I was a bit taken aback by the title on a recent blog post by Dr. William Davis at his Heart Scan Blog
Why doesn't your doctor try to CURE diabetes?
Dr. Davis paints the medical profession with a rather broad unflattering brush. Are there docs out there who are more concerned about profit over your health? Yes. Are there doctor-drones who reflexively reach for the prescription pad? Again, yes. But I believe that most doctors -- and I know several since before they became docs -- do care about their patients and dole out advice based on what they believe to be the best course of action.
Certainly the statement that "Adult diabetes is the one chronic disease that nobody cares to cure" goes more than a bit over the top!
Davis goes on to say that most docs don't think it can be cured, and that is probably true. The old school re: type 2 would be based on when the disease was more rare and probably not detected until progressed significantly to the point of beta-cell impairment. But nowadays, with earlier onset and screening, it really can be reversed and "cured" by ..... drum roll please ..... eating less and moving more! Reducing fat stores below the max fill line (caloric deficit) and exercise work in conjunction to reduce insulin resistance. I believe successful early intervention can indeed cure the disease.
Why doesn't your doctor try to CURE diabetes?
Dr. Davis paints the medical profession with a rather broad unflattering brush. Are there docs out there who are more concerned about profit over your health? Yes. Are there doctor-drones who reflexively reach for the prescription pad? Again, yes. But I believe that most doctors -- and I know several since before they became docs -- do care about their patients and dole out advice based on what they believe to be the best course of action.
Certainly the statement that "Adult diabetes is the one chronic disease that nobody cares to cure" goes more than a bit over the top!
Davis goes on to say that most docs don't think it can be cured, and that is probably true. The old school re: type 2 would be based on when the disease was more rare and probably not detected until progressed significantly to the point of beta-cell impairment. But nowadays, with earlier onset and screening, it really can be reversed and "cured" by ..... drum roll please ..... eating less and moving more! Reducing fat stores below the max fill line (caloric deficit) and exercise work in conjunction to reduce insulin resistance. I believe successful early intervention can indeed cure the disease.
Dr. Davis goes on to describe a scenario whereby you present at the doctor's office with a FBG of 156 and an HbA1c of 7.1%. The doc puts you on metformin and the ADA diet. Now this scenario is presented as if this is some uncaring robo-doc basically going with the flow recommending a course of action with no track record towards improving patient health. He also presumes there is no prior treatment history here. I would venture to guess that most of those who get the diabetes diagnosis from their docs have previously been diagnosed (formally or cautioned) as pre-diabetic and counseled to lose weight .. perhaps on multiple occasions. IOW, this isn't the first attempt at intervention in the progression of the disease and the patient has failed to make the appropriate lifestyle changes.
OK, so we could argue until we're blue in the face what diet is preferable for weight loss, but there's such a high correlation between obesity and T2 that some have taken to calling it diabesity, and there is ample evidence that just modest weight loss alone can cure it. LC advocates would blame the doctor for recommending a "failed" low fat diet, but they would be ignoring the fact that many people fail to lose weight on low carb diets as well (and/or fail to maintain it).
If my doctor counsels me to lose weight and I come back 6 months later weighing the same or more, whose fault is that? The doctor can't hold our hands and can only take our word for it that we tried to lose weight but couldn't or how hard we really tried (vs. compliance was not so hot). Given the deleterious impacts of glycylation, the doc is doing the responsible thing to lower HbA1C as rapidly as possible with the metformin. If a patient has not demonstrated an ability to reverse their insulin resistance through lifestyle change, the doc has no choice but to resort to pharmaceutical intervention.
There is emerging evidence that early intervention with metformin is more effective. In other words, use metformin to attain glycemic control in the early stages and there will be LESS of a need for other medications down the line (or their need will be postponed). So could it be that the doctors are trying to cure diabetes after all? Metformin may reverse the condition more rapidly in the short run, and if patients adhere to a reducing diet (even that of the ADA), their diabetes can be cured.
But Davis will infer no such positive motive on his colleagues. He presumes that patients will gain 10-15lbs a year on the ADA diet, thereby inferring that in prescribing the diet the doctors intend for their patients to do so. Huh?! There are obese/overweight people with serious health issues due to their weight and even those don't "scare them straight" to adhere to a weight loss plan. I am not condemning or criticizing those people -- I was one although w/o the serious health issues. But Davis ignores the reality that losing and MAINTAINING weight is both difficult and rare for any number of reasons not related to the composition of one's diet. The ADA formula of counting calories is a little too low in fat and protein for my tastes, but I hardly see recommending a reducing diet -- any reducing diet -- as irresponsible. Certainly since weight loss has been shown to reverse (aka "cure") T2, especially if caught early, this advice is what Martha would call a "good thing".
