Anyone been reading Peter Attia?

I forward very few items to my friends and relatives. I sent this link when you posted it before. It provided insight into T2D and informed newly deepened empathy with weight issues and T2D -- issues around shame and judgment.

I enjoyed last weekend in your fair city. Warm and pretty!

(Plz parden my link grammar!)

parden...pardon??! Now do I apologize for my apology?

LADA is type 1 that occurs in adulthood. It has a different progression than childhood T1 diabetes because the immune system of children is much more responsive/reactive than that of adults. With children the immune system kills off the beta cells relatively quickly. While in T1/LADA adults, the immune response typically takes years. In the LADA diabetic insulin production decreases over years as the immune system attacks the beta cells.

It is pretty well documented that type 1 diabetics of the LADA variety have insulin resistance. If you have data to the contrary, please provide it. The research I linked above ("Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients") showed that when BMI was taken into account their insulin resistance was equivalent to that of T2 diabetics. Maybe it is a little lower than that of T2s, but insulin resistance is common among LADA diabetics. This is also why diagnosing LADA can be problematic because it looks a lot like T2.

So it begs a few questions like....
1. Why do LADA diabetics have insulin resistance that appears similar to that of T2 diabetics? and
2. If obesity is what triggers insulin resistance resulting in T2 diabetes, why do so many very obese people not have T2 diabetes?

So as I said, maybe simply running high BG levels without enough insulin was the primary cause of the insulin resistance in type 2s, and it (or perhaps some other metabolic issue) triggered the midsection weight gain. Correlation is not causation.

http://www.ncbi.nlm.nih.gov/pubmed/17234296

Again, anecdotal, but most LADAs who post here on TuD are insulin sensitive (also not obese).

I supposedly have what is called lada- I call it late onset type 1 and I don't have insulin resistance. I have read online that "lada" have insulin resistance at one or two websites and that surprised me since that isn't true for me- I'm insulin sensitive. I don't think that the large majority of late onset type 1 have insulin resistance. They have usually have low c peptide also at diagnosis. That said as a type 1 if you gain fat weight your insulin needs will prolly increase, again, insulin needs are so variable for everyone. I think this is true for anyone with D on insulin.

Scott A, I think the title of the study "Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients" is causing some confusion.

The study says that T2's and LADA's have equivalent insulin resistance for equivalent BMIs, not that T2's and LADAs have equivalent insulin resistance as the title might imply.

I don't have any statistics but many/most of the LADA's here on tuD, like Shawnmarie, seem to be in the normal BMI range and thus show little or no insulin resistance.

Thus your statement "It is pretty well documented that type 1 diabetics of the LADA variety have insulin resistance" is incorrect and needs some qualifiers added to it.

I find this discussion interesting. I am a T1D who experienced slow onset diabetes with a T1D diagnosis at age 30. I never had any antibody tests done, so I'm unsure if LADA, but I am sure it was slow onset.

While my weight was in the normal range I was insulin sensitive. When I started to slowly gain weight and move into the overweight category, I became insulin resistant (IR). At my highest weight my BMI was 27.5 (25-30 is overweight, >30 is obese). At that point my insulin usage had doubled and my BG control was poor.

I lost over 20 pounds and my BMI went down to 24.3 or normal weight. My insulin needs were cut in half and consistent, predictable insulin action returned. My sensitivity to insulin returned.

I can only conclude that my IR varies directly with my weight.

In my case, while I share IR characteristics with T2D, my diabetes diagnosis occurred before my weight gain and increased insulin resistance was concurrent and driven by weight gain. When I lost enough weight, I lost my IR.

I don't think that T2D IR and weight gain relationship is as simple as my experience. There appears to be more going on and as many have stated here, correlation is not causation. If causation between weight gain and IR is asserted, what is the direction of causation? Did IR cause weight gain or did weight gain cause IR? In the end, we may very well find out that weight gain in T2D is merely another symptom of the disease.

I also think the mechanism of insulin resistance in type 2 may be different from a type 1 who gains weight- from what I have watched in a video a few months ago. I would have to review this again because I can't remember exactly what they said now.

I had assumed that insulin resistance with LADA was generally accepted. Most of the research I have seen supports it. Yes, I was talking about statistical groups and not individuals, but it isn't just one study showing LADAs with greater than normal insulin resistance. Again, if I am wrong about the research, then toss out some studies that counter it.

What the study apparently did was it corrected for BMI and then looked at insulin resistance because LADAs as a group are skinnier than T2s as a group and we know that there is added insulin resistance with the additional weight, so if you want to accurately compare the insulin resistance of T1/LADA to T2s, you really need to correct for BMI.

