Does the Atkins diet damage blood vessels?
Today I’ve been inundated with comments, emails and even a phone call or two about the ‘study’ that hit the news this morning allegedly showing that the Atkins diet causes blood vessel damage, and increase in ‘bad’ cholesterol and increased levels of inflammation. I figured I would take this opportunity to describe how this kind of information gets out there and discuss this ‘study’ in particular.
To begin with, this isn’t really a scientific study published in a peer-reviewed journal. It was a brief presentation (about 15 minutes including questions) made at the annual scientific meeting of the American Heart Association in Orlando, Florida a couple of days ago. To better understand where presentations like this one fit in the hierarchy of the scientific world, let’s take a look at how these huge meetings are organized.
The annual Scientific Sessions of the American Heart Association is an enormous meeting with thousands and thousands of attendees. This year’s meeting, which is still going on, is being held at the giant convention center in Orlando, Florida. When the organizers of these kinds of meetings start working on putting them together – which they do years in advance – they begin to contact all the big guns for the major lectures. These lectures are presented during the prime times of the conference when nothing else is going on and they can be attended by all attendees. These lectures held in the huge auditorium are usually by well-known, established researchers who present the data from many years of their work on specific inquiries.
Scheduled in around these giant lectures are concurrent meetings, which are held in small conference rooms holding 50-60 or so people. (The photo at the top of this post shows the typical size of one of these sessions) These smaller lectures compete with other lectures taking place at the same time. Usually there are four or five sessions going on at once, which is a major pain if you’re an attendee because invariable two lectures you want to see are going at the same time. (Fortunately, in our case, MD can go to one and I go to the other, so it’s not so bad.) These lesser presentations are often, but not always, made by graduate students or newly minted Ph.Ds or physicians doing postdoctorate work.
At the bottom of the food chain in terms of importance are the poster presentations. These are usually held in a large room and involve a bunch of people with posters describing work that they have done or research in progress.
In between the poster presentations and the concurrent lectures are oral poster presentations. These are lectures about work in progress or small or preliminary studies that have been done but haven’t been published. The ‘study’ in question is an oral poster presentation.
When the organizers of these meetings are in the preparation stage they send out a call for abstracts. They get inundated with abstracts and arrange them sort of in terms of significance with the most interesting or scientifically significant ending up being presented as a concurrent lecture. The next down the list are the oral poster presentations, then finally the posters.
The important thing to understand about these presentations is that they are not peer reviewed as they are if and when they show up in a scientific journal. They are sort of peer reviewed on the spot in the sense that other researchers familiar with the specific field ask questions of the presenters or of the people with the posters. But that’s it. There is no scientific review of the data as there is when it is published in a journal. So people can present all kinds of data with no one looking it over other than the folks who ask questions. And sometimes the exchanges at these meetings can become spirited to say the least, which means that those lecturing are often present data much at odds with what other scientists have found doing the same kind of studies. That’s why it’s always good to take anything that comes from a meeting like this one with a huge grain of salt.
If you take a look at the monster program for the 2007 Scientific Sessions of the American Heart Association (click here) you can find the presentation in question on page 407. It is session #3610. You should roam through this program a little just to get a feel for the scope of a meeting of this size and to see just how much is going on at once, which puts perspective on any given oral poster presentation.
These giant meetings are open to the press, members of which get these huge programs just as do the scientific attendees. The folks with press passes go through these programs looking for lectures that they think will give them a headline. They don’t care how insignificant the talk is, who is giving it, whether it’s a poster or an oral poster presentation – they are looking for headlines. And what better headline than that there is a problem with low-carb diets or even better, the Atkins diet itself.
So the stage is set. I would imagine that of the 30 or 40 people (if that many) who attended this talk a large number had press passes. These media types stay after and talk to the speaker to get a few quotes, then head off to the press room, dash off a few hundred words, send it to their service, and head back off for another headline-grabbing talk (or the bar).
Now that you know the genesis of the news report about this oral poster that many of you have read and maybe worried about, let’s take a look at the study itself.