I continue to be concerned over whether LC diets that either do not produce weight loss and/or are not consistently complied with present a significant improvement over a HCLF diet. BOTH elevated glucose and NEFA/FFA produce deleterious results, and it is the NEFA that contributes to insulin resistance. LC can lower 24 hr AUC glucose, but if IR persists you haven't "cured" a thing -- only masking a down-line symptom in the progression of a disease. Metformin, OTOH, increases insulin sensitivity and reduces gluconeogenesis. Perhaps early NEFA lowering pharmaceutical intervention is an avenue to pursue (metformin's action on lipolysis is inconclusive, it lowers NEFA in some while having no effect in others).
I would agree that all too often patients request a pill and/or doctors reach for the prescription pad to solve medical conditions. But in progressive lifestyle diseases like this, by the time it gets to the point of diagnosis, lifestyle changes alone may be either too slow or ineffective. The boat has sailed. But pharmaceutical intervention need not be for all eternity. It may well be that just as chemo "cures" cancer by killing off the cells, early intervention to lower circulating glucose and NEFA may well "cure" diabetes provided the IR inducing lifestyle (diet and inactivity) is altered and modest weight loss achieved.
What does it mean to be "cured" of diabetes? That would be normal basal insulin levels, normal fasting glucose and NEFA's and a normal insulin response to carbohydrate. If a low carber can't eat a bowl of rice without blood sugar going out of control, I contend their diabetes is not cured but rather controlled.
Comments
I think you are a little too anti-low carb, Carb Sane. Think it through - what meal plans would you make for a person with T2D?
You seem convinced that a high fat low carb diet is "best", and your super slow method is the "best" exercise. That is your opinion, and I suppose Dr. Davis' as well. But I do not see that this position is substantiated by the science as I've been reading. I've posted quite a few studies now demonstrating that good old fashioned moderate cardio is very effective in reversing insulin resistance.
Just because, say, HIIT is effective for one aspect, does not render other forms of exercise moot.
We didn't evolve to eat the infant food of other species and any product made from them. We didn't evolve rendering fats from prey and swigging coconut and MCT oils. Even the Eaton paper cited in The New Atkins by Westman, Volek and Phinney as justification for Atkins basically says no such thing. The best estimates is that we evolved to eat 35% carb (mostly from fruits and veggies and some honey), 35% fat and 30% protein. We did not evolve from the Inuit.
I'm not anti-LC, I'm trying to assess for myself whether it is the most healthful WOE for the long term. Not everyone who does LC loses weight -- some have to count calories (or adopt deliberate efforts to control them) as well. If I were diabetic I would have my NEFA levels checked and not just the HbA1c/FBG.
VLC does not "cure" diabetes, it masks the impaired glucose metabolism. Diabetes is a "bad" disease because of all the things that go along with insufficient insulin and/or insulin resistance. Insulin plays a huge protective role in our bodies apart from it's function to stimulate glucose clearance from our blood. If a T2 has IR, a "healing" strategy would be one that is best to reverse that. If a T2 has progressed to the point of beta cell impairment, pharmaceutical intervention (or certain protein's apparently) to improve the insulin response are an appropriate strategy and lowering the insulin response through diet would not be desired.
The ADA diet does seem too carby for me. But I am not sure a high fat VLC diet is any better.
A general observation: People (including the many diabetics who frequent LC discussion boards) seem to become more and more carb intolerant the longer they do low carb. Even if they are not diabetic, they will fail a standard OGTT and are essentially "diabetic". Their insulin signalling/responsiveness gets progressively worse, not better, even in those who have lost a lot of weight and maintained that loss.
Y'know, IMO, for most being obese is such an unhealthy state that just about any means by which to lose the weight are worth considering even if they have long term implications (e.g. bariatric surgery). I'm content with myself that I did what I had to do to lose the weight. I'm still re-evaluating the road ahead.
