The first thing to say is that it's extremely difficult to extract any hard data from the study. Many of the results are expressed as derived from "intention to treat" analysis. To appreciate quite how difficult this makes any sort of deconstruction, you have to read Dr Eades on this subject. Much of the HbA1c data are presented as the value before any medication change occurred. A change could be up or down (both occurred) and could have occurred after one week or after 73 weeks on the diet. The HbA1c value from just before the change in medication gets carried forward throughout the rest of the graph of HbA1c that features in the discussion, see later.
But let's take the study at face value. I'll begin with the top section of Table 2.
Now you may be forgiven for skipping down to the carbohydrate intake line where the massive increase from 47.7% to 66.3% is noted. This would be a mistake. First line to note is the SPONTANEOUS drop in caloric intake noted in the vegan group. 1798kcal/d to 1366kcal/d. This compares with the ENFORCED caloric restriction on the ADA diet, which did not alter the macronutrient ratio in any way from the pre study diet. This is where Stephan found the study interesting. I have a couple of concerns about the explanation of the vegan diet providing limited reward which I would need to see addressed before going along these lines:
No one sells a diabeso-genic diet for rats based on starch. There are two main techniques for making rats fat and glucose intolerant. The first is sucrose, the second is Crisco. You can also do it with lard, but that's a rat oddity and I doubt it applies to humans, as far as I can see.
The vegans reduced their caloric intake percentage of trans fats from 2.3% of calories to 1.1% of calories. The ADA dieters didn't. p < 0.0001.
If you want to look at either total fructose or HFCS or table sugar intake comparison between the two groups I'm afraid you will have to ask Barnard for this information, it's not in the paper. But I think it's safe to assume the vegan diet included the advice to consume minimal sucrose/HFCS and the ADA, with it's role in promoting diabetes to maintain medication sales, had some. Possibly quite a lot. Who knows? Well of course, as I said, Barnard knows; but he's not saying. Let's just assume p < 0.0001 again.
I would want these two factors to be controlled for before I would become interested in looking at food reward effects of the relative diets, important though this might be.
You may have noticed that the concept of components described as "a percentage of calories" has already sneaked in.
So next we have to look at that % of calories from carbohydrate expressed as a number of grams per day of carbohydrate, especially on that vegan "high carbohydrate" intervention.
Pre study the vegans were eating 47.7% of 1798kcal as carbohydrate, ie 858kcal or 191g/d. By week 74 of the study they were eating 906kcal/d or 201g/d of carbohydrate (66.3% of 1366kcal).
So the total carbohydrate intake increased by 10g/d. Did you notice that on initial browsing of Table 2? Tee hee.
Two other factors have to go in. Fibre, included in total carbohydrate, increased from 10.8g/d to 21.7g. Most of this was insoluble fibre, ie it literally became vegan cr*p. You know, wipe, flush... Let's see, 201g-11g=190g! Wow!!! I couldn't have asked for the arithmetic to work out that neatly, just a happy coincidence. Made me laugh anyway.
So, is this a high carbohyrdate diet, compared to the SAD? No. NO.
Weight loss. For the later months of the study subjects were weight stable. During this phase the vegans and ADA dieters deteriorate at remarkably similar rates. During the initial few months, when both groups demonstrated a very small improvement in HbA1c, there will have been marked weight loss. We don't know what the calorie intake was during this phase. If it was less than 1366kcal per day with a similar % of calories from carbohydrate this might actually have been a carbohydrate restricted diet!
If we briefly scan the HbA1c graph
it is pretty obvious that the ADA dieters stopped losing weight at 11 weeks and the vegans stopped losing weight at 22wks. End of weight loss is the time at which you would expect HbA1c to stop dropping and metabolic deterioration to set in for both arms of the study. Please note that we have no idea how many patients at a given time point are providing true HbA1c values or how many data points include "carried forward" values before a medication "change". Over 74 weeks 17 vegans actually reduced their meds by an unspecified amount and 10 increased them, again by an unspecified amount. So 17 out of 49 subjects provided "hypothetical" HbA1c values for some unspecified amount of the study period. Go figure. Must have been written by a low fat vegan!
