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Discussion Starter · #1 ·
Hi everyone,

Just read and learned something. Just want to share it in the way that I understand it. So here goes...

To understand the symptoms of diabetes, we need to know a bit about the way our bodies normally handle glucose. A hormone called insulin controls the level of glucose in our blood. A hormone is just a chemical that travels through the bloodstream to another part of the body to do its work; eg. insulin works like a key to open a cell so that glucose can enter to provide energy to our bodies. Insulin is also known as the builder hormone because it helps muscle to form. In addition to that, it helps storage of glucose in glycogen form for use as fuel later. Basically, we can’t survive for long without insulin.

So without insulin, or if our insulin is not working effectively in our bodies, glucose starts to rise in our blood; it can’t go into the muscles so it stays in the blood. When it is above 180mg/dl, glucose begins to spill into the urine and make it sweet. This loss of glucose into the urine leads to many short-term complications.

Here a the most common early symptoms of diabetes. If you have one or more of these symptoms, you should get tested.

Extreme hunger: Because glucose is not delivered into the muscle cells, a feeling of hunger develops despite all the glucose that is floating in the bloodstream. It is more popularly known as “starvation in the midst in the midst plenty.

Blurry vision: Because the glucose level shift to higher, the lens of our eyes swells due to water intake. The causes blurry vision because the eye lens can’t adjust soon enough to correct the change in focus due to swelling.

Frequent urination and thirst: The glucose in the urine draws more water out of our blood and more urine in the bladder causes frequent urination. As a result, we feel thirsty and drink more frequently - and start the process all over again.

Weight loss: it occurs among some people with diabetes due to the lack of insulin in their bodies. Without insulin, the body starts to breakdown - muscle tissues and fat tissues into glucose and small fat particles, respectively - and pass out of our bodies in the urine. This breakdown causes weight loss.

Fatigue: Without insulin or sufficient insulin, glucose cannot enter cells to fuel them to produce energy. This lack of energy causes us to feel tired and fatigued.
 

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Do not forget a fruity-smelling breath, from the ketones due to fat breakdown ... but dieters may get this too.

My oldest daughter got it any time she was sick b/c she would quit eating for days.
 

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what about Gum Disease ? sometimes u might find blood when brushing... Esp diabetes cope it..

And tiggling or numbness on the toes?
 
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Very nice summary, but it seems to emphasize shortage of insulin. This is universal with type one or slow-onset type one but is the exception not the rule with T2s - at least in the early stages of progression.

The usual progression begins with elevated insulin which is caused by diminished responsiveness of cells to insulin. More and more is needed to facilitate the uptake of the same amount of glucose. The pancreas keeps producing abnormally high amounts of insulin to compensate. This typically goes on for many years. In late stage T2, after the body's insulin-producing capacity has been severely damaged insulin deficiency can ensue making the condition resemble T1 in that regard.

Also, another nickname for insulin is the "aging hormone" because of the many harmful effects of elevated insulin on the body.

Interesting the connection between cell starvation (insufficient ATP) and hunger. I don't remember hearing that before. I'm often curious how little attention is paid to the "end" of this process. All the emphasis seems to be on the excess circulating glucose which couldn't get where it needs to be (in the cells for ATP), but what about the effects of this "starvation" on the cells themselves? This is why my focus is on providing alternative sources of ATP for my cells.

But I wonder what are the long-range effects of cells not getting enough ATP? If you treat with insulin, this is overcome and the remaining problem might be too much insulin in circulation but if you treat with things like Metformin and other medications and some carb reduction short of inducing ketosis which provides abundant ATP to the cells from FFAs and ketones, what impact does this have on the cells which logic says would still be "starving", i.e., not getting enough ATP?
 

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But Salim, many T2s are diagnosed with shut-down beta cells due to glucotoxicity, too. It is seen increasingly -- and is one reason I was overlooked as a LADA!

But I agree -- many people are apt to read those symptoms and say, "Oh, I am not having THAT, so I must be fine!" ... and that's DANGEROUS! Kinda like my reaction to the ADA quiz, for years and years.
 

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I think that the only symptom the average Joe will recognize as possibly diabetes is "Frequent urination and excessive thirst" and even then I recall me and my friends refering to ourselves as "drink-a-holics".

ColaJim
 

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Exactly! Think about what you just said. "shutdown beta cells due to glucotoxicity". Where did the high glucose come from BEFORE the beta cells began shutting down? Is it both the cart and the horse?

Something ELSE had to cause the rise in glucose in order for it to then cause (or probably more accurately, ADD TO) beta cell shutdown. That something is insulin resistance, the key difference between T1 and T2. LADA of course is not typical T2 and is really more like T1, just slow onset, right?