Reading through your old blog posts, and I'm confused, and trying not to freak out about what the heck I'm supposed to eat let alone feed my family. I'm really confused about the insulin resistance caused by eating VLC. I had bought the argument that it was important for VLC to cause peripheral IR in order for glucose to be shunted to the brain. However, now I learn that insulin is not required for glucose to be taken up by cells. So, what are the negative effects of the IR caused by VLC? And what does IR have to do with blood glucose? What does it matter if cells are IR if they can take up glucose without insulin? I'm sure these are all very basic (stupid even) questions, but I'm really unsure where to go for a reliable source of info. If you could point me to a paper, or good web site that would be appreciated. Thanks.
Insulin has functions in the vascular system that are seemingly independent from glucose metabolism. So I think this is where I have my concerns. See for example this blog post: Vascular Functions of Insulin.
" What does it matter if cells are IR if they can take up glucose without insulin? "
Here's the crux of the matter. It doesn't for glycolysis. Hyperglycemia is due more to IR in the liver where insulin fails to perform its inhibitory role in gluconeogenesis. This shouldn't be a problem with VLC as most VLC'ers make glucose just fine. If you're experiencing the symptoms of hypoglycemia doing LC, perhaps
IR is exhibiting undesirable effects.
BG meters and strips are relatively cheap. See how your body responds before freaking out!
I don't think systemic insulin resistance is a foregone conclusion eating VLC. For one, higher protein should maintain the postprandial insulin response and/or a non-fatty acid contribution to the energy fuel mix (as in that Protein for Energy post). It also seems that most studies looking at diet-induced IR do so with a large fat meal. If one eats high fat, then perhaps spread it around a bit?
It seems to me that the concerns are different for obese vs. the lean (or moderately overweight). It is the overstuffed fat cells that lead to IR because of the fatty acids released from the fat store. So this may be one key where IR isn't really significant if VLC is in energy balance. I'm glad I didn't read any of this back when I was losing weight and hope all those FFA's that were probably coursing through my veins didn't do much permanent damage!
That said, the sudden cardiac death and NEFA stuff still scares the bejeebers out of me. Again, I would really LOVE to find the caveat that so long as XYZ, it's all good.
I think our best bet is to find what keeps us at a healthy (not necessarily "ripped") relatively STABLE weight, and reasonable level of physical activity. I honestly try not to sweat the small stuff (stress isn't good for you anyway, and I have enough of it from other sources!!)
Thanks for replying. I really appreciate it.
I do have a BG meter. I've never have a low BG episode while on low carb. I did a little test on myself today with a bowl of oatmeal. It's only ~25g carb I know, but I've been on Atkins Induction for the last 3 wks (I'm giving it one last shot.), so that's a lot at one sitting for me. So, 1hr: 148, 2hr: 129. Not great I know, but maybe not bad for having been on induction? I know you're not my Dr. and I don't expect a diagnosis. Just sharing. However, the most striking thing about this experiment was that I was very hungry at 1.5hrs. I made myself wait until the 2hr mark to I could test my bg, and by then I was RAVENOUS. The oddest thing though, was that my stomach was growling like crazy. I realized that in the last 2+ yrs that I've been low-carbing I can't remember the last time I heard it growl. I even did an IF day last week, and I don't remember it growling, at least not like this! It was so strange to hear it. So, maybe carbs do make us hungry, but the mechanism has nothing to do with insulin?
Well, not sure what I'm going to do. I have the problem you mention where I've lost 20 pounds and normalized my BG, but stuck stuck stuck with 20 pounds to go. I'm strongly considering carb-cycling, but I'm not sure after this oatmeal episode. Have to do more experiments. I also have the stomach fat problem you mention in a later post, and it's disturbing to realize a lot of the low-carb celebs have it too.
Sorry for the super-long post. Thanks for your time.
I must say I'm pretty confused too ;-). My main question is if IR is equivalent to impaired insulin signaling on a systemic (all tissue) scale. I really don't like the horrible OGGT-results low carbers get. And this high NEFA-arrhythmia link is scary indeed. If VLC means systemically impaired insulin signaling, it would give us a neat explanation for the massive osteoporosis in traditional Inuit (they were brittle, if I'm correct), as per the article I linked to previously.
There are some seemingly contradicting observations.
Strict 'paleo' seems to massively improve insulin sensitivity (insulin signaling?). Staffan Lindeberg’s results were quite convincing.
The same can be said from calorie restriction and intermittent fasting (whatever the downsides).
VLC seems to make people insulin resistant.
AFAIK all these interventions would logically elevate NEFA’s, right?
Hope this posting comes through. Failed several times.
If I understand your comments correctly you are wondering if the skeletal muscle IR is indicative of system wide IR/messed up insulin signaling, and this is what concerns me. Insulin has functions outside of glycemic/metabolic control.
