Low Carb & Diabetes: Critical Review & Evidence Base
AlabasterVerve
Posts: 3,171 Member
Here's an article that should interest those following a low carb diet or have diabetes. Or at least I found it interesting and worthwhile.
Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base:
http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext#bib94
Here's the part where they attempt to define low carb which seems to be a common question:
Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base:
http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext#bib94
Here's the part where they attempt to define low carb which seems to be a common question:
Very low-carbohydrate ketogenic diet (VLCKD)
Carbohydrate, 20-50 g/d or less than 10% of the 2000 kcal/d diet, whether or not ketosis occurs. Derived from levels of carbohydrate required to induce ketosis in most people. Recommended early phase (“induction”) of popular diets such as Atkins Diet or Protein Power.
Low carbohydrate diet: less than 130 g/d or less than 26% total energy
The American Diabetes Association (ADA) definition of 130 g/d as its recommended minimum.
Moderate Carbohydrate Diet: 26 - 45%
Upper limit, approximate carbohydrate intake before the obesity epidemic (43%).
High Carbohydrate Diet: Greater than 45%. Recommended target on ADA websites
The 2010 Dietary Guidelines for Americans recommends 45-65% carbohydrate. The average American diet is estimated to be about 49% carbohydrate.
Carbohydrate Consumption (NHANES) :
Men - Year 1971-1974 - 42% (∼250 g for 2450 kcal/d)
Year 1999-2000 - 49% (∼330 g for 2600 kcal/d)
Women Year 1971-1974 45% (∼150 g for 1550 kcal/d)
Year 1999 - 2000 - 52% (∼230 g for 1900 kcal/d)
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Interesting because there are studies that have shown no difference in HBA1C and FBG levels between low carb and 'balanced carb' eg.reviewed in this meta-analysis and systematic review. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090010/ They also report that long term adherence is a problem with low carb diets. I acknowledge that it is hard to compare different studies though because of differences in classifying diet as low/balanced/high etc.
It does seem like the article in the OP is pushing the low carb agenda. When I was looking at some of the cited references, they didn't actually provide the evidence for what they stated in the article.
I'm interested about any possible benefit of low-carb for people with IDDM. Even going very low carb, some background insulin would still be required..? That's often what's done to workout the background insulin dose. I would be interested to hear if any Type1 diabetics have ceased insulin altogether due to low carb diet though....or maybe ceased their fast acting insulin and only have their background insulin?
I don't believe that dietary carb restriction should be the first approach. My take is that diabetes should be managed on a case by case basis.
JMO. Thanks for posting the article. It was an interesting read even though I don't necessarily agree with it, or find it particularly rigorous.0 -
Here's an article that should interest those following a low carb diet or have diabetes. Or at least I found it interesting and worthwhile.
Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base:
http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext#bib94
Here's the part where they attempt to define low carb which seems to be a common question:Very low-carbohydrate ketogenic diet (VLCKD)
Carbohydrate, 20-50 g/d or less than 10% of the 2000 kcal/d diet, whether or not ketosis occurs. Derived from levels of carbohydrate required to induce ketosis in most people. Recommended early phase (“induction”) of popular diets such as Atkins Diet or Protein Power.
Low carbohydrate diet: less than 130 g/d or less than 26% total energy
The American Diabetes Association (ADA) definition of 130 g/d as its recommended minimum.
Moderate Carbohydrate Diet: 26 - 45%
Upper limit, approximate carbohydrate intake before the obesity epidemic (43%).
High Carbohydrate Diet: Greater than 45%. Recommended target on ADA websites
The 2010 Dietary Guidelines for Americans recommends 45-65% carbohydrate. The average American diet is estimated to be about 49% carbohydrate.
Carbohydrate Consumption (NHANES) :
Men - Year 1971-1974 - 42% (∼250 g for 2450 kcal/d)
Year 1999-2000 - 49% (∼330 g for 2600 kcal/d)
Women Year 1971-1974 45% (∼150 g for 1550 kcal/d)
Year 1999 - 2000 - 52% (∼230 g for 1900 kcal/d)
The high carb diet is the one recommended by the ADA because they say that they want a diet people can follow long term.They should provide people good information.0 -
I tend to agree. I manage well on moderate carbs. I know others that thrive on LCHF. Finding a sustainable dietary approach depends on the individual. Food preferences? Particular foods that spikes blood glucose? Activity level?My take is that diabetes should be managed on a case by case basis.0 -
I've only sort-of read the paper in the OP, but it seems to me that figure 4B really makes a case against their conclusion that Low Carbohydrate Diet (LC) diets are required.
4A shows that people can lose weight on a LC Diet more so than on a calories than those on a Diabetes UK "Healthy Eating" diet. But in 4B they show that weight loss per se doesn't correlate with HbA1c levels. In fact, in 4B they show that people on both LC and Low GI diets (the fact that they used different studies in one figure here is somewhat confusing) both lower their HbA1c levels to similar extents. I haven't looked at the ref for 4B yet to see what they say about the significance of these findings.
iow: low GI and low carb both reduce markers of diabetes.
Some of the comments in the Introduction got my spider senses tingling that the authors here have an agenda, and looking at their Declaration of Interests makes that agenda quite clear...
The whole 12-point scheme is kinda strange to. It's like they are trying to make a circumstantial case rather than a scientific one (in fact, they even make the point in the discussion that this is more of a legal analysis than a scientific one). I also get the impression that there is substantial cherry picking of what data they do present.
So, overall, while I do think that people with diabetes should definitely be aware of their carbohydrate intake and probably lower it to moderate levels if possible (replacing carbs with protein, as they suggest), I really don't this paper makes the case that very low carbohydrate diets should be the automatic recommendation for every diabetic.0 -
Richard;I've only sort-of read the paper in the OP, but it seems to me that figure 4B really makes a case against their conclusion that Low Carbohydrate Diet (LC) diets are required.
