As probably many of you LADAs know, Dr. Bernstein writes in his famous book Dr.Bernsteins diabetes solution about the indefinite preservation of remaining beta cells.
I quote: " Based upon my experience with a fair number of type 1 diabetics I 've treatedfrom the time of diagnosis, I'm convinced that the honeymoon period can be prolonged indefinitely. The trick is to assist the pancreas and keep it as quiescent as possible. With the meticulous use of small doses of injected insulin and with the essential use of a very low carb diet, the remaining capacity of the pancreas, I believe, can be preserved."
Now, when I first was diagnosed with LADA about 6 months ago and read this, I was very excited. And since then, have been trying very hard to do exactly what he recommends, I inject when I need to and am on a low carb diet. But even so, I certainly don't achieve his recommended goal of "keeping BG around 85 at all times" (I mean, HOW ON EARTH???)
I have been reading about so many cases/stories of LADA since, and NOT ONE seemed to have accomplished what Berstein claims – the beta cells just seem to give up, sooner or later.
I feel almost more frustrated at the thought that there is this theory out there, and if I tried REALLY REALLY hard, I could maybe protect my remaining beta cells, but in practise it is just not accomplishable.
I would like to know about other people's experiences and thoughts, and if there are actually people (apart from Bernstein himself) who have seen this work – over many years.
Thank you for sharing!
I guess I have a more conservative view of Bernstein's statement. The typical story of T1 diagnosis was that you didn't bother catching things early and when you ended up in the ER with a dangerously high blood sugar, then insulin was started. Over time, many in the medical community (far beyond Bernstein) have come to believe that loss of beta cells is dramatically accelerated by high blood sugars (so called glucotoxicity). So we hear many recommendations to start insulin early to keep blood sugars from accelerating the decline of your beta cells.
But what exactly is a honeymoon? Is it the time during which your beta cell function declines, or just the time during which it declines due to the autoimmune response? Bernstein's regime won't stop your autoimmune attack, it can only avoid making it worse because of high blood sugars. And everybody is different. If your autoimmune response destroys almost all your beta cells, then the end result, whether you follow his recommendations or not won't be any different. But almost all T1s have some level of residual beta cell function, and any response is better than none.
We are all experiments of one. We can do things, but we will never be sure of how it affected the outcome. No T1 that follows Bernstein would ever be able to tell you that it "worked." How would they know?
I realize you are frustrated after working so hard. You had hopes that maybe you could get along with T1 that was "not too bad." Well, any diabetes is bad. Perhaps it is time to just give yourself a bit of a break.
An obsessive compulsive person myself, I agree that we have to not be so hard on ourselves. But I see too many diabetics use that as an excuse to fall off the wagon and eat what they call "normal" food, which isn't really normal, it's just the same doo doo that people without diabetes eat, and it doesn't do them any good either. I'm a T2 who read Bernstein first and took his advice to heart. It has kept my blood sugar very well under control so far (A1Cs between 4.9 and 5.4), but no matter what I do I gain weight. 900 calories a day for 45 days, less than 30g carb, and I still gained weight. The doctor said, "eat less fat" without even asking what I was eating. Makes one want to beat their head against the wall. The thing we have to do, I think, is give ourselves a break by acknowledging that we don't have control over our bodies, but we can still use our brains to take good care of them. I can tell right away if what I eat isn't good for the body, my blood sugar tells me that. If I feed it the right stuff and the stupid carcass can still figure out a way to make fat out of it, then I have to work on my attitude. Not that I'm giving up and eating donuts, it's just not worth it. Julez, I feel your frustration. I think nothing but good can come from knowing as much as you can, though, and then coming up with your own solutions.
"Some beta cells" and "enough beta cells" are two different things. A T1 by definition does not have enough beta cells to maintain their BG and needs exogenous insulin. That's why it is also called IDDM - insulin-dependent diabetes mellitus.
It is true that almost every T1 has *some* remaining beta cells. They have been found in the pancreas on autopsy of people who have had diabetes for most of their life. It's just that a handful of beta cells make little practical difference.
