Scientific journals aren’t for everyone. Journal articles use technical writing and can be rather dry. They can be long, they can be dull, they can show nothing new and exciting, or the research they describe can be so poorly thought out you wonder how a reviewer ever allowed the paper to go to the presses. Many good article are behind pay walls, so even if you want to read them, sometimes you can’t.
Fortunately an abstract of most papers can be found for free. An abstract is a brief summation drawn up by the authors to get their point across. Maybe it’s just me, but I sometimes think that abstracts can be a bit like movie trailers- they introduce the major players and they give you a general plot of the movie (and they try and hook you in by showing you all the good scenes).
Like a movie trailer, abstracts can be deceiving. Take the trailer for The Matrix Reloaded– how excited were you when you first saw that trailer? How much did you wish the movie had never been made after you saw the actual feature?
Unfortunately, while in the cinematic world people are unlikely to act like they’ve seen the whole movie when all they’ve done is watch a trailer, in the world of scientific literature it often seems that people assume that reading the abstract is as good as reading the paper.
It is not.
The list of examples is endless, but this morning I stumbled across an example of this that finally pushed me to write about abstract abstraction.
It all started when I saw a tweet proclaiming “A high saturated fat mixed meal induces inflammation & insulin resistance & elevated glucose cf [compared to] other types of fats”. Considering my interest in fats and my particular fondness for saturated fats you may not be surprised to hear that I decided to dig a little deeper.
The paper is from an open access journal. The full text is available here.
To be fair, the title of the paper is not quite as sensational as the tweet that led to it- The effect of two iso-caloric meals containing equal amounts of fats with a different fat composition on the inflammatory and metabolic markers in apparently healthy volunteers– but the “conclusions” offered in the abstract (the line that anyone who is just skimming the article will jump to) is rather dubious:
Metabolic and modest inflammatory changes occur within a few hours after the ingestion of a high SFA meal in apparently healthy adults.
I don’t have the time or the inclination to totally dismantle this paper (I really wonder how they did their statistics to show there was a significant difference), but I do want to point out how unwise it can be to draw conclusions from this abstract.
Let’s compare the methods sections. In the abstract, the authors say that healthy participants “were given two iso-caloric meals with similar amounts but different composition of fats: a meal high in monounsaturated fats (MUFA), and a meal high in saturated fat (SFA).”
The methods section in the paper reveals more detail:
The chosen meals represented two very popular meals habitually preferred by the general population: 1. Chicken sausages with fried potatoes, ketchup and mayonnaise (defined as SFA); 2. Pasta with olive oil, ketchup and nuts (defined as MUFA).
Seriously?
Two entirely different meals, and we’re supposed to believe that any differences in blood markers (of which I am skeptical) are due to the change in the type of fat- fat types that aren’t particularly well represented in at least one of the meals. Chicken is not high in saturated fat. Chicken fat is predominantly unsaturated, a combination of MUFA and polyunsaturated fats (PUFA), with less than a third of chicken fat being saturated. What were the potatoes fried in? These days most things are fried in PUFA rich vegetable oils not SFA rich animal fats or coconut oil. And mayonnaise? Mayonnaise contains very little saturated fat (because it’s usually made with PUFA-rich vegetable oils). At least the second diet utilizes olive oil, which is rich in MUFA.
The authors state that they used the Israeli Food Database to calculate the breakdown of SFA:MUFA:PUFA in each diet and that the “SFA” and “MUFA” diets contained 24:33:17g and 8:51:14g respectively. Without knowing more about the ingredients (what fats and oils were used in the SFA diet and what nuts were used in the MUFA diet) it’s hard to know if the breakdown is accurate. The meals are so different in every regard, it’s silly to quibble over the exact proportion of each fatty acid type.
The point of this post isn’t (or wasn’t) to pick this paper apart. The purpose was to show that we should be cautious when drawing conclusions from abstracts.
The authors chose to say that any changes (that may or may not be real) occurred after “the ingestion of a high SFA meal”, but they could equally have said “after the consumption of mayonnaise (or potatoes)”… Likewise, they could have claimed that pasta (or nuts) “protects against metabolic changes induced by ketchup”. Of course, all of these claims would be ridiculous- though perhaps less ridiculous than suggesting any changes were due to ingestion of a high SFA meal (something they didn’t even test)!
