I had a little scare this week.
I was seeing flashes of light when it was bed time and I turn the lights off. But I just figured it was nothing. The next day it went away and the day after that I had a new giant dark floater.
I’ve had them before but never as big or dark so I went in to see an ophthalmologist.
I had a vitreous detachment which sounds horrible, but really it’s a normal thing that happens as we get older. Some of the gel in my eye became adhered to my retina and then broke away leaving the floater.
So no bleeds and no tears in my retina.
He also said that at my age of 59 and with type 1 for 38 years, it’s very unlikely I will ever get problems with my retinas.
He said less than 2% so that was surprising. He said that most retinal tears and bleeds happen within the 15 years after dx. And if you pass that, you probably never will not have the issue.
That was new information.
I was not in great control my first 10 years, but now in very good control mostly. So going into this appointment I was very worried.
Gets me to think though, some people have lots of complications and some people do not. My a1c was mid 7s until I started pumping. So it’s not like I had stellar control at the beginning.
I can still say 38 years and no complications, but I do have dupuytrens contracture in both my hands and feet, but there is no direct link, and I’ve had frozen shoulder which is also a risk factor of diabetes but no direct cause and effect. And my other family members also have dupuytrens and no diabetes.
Luckily no eye issues no neuropathy and no kidney issues, as far as I know no vascular issues beyond being 59.
Makes me wonder what is the difference between people who get lots of complications and those who do not.
It sort of baffles me.
I have Dupuytren’s in my right hand but no retinal detachment issues. I’m 65 and have suffered from diabetes since the start of 1972, 53 years. I’ve never paid any attention to it until recently and so my control was not at all good. My HbA1c was certainly well over 8%, now, over the last 5 or so years, it’s better 6-6.5%.
Dupuytren’s is not auto-immune. It is hereditary and this is the cause of the false correlations; think male and Norse (not “northern european” because that would include Germanic tribes). Heavy drinkers, heavy workers; people who traditionally work with our hands. Every time I cut down a tree my Dupuytren’s gets worse.
I have retinal damage but not detachment. That said it’s easy to do. I believe my issues probably came from doing a head plant a couple of years back while skiing; I’ve had an ongoing blot clot near my optic nerve in my right eye. It’s getting better. I feel lucky for not having suffered any detachment then; the non-D I know who suffered from it recently was told point blank to lie down and not look up. He was cutting trees too at the time; if you go for folklore don’t cut trees down.
I also have the traditional diabetic vision issues; my eyesight is measurably worse if my BG is high when it is tested. That’s because of the sugar in our blood increasing the density of the fluid in our eyes and therefore making us short sighted. Since I start out at -9D it just gets worse.
Timothy, I didn’t have any complications until I was at the 50 yr mark. My eyes were perfect for the first 60 yrs. I then had a bleed but haven’t had any reoccurrences.
I really thought I was safe from complications until I wasn’t. I was diagnosed in 1959 and my control wasn’t very good while urine testing. I have had diabetes for 66 yrs and I actually feel pretty
fortunate to be doing as well as I am. I have had very tight control for the last 20 yrs.
Well that sort of flies in the face of what my doc told me, but maybe you are in that 2 percent.
I got dx when I was already 21 so hitting the 66 yer mark won’t come till I’m 87. Not entirely sure I’ll live that long
Still you are 66 with just that one bleed. It’s pretty remarkable.
I wish I knew what the trick is.
I know people 15-20 years in who have retinal tears and bleeds and kidney failure. Neuropathy etc.
I know tight control is the only thing we can control, but there has to more to it than that
I think that luck has something to do with it.
I was diagnosed when I was 8 and am very happy that I have made it to 74 so far. I think I might make it for another 10 years if I am lucky.
I just went through a lot of tests on my heart and it appears to be fine. I deal with fatigue but part of that is age. My kidneys are fine as far as I know. Only time will tell.
We are in a similar situation except I was 21 at dx. I’m a little shocked that I don’t have complications, and every time I go to the doctor I feel like this time it is something serious.
I often wonder if type 1 has some benefits.
Of my mother and siblings my dupuytrens is the least severe. I don’t even have any limitations
My heart is fine, I just had an extensive work up, and my 2 non diabetic brothers both have early signs of atherosclerosis.