See the following paper, for example:
Abstract Aims/hypothesis: Type 1 diabetes is widely held
to result from an irreversible loss of insulin-secreting beta
cells. However, insulin secretion is detectable in some people
with long-standing type 1 diabetes, indicating either a
small population of surviving beta cells or continued renewal
of beta cells subject to ongoing autoimmune destruction.
The aim of the present study was to evaluate these
possibilities. Materials and methods: Pancreatic sections
from 42 individuals with type 1 diabetes and 14 non-diabetic
individuals were evaluated for the presence of beta
cells, beta cell apoptosis and replication, T lymphocytes and
macrophages. The presence and extent of periductal fibrosis
was also quantified. Results: Beta cells were identified in
88% of individuals with type 1 diabetes. The number of beta
cells was unrelated to duration of disease (range 4–67 years)
or age at death (range 14–77 years), but was higher (p<0.05) in individuals with lower mean blood glucose. Beta cell
apoptosis was twice as frequent in type 1 diabetes as in
control subjects (p<0.001), but beta cell replication was rare in both groups. The increased beta cell apoptosis in type 1 diabetes was accompanied by both increased macrophages and T lymphocytes and a marked increase in periductal fibrosis (p<0.001), implying chronic inflammation over many years, consistent with an ongoing supply of beta cells. Conclusions/interpretation: Most people with long-standing
type 1 diabetes have beta cells that continue to be destroyed.
The mechanisms underlying increased beta cell
death may involve both ongoing autoimmunity and glucose
toxicity. The presence of beta cells despite ongoing apoptosis
implies, by definition, that concomitant new beta
cell formation must be occurring, even after long-standing
type 1 diabetes. We conclude that type 1 diabetes may be
reversed by targeted inhibition of beta cell destruction.
Keywords Autoimmunity . Beta cell apoptosis . Insulin
The conclusion they make is that in many long standing diabetics, beta cells are still being formed and killed off, so there may be some hope of regeneration if the autoimmune destruction could be turned off.
The other interesting thing is the paper says is that there was more beta cell mass in diabetics who had lower BG.
Hi Julez: There are several people here on TuD who were diagnosed with Type 1 diabetes as adults and who appear to have some remnant insulin production. I am one of them, Zoe is another. I have had Type 1 diabetes for 17+ years, and use a low TDD (total daily dose) considering my height and weight. Certainly I have had tight control most of the time, and have used an insulin pump for 14+ years (and have now added a Dexcom CGM), but I don't follow Bernstein. Recently, I was asked to participate in a clinical trial at UCSF Diabetes Center to determine if I actually do have endogenous insulin production. Maybe others will speak up as well, those who have long-standing Type 1?
Well Dr. B himself uses very little insulin and he has vast experience with diabetics so makes you wonder if he has something there. Possibly glucotoxicity is a factor that letting the BG go above normal finishes the Beta cells off. Some diabetics probably type 2 can go on insulin and the pancreas recovers enough to go off the insulin later. You wonder if that applies to some type 1 also. also I don't know how to get the BG to 85 at all times possibly by cutting carbs to his recommended levels.
Wow. Really good.
Theories are just theories is my attitude. It would be great if they turn out to be true, but its not the end of my world if they do not. Time will tell and sort it all out. Until then, all we can do is all we can do (if that makes any sense).
I would have to agree with Capin101. As they learn more, they will find out that there are far more types of Diabetes than is accepted now. This is also even among type 2s, there are so many differences case to case which are not easy to explain. The whole one size fits all thinking is just silly.
There is no doubt about the role of diet as it relates to controlling your BG. To discount it is as silly as the one size fits all mentality mentioned above. Low carb, or at least lower carb, is a must - implementing it can be a challenge. If you have a higher activity level, you can get away with more carbs.
I would encourage folks not to forget the mental part of the equation. Stress influences your BG almost as much as food if not more. With no change in diet, my BG went up over 50 points when a close cousin passed away. It stayed high for three months, long after I thought I was finished grieving. Being obsessive about your numbers can do the same thing - or lead to burn out. Stay calm, breathe, relax. Easy, right? I wish.