas go for about a hundred dollars, (or much more!) a piece. Buy two with AARP’s 20% discount and you have more than recovered twice your membership cost. (And, yes, they have phone plans, but I got all excited when I saw Cirque.)

That is the memo from my thrifty side. Now we can hear from my practical side.

My practical side says invest in power strips. We have a substitute cleaning person at the office. She unplugs my extension cord every time she cleans! Ahhhhhh!!!!!! That means I have to crawl around the furniture trying to get everything reconnected so I can plug in my CCTV. I will assume you have tried to plug something into an outlet in a dark corner before. With limited vision it is an exercise in frustration.

The answer is power strips! Plug those babies in one time. After that you can pick them up out of those dark, dreary corners and hold them in the light so you can see what you are doing. A thousand times easier to plug in my CCTV.

What else? Well, have you seen the research suggesting baby boomers have less AMD than their parents? And those who are coming after us – we who were born between 1946 and 1964 – seem to have even less.

Of course, it is sort of hard to prove by me with GA (geographic atrophy) in both eyes but supposedly the risk of developing AMD has been decreasing by 60% every generation. Seriously. Cross my heart and hope to die. Science Daily says they got the information from the JAMA Research Journals. JAMA apparently got it from Beaver Dam. [Lin/Linda here: The Beaver Dam Eye Study is a often-quoted research project funded by the National Eye Institute.  The purpose of the study was “to collect information on the prevalence and incidence of age-related cataract, macular degeneration and diabetic retinopathy, which are all common eye diseases causing loss of vision in an aging population.” ]

This does not mean there are fewer of us. There are many more of us. This is because our generation is so freakin’ BiG a smaller portion of us still gives us the bigger numbers. Got it?

There are articles on the web suggesting this is not just happening in the States. The proportions are going down in Europe and in Australia, too.

Why is right now just speculation. The folks who wrote the JAMA article suggested we just may be healthier. Rates of cardiovascular disease and dementia are also down.

Same underlying factors? Different ones? No clue at this point. However, the take home message is this: things are getting better. Keep exercising your good health habits. Encourage your kids in good health habits. We may have no clue what we are doing, but keep doing it!?

Written March 10th, 2018 Continue reading “Things Are Getting Better”

Another $64,000 Question

Last time I discussed why we believe clinical trials and experimental evidence are so much better than anecdotal evidence. A reason that I did not include for truly appreciating scientifically derived data is a little thing called peer review.

Wikipedia describes peer review as the evaluation of work by one or more people of similar competence to the producers of the work. It is a form of self-regulation by the members of a professional or scientific community.

In order for peer review to occur, research has to have a certain level of transparency. Experimental procedures and results must be put out there for scrutiny. And that is where this page comes in.

Seekingalpha.com publishes stock market insights and financial analysis. They had a source at the 2018 Macular Society meeting where Apellis presented their findings on APL-2. Gleaning information from the PowerPoint slides, an author for seeingalpha.com developed the opinion APL-2 may not be all that Apellis has been cracking it up to be. [Lin/Linda: the full research results have not yet been published.  The slides from this meeting is the best source we have of the preliminary results.]

Why? Well, for one thing he said the rate of conversion from dry to wet AMD was 21%. Ouch. That is just about 1 in every 5 subjects. The average number of dry AMD patients who convert to wet is between 10 and 15% (although in the trial, there was only 1 person or 1% of those in the sham group who converted to wet; that’s slide 14). Rounding it off, that is about one patient in 8. There may be something in APL-2 causing an increased conversion rate.  [If you look at slide 16, they have some theories on why this happened.]

Another issue the author of the article had had to do with what should be the primary outcome measure. Apellis measured the rate of growth of the lesion. That slowed down. There was no one debating that. What was being questioned was why visual acuity was not used as the primary outcome measure. After all, if you can see, who cares how big the hole in your retina actually is?

Speaking as me, Sue, I would have assumed the size of the lesion is related to how well you see. Slower growth would mean better retention of vision, right ? Not necessarily. While Apellis reported a modest, positive difference between monthly treatment and sham at 12 months into the project, this positive difference did not persist. While at 12 months monthly treatment had lost 3.3 letters on the chart and sham had lost 4.4, by month 18 monthly treatment had lost 7.7 and sham had lost 6.4. What the hell????? The data suggested a greater loss of acuity with the treatment than without it.