As I understand it, if beta cells begin shutting down due to glucotoxicity (and or methyl glyoxal in excess), the root cause is insulin resistance and that is T2. If they begin shutting down due to auto-immune activity, that's T1. If I'm not mistaken, LADA is much more like the second one but most likely, all kinds of "hybrid" conditions are possible.


But Salim, many T2s are diagnosed with shut-down beta cells due to glucotoxicity, too. It is seen increasingly -- and is one reason I was overlooked as a LADA!

But I agree -- many people are apt to read those symptoms and say, "Oh, I am not having THAT, so I must be fine!" ... and that's DANGEROUS! Kinda like my reaction to the ADA quiz, for years and years.
 

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As I understand it, if beta cells begin shutting down due to glucotoxicity (and or methyl glyoxal in excess), the root cause is insulin resistance and that is T2.
I doubt that insulin resistance is the root cause of anything because I believe insulin resistance is the bodies defense mechanism against high insulin levels that may have been caused by excessive consumption of carbohydrates, like me drinking 4 liters of cola a day while living on noodles. Of course the gross malnutrition therein would make insulin resistance happen much sooner.

ColaJim
 

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Oh, I think we agree that IR is more of a concept than a thing, they really have no clue. Could well be autoimmunity to receptor protein, or any number of other things.

And they clearly jump to a lot of conclusions ....
 

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This is exactly what I believe except that I would have said "the body's defense mechanism against excessive glucose being metabolized ... that have been caused by excessive consumption of carbohydrates and protein (in other words: under-consumption of fats), in terms of proportions."

Which is practice is about the same thing since processing lots of glucose goes hand in hand with excessive levels of insulin. Nevertheless, if beta cell death is not caused by auto-immune problems in the prototypical T2, what is it caused by? As I understand it, the general belief is that insulin resistance usually precedes both elevated glucose (because in the early stages lots of insulin production just handles it) AND beta cell death.

This makes the progression and apparent causality:

==> excessive metabolizing of glucose, but normal BG and insulin
==> insulin resistance
==> excessive insulin but normal BG
==> elevated insulin AND BG

If, as the previous post suggested, beta cell death is caused by exessive glucose, that didn't happen until the fourth stage above. This hypothetical sequence of events is supported epidemicologically by the huge uptick in T2 which coincided with the huge uptick in glucose-producing foods and their share in diet over the last 40 years.

I believe that the entire chain of events begins with step one and for those susceptible progresses through the steps. And, I suspect methyl glyoxal - a by-product of [successful] glucose metablism - is the mechanism or agent of that progression. We'll see what future studies and investigations bring.

Methyl Glyoxal - Superglycator

I doubt that insulin resistance is the root cause of anything because I believe insulin resistance is the bodies defense mechanism against high insulin levels that may have been caused by excessive consumption of carbohydrates, like me drinking 4 liters of cola a day while living on noodles. Of course the gross malnutrition therein would make insulin resistance happen much sooner.

ColaJim
 

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I would throw in the following symptoms. It may not be a 100% "you got diabetes" litmus test but warrant talking to a doctor and getting tested.

* Red, swollen gums
* Wounds that don't heal quickly
* Chronic infections (e.g. sinus infections 4x a year)
* Feeling lethargic/sleepy after meals
* Frequent headaches that come and go based on when you last ate
* NEEDING something sweet after each meal
* Experiencing hypoglycemic symptoms if you skip a meal (e.g. dizzy, shaky hands, being "not all there") or after eating a meal
 

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Discussion Starter · #12 ·
Very nice summary, but it seems to emphasize shortage of insulin. This is universal with type one or slow-onset type one but is the exception not the rule with T2s - at least in the early stages of progression.

The usual progression begins with elevated insulin which is caused by diminished responsiveness of cells to insulin. More and more is needed to facilitate the uptake of the same amount of glucose. The pancreas keeps producing abnormally high amounts of insulin to compensate. This typically goes on for many years. In late stage T2, after the body's insulin-producing capacity has been severely damaged insulin deficiency can ensue making the condition resemble T1 in that regard.

Also, another nickname for insulin is the "aging hormone" because of the many harmful effects of elevated insulin on the body.

Interesting the connection between cell starvation (insufficient ATP) and hunger. I don't remember hearing that before. I'm often curious how little attention is paid to the "end" of this process. All the emphasis seems to be on the excess circulating glucose which couldn't get where it needs to be (in the cells for ATP), but what about the effects of this "starvation" on the cells themselves? This is why my focus is on providing alternative sources of ATP for my cells.

But I wonder what are the long-range effects of cells not getting enough ATP? If you treat with insulin, this is overcome and the remaining problem might be too much insulin in circulation but if you treat with things like Metformin and other medications and some carb reduction short of inducing ketosis which provides abundant ATP to the cells from FFAs and ketones, what impact does this have on the cells which logic says would still be "starving", i.e., not getting enough ATP?
Thanks Salim for the post.
 