I would be willing to bet that the 17 vegans reducing their meds were all "carried forward" from the first 22 weeks and the 10 increasing their meds were in the >22 week period... You don't generally increase meds in type 2 diabetics during weight loss.
You can't lose weight for ever.
Once weight loss stops and human adipose tissue consumption ceases we are back to starch for diabetics and progressive HbA1c deterioration.
What would you expect?
It is quite clear that healthy humans can consume a very wide range of macro nutrient ratios. If you are glucose intolerant you cannot. Are you glucose tolerant? Are you sure? Russian roulette?
In summary: Any person with diabetes who considers that dropping their HbA1c from 8.05% to 7.71% (intention to treat basis) by following 74 weeks of low fat veganism will help them, is deluded. If they think it is going to get them out of the queue for dialysis, they're wrong. I suppose that weighing 4.4kg less in the dialysis room might give you a better self image, but this benefit might be wasted if you are blind by that stage...
Peter
A couple of add-ons:
Dr Haimoto in Japan produced this result by simply restricting carbohydrate to 137g/d of which 14g was fibre. The study was not intended to cause weight loss and it didn't, what there was was non significant. So this improvement in HbA1c is WITHOUT weight loss. Neat hey? Better end-study HbA1c values would need lower total carbohydrate intake.
Of course Dr Haimoto gives us all of the individual HbA1c plots and of course the individual weight change data. No intention to treat here, just numbers, including the data from the non compliers.
Then we shouldn't forget the Nielsen and Joensson study in Sweden
These people were asked to lose weight (not spontaneous). Note that maximum fall in HbA1c was at the time of max weight loss which occurred at the time of maximum compliance, here are the individual weight loss plots. No intention to treat fudge. Carbohydrate limit was recommended to be at 80-90g/d but some carb creep was noted... Despite this, note the downward trend in HbA1c over the years. Sorry there was no room to extend the graph to the full 44 months.
Oh, and for chopping off the top of the last graph!
31 comments:
"I have a couple of concerns about the explanation of the vegan diet providing limited reward..."
...What are these?
I personally am never "satisfied" without lots of fat: my stomach gets full, but I still want to eat more. Is it simply that with a very high starch diet, it's too difficult to eat enough?
The desire to eat is different with high fat and high carb: with the former, it's hunger; with the latter, it's "addiction." I think Emily Deans wrote about sucrose binges leading to anxiety but not fat (in rats)--to me it works the same with any carb source.
Also, for myself, low fat equals lean mass lost (without huge protein intakes).
Hi Peter, great post. I totally agree about their dodgy reporting of data.
“End of weight loss is the time at which you would expect HbA1c to stop dropping”
Did you mean this literally? Shouldn’t we expect a delay given the much faster turnover (after a diet change) of “weight” [fat mass] relative to “HbA1c?”
Thanks,
Bill
john, I would certainly want the trans oleic acid content controlling for, a simple lipotoxin without function in the human diet. It's hard to see how sucrose content could be controlled for but the wild type mice in http://www.ncbi.nlm.nih.gov/pubmed/14694219 have free access to sucrose/cornstarch but essentially leave it alone, preferring the lard/coconut combo.
Actually, it would be intereting to see what their response to having a fat/sucrose combo available would be in addition to the three macronutrient choice diet they had.
Knock out their BAT and they won't touch sucrose with a barge pole. They are then intensely leptin resistant too... Maratos-Flier also looked at them here http://www.ncbi.nlm.nih.gov/pubmed/9519718 (haven't got the full text for that second paper).
Bill, I agree, but within the limits of the relative infrequency of time points in all of the studies you can't pin this down. Also HbA1c will start to increase as soon as glycaemia deteriorates, even though full effect only shows after several months. To me the main message is that if you have broken your metabolism you will do the best job of patching it up long term with a high fat diet. Weight loss is only useful if you are overweight. Weight loss in already lean people tends to lead to being dead.
Peter
How can one differentiate reducing leptin resistance from food reward?
