I do not cook it
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Hi Brian,
Great to be on this forum with you.
The DPP was actually a clinical trial that measured the “efficacy” of metformin or lifestyle modification at prevention the “progression” of prediabetes to type 2 diabetes.
It’s important to remember than clinical trials are efficacy trials. The study didn’t measure the “effectiveness” of the intervention.
The effectiveness of translating the DPP into the real world is only as good as the practitioners. Facilitating behavior change is no walk in the park and unfortunately the vast majority of those who go through the DPP training are no sufficiently prepared to guide people toward adopting and sustaining the behaviors associated with preventing the progression of prediabetes to type 2 diabetes.
I think the confusion comes from clinicians having to navigate between two worlds. As a clinician there is a jargon what I just wouldn’t use with people I know did not have similar academic preparation as I did. This is not to say that the individual who is equally intelligent and has a different academic preparation is not capable of understanding what impaired glucose tolerance is.
It’s simply easier for the clinician to say “prediabetes” instead of impaired glucose tolerance.
I am of the opinion that if prediabetes or impaired glucose tolerance is indeed “stage one diabetes” what clinical criteria do physicians use to prescribe medication?
I believe the transitional stage “prediabetes” or “stage 1 diabetes” whatever you desire to call it affords the person who receives the “diagnosis” an opportunity to implement what the evidence base says is effective in preventing the progression of “prediabetes” to diabetes. Why prescribe medication when the individual is able to ,through changing behaviors, go from that transitional space of “impaired glucose tolerance” to glucose levels that are within normal clinical limits.
Thanks for the exchange.
You are correct, the DPP was a controlled intervention trial that compared both metformin and lifestyle intervention against a control arm that was treatment as usual. What really get’s my goat is the DPP trial was basically a failure, the majority of patients still got diabetes at essentially the same rate as the control arm and metformin was just as effective as lifestyle intervention. Despite that the health system “spins” the result to suggest that diabetes is caused by bad eating habits and lack of exercise.
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There are not good studies to measure the breakdown or digestion of resistant starch with or without fat, so I’m afraid I cannot answer your question. And yes, potato starch has >85% resistant starch if eaten raw, while Hi-maize has 50-60%. The difference is due to the structure of the starch granule. Hi-maize comes from a natural hybrid of corn that is very high in amylose, which is the long, linear chains of glucose. It may contain millions of glucose chains, and goes through a heat/moisture treatment that is thought to help line up the long glucose chains to make them more difficult to digest. The high amylose content elevates the temperature at which the starch cooks out or gelatinizes, so it retains its resistance after cooking. On the other hand, potato starch has mosty amylopectin, which is glucose chains in highly branched format. It has no process tolerance and cooks out or loses its resistance at any kind of processing. Does this makes sense? If you’re consuming it raw, then yes, potato starch has more resistant starch in it. I really cannot say if they would behave differently when you eat them with fat.
And yes, resistant starch is fermented and can cause gas. Some people report that the gas lessens over time as the microbiota adjust, while others report that it does not lessen over time. I’m sure it has more to do with the type of bacteria you have in your gut, which varies person to person a lot. If it is not fermenting, it is not working.
Hi-maize has been used in about 80 published clinical intervention studies, which is a lot! Raw potato starch has been used in three clinical trials that I know of. We know a lot less about resistant potato starch, but since both contain only chains of glucose that get to the large intestine, it has long been assumed that the studies done with resistant corn starch likely apply to resistant potato starch as well. Use whichever is easiest for you.
Brian, I am of the opinion that the people that were living with prediabetes progressed to T2DM because they didn’t maintain the behaviors. Remember, one of the outcomes was lifestyle modification (aka behavior change). From a theorectical perspective, (because this is what I do professionally) one can lapse or relapse into the very behaviors that predisposed them to “prediabetes.”