Bottom line for the seekingalpha.com writer was this: don’t sink a lot of money into Apellis stock. What is the bottom line for us? How about a few questions answered? Or at least a few, clever theories? I would like to know why saved macula does not equal saved acuity. That seems counterintuitive.

Another question would be how did they get through phase 1, safety and tolerability, if subjects were coming out in worse shape (if they were; I don’t know.) ? Are the acuity data for phase 2 all that different?

And the $64,000 question: should anyone volunteer for their phase 3 trials?….that one you answer for yourself.

Lin/Linda here: I was curious as to what the exact difference is between a placebo group and a sham group.  Here it is: “Placebo and sham treatment are methods used in medical trials to help researchers determine the effectiveness of a drug or treatment. Placebos are inactive substances used to compare results with active substances. And in sham treatments, the doctor goes through the motions without actually performing the treatment.”

Written March 3rd, 2018 Continue reading “Another $64,000 Question”

“Take This & You’ll Be Cured!”

Good morning! Back again.

I am sure you have noticed that this site has a real emphasis on information and research. We value the power that knowledge can give us. We also value the scientific method.

Some people may ask why that may be. It’s simple. The scientific method and controlled experiments allow us to know with a degree of certainty what is true and what works. Things are proven to within a shadow of a doubt.

Scientific method and scientific proof stand in contrast to anecdotal evidence. I would assume many of you know what anecdotal evidence is. However, for those who do not, allow me to take the podium for a second.

Wikipedia defines anecdotal evidence as evidence collected in a casual or informal manner and relying heavily or entirely on personal testimony. For example, “The world is flat.”

600 years ago everyone knew the world was flat. You look out on the horizon and everything just drops off. Terra incognita. Proceed at your own risk because you know you’re going to fall off. (Did you ever wonder what they thought you were going to fall off into? Just a random thought there.)

It took some intrepid explorers to go out and discover there was something beyond the horizon. They came back and told people just that. However, it was still anecdotal evidence. A handful of crazy sailors telling you that the world was round. It did, in fact, take a variety of explorers taking a variety of voyages (read performing experiments) to actually convince people that the world is round. These explorers proved to within a shadow of a doubt the world was round.

And you know what? I for one am glad people did not necessarily believe that handful of sailors. We should not accept everything without proof.

Very often, this reliance on anecdotal evidence happens in medicine. It happens to people looking for ways to treat their age related macular degeneration.

We hear testimonials all the time. “Take this and you will be cured!”  “It worked for my great aunt Tilly”! That someone truly believes a treatment worked for them is great. However, without scientific evidence we are not able to review it.

Nor should we. Operating on anecdotal evidence can be dangerous. Not only may you hurt yourself doing something dangerous, you could also waste valuable resources – yours and everyone else’s – on something with no value.

Why do we only talk about things that have come from clinical trials? Because the trials are controlled. That means they have tried to eliminate any confounding variables. Confounding variables are things that are outside influences that change the effects of the treatment. In other words with confounding variables we have no idea if what we tried worked. The results could come from something else entirely.

For example, you are going on a diet to lose weight. At the same time you also start walking two miles four days a week and take exercises classes three days a week. How much effect did your new diet exactly have? No way to tell, right? There are confounding variables.

Before we review anything and suggest the treatment may be promising, it needs research backing it up. We operate that way because it is the best way. We need to provide you with the best information we can. The best comes from clinical trials.

Written March 4th, 2018 Continue reading ““Take This & You’ll Be Cured!””

Supplies are Limited, So Act Now!

I tend to be pretty optimistic. I have said a couple of dozen times that this is the best time in history to be going blind and I stand by that. Because, you know what? It is only getting better!

A recent piece in healio featured APL-2. APL-2 met expectations in phase 2 clinical trials (proof of concept) and is rounding the base headed into phase 3. Go, APL-2!

Results of the phase 2 trials were, obviously, promising. There was a 29% reduction in the rate of growth of geographic atrophy lesions when APL-2 was administered monthly.

