Lagt ut av If you haven’t already heard there is a new low carb study out. It shows similar effects on weight compared to a low fat diet over 2 years, but better HDL results in the low carb arm. It’s a really interesting study, but I’ll leave it to others, like Jimmy to elaborate.
Once again this low carb study is from Gary Foster and colleagues. Foster has previously given us this one. Although containing a lot of interesting data the researchers once again insist on only presenting the data as intention to treat with missing data carried forward.
Statistics is definitely not my strong side, and if I’m way off on this one please show me why. And if there is a stat wiz out there who can tell me why this is the right way to present results, please do.
The researchers did do some sort of sensitivity analysis and tried to justify using the entire sample of 307 participants in the final analysis. But it still does not compare to actually giving us the data on the compliers vs. non compliers. A lot of people dropped out of the study. Of the 154 randomized to the low fat group, 49 was not assessed at 24 months. Of the 153 in the low carb group, 64 were not assessed at 24 months.
Now, intent to treat analysis is a perfectly fair method to use. But it means that the results cannot tell us which dietary approach is the more effective. If we want to know which diet causes the greatest weight loss we must look at the data from the participants that actually followed the diet, and only those. What the results of this recent study tells us, is the effect of being put on a diet as opposed to the effect of following one. Is it really so bloody impossible to include data on compliers vs non compliers? As interesting as it is to know the effect of being put on a diet I for one would also like to know the actual effect of following the diets.
Like many other studies using similar analyses, this one also show a regression to the mean, that is the results differ the most at 6 months and slowly merge into similarity as the low carbers eat more carbs, and the low fat group eat more total energy. Whether this is because of the type of analysis and the increasing number of participants discontinuing the treatment is beyond me.
The title of table 2 of the study says is all really, “Predicted Mean Changes…”. But what about the actual change and the actual effect of following the prescribed diet?
Richard Feinman has written this article, illustrating the trouble with using an intent to treat analysis.
Still, Foster has done a good job and provided interesting data. Looking forward to seeing how this study is going to be received.
Pål Jåbekk 
I understand that there are two separate effects that RCTs try to answer:
a) How effective is the treatment qua treatment
b) How easy/difficult is it to keep to the rules of the treatment.
The results of any particular study will mix up (confound) these two effects, and they cannot be separated unless one performs two analyses.
Check out this post
http://www.proteinpower.com/drmike/statins/the-adherer-effect/
and this entry
http://en.wikipedia.org/wiki/Intention_to_treat_analysis
Good luck.
LikerLiker
True Leon. The two effects are often mixed up. I realize there are two different questions to be answered. What I don't get is why the two questions aren't just answered in the same article? They’re both important and interesting questions, but could be answered by adding an extra column in one of the tables.
LikerLiker
The data are not separated because the authors have little scientific expertise. They blindly follow guidelines without applying any common sense. Also, Foster has said in public that they set out to trash the Atkins diet. They know that they will be in trouble if they falsify the data, but as in the first study, they try to put as negative a spin on it as possible. Intention-to-treat always makes the better diet look worse and so usually helps with trashing low-carb. What the study shows is that the conclusions of better controlled, more carefully done work by researchers like Volek and Phinney still show up in a sprawling poorly controlled study. I haven't actually read the whole paper or checked the reference. My prediction is that they do not cite Volek's work. Am I right?
Richard David Feinman
Professor of Cell Biology
SUNY Downstate Medical Center.
LikerLiker
Hi Richard. Good to see you agree. It's a strange scientific practice and I cannot see how it advances our knowledge. Didn't know Mr. Foster had been so blunt about his agenda in the past. It seems that the latest article is a step in the right direction though, overall it seems much less biased. And you're right, Jeff Volek is not in any of the 33 references, nor is Stephen Phinney.
LikerLiker
Pål and Richard,
I thought it was weird to have a TWO YEAR long trial without powering the stats sufficiently to prevent ITT… Academically speaking, two years is an ETERNITY and not cheap.
Aaaaahhh…! Thank you for the disclosures! It all makes sense. I thought it was hilarious that authors noted in the abstract (I haven't read the full article either) that low carb was associated with more 'adverse effects' than low fat.