That might be because I’m more careful about what I eat, because I have to be.
Whoever cracks the code that determines who will get complications and who won’t will win the Nobel prize.
I used to think that cpeptide has some preventative effect, but type 2 also have the same risks to nerves and kidneys and eyes. So it’s not that simple. Unless of course they are resistant to both insulin AND c peptide. Which could explain that.
Anyway, my new floater is a daily reminder that anything could happen.
The Beta cells make 2 hormones insulin and amylin. Amilin slows down digestion and is suspected to be anti-oxidant. Amylin is no necessary for life like insulin but it has some benefits that are poorly studied.
That may be true of c peptide, another orphan.
Short-term administration of physiological amounts of C-peptide to patients with insulin-dependent diabetes was found to reduce the glomerular hyperfiltration in these patients as well as augment whole body glucose utilization. It could also be shown that C-peptide administration increases blood flow, oxygen uptake and capillary diffusion capacity of exercising forearm muscle in IDDM patients, probably by increasing capillary recruitment in the working muscle. Studies under in vitro conditions have shown that C-peptide stimulates glucose transport in skeletal muscle with its maximal effect within the physiological concentration range. The findings in a clinical study in which IDDM patients were given C-peptide and insulin or insulin alone for 4 weeks in a double-blind randomized study design, indicate that C-peptide improves renal function by reducing urinary albumin excretion and glomerular filtration, decreases blood retinal barrier leakage and improves metabolic control. Preliminary findings suggest that C-peptide administration on a short-term basis (3h) may ameliorate autonomic neuropathy by restoring to near normal the heart rate variability in response to expiration and inspiration. Insight into a possible mechanism of action of C-peptide is provided by the finding that C-peptide stimulates Na+K(+)-ATPase activity in renal tubular segments. In conclusion, the present results suggest that, contrary to the prevailing view, C-peptide possesses important physiological effects.
The beta cells also make c-peptide; it’s a product of insulin synthesis just like insulin and is produced in precisely the same amounts. This is because insulin is produced as a single molecule, a protein, which is then sheared into two.
The shear cuts out a protein, the connecting protein commonly called c-peptide, to produce a complex protein composed of two molecules which could not otherwise have the structure that insulin has.
It is obvious that including c-peptide in insulin would more accurately mimic what happens in non-T1Ds. Since the bacterial synthesis of insulin has to produce c-peptide it’s anyone’s guess why it isn’t done. I would guess there is no money in it. There is, of course, a lot of money in diabetes complications so don’t sit around waiting.
On the other hand while it is asserted that several companies have tried c-peptide as a treatment in its own right (so, make money) only one seems to have progressed to trials and they found no benefit:
Most of the references to that company seem to have been removed, or is that cancelled? No one pays for bad news and no one cares!
As for Amylin Ozempic seems to fit the same bill of sale for T1Ds; GLP-1 analogs have the maybe undesirable effect of causing insulin production but that is obviously not a problem in T1Ds. See this paywalled paper or GIY (Google It Yourself):
The GIY results don’t point out the pretty much identical effect to GLP-1.
Ozempic. Good for everyone except McDonalds. Guess where the money is.
I’m certain that c peptide does something. Makes no sense for our bodies to make something that is 50% waste product.
As in pro insulin cleaves into cpeptide and insulin.
If there were some real extensive studies done, we might get to the bottom of it
If cpeptide were offered to me either by its self or combined with insulin, I would try it
Interesting - my endo said this (or something very similar, I can’t remember the exact number of years, and I think he was talking about complications generally)to me several years ago. Yet, here I am at 35 years T1D and I was told 2 years ago that I have the beginnings of retinopathy in my eyes. I will say that I have been very lucky thus far but I wonder where doctors hear things like this?
C-peptide is a byproduct of insulin synthesis. We (humans) use it to prove the existence of T1D; we measure C-peptide because insulin only survives a few minutes in the blood stream whereas C-peptide lasts about 10 times longer.
So C-peptide ends up being a good indicator of insulin production. Consequently there might be pathways within our body which take advantage of that to alter other metabolic behaviour.
From the intelligent design PoV, which is what I assume you are arguing, the same applies; we, humans, use C-peptide to identify T1Ds. Intelligent design. Might have been better not to design diabetes in in the first place, but, whatever.