I emailed the publicist for the University of Maryland Medical Center for an abstract of this talk, and he kindly sent it to me within minutes. (I’ve converted it to PDF for you: miller-2007-aha-abstract-diet.pdf.) Remember, this is all there is. Just an abstract, not a real paper. We can tell only a little about what really went on in this study. But let’s take a look.
The people doing this study were obviously tired of hearing about the supremacy of the low-carb diet as a weight-loss tool, and they probably didn’t want to do yet another study comparing the low-carb diet to the low-fat diet for weight loss or lipid improvement or blood sugar normalization or blood pressure lowering because they knew what that outcome would be. Those studies have been done again and again and the low-carb diet always comes out on top. So, these researchers decided to take a different tack.
They wanted to see what happened when subjects stayed on the diet after reaching maintenance, so they took 18 subjects (they started with 26, but only 18 made it through the entire study) and put them on one of three diets: the Atkins diet, the Southbeach diet or the Ornish diet. The subjects stayed on one of these diets for 4 weeks, then followed their normal diets for 4 weeks, then went on another of the three diets for 4 more weeks, then off for 4 weeks, then on to the last of the three diets for 4 more weeks. But the researchers didn’t put the subjects on the weight-loss versions of these diets, they put them on maintenance versions. They did this by weighing the subjects at the end of each week and adjusting their caloric intake so that they neither gained nor lost weight.
By keeping the weight of the subjects stable, any changes wrought by the various diets could be attributed to the diet and not to the lost weight. Many people believe the changes brought about by low-carb diets occur not because of the diet but because of the weight loss the diet induces. And since in most studies subjects on the low-carb arm lose more weight than those following low-cal diets, it seems reasonable to suppose that it is the lower weight and not the diet composition that results in the better lipids, normalized blood sugars and lowered blood pressure commonly seen in the low-carb group.
In this case the weights stayed the same for all the subjects during the various diets, and as you can see from the abstract, the LDL levels went up (although not significantly) in the Atkins group while LDL levels dropped in the other two groups. The abstract says that the researchers drew blood at the end of each 4 week phase on the different diets, and I assume that they also drew blood at the start of each 4 week dietary trial, but the abstract doesn’t say. For all I know, they could have drawn blood for baseline values at the very start of the study and compared the lab values at the end of each 4 weeks to this baseline number, which would make the later numbers suspect. This is one of the problems with ‘studies’ like this one. These questions would all have to be answered before such a study could be published in a peer-reviewed journal. But in a conference, pretty much anything goes. It would be left up to an attendee to ask such a question.
Along with the LDL levels, the researchers also looked at a number of fairly arcane measures of inflammation: ICAM2, SELL and SOD1. As far as I know, these are not lab studies that the average doctor can order, but are ones that are done in research facilities for research purposes. In any case these indicators went up on the Atkins diet and stayed the same on the Southbeach and Ornish diets.
Finally, the researchers performed a brachial artery reactivity test (BART), which is a somewhat controversial but nevertheless commonly used test to measure endothelial function. (About halfway this old post is a description of how BART works. If you want a more detailed explanation with a discussion the controversial nature of the test, read this full text article.) As to the outcome of BART, the abstract simply reports the following:
BART testing revealed a significant inverse correlation between flow-mediated vasodilation and intake of total fat, saturated fat and monounsaturated fat.
We’re not told if this correlation holds irrespective of which diet the subjects were following or if these were the numbers while they were following the Atkins diet. From the wording of the abstract one would have to think that these values were reported for all the diets. If so, then the researchers have extrapolated from these numbers that the Atkins diet causes more endothelial dysfunction simply because it contains more fat and certainly more saturated fat than the other two diets.
Based on the abstract we find that
In the absence of weight loss, the high fat Atkins diet is associated with increased LDL-C, reduced endothelial vasoreactivity and increased expression of biomarkers of atherothrombosis. As such, these data suggest that isocaloric conversion to the Atkins diet may negatively impact cardiovascular health as compared to the South Beach or Ornish Diet.