How about the adverse effects of low fat?
–diabetes
–heart attack
–cancer
–failure and frustration to lose AS MUCH FAT/WEIGHT
-G
LikerLiker
Speaking of disclosures Dr. B G. Just read that Foster recently did a study for Coca Cola which involved giving fortified diet Cola to overweight as a weight loss method. Wonder how that turns out?
In the Sacks et al (2009) study the authors wrote this, “A smaller group of studies that extended the follow-up to 1 year did not show that low-carbohydrate, high-protein diets were superior to high-carbohydrate, low-fat diets.” The studies they refer to are Stern et al and Foster et al, both using ITT analyses thus covering up the real effect. I still don’t understand how the Sacks study got into NEJM. I thought it was a horrible study.
James O. Hill, one of the other authors of the recent Foster trial wrote this in a document for The Sugar Association; “One popular theory indicts sugar and points to foods with a high-glycemic index. However, the theory that dietary sugar equals high insulin levels equals excess fat deposits is unproven and makes little biological sense.”
LikerLiker
I suggest Richard Feinman is being professionally kind to fellow practitioners.
Rather than presenting another table or column of data, upon which they might have to make reference in the abstract, they present the data in a way which justifies a result they are trying to «beat out» of the data!
I'm somewhat of a cynic.
LikerLiker
There is no need to be cynical. All of the other authors have spent a career, up until the publication of the paper knocking low carb diets some in publications, like Hernandez, et al. in a devious and dishonest way. Their conclusion that the diets are equal requires ITT because almost every study that looks at the effects on compliers shows that the low-carb arm is better. I suspect you will see that if we can get access to the data. You don't have to do a special analysis. You plot weight loss of compliers vs. carbohydrate consumed. They give themselves the privilege of not doing that because they are made men and nobody will disagree with them (nobody that wants their grant funded and their paper published).
RDF
LikerLiker
LeonRover,
More crooked mouths?? *haa*
Pål and Richard,
Harv-tards Wm Willet and Mozzafarian and cardiologists (like Davis, heartscanblog) all advise omega-6 PUFAs ~20% daily of diet and saturated fat only 8%.
To me (and you'd probably concur) this is akin to murder, a slow drawn out painful mentally-detained death from either cancer, thromboemblic events or heart failure. Sadly here in the States our tax dollars for Medicare cover the the chemo/radiation for cancer, Medicare D health insurance + drugs and disability from the fallout of these advised pro-inflammatory diets… When can we collectively vote these people off the island? Their dietary advice is literally bankrupting our health and nation's treasury…
Mozzafarian conversely had one of the most convincing impressive results in the U.S. for the clincal benefits in coronary regression with high saturated fats. Sad. Is he a made man? I believe he has clearly switched his brain off…
http://www.paleoforlife.org/article/dietary-fats-carbohydrate-and-progression-of-coronary-atherosclerosis-in-postmenopausal-women.15531663.html
-G
LikerLiker
Like many others in the same situation, it seems that Dariush Mozaffarian has been trying to make the whole saturated fat business go away, by working with trans fats and omega 3.
Still, this is from a recent article:
“Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.” Here http://www.ncbi.nlm.nih.gov/pubmed/20354806
Unfortunately, as you subtly pointed out, Mozaffarian suggests replacing sat fats with PUFA, and not only the o3 type.
And if you think it’s bad in the states you should hear the nincompoops in Norway. When I read the draft for the new Norwegian dietary guidelines I felt something like what, John Stewart felt here (I give up): http://www.thedailyshow.com/watch/wed-august-4-2010/i-give-up—9-11-responders-bill
LikerLiker
Pål,
Actually I meant advised diets of 11-16% o6 PUFA (half of 30-40% fat diet after 8% sat fat deduced, respectively).
I guess anything >> 2-4% o6 is exponentially higher and contrary to our receptors and ancestral background consumption. The epigenetic consequences are SEVERE… Countries like Israel, India and others which have switched exclusively to o6 and limited schmaltz, ghee and other ancestral hard saturated fats have lost their longevity and now see epidemic cancer rates. Women are actually most susceptible it appears.