One thing I tend to think re: Paleos is that they weren't obese or overweight. Thus their released NEFA's - and the NEFA's released during fasting - are not on the order of the elevated levels in the obese. Too late for me to worry over it now, but I really do wonder what VLC did to my NEFA levels back when I lost weight rapidly in 2007.
I was not aware of a link between IR and osteoporosis. The Inuit diet was very rich in O3's which (in at least one article I just found that I'll blog on soon) tend towards promoting IR a bit.
My own experience is that whatever I did VLC'ing I did right by my bones. I had one of those osteoporosis screenings done, and while they're probably not super accurate, I'm in like the 98th percentile for a 30 y.o. woman! Explains at least a little of my density!
The "a carb is a carb" and it's all rat poison theory is ill conceived IMO. Maybe I'm lucky, but this former binge eater is not triggered in the least by carbs these days. The other day for lunch I had a bowl of white rice (about 2/3c. leftover from the hubby) stir fried with a big old handful of sprouts, and a little later two slices of deli roast beef. I wasn't hungry until like 7pm.
At least your BG experience tells you that the hunger you experienced is not due to hypoglycemia or wild BG swings. Curious - what was your BG before the oatmeal?
Let's assume that tissue that communicates through insulin can become insulin resistant. I guess that's about any tissue except RBC's. From the article I send we learn that impaired insulin signaling in bone cells induces systemic insulin resistance and several features of 'metabolic syndrome' in just a couple of weeks. Would it be far fetched to suggest that prolongued insulin resistance in any tissue (be it the liver, adipose tissue, bone cells or even the brain) will adversely affect the whole system?
I have probably missed it in your extensive writings, but have you seen evidence that elevated NEFA's cause insulin resistance, in stead of being an innocent bystander? Many people with stubborn overweight, glucose intolerance, etc. seem to do really well on a paleoish, low carb regimen. If anthing, their glucose tolerance improves. They must have 'elevated' NEFA's, but they get better insulin sensitivity. Or is this a wild assumption (I mean, are they 'secretly' insulin resistant while at the same time showing all the typical improvements usually associated with insulin sensitivity)?
On the other hand there are slim, fit, young people who become severely insulin resistant on a low carb diet. I was shocked by a test done by the Swedish lowcarb doctor Andreas Eenfeldt. He did a prolongued OGTT after eating a typical (high but not sky high carb) lunch at an obesity conference in Stockholm. His numbers were horrible, hovering aroud 8 or 10 mmol/l for hours, if I remember well. My biggest question is: is this (reversible) insulin resistance a bad thing? Will it trigger bone loss and other unpleasant things in the long run?
Let's assume that tissue that communicates through insulin can become insulin resistant. I guess that's about any tissue except RBC's. From the article above we learn that impaired insulin signaling in bone cells induces systemic insulin resistance and several features of 'metabolic syndrome' in just a couple of weeks. Would it be far fetched to suggest that prolongued insulin resistance in any tissue (be it the liver, adipose tissue, bone cells or even the brain) will adversely affect the whole system?
http://www.springerlink.com/content/h7628r66r0552222/fulltext.pdf
http://www.the-scientist.com/article/display/57704/
To provide evidence that this isn’t just a mouse phenomenon, Karsenty investigated the osteocalcin and insulin levels in patients suffering from a disease called osteopetrosis, in which a reduced number of osteoclasts leads to a lack of bone resorption and very dense bones. These patients had significantly decreased levels of active osteocalcin and low serum insulin levels, even though their osteoblastic insulin receptors were intact. This supports Karsenty’s hypothesis that bone resorption is also an important step in insulin’s effects on bone.
More to look into there for sure. Definitely solidifying my impression that insulin sensitivity is important, not lowering insulin.
Low insulin is a good sign as long as it is reflecting excellent signaling. The great question is: does VLC impair signaling????
I'm so sorry for the slip. Ugh, how embarrassing.
It's been interesting. I've decided to "carb-up" to see if I can get normal BG after a bowl of oatmeal. I'm using oatmeal because it's the only carby thing I have in the house, and it all converts to glucose so no fructose to muddy the waters. So after two days I've managed to lose a pound. Could be a fluke, but I could not budge my weight on VLC. If I eat the oatmeal with a protein (eggs, meat) I don't experience the ravenous hunger. Too early to tell anything yet. I guess I can keep you posted. (If you care. Who the heck am I?)