What if our brains make us sort of anxiously hungry if the brain is blind to the the circulating leptin? The reward system is there for a reason - if leptin is part of it and we screw it up with high trygly and lectins from a high carb diet - it would be broken - but is it permanently?
A large percentage of the "calories" in a normal complex carbohydrate based vegan diet are unavailable and simply get flushed down the toilet bowl.
Young females, in particular, love these vegan diets as they can eat a lot of food and still lose weight (despite eventually developing severe malnutrition).
Basically veganism is simply gradual starvation. I've never seen a dedicated long-term vegan who isn't skinny and almost devoid of muscle.
I think we just eat until we get all the nutrients we need. Then we stop. How this works nobody knows. In 50 years we will probably be no nearer to the truth.
Unfortunately medicine has wasted the past 70 years on looking for magic bullets to cure lifestyle diseases. The process is an exercise in utter futility. No magical pill will ever prevent or cure obesity, diabetes, schizophrenia, CHD, cancer, MS etc. There is simply no substitute for vigorous exercise, a meat-based diet and strong social networks.
I have heard from thousands of people with diabetes over the last five years. I hear about all kinds of things they've done that have improved their health. None report that they normalized their blood sugar with a vegan diet. The only people who have emailed me about the wonders of vegan diets are people working for PR agencies.
Barnard is not a diabetes expert and has no training in endocrinology. He does not treat people with diabetes. His advice is driven by a religious belief not medical expertise. It's shameful the way he's been able to manipulate the media.
"weighing 4.4kg less in the dialysis room might give you a better self image, but this benefit might be wasted if you are blind by that stage..." Brilliant! Too many folks confuse "looks" with "vision." Nice the way you worked in a "barge pole," too. Another great post. Thanks.
Jenny - Thanks for your comment. Clearly, Barnard is well done the "Road from Foolishness to Fraud."
Hi karl, I guess you could describe Crisco as a high reward food, although I'm not sure it would act this way without carbohydrate, so maybe I'm misunderstanding food reward...
Of course you can view the whole debate from the vantage that modern food is too rewarding and we only see metabolic syndrome because this is intrinsic to those over rewarding foods. If lean steak was utterly rewarding compared to fatty steak or Twinkies we would have a different "metabolic syndrome" based on excess protein in take and hyperammonaemia. No doubt there would be many shades of "rabbit starvation" for the nutritionists to recommend overall caloric moderation for and us hard core healthy eaters would be yelling for protein restriction to less than 70% of calories, or (gasp) less than 30% and be being described as quacks (don't you know your brain needs "xxxx" amino acid to function etc). All potentially hysterical.
But we're where we are today and I still consider the issue is metabolic rather than behavioural, but where's the difference, ultimately?
blogblog, I read a detailed account of a young, female, post-anorexia vegan eating a documented 8000kcal per day of mostly leaves. Quite well substantiated. The mystery to me was how she managed to get off the loo for long enough to eat this much in the way of leaves. She was, needless to say, very thin. And probably very malnourished. Probably had a sore bottom too.
Jenny, he has blood on his hands.
Peter
Pete B, you're welcome
Oh, and before anyone calculates exactly what 8000kcal of spinach looks like I think there were some lentils going down the loo too. Probably whole! It was a long time ago.
Peter
I wasn't going to calculate it, but then I saw it was 8000 kcal not 800 kcal so I just had to for grins.
8000 kcal of spinach is something like 77 lbs and 9.5 cubic feet.
I certainly hope there were lentils involved.
"I read a detailed account of a young, female, post-anorexia vegan eating a documented 8000kcal per day of mostly leaves. Quite well substantiated."
Veganism is a religion. You just have to see 30bananasaday.com. Its really sad that people actually think that eating 10kg of fruit per day is healthy. Almost as crazy as those who think that eating lard is heart healthy :).
Hi, Peter!
