If you're short on time, the brief answer is "for most people, no, not really". The longer answer is very interesting. Here's the summary of the 2-year followup, straight from the source:
Unfortunately, the researchers didn't see fit to publish their complete results - there is no scatterplot here, for example, which would be rather more informative than averages. Even so, the outcome looks pretty mediocre:
1) Out of 298 participants split randomly into an intervention and non-intervention group, only 17 members of the intervention group lost more than 15kg of excess bodyweight at 24 months; 3 of the non-intervention group did. The mean bodyweight difference was 5.4kg between the two groups. This is unimpressive considering that the researchers maintain that remission is a direct consequence of weight loss.
2) They assert that 35%+ of the intervention group were "in remission" at 24 months. They define "remission'' as HbA1c<48mmol/mol. Mean HbA1c decreased from 60.4 (SD=13.7) to 54.4 (SD=15.9), implying (a) that 15% of the intervention group started off with their HbA1c less than 48mmol/mol in the first place and (b) Only ~20% of the intervention group actually ended up with HbA1c in the "normal" range (<42mmol/mol).
3) 39.5% of the intervention group were still receiving diabetes medication (presumably metformin) after 24 months.
If (2) and (3) genuinely count as diabetes remission, well, I'm a catwalk supermodel.
So why doesn't it work?
Well, there's really no reason why it should. After the initial 8-week starvation diet, patients are explicitly told to go back to "eating normally", albeit with "reduced calories" and some halfhearted exhortations to avoid processed starches. This is exactly the same advice that has been handed out by mainstream organisations such as the ADA and Diabetes UK (unsurprisingly, since the ND study was funded by Diabetes UK). This has been repeatedly shown to be only marginally effective, at best, and is completely at odds with known physiology.
The patient is essentially told to eat a diet of fresh air and protein, avoiding fats and carbs. Humans are not carnivores: we use protein for energy inefficiently, and a certain quantity of either fat or carbs is needed to burn protein at all. A protein-only diet results in rapid death. The usual outcome of a high-protein low-fat low-carb diet is that the patient becomes ravenously hungry and "falls off the wagon" - hence, I suspect, the rather high dropout rate in the intervention group.
As for the idea that diabetes is caused by obesity, and is put into remission by weight loss, this is easily disproved from two directions:
a) About a third of the cases presenting with T2D symptoms are not overweight.
b) Low-carb protocols drive an almost immediate improvement in blood glucose control, long before any significant weight loss is observed.
Since their hypothesis is wrong, it's not really surprising the treatment doesn't work.
Let's have a look at a couple of alternatives.
Dr David Unwin has been praised for his low-tech, commonsense approach: he basically tells people to stop eating junk, keep carbs to a minimum consistent with palatability, and not to be afraid of fat. Unwin reports:
1) 50% remission at 21 months (his definition of remission is <42mmol/mol) with nobody over 48mmol/mol. In other words, if we take the Newcastle University definition of "remission", he's achieving a 100% success rate.
2) mean 10kg weight loss.
3) A high rate of compliance with an essentially enjoyable diet plan.
Unwin is working with a group who have somewhat different baseline characteristics, compared to the ND study - more in the prediabetic than diabetic range. Nevertheless, his results are a lot more impressive, with a far simpler intervention that patients are happy to comply with.
And then there's standard LCHF. Unwin takes a conservative position, advising patients that carbs are OK in moderation, and that fat is not to be avoided. LCHF goes a little further, advising carbs (for diabetics at least) below 50g/day, with most of the patient's energy-calories from fat. The leading proponents of this approach are Virta Health in the US, reporting:
1) An average 14kg bodyweight loss;
2) HbA1c reduction from 59.6 ± 1.0 to 45.2 ± 0.8 mmol/mol (ie., 100% success according to N.U. criteria)
3) A good level of compliance (16% dropout compared to 9% for controls).
4) Improvements in many other health measures, including cholesterol panel and blood pressure.
Many of the study participants remain on metformin, but it's not entirely clear how necessary this is:
I find the psychological aspects of this really fascinating. I think there's a lot more mysticism and shamanism in modern medicine than the medics like to admit. The ND is nasty, and medicine has to be nasty or it won't work ... right? The straightforward portion-based advice for diabetes control that you regularly mention might be far more effective than the ND, but it's too simple. So it can't possibly be 'real medicine', and therefore it doesn't work. QED.
I honestly can't tell if the ND people actually know that their diet is flimflam and snake-oil, but sell it anyway because they know it appeals to something deep in the human psyche that wants medicine to hurt ... or whether they genuinely think their theory is correct.
>> Any success from the Newcastle diet is probably due to it being a reduced carbohydrate, albeit poorly balanced diet.