"...only sort-of read(ing) the paper..." and then cherry picking two charts that (ostensibly) support your biases "...really makes a case against (your) conclusion" (IMO, of course)
Perhaps a full reading (including those parts with which you are predisposed to disagree) might enlighten.
http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext
Nowhere in the Conclusion can I find words which might support YOUR statement that "....LC diets are *required*.
It does state; however, that,
"Given the current state of research funding and the palpable bias against low-carbohydrate approaches [4], it is unlikely that an RCT can be performed that will satisfy everybody. The seriousness of diabetes suggests that we have enough evidence of different types to re-evaluate our current recommendations for treatment."
and that,
"This review has described 12 points of evidence based on published clinical and experimental studies and the experience of the authors. The points are supported by established principles in biochemistry and physiology and emphasize that the benefits are immediate and documented while the concerns about risk are conjectural and long term."
As do yours as well.Some of the comments in the Introduction got my spider senses tingling that the authors here have an agenda, and looking at their Declaration of Interests makes that agenda quite clear...
Circumstantial vs Scientific (as used in this context) is VERY much in the eye of the beholder and a question of semantics.The whole 12-point scheme is kinda strange to. It's like they are trying to make a circumstantial case rather than a scientific one
The "study" is NOT what I (or probably most people) would consider a study (as in a clinical trial which actually IS scientific, bound by the constraints of the scientific method, and subject to peer review. We can thank the medical, governmental, and scientific communities for the confusion but it seems they fall prey to the same inability as MSFT does when it comes to recycling the same words to mean different things.
This "study" is more along the lines of a meta-data analysis wherein a number of previous study's results and conclusions are incorporated in an attempt to provide statistical justification for results that, on their own, might not appear significant (in the general useage sense of that word, not the scientific).
Meta-data "studies" are common (likely far outweighing the number of actual "clinical" studies).
They are NOT bound by regulation as to the number of studies included or even if those included are "clinical" or merely "observational". The results of the "studies" may be based on thousands of participants, hundreds, or a few. They may or may not have included double blind or even statistically equivalent test group populations.
Point being, in this case (as in all cases involving meta-data) it's very much "take it for what it's worth" (but not necessarily bad or good). The "study" can only, ever, be as "good" (reliable) as the original study results selected for inclusion, the weight assigned by the author to each, and the author's integrity in designing the parameters.
No they do NOT, go back and read it again.(in fact, they even make the point in the discussion that this is more of a legal analysis than a scientific one).
They used the legal (courtroom) analogy to make a point relating to overcoming the biases. (The existence of which has obviously been very well demonstrated).
"What evidence would be required to change the current recommendations for dietary treatment in diabetes? Evidence based medicine tends to emphasize random controlled trials (RCTs) as a gold standard. Such absolute requirements, however, are unknown in any scientific discipline. As in a court of law, science admits whatever evidence is relevant [98]. Following the legal analogy, one has to ask: Who decides on the admissibility of the evidence? The parody by Smith and Pell [99] has been described as both funny and profound in illustrating how there is not a single type of experiment that fits every scientific question."
As to the "...whole 12 point scheme..." Your choice of the word "scheme" belies any semblance of objectivity you might otherwise profess.
It's not a "scheme" - it's more like a listing of the hypotheses any reputable scientific study would require and which the study would then attempt to prove (or disprove) and validate (or which subsequent investigation invalidates).
Pretty standard stuff in the scientific community.
That you chose to label it "circumstantial" goes right along with your choice of the word "scheme".
Neither do I, and neither did the authors ever make any such proclamation (see above).I really don't this paper makes the case that very low carbohydrate diets should be the automatic recommendation for every diabetic.
Might the author (and subsequent commentators) have brought their own opinions and biases to the study?
Of course, and one need only look at the individual bios to realize that many are, in fact, in the LC "camp" based on (one might assume) their history and years of involvement researching the issue.
But do you really believe that the corn guy, or the Eli Lily guy would sign on to something they believed was provably incorrect simply to get their name in print?
Everything in the public domain is subject to comment and challenge by anybody (including you) - if you have "proof" that any of your accusations, inferences, or beliefs disprove the conclusions (or the research upon which they are based) - have at it.
If, however, it is just what you "want" to believe, I'd suggest you spare yourself the embarrassment.
Your stating it on any forum, (however many times), simply can't change fiction to fact just because you want to believe it will. (Well, let me modify that somewhat, it probably can change fiction in the minds of the "true believers" who live in the fact free zone and agree with the dogma and myth but can't be bothered to even read the basis of that with which they are agreeing.)
So if it doesn't "prove" to your satisfaction (as it doesn't to mine) that the issue is settled, what does it "prove"?
(hint....I already gave the answer above (search for "courtroom") - it's a trick question)
Pot......Kettle"I also get the impression that there is substantial cherry picking of what data they do present."0 -
Men in my family are all diabetic or ''pre'' diabetic and all are on low carb diets. But I should add, that it's processed or white starchy carbs that they are told to avoid, not carbs found in whole grains and fruits and vegetables. My dad aims to stay under 90 grams a day.0
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Does anyone else ever look at the Declaration of Interests and decide just to not even read the article, I know I do.0
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Interesting because there are studies that have shown no difference in HBA1C and FBG levels between low carb and 'balanced carb' eg.reviewed in this meta-analysis and systematic review. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090010/ They also report that long term adherence is a problem with low carb diets. I acknowledge that it is hard to compare different studies though because of differences in classifying diet as low/balanced/high etc.
It does seem like the article in the OP is pushing the low carb agenda. When I was looking at some of the cited references, they didn't actually provide the evidence for what they stated in the article.
I'm interested about any possible benefit of low-carb for people with IDDM. Even going very low carb, some background insulin would still be required..? That's often what's done to workout the background insulin dose. I would be interested to hear if any Type1 diabetics have ceased insulin altogether due to low carb diet though....or maybe ceased their fast acting insulin and only have their background insulin?
I don't believe that dietary carb restriction should be the first approach. My take is that diabetes should be managed on a case by case basis.
