I had someone tell me a story today about a friend who supposedly ‘cured’ their diabetes through some radical diet.
I don’t believe it.
But I’m wondering, on average, how many type 2’s manage to successfully control their sugars through diet and exercise, without medication.
I’m asking because I get the feeling that people believe it is a disease caused by laziness or lack of control.
Yes, it can be well controlled, and you can live a long health life with it, cured no, once you have it you have it, it is or can be partly genetics also, I have seen many fairly young and non-over-weight people who you’d never guess having type two but they do, so it is not just the lazy or over eaters and non-exercising crowed, people need to be better educated…hope this helps
T2 is a serious challenge because there is a long term development behind the scenes. The genetic predisposition has many effects and the growing resistance to insulin is one of them. To overcome the resistance the insulin production increases until the maximum level of production has been reached. This means that insulin peaks for food can not be supplied as needed. By reducing his weight the T2 can reduce the need of his body for insulin (if he is not already slim). This means that he can reach a weight where the insulin production will be sufficient again. I am sorry to say that this does not mean healing (Halle Berry is not healed). It is a state that should be reached and preserved as long as possible. So the great effords for controlling weight, physical exercise and medication are rewarded. How long this situation will be stable depends on the further development of insulin resistance and insulin production. Often you see a continuous degredation over time and therefore it is good to keep an eye on the blood glucose level - even if the A1c is good now. Just to see the point where better medication is advisable. As a bottom line T2s can follow some strategies to improve their situation without medication. But it is a serious illness and very often medication is the only way to control it - at least it should be taken as a great chance if the Doctor recommends to do so. Todays eating habbits are just fueling the illness with an oversupply of carbohydrates. In every country where the eating habits turn to carbohydrates the T2 numbers grow rapidly (China, Phillipines and many others). Why the genetic predisposition of T2 is so widespread over the world is not known today. Some scientists argue that T2 was a benefit in ancient days since increased insulin levels improve carbohydrate processing. With the increased life expectancy this benefit shows its negative side effects. But this is just a theory.
For me yes it can be controlled by diet and exercise.
It’s been 3 months since I was told I was diabetic, I went in with another bout of what was becomming cronic IT infection. My gloucose level was 341! 2 days ago my Dr. took me off Metformin. My numbers were all well within the accepted levels, ie: under 110 fasting, under 140 2 hours postmeal. The problem for me is that in order to get them to that level I had to cut carbs to less then 60 a day and when I finally was able to see a diet/ nutrition nurse i was told I’m not getting enough Carbs. I’ve tried to increase carbs but anything over 60 a day makes the BG levels rise. Still not over the ADA recommendations, but too high for me. ( I’ve become a fanatic!) I’m not hungry and I do get enough exercise so my dilemma is wether or not to raise carbs and go back on metformin or risk not getting enough nutrients (I do take a multi vitimin, an omega 3 and if I think I"m not getting enough fiber I’ll take that as well)
There are several factors that contribute to whether or not T2 can be controlled through diet and exercise (Intensive Lifestyle Management – ILM) without the addition of either oral medications or insulin.
The first of these should be obvious: how early is the persistent hyperglycemia, impaired glucose tolerance (IGT), and/or insulin resistance (IR) – the three main symptoms and/or predecessor conditions of T2 diabetes – detected? If these tendencies are detected while there is still significant beta cell function, and the cause(s) of the individual’s IGT and/or IR determined, then ILM can be used to retard or arrest beta cell decay.
Holger Schmeken writes, By reducing his weight the T2 can reduce the need of his body for insulin (if he is not already slim). This means that he can reach a weight where the insulin production will be sufficient again.
What I have been reading recently suggests that the issue is not simply weight loss, but rather that there are specific lipokines (like hormones, but produced by adipose tissue) that inhibit insulin metabolism and stress the endoplasmic reticuli (ER) of other body cells, resulting in insulin resistance. Weight loss shrinks the size of the adipocytes, reducing serum lipokine levels.
In addition, exercise in general has been shown to increase insulin sensitivity, and regular intense exercise (at the aerobic/anaerobic threshold) may improve glucose tolerance to non-IGT levels.
Now, if T2 has been diagnosed later on – the description I was originally given was, “after more than 50% of beta cell function has been lost”, but the current seems to be “after more than 80% of beta cell function has been lost” – it is less likely that the remaining beta cells will be able to produce sufficient insulin to suit the body’s needs without some assistance. This assistance may be in the form of pharmaceuticals that improve insulin sensitivity, increase insulin production, and/or inhibit glycogen conversion to glucose – or in the form of animal or analog insulin.
The third factor is the patient’s commitment to ILM. Many T2s I know find exercise difficult due to other conditions (such as asthma or osteoarthritis); some find the costs associated with dietary change and intensive testing to be too high (both economically and socially). Even with an initial commitment to ILM, changes in one’s condition and one’s environment can lead to increasing restrictions upon one’s dietary intake with increasingly less positive change, resulting in the need to add medication to one’s regimen.
While the progression can be arrested (or at the least, significantly retarded), in no case is anyone “cured” of IGT, IR, or T2 diabetes, once s/he has been diagnosed. Nonetheless, the twin misperceptions persist of glycemic control through ILM equating “being cured of” diabetes, and its polar opposite, that laziness is the only bar to controlling T2 through ILM. Both of these misperceptions need to be addressed and corrected.
I went off Metformin in January 2004… so I’m about 4.75 years with ILM… though I spent a much shorter time off BP meds (June? 2004 - May 2006?).
Wow. You guys are an insane wealth of information. This gives me so much more food for thought about the issue. It’s much more complicated than I had imagined.
“Diabetes” is complicated. Even in “Type 1” diabetes, there are multiple potential causes and multiple potential triggers, ranging from the genetic to the viral to the environmental. Medical researchers are still discovering additional etiologies – causes and progressions of illness – of persistent hyperglycemia. It is my personal belief that at some time in the future, “diabetes” – or its primary clinical signs, persistent hyperglycemia, impaired/absent glucose tolerance, and elevated glycosylated hemoglobin and fructosamine levels – will be considered as much of a diagnosis as “indigestion” is today. C-peptide, GAD antibody, gene scan, and lipid panel tests – or their more sensitive and specific successors – will be routinely performed to pinpoint specific disorders of glucose metabolism at the earliest suspicion of dysfunction and to suggest cause-specific therapy.