Quite. The shake formulation is proprietary, but I found the macro breakdown somewhere (I'm damned if I can find it again now). IIRC, it's about 50% carbs, 30% protein and 20% fat, ie., low-fat high-carb. 50% of 800kCal is 400kCal = 100g carbs, which is well above normal "keto" level, but given the extreme caloric restriction probably has the same effect as a VLCHF induction protocol.
That's all well and good, but because the experimenters refuse to accept that diabetics can't process carbohydrates efficiently, it all falls to pieces when everyone ends up on a low-fat diet with energy mostly from carbs ... and predictably enough, they remain diabetic. Mostly.
I would choose the one I felt I could follow!
Interestingly, the research you quote was to “
The purpose of this study was to evaluate if a new care model with very low dietary carbohydrate intake and continuous supervision by a health coach and doctor could safely lower HbA1c, weight and need for medicines after 1 year in adults with T2D”. On the Diabetes forum you tore my head off for suggesting the involvement of a healthcare professional.
The conclusions of that research are: “
These results demonstrate that a novel metabolic and continuous remote care model can support adults with T2D to safely improve HbA1c, weight, and other biomarkers while reducing diabetes medication use.” Even the researchers are happy that is about improvement and medication reduction. The model is about diet but, as importantly, continuous care/support. You never mention that and only ever talk about diet. You twist the research to suit your own ends of getting people to fit into your “method” and cement it by terminology such as poison and fault.
All of these experiments include results for compliance.
Do you disagree, then, that the ND had the worst performance on all measures out of the three interventions? On which measure(s) is it the superior choice?
>> The model is about diet but, as importantly, continuous care/support. You never mention that and only ever talk about diet.
Because nobody has ever needed care and support on LCHF. Unwin discusses this. He gets a few minutes with his patients to follow up. Such is life as a GP. They still stick with it. Once they understand it, and they try it, it just works. They don't feel inclined to stop doing it.
The ND is impossible to comply with because it is nutritionally deficient. Nobody ever complies with low-carb, low-fat, high-protein, calorie-restricted diets. They're horrible. Why NU should think "I'll work this time" is just beyond me. They don't even seem to realise they haven't done anything novel. People have been trying this stuff for decades, and it never, ever works.
>> You twist the research to suit your own ends
Give me one example of misrepresentation in my summary. Apart from the interpretation of mean and SD, I was merely quoting from the papers.
For those who are interested, three pieces of information.
“a) About a third of the cases presenting with T2D symptoms are not overweight.”
Studies have shown that becoming overweight is a major risk factor in developing type 2 diabetes. Today, roughly 30 percent of overweight people have the disease, and 85 percent of diabetics are overweight.7 Mar 2012k
“About a third of the cases presenting with T2D symptoms are not overweight.”
Studies have shown that becoming overweight is a major risk factor in developing type 2 diabetes. Today, roughly 30 percent of overweight people have the disease, and 85 percent of diabetics are overweight.7 Mar 2012k
Can you explain what you think these two facts mean?
There are different ways of tackling your insulin resistance.
Insulin resistance is not a disease. It's a normal, indispensable part of our metabolic machinery. Do you understand what would happen if there were no such thing as insulin resistance?
The Salisbury NHS leaflet makes the ND look better than it is by quoting preliminary results:
Of the ten people re-tested, 7 out of the 11 people remained in remission from type 2 diabetes.
The DIRECT trial shows 80% of the trial subjects (about 150 of them) either prediabetic or diabetic after two years, as I described elsewhere.
people are more likely to regain the weight that they have lost on a very low calorie diet without ongoing support from a health care professional.
In other words: they don't work.
I thought you has said your last??
On the question you pose - not all overweight people have type 2 diabetes - only 30% do. From the people who have type 2 diabetes, 85% of them are overweight. I am surprised that you could not fathom that out.
I wasn't questioning the statistic. I was asking you what inference you think can be drawn from those two separate observations. What do they mean? Or, if you prefer, what hypotheses are consistent with those observations and might be tested by experiment?
You had said that 1/3 of the cases of type 2 diabetes were overweight. The correct information was that 1/3 of overweight people have type 2 diabetes but, of those who have type 2 diabetes, only 85% of them are overweight. Just think you got your stats a little confused.
um ... if I did, it was a typo. I had intended to write that about 1/3 of diabetics are not overweight when diagnosed. I suppose it depends how you define "overweight". If you say it's 15% I'm not going to argue with that.
Anyway, the question still stands. Don't you think those numbers tell us something rather useful about the aetiology of T2D?
You seem to easily conflate "telling you off" with asking you a pertinent question.
That's telling you off, by the way. I'll stop doing it now.