Now, let’s probe a little deeper. And we don’t have to get very deep to see a major flaw in this study.
Before we get to the major flaw, though, let’s look at the LDL changes. As far as I’m concerned, they are a big Ho Hum. I mean, who really cares? How many studies do we have to look at to know that when you cut fat from the diet LDL levels decline? We already have dozens showing us this same finding. Dozens of other studies show us that when fat, particularly saturated fat, is increased in the diet that not only do LDL levels rise a little but HDL levels rise a lot. (I posted about this in the past.) So what little risk we might seem to accrue because of increased LDL levels is more than offset by the greater increase in HDL levels. It even gets better. The majority of studies have shown that when LDL levels increase due to high-saturated-fat, low-carb diets, the LDL particle size increases, making the LDL non-atherogenic. And while LDL levels fall with low-fat, high-carbohydrate diets, the LDL particle size decreases and becomes the small, dense type, which is highly associated with cardiovascular disease.
So, this study tells us that when the subjects went on the Atkins diet their lipid profiles actually improved as compared to the other two diets. Why didn’t the researchers just say that? One wonders. One also wonders why – if they went to the trouble and expense to check ICAM2 and the other markers of inflammation – they didn’t bother to check HDL levels or LDL particle size, especially since LDL particle size is lipid parameter that has the strongest correlation to the development of cardiovascular disease.
Back to the major flaw. The abstract doesn’t say how much these subjects weighed. So we can only assume. Let’s assume that they were average weight and required 24oo kcal per day to maintain their average weight. While these subjects were on the Atkins diet part of the study the abstract tells us that they were consuming 50 percent of their calories as fat. Let’s think about this for a minute and do a few back of the envelope calculations. Fifty percent of 2400 calories is 1200 calories. So 1200 calories were fat and 1200 calories were other than fat. Since other than fat means carbs and protein, that means that the other 1200 calories were divided between these two macronutrients. If we assume that 20 percent of calories were protein that calculates out to about 120 grams of protein per day, which is a fair amount and probably more than they actually got. But let’s assume 20 percent. That leaves 30 percent of calories as carbohydrate. Thirty percent of 2400 kcal comes out to 720 calories as carb. And since a gram of carb is 4 calories, dividing it out gives us 720/4 or 180 grams of carb per day. Does that sound like the Atkins diet to you?
Let’s give the researchers the benefit of the doubt and say that they had the subjects on 30 percent protein (180 grams), which I doubt because they would have been scared to death to give someone 180 grams of protein. But let’s assume they bucked up and did it. Running the same calculations on 20 percent of carbs gives us 120 grams of carbs per day – that’s a full 24 teaspoons of sugar’s worth of carbohydrates per day. Or two potatoes and a serving of pasta. Is that the Atkins diet?
See what I mean. It was a flawed study. I already linked to this post above, but it discusses the same issues, i.e., blaming a lab finding on saturated fat when the diet is full of carbs.
What do we care that a low-carb diet showed an increase in inflammation and worsening endothelial function when what was tested wasn’t really a low-carb diet?
In summary: no complete study, no peer review and no Atkins diet. Yet it made the news big time.
Now that you know the story, go back and read the press report of this oral report of a poster. See if your take home message is any different now.
Oh, and one other thing. According to the abstract the study started out with 26 subjects, but only 18 completed it. That’s a dropout rate of over 30 percent. One wonders why these subjects dropped out? And from which dietary protocol? It would be interesting to know, but I can make a pretty good guess.
Dear Dr. Mike,
I am living proof that Atkins and Protein Power work. After years of eating just like the ADA recommends, I GOT the Type II diabetes. Even though I didn’t even eat sugar. It was all the whole grains that did me in – that, and not enough fats!
I’ve been lowcarbing for 8 months now and lost 30 pounds. At 49 I feel great. My insulin levels dropped by 50 %. I also managed to bring my blood glucose down from 310 to around 120. That’s still not it, but it’s close, and I used no medications so far.