Stupidly I forgot to test my BG right before the oatmeal, but I did test it immediate after consuming and my BG was 61. I have to say it's never been that low normally. On VLC usually it's 80s fasting, and 90s post-prandial (doesn't really matter how long I wait).
I don't know if I have issues with gluten. I think I do have issues with wheat. I get a horrid crick in my back when I eat it. So far no crick, so maybe it's something else in wheat.
I agree!!
Low insulin is a good sign as long as it is reflecting excellent signaling. The great question is: does VLC impair signaling????
Yeppers. The question I seek an answer to. It is odd. The most IR folks seem to respond better to IR-inducing diets. Perhaps this is because they can't process carbs well for energy. But also, perhaps, this is why so many LC'ers "hit a wall" with weight loss, etc. They aren't restoring the proper insulin signaling that SHOULD accompany getting our fat stores below the "fill line"??? The research journey continues .......
I wanted to be sure of my results before reporting, but things are looking good! I gave myself a homemade glucose tolerance test with white rice. It was about 75 grams carbohydrate. I got 123 at 1hr and 109 at 2 hr. I'm so glad I've been able to get normal blood sugars! Another amazing thing is that I have better appetite control eating more carbs. I usually have a serving of some low GI carb with each meal (oatmeal, sweet potato), and a protein (meat, eggs). I never really got the spontaneous appetite suppression on VLC. I was eating at least 2600 cal/day to feel satisfied. If I tried to cut back I just ended up depressed. Eating the way I am now I've cut back to 1700 cal/day and feel better. I've also lost 3 pounds (total including the one I mentioned earlier). Even tho I'm eating a carb at each meal fitday thinks my carb intake is only around 20% of calories. That really surprised me. Well, I have to thank you for helping me get over my carbo-phobia and make some changes that have been really good for me so far.
I'm obviously not a doctor, but my research has me focused on two things where I'm concerned:
1. Maintain insulin sensitivity (it reduces with age :( )
2. Maintain pancreatic function/insulin production
Adequate to even a little excess protein, some carb regularly, and fat to maintain energy balance seems a reasonable dietary strategy to achieve these goals.
Do let me know how this works for you moving forward. :)
I think it is human nature to want to be able to blame someone else for our problems. And while doctors are supposed to be experts upon whose advice we're supposed to be able to rely, us patients must be proactive on our own behalves.
Diets don't really fail, people fail. That's the cold hard truth. Now it is true that certain diets require Herculean efforts to comply with, so it's not really the person's "fault" that they are human, but that is different than saying the diet doesn't work. Most of those cases where the diet doesn't work it is because it is not suited to the person and that person needs simply (yes, not so simple but ...) to find an approach that is suited for them.
Eating to meter is a great tool. Even as a non-diabetic, I found using one to understand how it was my body handled carbs was invaluable for me.
Y'know one thing that continues to bother me is the LC effort to lower insulin levels. Clearly insulin is a beneficial hormone in the body, as demonstrated by all the problems those who lack it entirely (Type 1's) have.
LOL, is 123 at 1hr considered a "spike"? OMG, are doctors actually medicating people because their bg is "spiking" up to 123? I'm appalled and yet somehow amused by this. Maybe blood sugar is the new cholesterol -- the lower the better? Well, I'm using the numbers I was given when I was diagnosed with gestational diabetes during my third pregnancy (in 2008). Those were under 140 at 1hr, and under 120 at 2hr. I know those numbers are a lot lower than the typical goal numbers given to non-pregnant diabetics. There seems to be a consensus on the net that those are "normal" numbers. Not that internet consensus should be my justification for anything. :) I had a few pretty bad bg spikes when I was prego before I figured out things like potato salad is a bad idea, and I should probably never eat pizza again. I think the pizza sent my bg up to the 180s. Now that was a spike! (I had a normal healthy baby, btw. He weighed 8lb, 5oz. The doctor was happy with his weight and his Apgars were 8 and 9.) Anyway, now I'm usually under 120 at 1 hr, and sometimes even under 100. I'm sure the Kitavans probably never go above 85, but I think for my situation I don't care.
Might just be. A year or so back I got a meter to check if I had issues and, of course, I went to various websites to see what "normal" was. I recall coming across an article from early 2000's discussing how they had recently reduced the BG levels for pre-diabetes and diabetes diagnoses by 10 or even 20 points on the fasting level (this was a long time ago so I'm not really sure). There was no explanation as to why, no research cited, not even a lame study taken out of context. This would increase the numbers diagnosed with pre & diabetes when nothing changed about the population. I hate to be a conspiracy theorist, but you just have to wonder sometimes. This reminded me of when some major cholesterol study came down the pike and they lowered the acceptable levels even lower. The subtext was that something like 40% of Americans should be on statins as a result.