The estrogen receptor (ER) appears to exhibit a special capability for upregulating linoleic acid (o6), esp in tumours. ERs are ubiquitious nuclear receptors (like VDR, vit D). Perhaps the rare LA in ancestral environments programmed rapid wt gain/inflammation for hibernation IMHO at the end of summer?? There is a practical purpose. Anyway, men have ERs too — this is particularly a problem for excess E1 E2 (not E3) and increasing prostate CA risk. On the other hand, conjugated LA is anti-oncogenic (grassfed lamb/beef/goat, dairy/ghee). BUTTER IS BEST.
http://www.ncbi.nlm.nih.gov/pubmed/12500930
http://www.ncbi.nlm.nih.gov/pubmed/10355854
http://www.ncbi.nlm.nih.gov/pubmed/12163849
I am sorry about Norway. You like Jon Stewart too??! *haa* The hilarious couple at the end CRACK ME UP.
Did Dariush trade the red pill for the blue…?!
SAD!!! His review of the ERA trial strongly suggested the dangers of high o6 — ~3X increased plaque progression (diameter reduction) in women with CAD associated at intakes of 7.5% o6 versus 3.9%. A proposed national 11-16% o6 intake is clearly insane… he knows.
-G
LikerLiker
B.G. So interesting about the o6 tumor growth and ER. Uncertain how humans and rodents differ in these factors. Do you know if there are any populations whos traditional diet was high o6 low o3?
Oh, and yes Stewart fan. Great show!
LikerLiker
Pål,
We are more metabolically complex than rodents and we do not endogenously produce vitamin C, a major antioxidant and anti-angiogenic factor. I dunno…
I have also wondered who may have evolved under high o6/low o3! The Pima Indians and other native N Am descendants? Northern and Eastern Europe and Russian that are mountainous away from marine-based resources?
http://www.ncbi.nlm.nih.gov/pubmed/12690461
Pflugers Arch. 2003 Apr;446(1):42-5.
Evolutionary adaptation of a mammalian species to an environment severely depleted of iodide.
This article provokes thought that some humans can be selected to retain environmental minerals (iodine). Unfortunately in polluted neolithic times this can be a detrimental trait against longevity and survival.
Perhaps natural selection for o3 retention or eicosanoid enzymes (SNPs) which promote higher endogenous o3 has occurred also?
Apo E4 incidence increases with latitude…Old World and New World. Environmental o3 decreases with latitude.
Please consider this: what if saturated fat substituted for the role of o3 in humans going into the northern latitudes (geographically away from o3-rich marine-sources)?
Some of the biological benefits overlap betw sat fat and o3:
–immunoprotection
–increased HDL and particle buoyancy and therefore antioxidant carrying capacity
–ketogenic value, mitochondrial FAO (peripheral insulin resistance can incr with both sat fat and o3 — never could I explain this identical resultant effect though some o3 studies show insulin sensitivity, it's not equivocal to me)
–neuroprotection — even more important in cold northern climates
–??induction of BAT, again vital in frigid north temps (esp no vit D??? contrast with marine sources of o3 which would naturally incl vitamin D)
Very CURIOUS!
-G
LikerLiker
Oooo! So much to think about and so little time.
Thanks for the input. Going to sit in my thinking chair now.
LikerLiker
I have a friend who spent a long time in academic medicine – produce or someone else will take your lab space and produce for you! All hubris, no doubt is REQUIRED to fight off the others nipping at your heels. It is so much easier to have your own space to postulate and prove in the limitless blogosphere.
LikerLiker
Hi Emily.
I don't like it when science turns into a battle requiring you to fight off those wanting to replace you. So, much easier with a blog, and speaking of blogs, I just discovered your great blog! Looking forward to read it all.
LikerLiker
Dr. Feynman:
> Foster has said in public that they set out to trash the Atkins diet.
Could you give me a reference to that public statement? Thanks!
Regards,
Zooko
LikerLiker
Pål,
Another update on this notorious trial… from Mr. Naughton of Fat Head blog.
http://www.fathead-movie.com/index.php/2010/08/30/inside-information-from-fat-throat/
-G
LikerLiker