I've met a reference to this study (on Keto diet for epilepsy treatment) in a debate on atherogenic effects of ketogenic diets. From an abstract:
At 6 months, the high-fat ketogenic diet significantly increased the mean plasma levels of total (58 mg/dL [1.50 mmol/L]), LDL (50 mg/dL [1.30 mmol/L]), VLDL (8 mg/dL [0.21 mmol/L]), and non-HDL cholesterol (63 mg/dL [1.63 mmol/L]) (P<.001 vs baseline for each); triglycerides (58 mg/dL [0.66 mmol/L]) (P<.001); and total apoB (49 mg/dL) (P<.001). Mean HDL cholesterol decreased significantly (P<.001), although apoA-I increased (4 mg/dL) (P = .23). Significant but less marked changes persisted in children observed after 12 and 24 months.
I wonder what's your take on this?
I think the problem that modern food is actually very "unrewarding". It has so little nutritional value that we must eat huge amounts of empty calories in a futile attempt to get adequate essential nutrients. Sugar has no nutrients (except calories) so in theory and practice it should have no ability to satisfy our appetite.
Yet highly nutritious foods such as liver are obviously extremely "satisfying" because we only eat small quantities of them.
@blogblog "I've never seen a dedicated long-term vegan who isn't skinny and almost devoid of muscle."
I'm not a vegan, nor do I advocate a vegan diet. But if you've never seen a muscular long-term vegan, you haven't looked around much. I know plenty of muscular long-term vegans. (And plenty of complete wimp vegans, too.)
If there's nobody in your neighborhood, just Google "vegan bodybuilder."
I can tell you one thing, though: the vegans amongst bodybuilders really pay attention to their diets and make sure they stuff up on protein powders (mostly pea protein, although hemp is becoming popular).
What I've to see is a muscular long-term raw foodist.
Peter,
I'm an Internal Medicine doc who aggressively integrates LCD in managemnt of DM, HTN, CAD, etc. I've come to believe "food reward" or "food cravings" as operant conditioning.
Many patients with broken metabolism have disrupted autonomic functioning with decreased cerebral perfusion due to sympathetic withdrawal and baroreceptor dysfunction.
Consumption of processed carbohydrates leads to a temporary surge in sympathetic discharge, increased cardiac output and a release of catecholamines all which serve to temporaily improve cerebral blood flow and make patients feel better.
I can dramatically reduce craving or "food reward stimulus" by increasing their salt intake. As you know, this will increase intravascular volume and also improve cerebral blood flow. I believe the same phenomena is responsible for a pregnant women's craving of pickles and ice cream (salt and processed carbs) to manage with the common relative hypovolemia of pregnancy.
I perform autonomic testing on the majority of patients I work with (most sick from insulin resistance) and the vast majority have a weakened sympathetic autonomic functioning during 5 min standing test that leads to orthostatic intolerance and poor cerebral perfusion.
The simple test to see if this is at play is to have a patient drink a cup of chicken broth 3 times a day and see how quickly their cravings for carbohydrates disappears.
@David.
I googled "vegan bodybuilder" and came away totally unimpressed. Most of them looked more like triathletes than bodybuilders. Few of them appeared to weigh any more than about 75kg.
Dr. N,
Salt is a dopamine stimulus, so I don't know how it would reduce cravings. It is more likely to increase them.
Salt causes a reward response in the limbic system because we never had it as we evolved. We were forced to search for it and load up when we found it, therefore it is labelled "good" by our brains, just like sugar.
I found that taking out salt for a few weeks made me crave it much less (and hence the foods it was loaded with), and that when eating in mixed company, I would find things very salty to me which were not salty to anyone else. I think this shows my reward sense is becoming more sensitive.
@Gunther,
there is an old food technology saying "salt only enhances the flavour of salt".
People become accustomed to certain salt intake and readily notice higher or lower levels than they are used to. However most people can become quickly accustomed to very high or very low sodium intakes. (100-10,000mg/day).
Personally I absolutely hate salty foods like bacon, asian sauces or salted peanuts.
@Dr N,
so your are an internal medicine doc now? Weren't you telling us recently that you are an HIV/AIDS researcher?
Consumption of processed carbohydrates leads to a temporary surge in sympathetic discharge, increased cardiac output and a release of catecholamines all which serve to temporaily improve cerebral blood flow and make patients feel better.