It is possible within a year or so dry AMD will no longer be considered a disease with no treatment. In other words, there will be a lot more hope.

Now granted, these treatments are not cures. But they are better than nothing. Nothing being pretty much what we have now. Would you prefer to go blind in 7.5 years or so without the treatment or in 9 or 10 years with the treatment? Yep. Thought so.

Admittedly, some subjects developed wet AMD with the treatment. Nasty side effect but they will work on that. It did not happen to a large number of folks.

As I have also said before, discoveries build on what came before. The APL-2 study targeted the C3 complement factor and got results. This lends further credence to the theory AMD is a function of the complement immunity system. There is now a strong suggestion we have the right target. There will soon be other treatments ‘leveled’ at that target. More progress will be made.

Phase 3 studies are to start sometime in 2018. According to the Apellis announcement they will be recruiting 1,200 subjects divided among several locations. I looked at clinicaltrials.gov but there is nothing yet listed. Be sure to watch that site for developments. Also, talk to your retinologist about getting into the study pretty dang soon. Lin told me one of the face book members has already been approached by her doctor. There are only 1,200 slots. “Supplies are limited, so act now!”?

Lin/Linda: Since sue wrote this page there has been additional, potentially contradictory information come to light. As usual, we would ask you to gather all necessary information for yourself and make an informed choice on any treatment. We are only one of many sources. And us? We have a few leads and will be following up on the contradictory information. Lin and Sue, girl detectives at your service! Stay tuned and if you have any clues, please share.

And if you want to advance scientific knowledge without subjecting yourself to an experimental treatment, the NEI is looking for subjects for a natural history study. Several measures will be taken, including genetic testing. They will be documenting the natural development of AMD and seeing if they can see any patterns and/or relationships. Not the type of study that will actually treat its subjects, but if you are needle phobic, it might be for you. Remember, Sun Tzu said if you know your enemy and you know yourself you do not have to fear the battle. This study, also discussed in healio, is being designed to let us know the enemy. Knowing yourself is your own problem!

So that is that for now. Hope you are staying positive. This really is the best time in history to be going blind!

Written March 3rd, 2018 Continue reading “Supplies are Limited, So Act Now!”

Advanced AMD (wet or geographic atrophy) in both eyes

Advanced AMD (wet or geographic atrophy) in both eyes

No one with this combination was included in either AREDS or AREDS2.   Some doctors tell their patients with geographic atrophy (advanced dry AMD) in one or both eyes to take the supplement to prevent their eyes from progressing to wet AMD (it’s possible to have geographic atrophy AND wet AMD).

Notes
  • Stages: In order to simplify the results of these studies, we have ‘stretched’ the stage assignments from how they were actually done in the studies.  For example, in AREDS, they looked at the lead/most advanced eye & assigned the participant that stage.  So someone with one eye at the intermediate stage & the other with no AMD, early AMD or intermediate AMD would be assigned the intermediate stage.  AREDS2 used a slightly different method.
  • Source of supplements: There are many ‘eye vitamins’ sold as AREDS or AREDS2 but they do not all have the exact ingredients that were a result of the extensive AREDS & AREDS2 research (see References section below for full study articles).
  • Importance of reading the labels: The ingredients & dosages from AREDS were antioxidants 400 IUs of Vitamin E, 500 mg of Vitamin C and 15 mg beta carotene.  Beta carotene was found to be linked to lung cancer in smokers so for that and other reasons, AREDS2 removed the beta carotene & used 10 mg Lutein and 2 mg Zeaxanthin.  The formulations from both studies included zinc (because of zinc, copper was also included), 80 mg in AREDS and both 80 mg and 25 mg zinc in AREDS2.   It was these exact ingredients that produced positive results (“showed reduction of risk  of developing advanced AMD”) so read the labels of any products carefully to make sure they match the study formulation as closely as possible.  There are 2 webpages in References below that compare selected products.
  • Warning about zinc: Several years ago, warnings were issued about the high dose of zinc in the study formulations (80mg). Those warnings were confirmed by 2018 research that found that 15% of patients with a specific combination of genetic risk variants nearly tripled their risk of developing wet AMD when treated with the AREDS formulation with 80mg zinc instead of a placebo.  For more information about genetic testing, see References below.
References

Go back to The Guide

 

 

Intermediate AMD in one eye/advanced (wet or geographic atrophy) in the other eye

Intermediate AMD in one eye/advanced (wet or geographic atrophy) in the other eye

Studied in AREDS & AREDS2: showed reduction of risk of developing advanced AMD over 5 years.