I don't know about the LADAs in this forum. I personally am LADA (positive on antibody tests and low c-peptide) and have a fair amount of insulin resistance. Additionally, it is generally hard for anyone who isn't skinny to get a LADA/T1 diagnosis so maybe that is playing a role here. Someone who is a little overweight (like most Americans) will likely be treated like a T2 and eventually be put on insulin as a T2. Most doctors wont bother with the antibody tests on them and will assume that lost insulin production resulted from burnout.

You defined LADA to include it, not the researchers. Since insulin resistance was their dependent variable, they wouldn't have used it as a criteria for group selection. The typical criteria for identifying T2 diabetes also catches LADA diabetics, and the common practice for figuring out which ones are actually LADA/T1 is to give them the additional blood work (antibodies, c-peptide).

My guess is that they took a bunch of people previously diagnosed as T2 and LADA/T1, and then gave them all the blood screenings for LADA/T1 to sort them.

But doesn't the Pima research shows that the underlying cause is genetic, and a stringent diet coupled with exercise can suppress the expression of that gene? Eating a similar diet, their rate of T2 diabetes is 5-6 times that of Americans. Few Americans are eating a subsistence diet and exercising a few hours each day, so maybe what differentiates Americans who get T2 diabetes from Americans who don't could very well be some underlying metabolic differences with the obesity being a symptom of those metabolic differences and not what is actually causing T2.

"Isn't insulin resistance a "clinical manifestation of T2DM?" By defining LADA to include it, they pretty much determined the outcome before they started."

You defined the clinical manifestations to include 'insulin resistance' which generally isn't measured by doctors making a diagnosis. The standard measures of higher A1Cs, and high BG levels (and physical symptoms) were probably used. Perhaps, fast onset type 1 diabetics who developed it later in life might avoided appearing like a type 2 diagnostically and gotten a quick T1 diagnosis, but I'm not sure they should be included with LADA diabetics in research.

I think it's safe to say that there are some LADA's who have lower BMI's and no insulin resistance and others who have higher BMI's and insulin resistance.

Perhaps it's not such a good idea to try to shoehorn people into too tight/too few categories

I see your point, that the Pima example doesn't really address the issue of whether weight gain or insulin resistance is happening "first". Clearly, weight gain is happening at the same time that insulin resistance is getting worse, and as far as can be observed externally they are happening together. I was really addressing the underlying issue that weight gain and insulin resistance are both determined by a person's diet and exercise - which is what I think the real consensus medical view is.

In fact after now listening to his Ted talk, I think he is mis-representing the consensus medical view in order to create a straw man argument that he can set ablaze. I'm afraid I'm not impressed.

The Defronzo article, the one I posted first in the thread, explains that both weight and IR are related to different genetic issues. It's a pretty heavy read (I would have to print it, I can't read stuff like that on the computer, at least until next week, when my new specs get here!!) but goes into the details and explains why it's not entirely diet and exercise. It's a really great article. It made me think that T2 is a lot harder than T1, even without the aggravation of the diet/exercise mantra all the time.

I'm totally dismissive about IR. If you need insulin, take it. Figure out how much you need and take it. Take as much as you need and, if you need U500 or something, it shouldn't be as much as a used car/ bottle.

"Skeletal muscle plays a pivotal role in determining systemic IR, as it is responsible for up to 80% of insulin-stimulated glucose uptake (DeFronzo et al., 1992). Skeletal muscle IR is a known feature of T1D (DeFronzo et al., 1982) and is due to decreased glucose transport into myocytes (Cline et al., 1997; Vuorinen-Markkola et al., 1992) from impaired insulin-stimulated upregulation of GLUT4 mRNA (Yki-Järvinen et al., 1992). "

Autoimmunity & insulin resistance in T1D

Thanks for posting this study. I don't read much out of Brazil but it makes sense that that robust economy and significant population would produce work like this.

Here's my take home:

The results obtained herein demonstrate that clinical and laboratory parameters can be used to discriminate DM1 patients with IR. Early detection and appropriate treatment of IR could help to prevent diabetes-related complications.

I had to discover, understand the significance, and determine a treatment for IR without help. I would have been happy to be measured and found to carry markers of IR and counseled to adopt corrective measures.

Do you have a connection to Brazil?

Excellent study -- thanks for posting. Here's my interest:

IR is also a powerful cardiovascular risk factor, and lowering IR in patients with T1D is likely to be as important as glycemic control in prevention of long-term complications.

This follows my experience exactly. As a long-term T1D I grew insulin resistant until I lost weight a restored insulin sensitivity. I went to a cardiologist yesterday, concerned about my heart health. He did an ultrasound of my carotid arteries and he tells me to not be overly concerned. I have very little athlerosclerosis.

Thanks for pointing it out again. I'll try to get to it.