I have read many posts on this subject. I continue to have lingering questions though.
I think T2 is an umbrella for several different conditions which our doctors have not yet learned to differentiate. For those of us who lose weight and can maintain something close to euglycemia without pharmaceutical intervention, our hyperglycemia may be lipokine-mediated and there may be little or no loss in beta cell function (or, our beta cells may be used to putting out insulin at greater rates than in people who have never been diagnosed with T2, thereby covering up for any damage they might have incurred from lipokine-mediated changes to our glucose metabolism.) For those of us who lose weight and still decline, there may another trigger – possibly genetic and more closely related to MODY than to T2 per se – especially if their diabetes was diagnosed early on in its progression.
FWIW, I was diagnosed with diabetes in July 2002 at a weight of ~222lb with a fasting BG of 170 and an A1C of 7.8. I semi-deliberately dropped about 90 lb (of which about half have unfortunately returned), bringing my A1c and BG readings down low enough to be able to drop the metformin I had been taking. I have been on diet-and-exercise only since January 2004. Which suggests either that what I had was not diabetes, but excess fat – or that what functioning beta cells I have remaining are working overtime – or that there has been, somewhere, some beta cell regeneration (i.e., a temporary “cure”).
That said, my numbers have been deteriorating over the past year or so (I’m sure weight and age have something to do with it) so rather than suggest I might have been “cured” of diabetes, it would be more appropriate to say that its symptoms had “gone into (or been driven into) remission”.
I’m a newbie type 2, and so I am just getting up to speed on a lot of this. I didn’t know that beta cells can regenerate under any circumstances. I thought you lose what you lose, and through managing your BG you try not to lose any more.
My doctor told me that if I lose 100 lbs., I will still be a diabetic, (a thin diabetic). But the amount of flesh that needs to be serviced by my blood will be less, so the work load on the remaining beta cells will be lower.
I recently lost 11 kgs, while being on the dr.Barnard diet, as I couldn’t lose weight eating low carb.
So I consume a lot of carbs now, though always low GI. But this loss of weight didn’t really improve my insuline-sensibility, though it did lower my cholesterol and bloodpressure (now 110/70) gigantically. Although I know better, I am still hoping to be able to ‘get rid of diabetes’ one day, after losing another 11 kgs (then I will be skinny).
My endo told me that I wouldn’t be a diabetic anymore if I lost enough weight. That really is a stupid thing to say, because everybody in my family gets diabetes someday, and I am the only one who is overweight (my dad’s Indian).
Thanks for the welcome. I’m sure everybody on here knows how depressing this is. And, I don’t have any friends with diabetes so its no use talking to anyone who doesn’t know. Lately I have had alot of highs and lows. Its like being on a treadmill - if I eat something I shouldn’t, I’ll take my full dose of insulin (30 units which on a normal day is way too much) and then wake up really low. Once, I was actually taken to the er because I was unresponsive. I could hear the emt’s talking around me but I couldn’t reply. They quickly caught on and gave me some orange juice and I came to - but talk about scary. I know when I lose even 10lbs everything seems better so I am off to a new diet.
The TedX seminar on curing diabetes that was shown a few weekends ago on here had several scientists talking about Beta cell regeneration. Like other cells in our bodies, the beta cells are continuously dying and being replaced. They do regenerate and he showed pictures of pancreatic beta cells in T1 patients after death - the quantities are much lower than in non-T1 people. But they don’t regenerate fast enough to replace the destruction caused by the autoimmune process in T1. He didn’t talk about T2… but I suspect that the destruction processes in T2 (overuse, etc) again may be faster than regenerative processes. And there is still the issue of absolute insufficiency due to insulin resistance and (for some) extra mass.
So, you’re asking the $64 million question? I wish I knew the answers!
I HAVE read that there is at least one study that showed an auto-immune attack on (I don’t remember which) either the fat cells or the insulin receptors, but I know no more than that. If this is true, then Type 2 is also an auto-immune condition, but the target of the attack is different from Type 1.
Also, there does seem to be some unknown process, possibly beta-amyloid, damaging the beta cells in Type 2’s regardless of weight – C-peptide is often higher than normal to begin with and deteriorates over the years. But that apparently doesn’t happen in everyone – some Type 2’s remain very stable for a long time, and others deteriorate. Which just reaffirms what I’ve been saying – Type 2 is a garbage can diagnosis for everyone who doesn’t fit the strict definitions of Type 1 and LADA. It’s likely that there are multiple possible disorders in those who are called Type 2, and so there will never be one definitive answer to your questions.
Now I’m going to go read what everyone else has said!
You may find this interesting: National Institute of Health report
Some of the ‘Related Citations’ on the right side of that page are interesting as well.
Here is another text/comment on energy balance and insulin resistance and working of the skeletal muscle cells.
Some of latest thinking clearly suggests that skeletal muscles can only take so much glucose then they turn off body’s own insulin as defensive response to prevent too much glucose into cell and causing damage and wreckage.