JMO. Thanks for posting the article. It was an interesting read even though I don't necessarily agree with it, or find it particularly rigorous.
First, it is very important to note the difference between type 1 and type 2. This is mostly for those who don't know the difference and are reading this:
Type 1 - Do not make insulin. This is most commonly caused by an auto-immune disease where the immune system kills beta cells in the pancreas. This is caused by genetics and the genes have even been identified, which is a different topic altogether, and a trigger for the auto-immune response. Someone who is type 1 will always take insulin, and will die if not. This disease is not caused by being fat. A type 1 will need insulin even if s/he is eating nothing.
Type 2 - Are resistant to insulin. Sometimes it is said that type 2's do not make enough insulin (because they need to make more than most because it isn't being used at 100% effectiveness and can't). It is important to note that many of these explanations are misunderstood, and type 2's are resistant to insulin (ANY insulin), and that is the only commonality. I clarify this because I am someone who has both type 1 and type 2 and a lot of people get confused. I take artificially made insulin because I am type 1. I take medications and require a large amount of insulin to be injected because I am type 2. These are not the same disease, and you cannot switch from one to the other. Being overweight can lead to type 2 diabetes, and the treatment is either weight loss, pills, and/or insulin. When a type 2 (with only type 2) starts taking insulin, s/he does not become a type 1. Treatment does not define the disease. **The ignorance on this topic is a real annoyance for me, as you might guess.**
The question about basal insulin (this is the insulin that is always needed by type 1 diabetics who have no insulin otherwise) and bolus insulin (additional insulin to cover food and/or to correct high blood sugar) is a good one. Personally, I do not believe it to be possible to eliminate bolus insulin for food. I say this because protein is also converted to glucose, but at a much lower rate, and over a much longer time period. Most of us diabetics eat a small enough amount of protein that we do not notice it. If we were to stop eating carbs, we would need to replace at least some of those calories elsewhere. That means we are eating more protein (and fat, which is converted at even less and over an even longer time period), which is probably enough to require some boluses. The challenge is timing. The best way to handle that is with consistency in amount of protein eaten and what time it is consumed. By doing that, it would be easiest to increase basal insulin because of the length of time over which the insulin should be active.
Does that make sense?0 -
So, overall, while I do think that people with diabetes should definitely be aware of their carbohydrate intake and probably lower it to moderate levels if possible (replacing carbs with protein, as they suggest), I really don't this paper makes the case that very low carbohydrate diets should be the automatic recommendation for every diabetic.
I think you're on the same page as the authors. They appear to be arguing that carbohydrate restriction should be the first line of attack for treating diabetes, not very low carbohydrate per se. Currently drugs are the first line of attack, perhaps with weight loss, and carbohydrate restriction is not a core part of the strategy or even mentioned in many cases. Diabetes UK for example advocate a "five types of sugar" breakfast for people with type 2 diabetes.
To the question about Type 1s and carbohydrate restriction here's one approach using education -
http://www.ncbi.nlm.nih.gov/pubmed/22650646
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This is a great discussion and what I'm hearing is that there isn't one right amount of carbohydrate, or even one type of meal plan, that is effective for each person. Paying attention to food choices, activity level, sleep habits, and stress management will help each person with diabetes understand what helps them manage blood sugar levels most effectively. Research gives us some ideas on what to monitor, and then each person figures out a plan that works best for them. ~Lynn /Glucerna0
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4A shows that people can lose weight on a LC Diet more so than on a calories than those on a Diabetes UK "Healthy Eating" diet. But in 4B they show that weight loss per se doesn't correlate with HbA1c levels. In fact, in 4B they show that people on both LC and Low GI diets (the fact that they used different studies in one figure here is somewhat confusing) both lower their HbA1c levels to similar extents. I haven't looked at the ref for 4B yet to see what they say about the significance of these findings.
"First, weight loss is better in the VLCKD than the low fat diet: inspection of points along the x-axis shows that 70% of the low fat subjects lost less than 8 kg (right side of vertical dotted line) while 80% of the VLCKD subjects lost more than this amount, and along the y-axis, more than one-third of the low-fat subjects increased levels of glycated hemoglobin and only about 10% of the VLCKD did. Finally, as pointed out above, again by inspection, there is little correlation between the two parameters."
Point 3 argues that carbohydrate restriction can benefit HbA1c without weight loss, trying to break the obsession with weight loss as a T2D treatment (I know a few thin T2D people). The scatter of 4B makes the point about the lack of correlation.0 -
MidWest;First, it is very important to note the difference between type 1 and type 2. This is mostly for those who don't know the difference and are reading this:
Type 1 - Do not make insulin. This is most commonly caused by an auto-immune disease where the immune system kills beta cells in the pancreas. This is caused by genetics and the genes have even been identified, which is a different topic altogether, and a trigger for the auto-immune response. Someone who is type 1 will always take insulin, and will die if not. This disease is not caused by being fat. A type 1 will need insulin even if s/he is eating nothing.
Type 2 - Are resistant to insulin. Sometimes it is said that type 2's do not make enough insulin (because they need to make more than most because it isn't being used at 100% effectiveness and can't). It is important to note that many of these explanations are misunderstood, and type 2's are resistant to insulin (ANY insulin), and that is the only commonality. I clarify this because I am someone who has both type 1 and type 2 and a lot of people get confused. I take artificially made insulin because I am type 1. I take medications and require a large amount of insulin to be injected because I am type 2. These are not the same disease, and you cannot switch from one to the other. Being overweight can lead to type 2 diabetes, and the treatment is either weight loss, pills, and/or insulin. When a type 2 (with only type 2) starts taking insulin, s/he does not become a type 1. Treatment does not define the disease. **The ignorance on this topic is a real annoyance for me, as you might guess.**
(snipped)
The challenge is timing. The best way to handle that is with consistency in amount of protein eaten and what time it is consumed. By doing that, it would be easiest to increase basal insulin because of the length of time over which the insulin should be active.