Notes
  • Stages: In order to simplify the results of these studies, we have ‘stretched’ the stage assignments from how they were actually done in the studies.  For example, in AREDS, they looked at the lead/most advanced eye & assigned the participant that stage.  So someone with one eye at the intermediate stage & the other with no AMD, early AMD or intermediate AMD would be assigned the intermediate stage.  AREDS2 used a slightly different method.
  • Source of supplements: There are many ‘eye vitamins’ sold as AREDS or AREDS2 but they do not all have the exact ingredients that were a result of the extensive AREDS & AREDS2 research (see References section below for full study articles).
  • Importance of reading the labels: The ingredients & dosages from AREDS were antioxidants 400 IUs of Vitamin E, 500 mg of Vitamin C and 15 mg beta carotene.  Beta carotene was found to be linked to lung cancer in smokers so for that and other reasons, AREDS2 removed the beta carotene & used 10 mg Lutein and 2 mg Zeaxanthin.  The formulations from both studies included zinc (because of zinc, copper was also included), 80 mg in AREDS and both 80 mg and 25 mg zinc in AREDS2.   It was these exact ingredients that produced positive results (“showed reduction of risk  of developing advanced AMD”) so read the labels of any products carefully to make sure they match the study formulation as closely as possible.  There are 2 webpages in References below that compare selected products.
  • Warning about zinc: Several years ago, warnings were issued about the high dose of zinc in the study formulations (80mg). Those warnings were confirmed by 2018 research that found that 15% of patients with a specific combination of genetic risk variants nearly tripled their risk of developing wet AMD when treated with the AREDS formulation with 80mg zinc instead of a placebo.  For more information about genetic testing, see References below.
References

Intermediate AMD in both eyes

Intermediate AMD in both eyes

Studied in both AREDS & AREDS2: showed reduction of risk of developing advanced AMD over 5 years.

Notes
  • Stages: In order to simplify the results of these studies, we have ‘stretched’ the stage assignments from how they were actually done in the studies.  For example, in AREDS, they looked at the lead/most advanced eye & assigned the participant that stage.  So someone with one eye at the intermediate stage & the other with no AMD, early AMD or intermediate AMD would be assigned the intermediate stage.  AREDS2 used a slightly different method.
  • Source of supplements: There are many ‘eye vitamins’ sold as AREDS or AREDS2 but they do not all have the exact ingredients that were a result of the extensive AREDS & AREDS2 research (see References section below for full study articles).
  • Importance of reading the labels: The ingredients & dosages from AREDS were antioxidants 400 IUs of Vitamin E, 500 mg of Vitamin C and 15 mg beta carotene.  Beta carotene was found to be linked to lung cancer in smokers so for that and other reasons, AREDS2 removed the beta carotene & used 10 mg Lutein and 2 mg Zeaxanthin.  The formulations from both studies included zinc (because of zinc, copper was also included), 80 mg in AREDS and both 80 mg and 25 mg zinc in AREDS2.   It was these exact ingredients that produced positive results (“showed reduction of risk  of developing advanced AMD”) so read the labels of any products carefully to make sure they match the study formulation as closely as possible.  There are 2 webpages in References below that compare selected products.
  • Warning about zinc: Several years ago, warnings were issued about the high dose of zinc in the study formulations (80mg). Those warnings were confirmed by 2018 research that found that 15% of patients with a specific combination of genetic risk variants nearly tripled their risk of developing wet AMD when treated with the AREDS formulation with 80mg zinc instead of a placebo.  For more information about genetic testing, see References below.
References

Go back to The Guide

Early AMD in one eye/intermediate or advanced (wet or geographic atrophy) in the other eye

Early AMD in one eye/intermediate or advanced (wet or geographic atrophy) in the other eye

AREDS: showed reduction of risk of developing advanced AMD over 5 years.