But I seem to have a problem with inflammation: I have another 50 pounds to lose yet my weight won’t budge. I would also like to get rid of my BP medicine, but to my dismay, after 13 years of perfect control, my BP is on the rise. There are days when I don’t feel so good. I suspected inflammation and had my CRP checked – it was 300 % the normal level. That’s when I found your blog, read about the inflammation and started IF. After 3 weeks , I feel fine (I eat just one meal on workdays and 2 meals per day during the weekend). BUT: I gained 4 pounds and my CRP got worse (it’s 500% the normal level now). What could be the reasons? I eat a lot of saturated fat (raw butter and coconut oil) but it’s all organic. Also, my one meal per day is no binging, and I still stay LC all the time.
I read about the Anti-Inflammation diet by Dr. Monica Reinagel and she seems to think that saturated fats and some other foods are inflammatory. It’s quite confusing. I believe in LC and that fats are good. What could be the reason that LC eating – which suits me so well -and IF – which I easily adopted from day one – does not seem to be working for me and is not diminishing my weight, my inflammation, my blood pressure and my blood sugar?
Thanks for your valuable thoughts and best regards from Europe, Xenia
Hi Xenia–
I couldn’t begin to tell you what’s going on from the history you gave me. You could have an inflammatory process taking place that has nothing to do with your diet. But I don’t know because I haven’t examined you. I would suggest that you see your physician and discuss the situation with him/her. There are a number of tests you can have done that will uncover an inflammatory process at work that you may not be aware of.
Keep me posted.
MRE
The problem with the mainstream media is that they do not seem to feel the need to check the facts. Rather, they look for ways to sensationalize any claim in their headlines and then amplify it to fit their own biases by then getting pseudoscientists to comment on it and reinforce the message.
Precisely!
Here’s the latest attack on low carb.
Protein diets not so good
Tuesday November 13, 2007 (2108 PST)
http://paktribune.com/news/index.shtml?194471
A few excerpts.
“There are no long-term studies of these high-protein diets,” she says. However, scientific evidence suggests that the diets carry “great potential” risk of heart disease as well as problems for the kidneys, bones, and liver, she says (Alice Lichtenstein, DSc, a professor of nutrition at Tufts University).”
“A popular premise of high-protein diets is that excess carbohydrates cause elevated insulin levels, which in turn, promotes storage of body fat, according to the study.
Supporters of high protein diets say that the high amount of protein and fat relative to carbohydrates helps reduce insulin levels. The researchers counter, however, that protein stimulates insulin secretion, and changes in calorie intake do not influence insulin action.”
Inference: Protein is the same as carbohydrate.
If the preceding quoted statements are not deceitful then nothing is. No one is going to convince me that the authors don’t know the true facts of the matter.
Either they’re stupid or they have an agenda. Who knows which?
Cheers–
MRE
Thank you for your reply. I am aware you cannot diagnose me from overseas … I wish you could. But talking to doctors following official doctrine is so useless. I went to see my personal physician yesterday – she’s such a nice lady, but she knows less than I do. When I mentioned inflammation she thought I could try a rheumatologist …
She also thought my high CRP was nothing special.
When I mention my high protein diet to any doctor, they go: Aha! But I am sure meat and natural fats are not inflammatory. For the first time in my life my food feels so right. I have no cravings even though I eat only once per day now and that one meal is not excessively big. Most days I hardly eat any carbs. I eat an apple maybe twice a month and if I do eat any carbs, they come from raw vegetables and partly from dairy.
Well, the only thing I can do is muster on and see what happens. My insulin has come down beautifully, so my weight has to as well, doesn’t it? And when the weight comes down, so will blood sugar (I still have some 20 % to go) and my BP.
Hi Xenia–
As the weight comes down so should the blood sugar. It doesn’t always, but it usually does. I’ll keep my fingers crossed that it does in your case.