Does that make sense?
It makes perfect sense, thanks for putting it in words that most should be able to comprehend.
Sadly, you are absolutely correct regarding the general level of "ignorance" (or just lack of knowledge) regarding Diabetes (as if it's one disease). Sadder still is the fact that so many seem so unwilling to even consider approaching it with an open mind and learning what they don't know - so much easier to just bury one's head in the sand and "not read past those first 12 lines". That it occurs here is, I suppose understandable given the group speak atmosphere, but as is made obvious by the comments in the study conclusion, the biases exist at all levels of society.
Anyway, as you stated, until people can get past the basic misunderstanding that diabetes is diabetes is diabetes (or that T2D just naturally progresses to T1D) it's doubtful much will change.
I'm not a med pro, do not have T2D (or T1), no immediate family history, and the closest familial member that does is my FIL. My wife and I have been pretty actively involved in his treatment though, and we've been following the development of MannKind's Afrezza on his behalf. (I imagine you know of it but if not, encourage you to do so - the trial results were very impressive, including significant reductions in both basal and bolus in a number of participants (one of which I was in contact with during his participation in the trials). A secondary, but equally important benefit of the ultra fast acting qualities speaks directly to your mealtime and timing concerns.
That said (as background), we have also been following the research pretty closely on LC approaches to both T2D (on his behalf) and to weight loss in general (on both his and our own behalfs). I would say that our "position" on LC is best described as still uncertain but evolving. That we share your disdain for ignorance and even more so, closed minds, is something I really wish I could predict an end to in our lifetimes....unfortunately, that wish is becoming increasingly less likely day by day.
I would like to add a couple points to your excellent summary if I could and would welcome your correcting any of my understanding that is incorrect as your level of expertise on the subject obviously exceeds mine by orders of magnitude.
I should note that despite the amount of time we've spent with my FIL and researching diabetes in general, I seem to have developed something of a mental block regarding the "types" and can never quite keep it straight which is which (T1 or T2). Tried all kinds of mental crutches (2 is bigger than 1 or, it's backwards - 2 then 1, which works great except 10 minutes later I don't remember if it's backwards or not!). Anyway, so be it.
Not positive about the actual numbers but I think the last I saw at least 90% of all diabetics (US) were T2 a "fact" I'm fairly sure most are unaware of (I was). This doesn't, of course, take into account the relative severity or impact on the 1's vs 2's but I'm guessing most not only believe that "all" diabetics must use insulin, but think, as you stated, that 2 progresses naturally, to 1 automatically (it does not).
In fact though, type 2 is "progressive" in a highly predictive manner in most cases throughout it's course. Weight gain (loss) is a factor as is the eventual need for insulin but in the end it all comes down to "when", not "if" in most cases. When, the B-cells can no longer adapt to the body's impaired glucose tolerance.
I'm of the belief that, at least to some extent, our understanding of this progression is largely due to earlier detection, the formalization of the term pre-diabetic, and genetic predisposition. Unlike years ago, many individuals are now identified as PD's and increasing numbers of kids understood to be "at risk" at much earlier ages. The results of both situations being increased numbers of T2D's who have been "watched" if not "in treatment" for nearly an entire lifetime.
Regardless of the age of onset (and excepting those that are actually "cured" (or the progression halted) early on, for the vast majority of PD's and T2's it is absolutely progressive and on a highly predictable course. Mid course interventions can, and have, moderated the rate of progression (some more effectively than others) but stopping the progression in its tracks still remains an elusive goal.
We know "what" causes the progression (for the most part), understand the physiology, but still haven't been able to totally halt (or reverse) it - that remains the goal and if meds, low carbs, or magic mushrooms (or any combination) prove to be the means of achieving the goal does it really make a difference which one (or ones) it is?
Why would anyone dismiss out of hand ANY potential "cure" or even a more effective treatment protocol- even if it's not one cure for all or doesn't lower A1C any more than "x" (but does offer numerous other benefits)?
Shouldn't gaining a better understanding of which treatment mode is potentially more likely to be successful for an individual with certain indications trump what some "want" to believe?
I just don't get it and simply cannot accept the current level of bias against ANY mode - especially when the bias is based in ideology and ignorance.0 -
MidWest;First, it is very important to note the difference between type 1 and type 2. This is mostly for those who don't know the difference and are reading this:
Type 1 - Do not make insulin. This is most commonly caused by an auto-immune disease where the immune system kills beta cells in the pancreas. This is caused by genetics and the genes have even been identified, which is a different topic altogether, and a trigger for the auto-immune response. Someone who is type 1 will always take insulin, and will die if not. This disease is not caused by being fat. A type 1 will need insulin even if s/he is eating nothing.
Type 2 - Are resistant to insulin. Sometimes it is said that type 2's do not make enough insulin (because they need to make more than most because it isn't being used at 100% effectiveness and can't). It is important to note that many of these explanations are misunderstood, and type 2's are resistant to insulin (ANY insulin), and that is the only commonality. I clarify this because I am someone who has both type 1 and type 2 and a lot of people get confused. I take artificially made insulin because I am type 1. I take medications and require a large amount of insulin to be injected because I am type 2. These are not the same disease, and you cannot switch from one to the other. Being overweight can lead to type 2 diabetes, and the treatment is either weight loss, pills, and/or insulin. When a type 2 (with only type 2) starts taking insulin, s/he does not become a type 1. Treatment does not define the disease. **The ignorance on this topic is a real annoyance for me, as you might guess.**
(snipped)
The challenge is timing. The best way to handle that is with consistency in amount of protein eaten and what time it is consumed. By doing that, it would be easiest to increase basal insulin because of the length of time over which the insulin should be active.
Does that make sense?
It makes perfect sense, thanks for putting it in words that most should be able to comprehend.