Nowadays anyone can get a meter cheap. Just 10 years ago and certainly 20 years ago, most wouldn't even think to do so. Awareness of the dangers of diabetes and elevated BG is one thing, but it does seem we've gotten a bit out of hand with this.
A chronic elevated BG level will lead to glycosylation and the deleterious effects thereof. I think the level for this is somewhere north of 150. That does not mean, however, that an occasional spike for an hour or so over 150 is instantly damaging. I've seen diabetics claim that a single BG reading of, say, 175 will cause permanent damage.
First, I think most people do not get yearly physicals, although I could not find any hard data on the subject. This would mean that most people wouldn't get blood work done with any regularity.
On the off chance they got blood tests as part of a life insurance exam or because of a visit to the ER, doc's typically don't tell people with fasting BG of between 100 and 110 that they are pre-diabetic. If they say anything it usually goes something like this: "Your fasting glucose is alittle high but if you lost ten pounds that would drop right back down into the nineties."
In addition, a fasting BG between 90 and 99 is usually reported as AOK. But many studies show that fasting BG above ninety is an accurate predictor of type 2 diabetes.
On the negative side, Dr Davis motivated me to switch from high-carb to low-carb for a few weeks. That was a sickening experiment and caused me to gain about 5 pounds which I've since worked off via my usual high-carb diet. In retrospect, I think it was the novelty of all the new foods on the low-carb diet that caused me to go crazy, rather than the low-carb itself. I don't really love eggs, for example, but I haven't eaten them in ages. So the taste was new and I ended up eating the whole dozen at once and then returning to the store for another dozen. And so on. The reason I even bothered switching to low-carb was that I had gotten sick while traveling and then upon reading up on my sickness, I came across all this paleo thinking and became paranoid that I was killing myself by eating high-carb, even though I had always been healthy and lean with a high-carb diet.
Though if I were overweight, I would definitely try low-carb. A can of salmon, a dozen eggs, 3 x 10oz packs of spinach and other greens would be my preferred low-carb diet. The advantage of this diet is that it can be bought at any store, so I would be able to clean my apartment of all food and then shop daily until my weight was back to normal, thus removing the problem of temptation to raid the refrigerator.
I currently argue with Dr Davis on his blog about the anti-oatmeal stance. Oatmeal has long been my staple food and I am convinced it is enormously healthy for me, at least when balanced by canned salmon/mackeral/sardines (for omega-3 fatty acids and various other nutrients). The thing to understand about low-carb is that it down-regulates the ability to deal with glucose. Once down-regulated, it takes a few days for the body to up-regulate again. So yes, if you eat low-carb and then take a glucose-tolerance-test or eat a big bowl of oatmeal, your blood glucose will skyrocket. What you have to do is wait a week or so AFTER transitioning back to high-carb before running these tests.
Incidentally, I do not recommend high-carb for anyone who is at all overweight. Stick to low-carb until you are lean and have established a daily exercise program, then switch back to high-carb. Even if your metabolism is working fine, it is quite easy to overeat on high-carb, especially if you are older and hence have reduced metabolism compared to a younger person. And remember that high-carb/low-fat doesn't mean no-fat. There is no such thing as a sustainable no-fat diet. Even a diet of vegetables and brown rice has fat. Overeat on this diet and the body will burn the carbs and store the fat.
I'm beginning to think that as drastic as it seems, a protein sparing modified fast is probably the safest means by which to lose excess fat mass. Not whey shakes, but lean animal protein and some veggies. Unfortunately it is hard to sustain and not a permanent habit change for the long term, so "losers" will be especially susceptible to regain.
My personal belief is that we Americans are an overmedicated society. As a group we tend to want a quick fix to everything. A magic pill to undo the effects of chronically abusing our bodies.
Doctors also tend to look to meds first, lifestyle intervention second in too many cases. Far from ideal.
But if I were a doctor and a patient presented with full blown hyperglycemia, I would want that patient to at least consider pharmaceutical intervention in the immediate term and work with them to make changes that may reduce or hopefully eliminate the need for them in the long run.
I'm ever more convinced that long term VLC diets don't "cure" diabetes. To me, a cure would be re-establishing normal glucose tolerance.
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