There is a new study that will be published in a couple of weeks in a prestigious journal showing that low-carb diets containing meat and saturated fat reduce inflammation more than do low-fat diets. I’ll post on it when it’s no longer embargoed.
Cheers–
MRE
Sorry, I just forgot to add one thing:
Maybe toxins from the fat that I lost so far (30 lb) are now circulating in my blood and causing or furthering my inflammation?
I read that in many of the studies where scientists found meat and animal fats “pro-inflammatory” did not distinguish between industrially raised meat and truly organic, pastured meat. This could account for some negative reports on meat since not only is corn-fed beef actually second-generation sugar but it also contains pesticides, hormones and other harmful stuff. Plus, it contains arachidonic acid which indeed IS inflammatory.
I would have suggested the toxin release from the fat loss, but I didn’t know your actual history, so it would have been speculation on my part.
Actually, the new study I mentioned in the answer to your last comment demonstrates strong evidence that arachidonic acid is not necessarily inflammatory, an idea that will have to change my thinking. But it’s pretty difficult to argue with the data in this paper.
Cheers–
MRE
R Tamesis, sensationalism is why Atkins was alway invited onto national talk shows to debate and the Eades almost never. Atkins had a tendency to get confrontational on occasion, which fed right into the controversy that TV producers know gets bigger ratings. The Drs E on the other hand always remain informational instead of confrontational so they’re rarely invited on.
Once I mustered up the courage to do low carb, I began learning more and more about the truth. I know of cultures that have lived traditionally low carb lives that were, by far, the most extreme low carb lifestyle one can imagine. Yet, they had remarkable health. I learned about insulin stability, cancer prevention,glucagon, the mechanics of our precious organs. It is a good thing that I grew in my knowledge about low carb as a whole. I say this because of the way the “experts” want to dumb us down.
I have been a happy and healthy low carber for 5 years this Thanksgiving and I have not looked back despite the “sky is falling” warnings. I have medical training as a medical assistant and IV technician so I trust my brain’s ability to sort things out.Dr. Mike thanks for not dumbing me down.
Thanks,
Mary
It’s my mission to not dumb anyone down.
Cheers–
MRE
This is very late in coming, but I had to relay what I just heard Dr. Dean Edell say during his daily one minute radio segment this morning.
He quoted from this study without any qualification as proof that Atkins was an unhealthy diet!
He has always been strongly anti-Atkins, but the way he used this study makes me seriously question his motives and qualifications for reporting science.
It’s pretty apparent that he has a substantial bias against low-carb. It’s sad, though, that he would parrot that idiotic study without a little more looking into it.
Cheers–
MRE
In your opinion do statins have the capacity to alter the distribution of LDL particle size toward the large, fluffy type, like low carbing does? I’ve done some digging around on PubMed and found a handful of studies that seem to indicate they don’t.
My 48 yo husband started on Crestor about 4 years ago, and I’ve been fighting with him about it ever since. He has no family history of heart disease, no health problems, etc, but his dr. thought his cholesterol was a little too high. I think it’s criminal a guy this young, with no preexisting health problems, would be put on a statin.
He realized a week ago that he’s developed some hearing loss, and I’m worried it’s because of the Crestor, so am back in full attack mode again.
I hope to show him a number of studies linking small LDL particle size to heart disease, plus studies showing that statins (esp rosuvastatin) have no effect on particle size. He only believes what he reads in the media, so this whole ordeal has been incredibly frustrating.
Hi Amanda–
The literature (at least that which I’ve read) is inconclusive as to whether or not statins reduce LDL particle size. I’ve read a few papers presenting opposite viewpoints. If I were to make a bet as to how it will ultimately shake out, I would bet that there wouldn’t be a reduction in particle size with statins. But I could be wrong.
See if you can get your husband to read Lipitor: Thief of Memory. That might make him take a different view.
Good luck.
MRE
Hi Dr Eades
This is a very late reply, but I just found this post from Adam C’s blog.
