proliferative diabetic retinopathy - need help please :(

@PDR_T2 Yes, both eyes were proliferative DR. At different times, I lost complete vision in both eyes (this was in 1996). Vision was completely restored.

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I have had floaters my whole adult life. They look like hairs in front of me or like translucent spots.
They tend to settle lower and lower until I canā€™t see them anymore.
I really only notice them when I look up at the sky.
My doctor told me itā€™s nothing. So I think there are different kinds of floaters

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thank you @Timothy @Jimi63. Appreciate it. From your guys experience:

  • Does vision get blurry / faded after laser (PRP) treatments for a while and then it settles?
  • I donā€™t notice bleeding / hazy vision but there is blood on my retina. Do this blood create distorted vision / faded spots?
  • My biggest concern is my right eye . it has a blind (Empty) spot from central vision to bottom right. Do you or any one experience similar temp issue due to blood on retina? or this more of a permanent damage type of deal? Please see attached ā€¦ best explanation i can give in terms of missing spot in vision (while line)
    I will be asking my doctor as well (confirm with him again) but wanted to see if anyone experienced this as well.

I have had numerous laser treatments in my left eye, all several years ago. Itā€™s stable except for a cataract. My good eye finally went a few years ago. I had a few laser treatments, two Avastin injections. Holding steady right now. I will always see things floating around, that never went away. A dot in my ā€˜goodā€™ eye, and a little half circle in my left eye. When the bleeds happen, I get coffee ground or speckle sky plus some webby stuff. If it bleeds into my field of vision, I have to back off driving etc. If it bleeds to the sides, I can deal with it. My last round of major speckles took a full year to clear up. I see them in the daytime, but I donā€™t see them at night against a dark sky. Thefact that things eventually clear up is reassuring. I just keep dealing best I can. The only real problem is my husband has a new cancer diagnosis, which came during my last really bad episode. I had to get us rides everywhere. That feeling tho, when those speckles clear upā€¦Blessings to you. I hope things go well.

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From Bernsteinā€™s book ā€“ this is a recognized phenomenon:

Insulin-like Growth Factor 1 (IGF-1)

Rapid correction of very high blood sugars can, on occasion, cause exacerbation of a common complication of diabetes called proliferative retinopathy. This condition can cause hemorrhaging inside the eye and blindness. Such exacerbations are usually preceded by an increase in serum levels of insulin-like growth factor 1. A baseline level of IGF-1 in the blood should be measured in people with proliferative retinopathy. Repeat determinations should be made every two to three months. If levels increase, blood sugars should then be reduced more slowly.

Bernstein, Richard Kā€¦ Dr. Bernsteinā€™s Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars (pp. 64-65). Little, Brown and Company. Kindle Edition.

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Bernstein always measures IGF-1 at baseline, with new patients, and tailors his insulin regimen to adequately slow increase so as to prevent IGF-1 rising. This is a transient phenomenon, presumably having to do with providing adequate time for appropriate cellular adaptation (to lowered BG) via nuclear/gene expression. This generally requires several weeks to several months.
I scanned beacherā€™s reference but it does not discuss the role of IGF-1. But there are quite a number of studies that do this ā€“ include ā€œIGF-1ā€ with other keywords describing the retinopathy-BG phenomenon.
I cannot suggest quick remedies for damage done, but hopefully this is helpful for understanding what happened. Lowering BG is hugely beneficial in the long term, and will probably help greatly with healing, but this requires years (and patience and discipline) for most neuropathy regardless of cause. Bernstein is also a useful reference for his own case and those of many patients wrt to this.

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I would further comment that it is the BG transients, in response to meals, that cause virtually 100% of diabetic complications. Glucokinase-monogenic diabetes (aka MODY-2) illustrates this perfectly. So does the research of M. Brownlee et al.
I have a monogenic form of diabetes in which the fault is underexpression of insulin genes and proteins in beta cells (MODY-3 or HNF1-alpha diabetes). This is similar to type-1 and very much unlike type-2, phenotypically.
My impression is that a lot of the T1Ds reporting here tolerate a pretty high HbA1c, but nevertheless this only reflects long-term average BG. If the meal-induced swings are small there is no problem with a high baseline ā€“ the cells adapt. But for most diabetics a high HbA1c reflects large BG transients and not a high nonprandial baseline.

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P.S. And as I have written here before, prandial deficiency in islet secretion of insulin will produce excess islet secretion of glucagon. It is the excessive portal glucagon that causes the prandial hyperglycemia.
Even Bernstein is completely unaware of this, the fundamental mechanism of BG regulation by liver under islet-hormone control during meal absorption. So he does not understand the fundamental endocrinology at all. But he has a lot of clinical observational experience.
I do not know of many diabetics who understand the biology either. I think it is essential to making good choices about BG management, and understanding the crude and flawed compensation of peripheral (exogenous) insulin and its enormous limitations.

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thank you @Mac2. Appreciate it.
Have you had any eye issues by any chance? how are you now?