I actually was not arguing intelligent design but the opposite.
That is a lot of protein production to make proinsulin to then split that to make insulin and cpeptide if cpeptide has no function then it is wasted. Generally over millions of years unnecessary functions fade away because well they are unnecessary.
I know that cpeptide is a good tool for us, but clearly our bodies aren’t making it for that reason.
What I was trying to assert is that there likely is a biological function to cpeptide that we have not discovered yet.
Because unnecessary protein synthesis is unlikely from an evolutionary standpoint
The 1994 publication cited by Luis3 on the role of c-peptide is not the only research investigating its other functions in the body. For example, the article on C-peptide in Wikipedia (C-peptide - Wikipedia) states that
“In the first decade of 21st century, C-peptide has been found to be a bioactive peptide in its own right, with effects on microvascular blood flow and tissue health.[5]” ,
where Ref. 5 is the 2012 publication (Role of C-Peptide in the Regulation of Microvascular Blood Flow | SpringerLink). Unfortunately, this URL reveals only the Abstract and the References from this publication. I don’t have access to the full text of Ref. 5 and haven’t tried following up on the other papers cited by it that deal with research on the role of C-peptide. However, some of these References mention C-peptide in their titles. It seems that many scientists and physicians are interested in studying its role, contrary to the skepticism voiced by several authors in this thread.
I have been Type 1 for 58 years, and I was told a few years ago that if I did not have any ocular problems after all of those years, that I never would. Yeah, right. A few months ago, I woke up to a right eye that was fogged and looked like it had a screen over it. Turns out I had bleeding which the doctor treated with not-so-great laser surgery. A second laser surgery on that eye sealed off some more of the damage, but he could not complete what he wanted to do. I have since left his care. A third laser surgery with a new doctor was more successful, and I go in for a fourth at the end of next week as I now have the beginnings of proliferative diabetic retinopathy in both eyes. I thought I was free from worries about eye problems and loss of vision, but I guess the doctors and I both were wrong.
Why do they lie about this stuff. I remember the old “ diabetes will be cured in 5 years” story they used to say when I was first diagnosed. Or that we will live 20 years after dx.
So doctors don’t know it all, we all know this but it’s perplexing why they say things like this.
I am beginning to think that we can never think that we will be complication free in the future. No problems for me during the first 50 years of having diabetes. At 50 years I discovered that I had heart disease, at 62 a bleeder in my eye, and at 65 years in PAD which was a complete surprise.
I think many of us who were dx in the 1950’s and 60’s find that poor control in the past has caught up with us. Urine testing left a lot of us in the dark about our lack of control. For me, following a certain diet in middle age was just not healthy for me in the long run. I also have a bit of neuropathy caused by a statin, but most of the time it doesn’t cause a problem for me.
I hope that pumps and CGMs change the rate of complications for people diagnosed in the past few years.
And physicians should never tell us that we will be complication free in the future.
I was just now thinking about this in a larger scope.
My whole diabetic life I have been given predictions by doctors.
At first I was told that I would likely die in 20 years after dx.
Then came the many years of “ There will be a cure within 5 years”
Now I hear if you pass the 15 year mark with type 1 with no retinal issues, you won’t ever get retinopathy.
It’s just funny that they keep changing the predictions, but never stop predicting.
There is nothing I can do except keep my sugars tight, which I do for all the other reasons anyway.
Telling me that I won’t get retinopathy could cause me to not be checked if I have a symptom.
This is the opposite of everything I’ve ever been told about diabetes complications. I’ve always been told that damage builds up over time. Good control lessens that damage but doesn’t prevent it entirely and doesn’t reverse damage that occurred in the past. The home-free after 15 years is bizarre to me. Why would Joslin give out medals for going 25 or 50 years without complications if no one was going to get them once they got past the 15 year mark?
The comment was specific to retinas. And clearly it’s not true because some people have issues past 15 years. I think the doc was saying that if you gave retinas that are susceptible to retinopathy, it will show up within the first 15 years. But what he said was you have only a 2% chance after 38 years.
I think we cal all agree it was an add statement and he in no way was saying no complications. Only retinal issues. But eve that seems like an odd declaration