Get more hearty exercise and reduce carb ingestion and one will see the IR turn off. I have.
See attached text/comment and studies on this.
As regards genetics, possibly but in my mind the hunter gatherer gene - digestion system is far too efficient grabbing every possible cakorie/carb from eaten food and on todays 24/7 grain based food supply - corn sugar etc and couch potato cars, lap tops, video games and wide screen TV dropping all round energy burn resulting in massive energy imbalance in body and backing up liquid glucose in blood stream.
Adding more insulin - dead ■■■ stupid, answer why the Insulin resistance and what that is doing. Type 2 insulin resistant diabetics typically showed increased levels of insulin not the other way around as body attempts to force more and more glucose into the liver, fat cells, skeletal muscle cells and kidneys that are all ready stuffed to the gills. Current thinking has BLINKERS ON staring into dark unlighted tunnel.
6083-DiabetesMellitus_paper_williams_wilkins.doc (607 KB)
I only had time to skim the paper, but there is one aspect missing from the discussion. There are 2 types of abdominal fat: visceral and subcutaneous, and the paper does not distinguish between them, but merely talks about waist-hip ratio being a risk factor.
However, at the AADE meeting last August, one of the presentations I went to discussed the difference. A person can have quite a bit of subcutaneous abdominal fat, and little visceral fat, and thus have a “bad” waist-hip ratio, but not actually be at risk of insulin resistance or Type 2. A case in point was that of a 400-lb. man who developed diabetes, and was assumed to be Type 2. They did an MRI on him, and found that it was ALL subcutaneous fat, and then did antibody testing, and he turned out to be a Type 1.
An easy way to find out if your abdominal fat is visceral or subcutaneous is to expand your belly and poke it. If it’s hard, your fat is visceral; if it’s soft, it’s subcutaneous. In my experience, going on a low-carb diet, and IGNORING saturated fat resulted in a re-distribution of my weight. My belly used to be rock-hard, and now it’s soft. In the meantime, my lipid panel has become totally normal, actually on the good side of normal, and since I’ve lost weight, the only explanation is that I’ve lost visceral fat. And the only explanation of the subcutaneous fat on my belly instead of my hips is that I’m genetically programmed to store it that way.
So my reaction is to ignore the waist-hip ratio just as I’ve ignored BMI. I have diabetes because I lack insulin, which has been proven, and so for me, taking insulin is the obvious answer. I take about 25-26u TDD these days, and my weight is maintaining at exactly the healthiest place for my age, and I’m a scientific study of n=1. We each need to find out what is going on in our OWN bodies – I’m certainly not the same as you, and one size does not fit all. ANY study that does not take individual variation into account has blinders on!
I never said no insulin ever, as aging and pancreas performance will need extra insulin.
Prior to getting my mess under control I was on 26 units of 75/25 a day, my weight was climbing thru roof.
This is not argument that meets all. Current testing on type 2 is woefully inadequate on a multi organ system and so far only catches outright shut down issues and does not catch a complex analog system to identify hormone interaction and organ interaction playing a full role in this mess.
That said, I was on the ole just add ton of insulin - starlix/glyburide and 75/25 - 26 units and getting progessively worse at the end, on 1200 carb restricted diet with 2 miles walking , could not lose an ounce.
In the end, it was the liver over dumping glucose and major dawn effect that most endo’s and doctors do not subscribe to. The reason for that is present practice subscibes to the american manufacturing stratagy of load all the stuff - parts at front end of system and shove. BG too high- just add more insulin. There is no description about limits on glucose generation and effects - just add more insulin if BG is too high. And oh, by the way insulin resistance is just some sberration of body mi-susing its insulin.
If you start at the user end and a “pull system approach” of burning glucose, one learns that the liver, kidneys, fat cells, and skeletal muscle cells all store glycogen and have finite limit. One also learns that if the cells get too full they have the ability to turn off the human insulin - ignore it to stop sugar transfer., Insulin resistance?
The implications are huge here since BG regulation is based upon a storage approach of the body being able to send out insulin and store glucose - as long as there is room to do so. ALeaky liver always putting out excess glucose can sneakly and does load up the storage of thr body. STopping it is critical.
After getting liver stopped on metformin, then exercise and diet finally worked and my weight dropped from 330 pounds to now sub 250. My body finally through off all the extra insulin after 6 months on the same diet I have used for last 4 years and now find that I get good control on 2 to 4 units of insulin, 1200 calorie and 2 miles exercise.
The real tragedy is that there are many suggestive steps and research work out there that would be most helpful to T2 diabetics but sits there languishing for the last 4 years while a frustrating argument persists about how to tan the alligator hides and whether hand bags, belts or shoes should be made while the prime job should be first to get the damm swamp drained.