One’s motivation to change behavior as well as self-efficacy has to be assessed to determine whether the individual’s self-efficacy is high enough to continue to engage in the behavior s/he recently adopted. Lifestyle as operationalized by the DPP may not be suitable approach for the participants once the trial was over. Why would anybody continue with a “lifestyle intervention” that didn’t meet the needs of their “lifestyle.”
As I mentioned to you at the AADE last year, I am very passionate about DPP implementation. Where I feel the challenge is is included the very health care providers who were on the DPP intervention team on the health care teams when the DPP is implemented in real life.
What gets my goat is that I have earned all the credential academic and otherwise, I am a clinical exercise physiologist yet it is very rare that you will see a clinical exercise physiologist/cde on a DSME or DPP team. The DPP used exercise physiologists.
If you look at every DPP intervention that has been translated into real life, very few (I can count them on one hand) have utilized the knowledge, skills of exercise professionals.
I genuinely respect the work that RNs do but for the most part they implement they DPP. That really gets my goat!
Sadly I believe that many health care professionals believe this. Unfortunately the evidence doesn’t support this view. As I discussed previously, the results of the DPP showed that the vast majority of the patients progressed to diabetes despite any intervention. And the lifestyle intervention was not better than just taking metformin. I firmly believe that diet and exercise is important to managing diabetes, I just believe that telling the public that lifestyle changes can “prevent” diabetes" (and causes diabetes) is very harmful.
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Brian,
This is a deep conversation and way to complex to relegate to chat. I hope to have the opportunity to speak about it in depth with you at this upcoming AADE convention.
Best,
Jo
If this was not the case at all, wouldn’t as see the exact same prevalence of type 2 diabetes across every cross section of civilization, regardless of lifestyle? Seems to me that lifestyle is undeniably linked to development of diabetes… If not, as the American lifestyle changed over generations, why have rates of diabetes increased?
It’s not a black and white proposition like it’s always framed as. The two extreme philosophies always represented are always some variation of “slothful diabetics ate their way into this” or to be contrary “my lifestyle and choices I’ve made throughout my life have nothing to do with my current health.” It seems to me that the truth is a long way from either in most cases, but always somewhere in between.
I think the difference is in how you conceive of “cause.” Clearly modern diets cause (T2)to be “expressed.” But suggesting that diet and lifestyle “causes” diabetes is a misconception. If changing diet and lifestyle cannot reverse or cure diabetes that is a strong suggestion that diet and lifestyle is not a cause of diabetes. I propose that diabetes is in fact a genetic condition. It doesn’t matter what you do with diet and lifestyle, all these people still have diabetes no matter what they do.
So how would not eating a modern diet (to use your example-- one that I agree with) and therefore never reaching a point of “expressing” diabetes, differ from preventing diabetes?
There are no doubt genetic components, likely many of them, but I’d tend to believe that human genetics haven’t changed anywhere near as much over he past 100 years as human behavior, diet, and lifestyles, and that the rates of diabetes seem to correlate more with the latter group. Not entirely, of course, but enough that it’s important to acknowledge, and perhaps harmful to ignore.
I have friends, who were obese and inactive, reverse their diabetes by losing heaps of weight, getting physically active, and changing how they eat. Now totally normal blood sugars all the time. Of course the diabetes will return if they return to their previous condition, or may just with age, regardless.
Therefore, i believe that in type 2 diabetes / prediabetes is reversible, in at least some cases.
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To add more fuel to the fire. …
Maybe the intervention was not the right intervention?
Maybe some of the participants didn’t stick with it because they could see it wasn’t working. …
or maybe they did stick with it but were accused of not sticking with it because the results did not show what the medical professional wanted to see. …
I lost “heaps of weight,” became physically active, and changed my eating habits over a period of 7-8 years prior to diagnosis and my HbA1c was 11.8. Note - I was never diagnosed with pre-diabetes, nor was my glucose level a factor in my decision to lose weight or make the other changes.