Sadly, you are absolutely correct regarding the general level of "ignorance" (or just lack of knowledge) regarding Diabetes (as if it's one disease). Sadder still is the fact that so many seem so unwilling to even consider approaching it with an open mind and learning what they don't know - so much easier to just bury one's head in the sand and "not read past those first 12 lines". That it occurs here is, I suppose understandable given the group speak atmosphere, but as is made obvious by the comments in the study conclusion, the biases exist at all levels of society.
Anyway, as you stated, until people can get past the basic misunderstanding that diabetes is diabetes is diabetes (or that T2D just naturally progresses to T1D) it's doubtful much will change.
I'm not a med pro, do not have T2D (or T1), no immediate family history, and the closest familial member that does is my FIL. My wife and I have been pretty actively involved in his treatment though, and we've been following the development of MannKind's Afrezza on his behalf. (I imagine you know of it but if not, encourage you to do so - the trial results were very impressive, including significant reductions in both basal and bolus in a number of participants (one of which I was in contact with during his participation in the trials). A secondary, but equally important benefit of the ultra fast acting qualities speaks directly to your mealtime and timing concerns.
That said (as background), we have also been following the research pretty closely on LC approaches to both T2D (on his behalf) and to weight loss in general (on both his and our own behalfs). I would say that our "position" on LC is best described as still uncertain but evolving. That we share your disdain for ignorance and even more so, closed minds, is something I really wish I could predict an end to in our lifetimes....unfortunately, that wish is becoming increasingly less likely day by day.
I would like to add a couple points to your excellent summary if I could and would welcome your correcting any of my understanding that is incorrect as your level of expertise on the subject obviously exceeds mine by orders of magnitude.
I should note that despite the amount of time we've spent with my FIL and researching diabetes in general, I seem to have developed something of a mental block regarding the "types" and can never quite keep it straight which is which (T1 or T2). Tried all kinds of mental crutches (2 is bigger than 1 or, it's backwards - 2 then 1, which works great except 10 minutes later I don't remember if it's backwards or not!). Anyway, so be it.
Not positive about the actual numbers but I think the last I saw at least 90% of all diabetics (US) were T2 a "fact" I'm fairly sure most are unaware of (I was). This doesn't, of course, take into account the relative severity or impact on the 1's vs 2's but I'm guessing most not only believe that "all" diabetics must use insulin, but think, as you stated, that 2 progresses naturally, to 1 automatically (it does not).
In fact though, type 2 is "progressive" in a highly predictive manner in most cases throughout it's course. Weight gain (loss) is a factor as is the eventual need for insulin but in the end it all comes down to "when", not "if" in most cases. When, the B-cells can no longer adapt to the body's impaired glucose tolerance.
I'm of the belief that, at least to some extent, our understanding of this progression is largely due to earlier detection, the formalization of the term pre-diabetic, and genetic predisposition. Unlike years ago, many individuals are now identified as PD's and increasing numbers of kids understood to be "at risk" at much earlier ages. The results of both situations being increased numbers of T2D's who have been "watched" if not "in treatment" for nearly an entire lifetime.
Regardless of the age of onset (and excepting those that are actually "cured" (or the progression halted) early on, for the vast majority of PD's and T2's it is absolutely progressive and on a highly predictable course. Mid course interventions can, and have, moderated the rate of progression (some more effectively than others) but stopping the progression in its tracks still remains an elusive goal.
We know "what" causes the progression (for the most part), understand the physiology, but still haven't been able to totally halt (or reverse) it - that remains the goal and if meds, low carbs, or magic mushrooms (or any combination) prove to be the means of achieving the goal does it really make a difference which one (or ones) it is?
Why would anyone dismiss out of hand ANY potential "cure" or even a more effective treatment protocol- even if it's not one cure for all or doesn't lower A1C any more than "x" (but does offer numerous other benefits)?
Shouldn't gaining a better understanding of which treatment mode is potentially more likely to be successful for an individual with certain indications trump what some "want" to believe?
I just don't get it and simply cannot accept the current level of bias against ANY mode - especially when the bias is based in ideology and ignorance.
Right, so I'm not officially an expert, but have had both types of diabetes long enough and have had enough training to run circles around nearly every lay-person and even a lot of GP's. I'll try to address your questions as a non-expert. Also, please understand that when I refer to a type 1 or a type 2, I'm talking about a patient that, unlike myself, does not have both. This is for simplicity.We know "what" causes the progression (for the most part), understand the physiology, but still haven't been able to totally halt (or reverse) it - that remains the goal and if meds, low carbs, or magic mushrooms (or any combination) prove to be the means of achieving the goal does it really make a difference which one (or ones) it is?
Yes, absolutely! Someone diagnosed with type 1 will need to go on insulin immediately. A type 1 who stops taking insulin will become very sick very quickly. S/he will slip into DKA and die without insulin. DKA is rare for type 2's, and only happens to those who have progressed to the furthest states of being type 2.
Let's figure for example, that I go on a 5 day hike, and on the 2nd day, everything I have for insulin is gone. My insulin pump is broken, I have no syringes, and a bear ate my insulin anyway. If a helicopter cannot make it to wherever I'm at, I will die. It isn't enough for other hikers to carry me out, as that would still take 2-3 days to accomplish, as would someone else carrying in supplies. Conversely, a type 2 diabetic will likely survive that situation. S/he may be feeling poorly by the time s/he makes it out 2-3 days later. In fact, when I was young, I tried not taking insulin once. Chalk it up to being young and stupid, or just tired of the disease, or whatever... I was on injections (MDI), and took my last basal insulin on Friday evening. By Monday morning, I was in the ER. I was vomiting, urinating every few minutes, was extremely dehydrated, my fingertips were turning purple, I did not have the energy to even stand on my own, I could not see well. This is after consuming approx. 110g of carbs total on Sat. and Sun. My blood sugar was 938, and I had lost around 50 lbs. (most of which was water weight). I was in DKA, and close to a coma because I have type 1, not because I have type 2. Except for the worst cases, type 2's would not be in such an emergency situation in just 2 days. So yes, it does matter what kind because we do not have the same level of severity.Why would anyone dismiss out of hand ANY potential "cure" or even a more effective treatment protocol- even if it's not one cure for all or doesn't lower A1C any more than "x" (but does offer numerous other benefits)?