There’s some evidence that sometimes there is a small autoimmune attack in type 2. Not as large as in type 1. The question is, are these really type 2 or slowly progressing type 1 with some insulin resistance? They’re now finding that some of the type 2 drugs that reduce insulin resistance. help type 1. I think there’s more similarity to the two conditions than most people admit.
If anyone could answer question 2, they’d be on the short list for a Nobel Prize.
When people (well, Ok, just women) are pregnant, their beta cell mass increases in the third trimester to overcome the insulin resistance that is normal at that time. Then after the baby is born, the beta cell mass regresses. In some people, the beta cell mass doesn’t increase enough in the third trimester, and they get gestational diabetes. They’re also at great risk of progressing to type 1 because their beta cell mass can’t increase to overcome insulin resistance.
Obesity does increase insulin resistance, but fat people who don’t get diabetes are able to increase their insulin output to cover the increased insulin resistance. Fat people who do get diabetes may be able to go into remission if they lose the weight while they’re still able to produce enough insulin to cover a lower load of insulin resistance. But age also causes beta cell poopout (sorry for using a technical term), and they may see the diabetes return as they age.
There are undoubtedly many varieties of “type 2 diabetes” and many combinations of insulin resistance and defective beta cells, but we haven’t worked them out yet. We know that type 2 is “multigenic,” meaning many genes can contribute, and we may all have different permutations and combinations of mutations in those genes. Some studies have shown that most of the known mutations in type 2 involve not insulin resistance but beta cell function.
I know I have references somewhere in the 6-foot stack of papers waiting to be filed, but I can’t look for them at the moment.
I have more data and comment on my situation and in fact the period after stopping the liver on metformin and arriving at the current prescribed treatment is very bizzare and the following data was found:
a) it took 2 months on the reduced carb/calories diet, exercise and met on liver to finally see the liver do a proper liver dump and add glucose when BG at finger tips went below 70. There apparently was so much glucose lying around that the liver and brain didn’t care in the first 2 months.
Finally, the liver dump function started to work reliably as BG dropped below 70.
Next, at 6 months, suddenly I started having all sorts of lows. I first cut the starlix in 1/2 - still lows. Then removed all together. That was some improvent.
Next, after no starlix, the lows kicked up again and this time my Doctor decided to switch me off the the 75/25 crap and put me on 10 units of humalog lispro - standard every meal. Immediately, I found 6 units was better and no lows. Well, that changed to today where I take 4 units in am breakfast and 3 at lunch and dinner.
I had been using Lantos 15 units at night and finallly had to get rid of that after I went down to one shot at 5 units and still having trouble of lows.
The joke here was that I had been on 75/25 in am 26 units and starlix at meals for years without incident.
After removing the pressure of the liver glucose excessive dawn effect and excessive release on any of its functions to add glucose and 6 months later, I am removing insulin to beat hell. The pancreas that seemed non function in past was heaving in the bolus’s and I see easily on the CGMS just after eating.
What changed after 26 years I am unclear.I was not trying out new solutions and in fact working with my Doctor to rectify my solution.
My data seems to show:
Stopping the glucose excess pressure on the body by stopping liver leaks, cut carb diet back to create glucose under actual daily body needs and exercusing hearty 2 miles has an impact.on the body.
A type 2 body needs to have its excess glucose swept out by tight diet and exercise to see any improvement.
Once excess glucose gone, one can see if pancreas snaps back. Mine did. AFter 26 years when I thought mine was dead, after incidence of getting excess added insulin out, my pancreas was shown to be kicking ■■■.
Why - I have no idea. Key concern is that anybody on traditional add insulin cures need to be very carefull if they get the excess glucose under control, swept out and if the body decides to take over one will have 2 times as much needed insulin.
I make no claims here, I am an electronics engineer who tripped over the items documented here and then went looking around the web to see if any research, comment that made sense. Surpisingly there is and some of it under the ADA banner and up to 4 years old.
I was dying and everything heading under. Today my health has stabalized and key is to maintain energy balance and ensure body stoarge sites have room to store Glucose so as to keep BG regulated otherwise BG climbes and rots out body above 155.
Draw your own conclusions. My experience I was through my fautty liver max out the Insulin resistance each morning when liver hammered BG up to 238. For a year before the metformin fix was identified , I walked each am 2 miles to get the excess glucose out. By 1.7 miles I would see my BG drop down and see insulin sensitivty return as BG dropped to 140 and under.
This was each and every day for a year till My doctor and I modified the dose timing on the metformin for maximum effect.
In the morning when the BG was 238 plus, 26 units of 75/25 did absolutely nothing.
People who have had bariatric surgery report a faster back on the pancreas snapping back. My guess is that the tighter the starvation diet is on the body propably accelerates the improvement.
Doing this is dangerous for anyone who has been on the standard cures of extra insulin when the body decides to get back in control.
Natalie is correct on her dose and what she is doing. Until the pancreas recovers - if it can- the old dose and regimene is required or if pancreas has really burnt fully out.