@Laura_S hope you and your husband are doing well Laura. Please stay strong :slight_smile:

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P.S. (again): Best keyphrase and words would be ā€œlossā€ of ā€œdecrement of intraislet insulinā€ and/or ā€œintraislet hypothesisā€. This has been verified continuously by experiment since 1970 ā€“ the understanding or theory is as well proven as any, and I treat it as axiomatic.
T1Ds (unlike myself) should really be aware of the transformation of the alpha cells, epigenetically, that takes place over a few years after initial diagnosis. It is this transformation that makes T1DM ā€œinsulin-dependentā€ and generates susceptibility to ketoacidosis thereafter. Islet glucagon acts upon the beta cells to stimulate more insulin release ā€“ this negative feedback or regulation is lost in T1DM and/or other forms of diabetes in which almost all beta cells are lost.
But once insulin-dependent, a diabeticā€™s alpha cells lose responsiveness to hypoglycemia as part of the epigenetic sequelae ā€“ not totally, but in certain ways. Lag is increased and precision is decreased for BG regulation ā€“ i.e. phenomena such as hysteresis are introduced.
I think these fundamental phenomena are important to understand for T1Ds. MDs rarely know any of this. End of lecture.

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Hi PDR_T2, I was tested by Bernstein in 2014. I self-diagnosed in 2010. I had essentially all of the testable diabetic complications in eyes when tested.
Nobody that I know of does the type of testing that Bernstein does, but this is discussed in his book. I think an opthamologist probably can replicate some of it, albeit probably with different instrumentation.
None of positively-tested phenomena (e.g. multiple vision, serpentine vasculature, and maybe ten more) was I aware or conscious of before testing. I had a ā€œstaticā€ black spot that I would ā€œseeā€ in my motorcycle visor, and this was eliminated within one or two years after I began insulin therapy. Indeed, according to Bernstein most of the eye complications are amongst the fastest to resolve after BG is normalized. But my guess is that your retinopathy may take longer ā€“ that is just a guess. You can probably find some discussion of this in the clinical research literature.

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More generally, I am myopic and have used presciption eyeglasses since age 30 or so, roughly. But I am stable and I donā€™t think the myopia has anything to do with the diabetes.
I am 62 years old, and have been a diabetic for my entire life, but did not recognize it until over 50. My diabetes or intrinsic hyperglycemia is completely stable and pretty mild, being genetic. Fasting/non-prandial hperglycemia is mild but hyperglycemic response to protein is large, and to carbohydrate very large without possibility of predictable peripheral insulin compensation. Gastroparesis (due to substantial damage to vagus nerve) is probably the most important complication. I think I have had some neural regeneration of vagus nerve, but not complete recovery. I have Monckebergā€™s sclerosis (death and calcification of media/muscle of lower leg arteries) and complications in calves and feet. I think I have partly regenerated there too, but not completely. I have reduced what I now recognize as neuropathy in the feet ā€“ I run 8 to 16 miles twice weekly in deep woods. The pain that always emerged for less than an hour after running has diminished and disappeared for shorter runs.
You might want to consider consulting Bernstein. But he doesnā€™t work with insurance at all, and he charged $600/hr last I knew. He also does not, generally, do limited consultations and a new ā€œpatientā€ must sign up for his whole ā€œprogramā€. So any or all of this might be a showstopper. You can try talking to his office, though, to explore ā€“ the office admin is Samantha and she fields all prospective new patients.

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Taurine is interesting:

Dietary taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in streptozotocin-induced Sprague-Dawley rats

Taurine Protects Retinal Cells and Improves Synaptic Connections in Early Diabetic Rats

Taurine: The comeback of a neutraceutical in the prevention of retinal degenerations

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Thank you so much.

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I had a similar situation. I had a1c around 11 when I was diagnosed, then it dropped down to 6 within a short period of time and I had to go to an ophthalmologist who directed me to a retina specialist with PDR. I am not sure how severe it was but the photographer who did pictures with dye was shocked. They did Avastin injections and laser treatments over the next year. Everything have been stable since then (about 7 years have passed now). It took around another year or two for the vision to recover somewhat. I am not sure if it as good as before (it was never great) but there is a noticeable improvement since the last laser treatment. Ask the doctor about the empty spot, he knows what it is and what to expect about it. Overall, I think all I can do is to maintain as healthy lifestyle as possible, a1c included, and hope that the body would heal and take of itself.

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Thank you so much for your response.
If you donā€™t mind me asking. How many laser have you done and how many injections ?
Are you still on injections right now ?
Any laser side affects ?

Thanks.

I think I had around 2-3 injections and 1-2 lasers for each eye. I havenā€™t done anything else since then and I donā€™t notice any laser side effects.

Awesome. How long was each session of laser if you remember ?

From my end am to do about 4x laser in each eye. And 2 years worth of injections. 6 weeks apart for each injection.

Something that is not told to us is that a rapid drop in A1c is bad for the eyes and that is what has happened to you. Your situation is usually treatable so try not to panic.

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