Why? Because there are risks involved. Let's say that a type 1 were to try the "okra cure." That person might die. It is important to understand what one is doing. I dismiss so-called "cures" all the time, thought I wouldn't say it is "out of hand." It is because I understand the science enough to know when something is not worth the risk.Shouldn't gaining a better understanding of which treatment mode is potentially more likely to be successful for an individual with certain indications trump what some "want" to believe?
Yes, science should be taken over belief in nearly all situations. The exception is when a belief is so strong that the science will be thwarted, knowingly or not. What I mention is similar to the placebo effect, acting in reverse. Some situations provide one side or the other with such an advantage that the ultimate outcome is the same regardless. In the case of a type 1, no matter how much s/he wants a cure to work, s/he will not start making insulin by consuming okra infused water. There is no control that can be manipulated, consciously or sub-consciously, that will cause the patient to re-grow beta cells and start producing insulin again.0 -
Here's an interesting bit of diabetes history. Up until 1935 (and insulin) low carb was the treatment for even type 1 diabetics.
"The pre-insulin era
Childhood onset diabetes was rare – or at least, rarely diagnosed – in the pre-insulin era. Elliot Joslin collected such cases, despaired of by other physicians, and reported in 1917[1] that of 59 who developed diabetes before the age of 10, 38 had died within an average of 1.4 years. Their prognosis had however improved with a low carbohydrate ('Eskimo') diet. Death was from starvation, tuberculosis or diabetic coma."
http://www.diapedia.org/type-1-diabetes-mellitus/natural-history
Diabetic Cookery (published in 1917)
http://archive.org/stream/diabeticcookeryr00oppeiala#page/12/mode/2up0 -
Here's an interesting bit of diabetes history. Up until 1935 (and insulin) low carb was the treatment for even type 1 diabetics.
"The pre-insulin era
Childhood onset diabetes was rare – or at least, rarely diagnosed – in the pre-insulin era. Elliot Joslin collected such cases, despaired of by other physicians, and reported in 1917[1] that of 59 who developed diabetes before the age of 10, 38 had died within an average of 1.4 years. Their prognosis had however improved with a low carbohydrate ('Eskimo') diet. Death was from starvation, tuberculosis or diabetic coma."
http://www.diapedia.org/type-1-diabetes-mellitus/natural-history
Diabetic Cookery (published in 1917)
http://archive.org/stream/diabeticcookeryr00oppeiala#page/12/mode/2up
Early on, most type 1's died without being diagnosed. It would see that those who lived the longest had a longer "honeymoon" stage. Since type 1 is an auto-immune disease, one does not simply stop making insulin overnight. It takes quite some time for our immune system to kill all of the beta cells... months or years. Adults who get type 1 often see such a slow immune response that they are commonly misdiagnosed as having type 2 (these type 1's are often described as having LADA or type 1.5, but truly have type 1).
I've heard that type 1's were treated with alcohol before insulin was available. Processing alcohol can lower blood sugars. (That makes sense as to why it is on the list you posted.)0 -
Why would anyone dismiss out of hand ANY potential "cure" or even a more effective treatment protocol- even if it's not one cure for all or doesn't lower A1C any more than "x" (but does offer numerous other benefits)?
Shouldn't gaining a better understanding of which treatment mode is potentially more likely to be successful for an individual with certain indications trump what some "want" to believe?
I just don't get it and simply cannot accept the current level of bias against ANY mode - especially when the bias is based in ideology and ignorance.
Right, so I'm not officially an expert, but have had both types of diabetes long enough and have had enough training to run circles around nearly every lay-person and even a lot of GP's. I'll try to address your questions as a non-expert. Also, please understand that when I refer to a type 1 or a type 2, I'm talking about a patient that, unlike myself, does not have both. This is for simplicity.We know "what" causes the progression (for the most part), understand the physiology, but still haven't been able to totally halt (or reverse) it - that remains the goal and if meds, low carbs, or magic mushrooms (or any combination) prove to be the means of achieving the goal does it really make a difference which one (or ones) it is?Why would anyone dismiss out of hand ANY potential "cure" or even a more effective treatment protocol- even if it's not one cure for all or doesn't lower A1C any more than "x" (but does offer numerous other benefits)?
Why? Because there are risks involved. Let's say that a type 1 were to try the "okra cure." That person might die. It is important to understand what one is doing. I dismiss so-called "cures" all the time, thought I wouldn't say it is "out of hand." It is because I understand the science enough to know when something is not worth the risk.Shouldn't gaining a better understanding of which treatment mode is potentially more likely to be successful for an individual with certain indications trump what some "want" to believe?
Yes, science should be taken over belief in nearly all situations. The exception is when a belief is so strong that the science will be thwarted, knowingly or not. What I mention is similar to the placebo effect, acting in reverse. Some situations provide one side or the other with such an advantage that the ultimate outcome is the same regardless. In the case of a type 1, no matter how much s/he wants a cure to work, s/he will not start making insulin by consuming okra infused water. There is no control that can be manipulated, consciously or sub-consciously, that will cause the patient to re-grow beta cells and start producing insulin again.
MidWest;
Thank you for the input/info.
My choice of words (ANY) was poor - should have been more clear that what I was trying to convey wasn't "any" - but rather any potential treatment regimen that DOES have a basis in science (as opposed to "belief").
Additionally, despite (or maybe because of) the wordiness of my previous post, I neglected to say that my knowledge of T1 is pretty much limited to 1) T1 and T2 are totally different, 2) with T1 insulin is "life or death", with T2 it may or may not be required depending on where one lies on the progression, 3) there is no "natural" (or automatic) progression from 2 to 1.
As such (and I should have been clearer expressing it), my comments are almost exclusively relevant ONLY to T2.
