A while back, an author sought contributions from "young, thin women with Type 2 diabetes" here on TuD. The author was told that those "young, thin women with Type 2" were probably misdiagnosed and have Type 1 diabetes/LADA. In an email exchange with me, the author actually acknowledged that she had gotten so many responses regarding LADA. But sensationalism wins out, and Su Subramanian has published a horrible article in Women's Health magazine. The only sane person quoted in the article is Dr. Richard Bernstein, who says that the young, thin "Type 2" women are probably misdiagnosed and actually have Type 1 diabetes. Amy Tenderich over at DiabetesMine calls the article "c**p." I am really angry and appalled, because misdiagnosis can be so terribly harmful, and can lead to rapid onset of complications and even death due to DKA. What a terrible disservice to women (and all people).
Most people who are overweight are type 2 and those that are skinny/thin are type 1 at the beginning of their diagnosis from my personal and nursing experience.
@lisa: That doesn't work for me, and doesn't work for many others I know. I am overweight but GAD Positive with no c-peptide (33 years in). My daughter at 22, is thin, with an awful 1st phase insulin response (high BGs), which is the start of something. We are just waiting for antibody tests to come back for her. There are indeed thin T2s, who are not antibody positive and do not have MODY. There is a possibility she has PCOS with three burst ovarian cysts so far, but they were all singles and scans at the time don't put her in the PCOS class, according to her doctors, because they are looking for multiple cysts.
We are assuming here that we (researchers etc) know all there is to know about diabetes. I suggest we don't know and that we will find in years to come, more causes for insulin resistance in thin people, and more variants of all kinds of diabetes.
Nevertheless, for the percentage of diagnosed T2s who are actually slow-onset T1, it's a disservice to them that more doctors are not prepared to do any testing (for whatever idiotic reason) because it's thought that early insulin can prolong the health of existing beta cells. It also stops these people from being called non-compliant (as I was for many years), and hanging around with high BGs that often are not being addressed.
The tests are easily done and in my opinion, should be routine. I, like others, spent years fighting to be tested when doctors were saying, "impossible" because I'm in the overweight category of BMI. It shouldn't have had to be that hard! Meanwhile, I spent more than 10 years with huge spikes and some resulting damage and it slid me into diabetes burnout because I just wasn't prepared to go marathon running every time I ate something, to get by BGs down. It's really a tragedy in every sense of the word, because it all could have been avoided.
I had a debate with my current, soon to be former Endo about this very issue. I can keep relatively great BG's so long as I ride 125-175 miles a week and eat raw veggies and meat protein in very small amounts. I then feel drained because I am not taking in enough calories to fuel the amount of activity. The endo was more concerned with possible hypos then how I felt, he suggested I needed to increase the calorie intake to cover the activities. I have increased the daily carb intake from 130 average a day to 250 average a day, this has helped with the riding but of course my after meal spikes are often +100 bg's from the premeal numbers.
Diabetes is so simple(yet so complicated) but docs think we are unable to manage ourselves. I am told your numbers are not high enough to warrant an Insulin bolus, well that is easy to fix instead of 25-30g's of carbs I eat 50-70g's at a meal and I spike over 200 for a short while(I am now catching it with the meter, as soon as I feel sleepy I test, usually around 60-70 minutes after I start eating)The simple minded docs just don't get as a Type 1, I do not make enough Insulin to cover a small meal. Therefore I have to risk long term damage to my body to show an Endo that I spike after a meal high enough to increase the risk factors. The Endo looked at my c-pep test and stated wow "that's low, but that may be all the insulin your body needed to cover your carb intake". I should have said something along the lines, then why is my A1C 5.9, if I needed so little Insulin production from my Pancreas, to cover my intake, should not my A1C be more like 4.2?
Through all this I see that what ever number the doc feels like he needs to see, I can give it to him. But why? Why don't we be proactive and stop the high BG's with the proper treatment and trust, but verify, that I am constantly researching reading and learning what I must do to maintain proper numbers. I have detailed food logs, I have acquired the cable for my meter so I can print color graphs and all my bg's number in clear to understand forms and charts. I test religously, I have a Garmin GPS to log and verify my exercise 5-7 days a week, which I print out and bring to the Endo visits, I just don't get it why the Doc forces me to blow up my sugar to get him to get that I need a Bolos 3-4 times a day.
I think if doctors would err on the side of type 1 instead of type 2 it could solve this problem. A type 2 getting insulin is not going to kill him or her but lack of it can kill a type 1.
The antibodies test can be unclear but it should be done to at least rule it out.
I think if the 2 diseases type 1( auto immune ) and type 2 ( insulin resistant) were called different things entirely, it could help .
Agreed, especially as "insulin resistant" is probably also "autoimmune" -- just a different kind of autoimmune that results in insulin resistance rather than the direct destruction of beta cells.
Just to make this even more maddening, T2 also results in the destruction of beta cells over time, just not as rapidly nor via the same process that causes T1:
"In type II diabetes, an increasing demand for insulin places a substantial stress on the protein secretion system of the beta cells of the islets of Langerhans, which results in cellular dysfunction and, eventually, beta cell death. As the population of beta cells continues to diminish, the stress on the remaining cells increases as they struggle to produce the insulin necessary to mount a proper host homeostatic response. This feedback loop is thought to be responsible for the progressive nature of type II diabetes (1).
Cross-β-sheet amyloid deposits are generally observed in the islets of Langerhans of type II diabetic subjects (2) and their presence correlates with the loss of beta cells (3). Whether amyloidogenesis causes, exacerbates, or results from beta cell dysfunction in humans are key unanswered questions being intensely investigated (2–5). The primary component of the amyloid deposits is amylin or islet amyloid polypeptide (IAPP), a peptide that is co-secreted with insulin by islet beta cells (3). Human amylin is a highly amyloidogenic peptide based on in vitro experiments, and amylin amyloidogenicity in organismal diabetes models correlates with beta cell death, although to date, a direct cause and effect relationship has been difficult to establish (2, 6–8)."