I maintain that there is ample data to argue that environmental factors play a role in the development of myopia. Genetic models do not explain the prevalence rates of myopia, especially the drastic increase in recent generations in certain populations (i.e., Asian). It is also my opinion that there could be variants of myopia (i.e., moderate and pathological myopia subtypes) that may respond differently to environmental factors (e.g., quantity of near work). Studies utilizing large group statistics in a general population would fail to demonstrate a relationship between myopia and individual environmental factors (e.g, quantity of near work) if the variants are small in number and not subtyped a priori. It may very well be that the degree of nearwork may have little impact on folks with an inherited or otherwise acquired tendency toward simple or moderate myopia. But that may not be the case for ALL individuals with myopia. And there may also be other causative environmental variables at play as well.
I take such a stance not only because of my own interpretation of all the available data, but because in doing an informal study (highly anecdotal and subjective, I know) within my five sibling group, I can easily identify the quantity of nearwork done by each child during childhood and adolescence and the degree of myopia as an adult and find a perfect correlation. The odds of that occurring merely by chance are incredibly rare. Additionally, as I research my maternal history, including the deceased (several relatives have/had high or extreme myopia), those adults who were widely known as the "readers" or most educated in the family have/had the highest degree of myopia.
I love science. Sometimes it takes a preponderance of studies and creative ways to ask the question that leads to discovery. I say that the jury is still out.
Kg17 thanks for the input. Beware the tyranny of small numbers. Your family study group is seriously underepowered statistically.
Much agreed - I didn't mean to imply that I calculated a true correlation coefficient. Just want to provide food for fodder.
As is typical for medical research, however, sometimes it is the collection of "case studies" that provides the impetus for larger, better clinically controlled studies that attempt to answer the question in different, unique ways.
Interesting take on the issue kg17.
Given your response, would you advocate for a similar study, to the one above, replacing the population with a different ethnic group (I haven't actually read the article yet, but I'm assuming the subjects were all Asian) to see if the results held true? After all, isn't the true benchmark of sound science rooted in reliability and validity?
Remember correlation does not equal causation.
Yeh I do not believe for one second that near work leads to myopia or increases its progression, I don't even need to read the study, there is literally hundreds identical studies going back decades. That idea is a red herring that has led to a wild goose chase for decades and has wasted countless resources.
In any case it is a moot point in my opinion, we already know what the cause of the symptoms of severe myopia is, it is the progressive elongation of the eye beyond the growth years. The question is why does that happen? There are clearly defects in the collagen make-up of highly myopic eyes, very poor choroidal circulation, questionable IOP problems and areas of severe weakness in the scleral wall leading to the dreaded staphyloma. Now throw into the mix lifestyle factors such as diet (fish oil, vitamins), exercise (weight lifting - bad idea), occupation (i.e. active vs. sedentary), habits (eye rubbing, squinting = very bad) and you have some big problems just waiting to happen. Of course lifestyle plays a role and of course this is a multigenic (many genes) disorder but we essentially know what the underlying cause is and we can probably fix it already if resources were thrown in that direction. The comical thing is that all of the relevant information has been around for decades but no-one is even bothering to do the studies anymore and given most scientists and MDs inability to go to a bloody library and pull out a journal prior to 1990, we are now going backwards. I mean are we seriously still talking about NEAR WORK? Who bloody cares? People are losing their vision because of a bulge sticking out the back of their eye which you can see with your own eyes. What difference does it make if you studied for a BSc or a PhD or not at all. There are countless studies of teenagers losing sight to myopic degeneration. Was that because they started reading in the womb? No, it is because they have a bloody great big bulge out of the back of their eye and their axial length is off the chart. You can't blame the retina for cracking under the pressure, it has no other option than to crumble to pieces. Let's get real here and stop wasting money on pointless and pathetic attempts at scientific research.
Take diabetes to emphasise my point (it's easier for me). We know high blood sugar is the bad guy but even today we really don't know what causes it specifically. But you know that if you inject insulin, it will bring the glucose down. OK so let's do that if we can and allow people to live FIRST. We can deal with the ACADEMIC details later. Maybe this research will improve treatment later on (it is of course) but it will take time and money. It's the same scenario with myopia.
Pathological myopia is blinding, it does not lead simply to central visual loss, it leads to profound visual loss in it's worst form. We all know it, the researchers know it, the eye MDs know it and the patients know it. Lets just acknowledge the giant elephant in the room. We already know the cause of the symptoms, we probably know the best way to fix it, lets just do it.
Most MDs talking about myopia have never seen enough true pathologically myopic patients to comment on the condition with any authority. I have just come back from my posterior pole buckle surgery with Dr Ward and, hands down, he is the only eye MD in the western hemisphere who is TRYING to do anything for us as patients. I am not saying his treatment is the only way but at least he is trying and putting his reputation on the line. We need more like him.
"The odds of that occurring merely by chance are incredibly rare."
Actually no they are not. This is a classic type I error (under powered) and of course you are extremely biased. Also this is all one family and it is more than likely that there is a genetic factor in your family which does not apply at the population level. It's interesting but statistically useless. You also have no idea really how much near work they did. Did you count all the time they spent reading on the toilet? (an exaggeration but you get my point). You would have to compare multiple families before you can even begin to say anything useful here and I can tell you know from the already publsihed genome wide studies that are beginning to come out in myopia, it is a waste of time.
"I love science. Sometimes it takes a preponderance of studies and creative ways to ask the question that leads to discovery. I say that the jury is still out.
No you just have to ask the RIGHT questions.
"As is typical for medical research, however, sometimes it is the collection of "case studies" that provides the impetus for larger, better clinically controlled studies that attempt to answer the question in different, unique ways."
Ahhh the infamous "meta analysis". Otherwise known as fudging the data. Beware, the only time a meta-analysis is done is where there is lots of controversy in the field already. Stay away from them.
"After all, isn't the true benchmark of sound science rooted in reliability and validity? "
Exactly and this has already been reliably proven as very pathetic and pointless research decades ago. Come on, behave yourself.
Dukey - I haven't been here much lately - I take it the 7-mx didn't work out too well? Are you still taking it?
Can you tell us about the surgery? Lengthy surgery/recovery or quick? Does anyone do it besides Dr. Ward?
With all that off your chest, would you mind posting in depth the details related to your experience of the posterior pole buckling. Some of us are quite interested.
Hey yes I will, sorry for the rant haha!
I just need another week or so for my vision to recover a little bit better before I write a full review of everything. But in a nutshell all has gone well so far. There was some pain and very restricted and painful eye movement for a day or two but the key is to use it ASAP. That has 90% gone now 7 days post surgery. Redness is still there and will be noticeable for a few more weeks. Double vision is a problem at first but is pretty much gone as well as vision improves and as you do the exercises. Post surgery, vision is VERY poor, usually it is finger counting for a few days and then recovery from there on. I was 20/300 the next morning (from 20/25!) but now I am at 20/50 if I try hard but I can now see that my vision is there 100%, it's just my pupil and muscles are not quite working right so it will take sometime. It's weird, it feels like you are learning to see all over again. The atropine has not fully worn off yet either making my pupil a little larger than normal. Apparently I am ahead of the curve so all is very normal. The dreaded rise in IOP never really happened to me, pressure was 13 24h post-op (on Diamox) and today was measured as 13 again (off Diamox) (control eye = 11). Everything was very professional, very routine and very impressive. Only time will tell if it works long-term. I cannot tell you what the total cost is just yet but with insurance (who approved the procedure before hand) my cut will probably be around $2K.
I will post back later.