Prior to your posts, (and due to my lack of knowledge), I had never considered that some percentage are afflicted with both T1 and T2. It wasn't based on any factual knowledge but rather simply never having been something I had thought about. Thank you again for opening my eyes on that point.
Finally (and somewhat OT), since you are using a pump and you're clearly a research bug (as am I, it's meant as a compliment (g)), I'm guessing that you are familiar with Medtronic/MiniMed. While it's not the only pump out there, my understanding is that Medtronic does have the largest market share (never actually verified the numbers so it's an assumption).
Anyway the "history" is interesting in that Alfred Mann (as in Mannkind/Afrezza), while he (his company(s)) didn't actually invent the pump (as some mistakenly proclaim), he was the driving force behind developing the technology to the point where it became widely available and viable.
As a result of these (and other) efforts on the R&D front and his business acumen, he became a gazillionaire and has dedicated his life to finding the "cure" (or at least to improving the lives of those afflicted with either T1 or T2 or both).
He truly is not only a pioneer in the field but a man (pun?) on a mission.
Afrezza is likely last "mission" (as he's approaching 90) and some (myself included) believe it will be his crowning glory and define his legacy, but his work will live on in the form of the Mann Foundation in any case.
There is no finer example (IMO) of the American Dream or the definition of philanthropy when used to benefit the "greater good".0 -
deansdad101:
Those were the bits that jumped out at me during an initial quick read through of the pdf. I have it printed out on my desk at work and will go through it in more detail if time permits next week. As a prediabetic myself I will usually describe my own diet as "moderate carbs" so it isn't something I am dismissing out of hand. So while I may well end up agreeing with their conclusions (which apparently I had slightly misunderstood), that doesn't mean that there still can't be issues with the paper...0 -
deansdad101:
Those were the bits that jumped out at me during an initial quick read through of the pdf. I have it printed out on my desk at work and will go through it in more detail if time permits next week. As a prediabetic myself I will usually describe my own diet as "moderate carbs" so it isn't something I am dismissing out of hand. So while I may well end up agreeing with their conclusions (which apparently I had slightly misunderstood), that doesn't mean that there still can't be issues with the paper...
Richard;
Couldn't agree more with "...that doesn't mean....."
but neither does it mean that there are (issues).
My concerns are focused more on the dissemination of factual information (or maybe more importantly, on calling out those that pick and chose "snipets" that while true (perhaps), are clearly selected to embolden their preconceived "beliefs" and the myths so often repeated as to take on false legitimacy).
I'll confess to "assuming" that your initial comments did set off my "radar" on that count and I apologize for making the assumption - not because of your subsequent "..moderate carbs diet..." comment but because of your willingness to keep an open mind and revisit the study details in their entirety.
Assumptions are almost always a bad idea (as is obvious in both of our cases here) and I'm in no way saying this particular "study" is either flawless OR definitive. It is, however, a valuable contribution (at least IMO) to the knowledge base by an individual who has earned a degree of respect and is endorsed by a number of his peers. As such, it at least deserves to be considered (even if not agreed with) in its entirety.
We can agree to disagree on any of the details or the relative weight of the underlying studies assigned by the author when reaching his conclusions.
We can at the same time (and probably do), agree that the author didn't come to table completely bias free or that he didn't "want to prove" certain points in which he believed going in. But that's inherent in the nature of meta-data studies (all of them). It would be wonderful if we lived in a world of "pure" science where every question had a black/white, yes or no answer and every scientist influenced ONLY by the science, but.....
It's really not about debating points for me, but rather doing what I can to encourage those facing the challenges of diabetes to dig past the myth and the group speak and down to as close as they can get to actual "fact".
Unfortunately, too many (present company excluded) are too willing to rely on what they see posted on these (and other), forums...."I saw it on the internets, it must be true....bonejours".
DD0 -
Deansdad101:
Yes, I currently am using a Minimed pump (723, with sof-sensors for CGM). My first pump was a minimed, and I switched to Disetronic, then to Cozmo, and now back to Minimed. I remember I was just reading somewhere recently (it was information from 2-3 years ago, though) that Minimed holds 85% of the US market share for insulin pumps, but that is not nearly as high in other countries.0 -
Yes, it does make sense. I was curious not because I'm a diabetic, but because in my clinical training I worked in a hospital diabetes centre. I know the pathophysiological distinctions between types 1 & 2 well, but certainly where I worked the type 1 & 2 classifications were not used as much as ID or NID because many type 2s end up on insulin eventually. At the clinic we focused on education and management of diet and insulin using mostly carb counting. I didn't see anyone on a low carb diet, except to test the basal dose. The possibility of managing on an increased dose of basal insulin alone would probably be very appealing to some people.Interesting because there are studies that have shown no difference in HBA1C and FBG levels between low carb and 'balanced carb' eg.reviewed in this meta-analysis and systematic review. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090010/ They also report that long term adherence is a problem with low carb diets. I acknowledge that it is hard to compare different studies though because of differences in classifying diet as low/balanced/high etc.
It does seem like the article in the OP is pushing the low carb agenda. When I was looking at some of the cited references, they didn't actually provide the evidence for what they stated in the article.
I'm interested about any possible benefit of low-carb for people with IDDM. Even going very low carb, some background insulin would still be required..? That's often what's done to workout the background insulin dose. I would be interested to hear if any Type1 diabetics have ceased insulin altogether due to low carb diet though....or maybe ceased their fast acting insulin and only have their background insulin?
I don't believe that dietary carb restriction should be the first approach. My take is that diabetes should be managed on a case by case basis.
JMO. Thanks for posting the article. It was an interesting read even though I don't necessarily agree with it, or find it particularly rigorous.
First, it is very important to note the difference between type 1 and type 2. This is mostly for those who don't know the difference and are reading this:
Type 1 - Do not make insulin. This is most commonly caused by an auto-immune disease where the immune system kills beta cells in the pancreas. This is caused by genetics and the genes have even been identified, which is a different topic altogether, and a trigger for the auto-immune response. Someone who is type 1 will always take insulin, and will die if not. This disease is not caused by being fat. A type 1 will need insulin even if s/he is eating nothing.