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Discussion Starter · #13 ·
I would throw in the following symptoms. It may not be a 100% "you got diabetes" litmus test but warrant talking to a doctor and getting tested.

* Red, swollen gums
* Wounds that don't heal quickly
* Chronic infections (e.g. sinus infections 4x a year)
* Feeling lethargic/sleepy after meals
* Frequent headaches that come and go based on when you last ate
* NEEDING something sweet after each meal
* Experiencing hypoglycemic symptoms if you skip a meal (e.g. dizzy, shaky hands, being "not all there") or after eating a meal
Thanks, Daytona.
 

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Many people are suffering from diabetes but they are aware of it's symptoms. It is better to concern doctor in the early symptoms of diabetes. because will be easy to diagnose and find the real reason for diabetes and the type of diabetes.
 

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There's also some rather unknown symptoms especially for type 1 diabetes.
I had leg cramps at night (i think it was caused by potassium not being able to enter the cells) - a lot of type 1s experience this.
And I also suffered from acid reflux. Nobody has been able to give me any insight on this but all I know is that with the moment they started that insulin drip at the hospital it was gone. And I didn't change what I eat or anything like that
 

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I had none of the classic symptoms. I was very tired, and would eat sweets to try and get energy, only to become even more tired! I did have a bladder infection that, in retrospect, was probably due to sugar in my urine. Also, after regaining control of blood sugar, I realized that my big toes had been a bit painful to touch, maybe the start of a symptom.

Getting my BG tested at my physical was what resulted in my diagnosis.
 

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hyperlipid blog

This is exactly what I believe except that I would have said "the body's defense mechanism against excessive glucose being metabolized ... that have been caused by excessive consumption of carbohydrates and protein (in other words: under-consumption of fats), in terms of proportions."

Which is practice is about the same thing since processing lots of glucose goes hand in hand with excessive levels of insulin. Nevertheless, if beta cell death is not caused by auto-immune problems in the prototypical T2, what is it caused by? As I understand it, the general belief is that insulin resistance usually precedes both elevated glucose (because in the early stages lots of insulin production just handles it) AND beta cell death.

This makes the progression and apparent causality:

==> excessive metabolizing of glucose, but normal BG and insulin
==> insulin resistance
==> excessive insulin but normal BG
==> elevated insulin AND BG

If, as the previous post suggested, beta cell death is caused by exessive glucose, that didn't happen until the fourth stage above. This hypothetical sequence of events is supported epidemicologically by the huge uptick in T2 which coincided with the huge uptick in glucose-producing foods and their share in diet over the last 40 years.

I believe that the entire chain of events begins with step one and for those susceptible progresses through the steps. And, I suspect methyl glyoxal - a by-product of [successful] glucose metablism - is the mechanism or agent of that progression. We'll see what future studies and investigations bring.

Methyl Glyoxal - Superglycator
I think this adds some more about methylglyoxal.
Hyperlipid Methylglyoxal
More interesting things there as well.
 
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New to the forum and haven't got much education yet, but didn't know about any of the symptoms. Thought I was always hungry because I was overweight. Thought I needed reading glasses now because of blurry vision. Was getting up one or two times during the night urinating, which never happened before, because I was getting older, and drinking more because I like salty foods.
 

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There's also some rather unknown symptoms especially for type 1 diabetes.
I had leg cramps at night (i think it was caused by potassium not being able to enter the cells) - a lot of type 1s experience this.
And I also suffered from acid reflux. Nobody has been able to give me any insight on this but all I know is that with the moment they started that insulin drip at the hospital it was gone. And I didn't change what I eat or anything like that

I didnt know this was related to my diabetes, but I remember clear as the day how much cramps I had in my legs the last weeks before diabnosed. Especially the weekend before neing diagnosed;
we were visiting a friend and slept in sleeping bag. Woke up with really hard cramps in both of my legs and really struggled to get out of the sleeping bag.

Today I am really chocked my doctor didnt recognize my symptoms; I complained about always being thirsty and drank between 5 and 7 liter water each day (and urinated of bourse a lot), I went from 54 kilo to 46 kilo, and my vision was so blurry I felt like an owl in a flashlight. I frose all the time and really didnt feel good at all.
The doctor took a lot av tests, but didnt check my BG.
A diabetic friend lend me her glucosemeter, and I wrote down all my testings during a day. The highest said " Warning, high BG, over 33,3":eek:
When I went to the doctor the next day she didnt believe me wgen I gave her my desult, so they tested me there, FBG 18,6 and it rose to 26,6 after eating one ryecrackser with fish.
My Ac1 was 12,6 and then the doctor finally believed me.
Her excuse for not believing me being diabetic was my age (45 years)
 
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