Notes
  • Stages: In order to simplify the results of these studies, we have ‘stretched’ the stage assignments from how they were actually done in the studies.  For example, in AREDS, they looked at the lead/most advanced eye & assigned the participant that stage.  So someone with one eye at the intermediate stage & the other with no AMD, early AMD or intermediate AMD would be assigned the intermediate stage.  AREDS2 used a slightly different method.
  • Source of supplements: There are many ‘eye vitamins’ sold as AREDS or AREDS2 but they do not all have the exact ingredients that were a result of the extensive AREDS & AREDS2 research (see References section below for full study articles).
  • Importance of reading the labels: The ingredients & dosages from AREDS were antioxidants 400 IUs of Vitamin E, 500 mg of Vitamin C and 15 mg beta carotene.  Beta carotene was found to be linked to lung cancer in smokers so for that and other reasons, AREDS2 removed the beta carotene & used 10 mg Lutein and 2 mg Zeaxanthin.  The formulations from both studies included zinc (because of zinc, copper was also included), 80 mg in AREDS and both 80 mg and 25 mg zinc in AREDS2.   It was these exact ingredients that produced positive results (“showed reduction of risk  of developing advanced AMD”) so read the labels of any products carefully to make sure they match the study formulation as closely as possible.  There are 2 webpages in References below that compare selected products.
  • Warning about zinc: Several years ago, warnings were issued about the high dose of zinc in the study formulations (80mg). Those warnings were confirmed by 2018 research that found that 15% of patients with a specific combination of genetic risk variants nearly tripled their risk of developing wet AMD when treated with the AREDS formulation with 80mg zinc instead of a placebo.  For more information about genetic testing, see References below.

 

References

Early AMD in both eyes

Early AMD in both eyes

Only studied in AREDS. Not enough participants to generate a recommendation. Perhaps results of Awh, Zanke and Kustra (2017) may apply but it has not yet been studied.  The study found that those with a specific genetic makeup may be harmed by taking the antioxidants (no zinc).  See reference below.

There were no participants with early AMD in AREDS2.   Some eye doctors recommend that those with early AMD in both eyes take the AREDS or AREDS2 supplements.  Please make sure that you discuss the benefits versus the risks (ie, interactions with other medications and/or supplements) with your eye doctor.  If you decide to take the supplements, please read the notes below and talk to your medical doctor about them.

  • Stages: In order to simplify the results of these studies, we have ‘stretched’ the stage assignments from how they were actually done in the studies.  For example, in AREDS, they looked at the lead/most advanced eye & assigned the participant that stage.  So someone with one eye at the intermediate stage & the other with no AMD, early AMD or intermediate AMD would be assigned the intermediate stage.  AREDS2 used a slightly different method.
  • Source of supplements: There are many ‘eye vitamins’ sold as AREDS or AREDS2 but they do not all have the exact ingredients that were a result of the extensive AREDS & AREDS2 research (see References section below for full study articles).
  • Importance of reading the labels: The ingredients & dosages from AREDS were antioxidants 400 IUs of Vitamin E, 500 mg of Vitamin C and 15 mg beta carotene.  Beta carotene was found to be linked to lung cancer in smokers so for that and other reasons, AREDS2 removed the beta carotene & used 10 mg Lutein and 2 mg Zeaxanthin.  The formulations from both studies included zinc (because of zinc, copper was also included), 80 mg in AREDS and both 80 mg and 25 mg zinc in AREDS2.   It was these exact ingredients that produced positive results (“showed reduction of risk  of developing advanced AMD”) so read the labels of any products carefully to make sure they match the study formulation as closely as possible.  There are 2 webpages in References below that compare selected products.
  • Warning about zinc: Several years ago, warnings were issued about the high dose of zinc in the study formulations (80mg). Those warnings were confirmed by 2018 research that found that 15% of patients with a specific combination of genetic risk variants nearly tripled their risk of developing wet AMD when treated with the AREDS formulation with 80mg zinc instead of a placebo.  For more information about genetic testing, see References below.
References

Go back to The Guide

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