Type 2 - Are resistant to insulin. Sometimes it is said that type 2's do not make enough insulin (because they need to make more than most because it isn't being used at 100% effectiveness and can't). It is important to note that many of these explanations are misunderstood, and type 2's are resistant to insulin (ANY insulin), and that is the only commonality. I clarify this because I am someone who has both type 1 and type 2 and a lot of people get confused. I take artificially made insulin because I am type 1. I take medications and require a large amount of insulin to be injected because I am type 2. These are not the same disease, and you cannot switch from one to the other. Being overweight can lead to type 2 diabetes, and the treatment is either weight loss, pills, and/or insulin. When a type 2 (with only type 2) starts taking insulin, s/he does not become a type 1. Treatment does not define the disease. **The ignorance on this topic is a real annoyance for me, as you might guess.**
The question about basal insulin (this is the insulin that is always needed by type 1 diabetics who have no insulin otherwise) and bolus insulin (additional insulin to cover food and/or to correct high blood sugar) is a good one. Personally, I do not believe it to be possible to eliminate bolus insulin for food. I say this because protein is also converted to glucose, but at a much lower rate, and over a much longer time period. Most of us diabetics eat a small enough amount of protein that we do not notice it. If we were to stop eating carbs, we would need to replace at least some of those calories elsewhere. That means we are eating more protein (and fat, which is converted at even less and over an even longer time period), which is probably enough to require some boluses. The challenge is timing. The best way to handle that is with consistency in amount of protein eaten and what time it is consumed. By doing that, it would be easiest to increase basal insulin because of the length of time over which the insulin should be active.
Does that make sense?
Others would find the idea of carb restriction to that degree intolerable.0 -
Ugh, couldn't edit my previous post.
Regarding the quality of the article, I didn't check all of the references as I would if I was reviewing it for a journal, but one that was cited for evidence of success of low carb diets was the blog Authority Nutrition. To cite something like that instead of a peer reviewed source is very alarming and I question how they got it past the reviewers and actually published.0 -
Regarding the quality of the article, I didn't check all of the references as I would if I was reviewing it for a journal, but one that was cited for evidence of success of low carb diets was the blog Authority Nutrition.
Had you bothered to check you would have seen it was merely referring to a list of RCTs that is summarised on the authority nutrition blog, as a shorthand way of referencing them. It's the source of the graph below.
0 -
I tend to agree. I manage well on moderate carbs. I know others that thrive on LCHF. Finding a sustainable dietary approach depends on the individual. Food preferences? Particular foods that spikes blood glucose? Activity level?My take is that diabetes should be managed on a case by case basis.
I doubly agree. My pre-diabetes seems to flare up when I go under 100 carbs but my blood sugar is well within normal range when I consume moderate carb (around 150 g). My uncle on the other hand has to be low carb to keep his blood sugar under control.0 -
My take is that diabetes should be managed on a case by case basis.I tend to agree. I manage well on moderate carbs. I know others that thrive on LCHF. Finding a sustainable dietary approach depends on the individual. Food preferences? Particular foods that spikes blood glucose? Activity level?
AMM;I doubly agree. My pre-diabetes seems to flare up when I go under 100 carbs but my blood sugar is well within normal range when I consume moderate carb (around 150 g). My uncle on the other hand has to be low carb to keep his blood sugar under control.
I doubt that anyone on this thread (or in real life), disagrees with the sentiments that each "patient" must be treated as an individual and that there is NO "one size fits all" approach.
Your personal examples, while anecdotal (which doesn't mean they are wrong), are living proof, as are those of many of the previous posters.
Keeping an open mind regarding the various methods available in order to find the "best fit" treatment protocol is really what the discussion is (or should be), all about.0 -
Lol at your assumption. I checked as I was surprised at the citation. Authority Nutrition is a blog and NOT a peer-reviewed source of information. The data that was summarised by the blog author was not reviewed by the scientific community for accuracy etc, and therefore not appropriate in the context it was used.Regarding the quality of the article, I didn't check all of the references as I would if I was reviewing it for a journal, but one that was cited for evidence of success of low carb diets was the blog Authority Nutrition.
Had you bothered to check you would have seen it was merely referring to a list of RCTs that is summarised on the authority nutrition blog, as a shorthand way of referencing them. It's the source of the graph below.
You seem so defensive.....0 -
The chart clearly shows the results of numerous peer reviewed RCTs with references.
Is your issue that the chart itself hasn't been peer reviewed to check that the values are the same as in the studies ? It has now, as this article was published in a peer reviewed journal and it's at the bottom under " Uncited reference "0 -
duplicate0
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The chart clearly shows the results of numerous peer reviewed RCTs with references.
Is your issue that the chart itself hasn't been peer reviewed to check that the values are the same as in the studies ?
My big issue is using a non-peer reviewed source as evidence. This is simply because a non-peer-reviewed source hasn't been reviewed by the scientific community. That's a big one for me. For example, in his summary of compliance with LC diets, how did he classify a diet as low carb, how long did participants follow the diet, what was the participant profile etc. There are many variables to consider when summarising data and a simple comparison as presented with little explanation may not show the true picture. Of course, it may be very accurate, but without scrutiny and comment by the scientific community, it remains an unknown.0 -
I was diagnosed with type 2 diabetes six years ago, and by sticking close to 120-150g of carbs per day, I've been able to lower my A1C to 5.3 (as of July 2).
When my carbs were around 190g per day, my A1C stayed below six, but was higher, around 5.6 - 5.8.0 -
Yes, I commented on that earlier. I was surprised that it got past the reviewers. I would ask for a different source, or request that original articles be referenced. Fortunately for the authors, I don't review for Nutrition.It has now, as this article was published in a peer reviewed journal and it's at the bottom under " Uncited reference "0
This discussion has been closed.
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