The obvious conclusion is that, if a significant fraction of new T2D patients present without obesity, and obesity doesn't necessarily result in T2D, then obesity isn't the proximate cause of T2D. There are various ways you can test this conclusion: for example, you could predict that T2D symptoms might be treated more-or-less independently of obesity. As I noted elsewhere, it turns out that this is true: T2D can be dramatically improved in both obese and non-obese patients before any significant weight loss occurs.
The proponents of the ND diet are therefore wrong in their assertion that T2D is caused by obesity and that reversal is a consequence of weight loss.
A small number of those presenting with Type 2 diabetes are not obese - only 15%. This does not mean that obesity is not a cause of Type 2 diabetes but that it is not the only cause!! That said, many of the common, new diabetes medications also assist in weight loss.
There are probably a lot more! However, these show quite well both the connection between Type 2 diabetes and obesity and the effect on diabetes of losing weight.
Any significant weight loss, if maintained, will assist in lessening or removing insulin resistance.
Obesity correlates with diabetes. Sure. However, if you have the hypothesis "obesity causes diabetes", your next experiment should set out to disprove it. That disproof has been offered from multiple approaches (including at least one of your quoted papers).
- The second paper you quote explicitly points out that obesity is not a cause of diabetes, but that obesity and diabetes are symptoms of the same underlying disorder.
- The authors of the third paper are your typical diabetes researchers floundering around without any knowledge of control systems theory to guide their experiments. I've read the whole thing, and I can see very little of practical value there. Breaking a MIMO control loop as they have done can tell you something about the transfer function, but it's a damn difficult task. You must at least have completed a system identification procedure using standard methods (impulse or step response, say), and these guys not only haven't done that, they're not familiar with any research that has.
- The fifth paper points out that obesity in diabetics appears to be a protective mechanism (as I've asserted elsewhere).
- The sixth demonstrates correlation but not causation.
- The first and fourth links seem to be broken.
If you had a wonder drug that "removed insulin resistance", the patient would die within a matter of hours from multiple organ failure.
You do realise that insulin resistance is not a systemwide parameter, but something that each cell adjusts independently for itself? So "reducing insulin resistance" doesn't accurately describe what happens in diabetes remission.
Also worth pointing out that there is really no way for a diabetic to maintain any significant weight loss without removing the carbohydrate load on his body. The ND results demonstrate this with their reported weight-loss outcomes (something like 5kg at two years on general caloric restriction, compared to 10-15kg for LCHF-like interventions).
Your comment on the fifth paper, which you dismissed, has the following as its conclusions:
“We believe that the findings of obesity paradox should not change current clinical advice regarding the importance of weight reduction in patients with type 2 diabetes mellitus who are overweight or obese. We agree with Lajous et al. [54] who conclude that we should not recommend that patients with chronic diseases gain weight. A systematic review of randomized controlled trials of weight loss interventions for adults with obesity concluded that these interventions may reduce premature all-cause mortality in adults with obesity [55]. We believe that the literature also provides good support for recommending weight loss to overweight and obese patients who have type 2 diabetes mellitus. The Look AHEAD Study conducted an intensive lifestyle intervention in 5,145 overweight or obese patients with type 2 diabetes mellitus to assess whether this would reduce cardiovascular morbidity and mortality [56]. The intervention group succeeded in losing 8.6% of body weight by year 1 and 6.0% by the end of the study. Although this randomized controlled trial did not demonstrate a reduction in cardiovascular morbidity or mortality, no increase in either of these outcomes occurred, which might have been expected if excess adiposity conferred a survival benefit consistent with the obesity paradox. This clinical trial therefore has a 2-fold benefit as it argues against the obesity paradox and provides reassurance to clinicians that overweight and obese patients with diabetes may safely attempt to reduce weight.”
Perhaps you did not give it the full attention it deserved - or do you see all papers in the light of your own preformed views?
I didn't "dismiss" it. It's a good, rigorous review. I was simply saying it doesn't show what you think it shows.
The passage you quote doesn't offer any support for your position. It's just a statement of the experimenters' beliefs (the word 'believe' is used). As far as it goes, I wouldn't disagree with it: they are not arguing here that weight reduction "cures" diabetes, merely that weight reduction is a Good Thing in and of itself, which is fairly uncontentious. Notice that link [56] shows no widespread health benefits, suggesting that it did not address the inflammatory syndrome discussed in the body of the paper.
The bottom line is that obesity has been comprehensively disproved as a cause of obesity, so it's rather futile gathering papers suggesting that it might be - unless, and this is important, those papers can argue persuasively that the experiments disproving causation are themselves flawed. You would have to show, for example, that the rapid diabetes remission that appears with LCHF is nothing to do with insulin-response recalibration, but it primarily a result of bodyfat loss. Since there is no such bodyfat loss (at least not for several weeks), that seems like a tough ask to me.
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