I also have a friends who were diagnosed with diabetes or pre-diabetes who managed their condition with lifestyle changes - one of whom was put on insulin immediately on diagnosis, lost weight & became active and needed no medication… then years later, fell and broke a hip, and needed to go back on insulin almost immediately thereafter – it didn’t even require weight-gain for her diabetes to “relapse.” Sorry, but that doesn’t meet the definition of “reversing diabetes” in my book.
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I don’t have the references handy, but there have been those that claim that (at least in many cases) Type 2 is caused by “the thrifty gene,” meaning that people needed the “T2 gene” to survive in areas that had periods of famine. In fact, I recall reading that people whose families originated in areas that had regular or periodic times of hunger have a higher incidence of Type 2. There is a lot more available food of all types today with better food distribution, as well as a lot more movement of people away from area that even today suffer from famine. (And famine isn’t the only condition that maintaining some extra weight helps to improve survival – there are many illnesses where starting out with extra weight allows some people to be able to “last it out” better than those without it.) Isn’t it possible that the presumed higher incidence of T2D relative to times past is because those people with that “thrifty gene” survived better than those without it? People, like all species, with “survival genes” tend to, well, survive.
Before anyone jumps all over me on this, I do know that there have been many genetic markers that have been identified as possible causes of T2D, and likely many different routes to the disease that are likely completely unrelated to one another. Still there appear to be far more people with poor lifestyle habits than there are people with T2D. I agree with @Brian_BSC that the genetic link is far more important than the other “risk factors.” That is not to say PWD should not adopt a “healthy lifestyle” - EVERYONE should - but that doing so is no “cure.”
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It greatly depends upon how one operationalizes “lifestyle.” In another thread, there is a discussion about the use of the term “prediabetes” and how many feel it is deceptive. I am not of that opinion. It has everything to do with my academic preparation. I believe it is the same thing with the term “lifestyle.” Depending upon one’s academic preparation the term “lifestyle” can have a different meaning from one person to the next.
From a professional perspective, I look at the term “lifestyle” from an ecological perspective. In the realm of health education (where I am earning my doctorate) we call it social determinants of health. There are somethings that influence a person’s “lifestyle” that s/he cannot control that increase the risk of of him/her developing not only diabetes but other noncommunicable diseases. However, that same individual can be taught to reduce the modifiable risks associated with disease acquisition that s/he can change.
A person can change their behavior, however, it’s a little more challenging to change policy.
Thanks for your post.
What really upsets me is the poor science that has been done surrounding the DPP and attempts to treat type 2 with diabetes. As I mentioned in a post a little more than a week ago the results of the DPP are particularly underwhelming in the long-term. The majority of the patients progressed to diabetes anyway and the “lifestyle” arm was no better than just taking metformin. The DPP at best could be said to delay the diagnosis of diabetes in 1 in fourteen people, but to leap to saying that “reverses” or “prevents” diabetes is just unsupported by the evidence.
Make no mistake, I strongly believe there is evidence that “lifestyle” can help all of us manage our diabetes. But managing our diabetes is very different than reversing or preventing diabetes. Words make a huge difference.
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Did anyone study whether on TOP of a good lifestyle if adding metformin can delay progression? It wouldn’t surprise me at all if lifestyle works as good (or better) as metformin if the metformin people aren’t changing their diet. But what about doing both? And doing both WELL (meaning, maintaining a good A1C indefinitely). Progression in those people?
The DPP study had such a small effect effectiveness and was so expensive to run that it did not look at a combination of lifestyle and metformin. Presumably there would be some additive effect, but it is unlikely to have radically changed the result, lifestyle and medication both have a small effect in delaying the onset of diabetes. Over half of people with prediabetes progress on to diabetes in 15 years no matter what intervention is tried.
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So is your opinion that a prediabetic is doomed to get diabetes at the exact same time whether they change their ways and maintain ‘normal’ A1Cs or if they just let it all hang out and allow their A1C to stay elevated?