First thank you very much for posting about this. I haven’t had time to dig into it like you have, but I’ve been meaning to because it is of important to my current research.
I’m Cassandra Forsythe, one of the et al’s in Jeff’s lab. I was the team leader for this study that Adam has mentioned, and know that the responses are real.
However, I must point out that although our study did show reduced inflammatory markers, and it was truly low-carb versus a healthy low-fat, it was a weight loss study, whereas this abstract is weight-maintaining. So, some of our responses may have been a result of the great weight loss that our low-carb subjects had.
Now, I’m not saying that the same things wouldn’t be seen if it was weight-maintenance and true low-carb, but this is a point to keep in mind.
Currently, I am working on my dissertation to answer this question. I’m conducting a low-carb weight-maintaining feeding study (i.e. I cook and prepare all the food within the exact guidelines of a low-carb ketogenic diet) with a comparison between high SFA vs, high MUFA plus n-3 PUFA. The end points are the same inflammatory markers measured in our previous work, plus insulin sensitivity and blood fatty acid composition. It would have been nice to do BART again (we’ve done it before), but there just wasn’t any room (or money). The overall purpose is to determine if there is an ideal fat composition of a ketogenic low carb diet, or if it doesn’t matter due to the restricted nature of insulin-provoking carbs. The results will be very exciting and hopefully will be available in the next few months. Currently, I still have no idea what to expect, but know that this study will stimulate a lot more work and interest in low-carb research.
Thank you again. Happy Holidays. Best, Cassandra
Hi Cassandra–
Good point about the possibility of the anti-inflammatory results being due to the weight loss and not necessarily the low-carbs. My own bias is showing a little.
I’m really excited to see the outcome of your low-carb weight-maintenance study. I think you guys are doing the best low-carb science around. Keep up the good work. And keep me posted. I don’t want to have to wait until it’s published to find out what happened.
Happy Holidays!
Cheers–
Mike
Every time I’m sent to this site, as I was today, I am amazed that anyone would take you seriously. I don’t pay much attention to doctor blogs which are covered with ads for unproven methods and products, anymore than I do to the study you have deconstructed for us.
Thanks for stopping by. Your comment confirms everything this book explains.
Cheers–
MRE
Dear Dr. Eades,
I hope I’m not asking you a question that was covered elsewhere. I apologize if I am.
Are you aware of any evidence, be it published or otherwise, that shows a regression of arterial plaque due to low carb dietary influence?
It’s something that I often wonder about, personally, and it often comes up when I tell people that I think a lower-carbohydrate diet can be heart healthy.
I’d appreciate it greatly if you could direct me to such data or share some of your experiences from “the field”.
Thanks for your wonderful blog and your time and consideration.
Kind regards,
John Paul
As far as I know, John Paul, there has not been a human study showing this. There is some work with dogs that I’ve read showing that increasing insulin increases arteriosclerosis, and then reducing the insulin makes the plaque go away. But nothing like that in humans. Dean Ornish was involved in a couple of studies a decade or so ago that purported to show that his extremely low-fat diet ‘reversed’ heart disease, but the studies were kind of bogus. And the two groups studied didn’t just differ in diet, but in a whole host of things. I would love to do such a study, and am working on getting involved with a facility where I can. I’ll keep everyone posted.
Dr. Eades,
April 2009: The study is back: http://www.adajournal.org/article/S0002-8223(08)02336-5/abstract
Seems to be almost the same as the one you posted about 2 years ago. Probably dismissible for the same reasons… It does make me wonder about flow-mediated vasodilation since it does seem that high fat meals do temporarily decrease it. My biases make me think that’s not a big deal, but I haven’t been able to find a reason for that.
If high saturated fat meals do lower flow mediated vasodilation, do you know of a reason why that’s not worth worrying about?
Thanks, Dan
I actually haven’t had the time to give this paper a critical read. I’ve got it pulled and printed, but I just haven’t delved into it yet. I suspect that it is similar to the other, but can’t tell until I’ve read it. If it is of interest, I’ll post on it.