Strangely enough my exercise physiology textbooks said the exact opposite. They said that hypoglycemia causes a surge in cathecholamines to mobilise glycogen and FFA. This typically results in feelings of stress and can cause anxiety attacks. The simplest way to treat this is by eating a small amount of carbohdrate.
I can dramatically reduce craving or "food reward stimulus" by increasing their salt intake. As you know, this will increase intravascular volume and also improve cerebral blood flow..
Have you been nominated for a Nobel Prize for this brilliant discovery?
Most of the fat people I've seen have a very high salt intake. Processed carbohydrate foods are chock full of the stuff.
The simple test to see if this is at play is to have a patient drink a cup of chicken broth 3 times a day and see how quickly their cravings for carbohydrates disappears.
Why wouldn't they just put a bit of extra salt on their food?
@blogblog Well played. I was getting sick reading that from Dr N. Its time to open a biochemistry book and not go to a weekend seminar selling BIA's or HRV monitors. The QUILT (Dr K)
Hi Peter, those BAT-less mice are really something!
Regarding the relationship between HbA1c and body weight, what do you think was happening in the 90ug BID group between weeks 39 & 52 (fig 1, PMID: 12610038)? A glitch? oddly enough the same thing happened here: fig 1, PMID 11919132 (so in both type I and type II diabetics). I’m happy to chalk it up to ‘chance,’ just curious if you thought otherwise.
Thanks, Bill
Bill,
I can't see that we have any information in either study looking at food intake. Amylin clearly slows glucose uptake and suppresses hyperglucagonaemia, probably suppresses appetite. The effect under the lethal ADA diet is very modest, certainly compared to not eating some sugar. But if I was a type one with HbA1c of 6% on LC I might be interested... Am I missing something?
Peter
Gunther gather - I generally agree but in patients with autonomic dysfunction, they have poor cerebral perfusion due to baroreceptor function. The salt in this case increses intrasacular volume and improves their hemodynamics. Easily measure with orthostatic bp/pulse measurements.
BlogBlor - testy aren't we. I am an Internal Medicine specialist who has cared for HIV patients for 20 years.
The salt phenomena I describe is the exact reason why the updated Atkins encourages patients to drink chicken broth (i.e. salt) a few times daily for the first few weeks until autonomic function recovers with lower carbohydrate intake. I don't think I deserve the credit but maybe Drs. Westman, Phinney and Volek do.
@gunthergatherer
That's Stephan Guyenet nonsense.
Dopamine prevents metabolic syndrome, so any dopamine agonist/stimulus will result in decreased eating behavior. Your logic is informed by poor prior understanding, which in turn is informed by idiots like GUyenet.
The fact that fat people are dopamine insensitive does not suggest that fat people are food addicts. Yes, meth addicts are dopamine insensitive, but for TOTALLY different reasons than are fat people.
Giving fat people more dopamine helps them to not be fat people anymore, which is not the expected outcome of a supposed "addict" chasing a dopamine high.
It seems that compulsive eating and obesity is the result of having no dopamine sensitivity... and this is true REGARDLESS OF HOW the dopamine insensitivity develops. Low dopamine is a powerful sign to the body to prepare for starvation. Dopamine along with melatonin are seasonal indicators and integral in controling hibernation.
These dumb dumb idiots like Guyenet and other researchers take some isolated findings and jump the grand canyon with it.
That the obese lack dopamine sensitivity doesnot mean they ate their way there.
Remember: drug addicts of any kind become obese and overweight and eat a lot more after you take them off their drugs. This is purely an effect of dopamine deficiency. The addict got there by burning out their dopamine receptors. The obese person got there by very different mechanisms (I will speak of this in the next response). It is SPECIFICALLY dopamine insensitivity and not any kind of personality deficit/addictive response that causes the over eating behavior.
The same over eating/weight gain can be produced by giving a normal person zyprexa or haldol (dopamine receptor blockers).
Watch as they become apple shaped, overweight, diabetic, demonstrate emotional apathy and fatigue and want to eat ALL THE TIME.
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