If they were testing a proposition that was going to be subjected to universal skepticism, such as “coke has an anti-inflammatory profile superior to that of green tea “, they would try harder to design an experiment that would actually show this.
Because they are saying something that most people now believe to be true, they get a free pass. Skepticism need not apply.
To convince people that cigarettes cause lung cancer, or that contaminated water was spreading cholera, or that the atom was divisible, other scientists had to devise experiments that not only showed clear results, but that would stand up to the most skeptical nit-picking. It was often a case of “back to the drawing board” after taking the objections of skeptics on board.
The MUFA meal had 3 sources of antioxidants, the “SFA” meal only one (ketchup). You have to remove these inequalities to prove anything.
Actually it has been done: http://www.ncbi.nlm.nih.gov/pubmed/9844997
(full text pdf http://www.dragaonordestino.net/Drachenwut_Blog_DragaoNordestino/Ernaehrung/fette_oele_arquivos/linoleic_acid_stress.pdf )
In this study, high oleic oil was more inflammatory than the high-SFA butter-based diet consumed by controls and by the oleic and linoleic groups at baseline.
Thanks for the links to the paper, and for the comment. You are definitely right that people get away with a lot more when what they say supports common presumption, but this paper was just so off in what it said it showed and what it actually tested I couldn’t ignore it…
The paper you shared is interesting- I hadn’t seen it before. I’ll disagree with your take of it though- I think the controls were eating their normal diet throughout, not the butter rich “loading” diet of the treatment groups, though it’s not particularly clear. Either way, the apparent increase in oxidative stress seen with the high LA diet does not surprise me (though reaffirms my anger when I see PUFAs being touted as “heart healthy” as in this new Consumer Reports article
You may be right about the controls. However, all their scores improved during the experiment just as the others declined. If this was a placebo effect produced by participation in the experiment, presumably common to all groups, then the pro-inflammatory effect of both the oleic and linoleic diets was especially great; the oleic diet, tho not as bad as LA, doesn’t come out of it particularly well.
But perhaps the participants were just depressed by the vile food they had to eat, and this accounted for the difference.
Here’s an interesting find from MDA – even artificial trans-fats aren’t all bad, it seems. http://ajcn.nutrition.org/content/early/2013/02/12/ajcn.112.045468.short
Perhaps it is also the linoleic acid, the destruction of omega 3s (longest chain FAs are first to be hydrogenated in partial hydrogenation) and the empty calories that make hydrogenated oils and spreads harmful.
I remember R.D, Feinman saying that the evidence that artificial trans fats are a big factor in human diet-related disease isn’t as strong as we think. Not that i’m likely to eat them, just sayin’ is all.
As for Consumer Reports, if you lump in studies where fish oil consumption is increased and total fat (including linoleic acid) decreased, and if you ignore mortality and just focus on events, then you can get that result, but it begs the question why they ignore all the other Cochrane studies showing that saturated fat as an independent variable has no effect on CVD death rate whatsoever.
Excellent criticism, that study definitely doesn’t say much, it’s too confounded and as likely to be oxidized n-6 as the smaller amounts of SFAs if we only take that study into account.
I never even knew about that paper on linoleic acid sunflower oil replacing SFAs, that’s a critical piece of the puzzle, we already know that replacing SFAs with linoleic acid increases overall mortality, and the 1998 paper is especially good because it reduces LA to less than the theoretical cutoff of 4% of energy (fabled to be the driving force beyond the Lyon study’s amazing efficacy). Thanks for that one! 😀
I have a bit of a different take on the effects of dietary fatty acids in the postprandial period. It is possible for lipotoxicity to increase in response to a high fat meal, and SFAs may be the most potent fatty acids, though it might also be the discrepancy between certain antioxidants like you mentioned. This paper shows butter being worse than other fatty acids and macronutrients http://atvb.ahajournals.org/content/25/6/1274.long However it’s not like it’s fat’s fault, it’s the lack of nutrients and hormonal and inflammatory chaos that most people are experiencing that produces cellular lipid overload in the first place.
http://www.ncbi.nlm.nih.gov/pubmed/11679024
http://www.ncbi.nlm.nih.gov/pubmed/9388088
http://www.ncbi.nlm.nih.gov/pubmed/20555373
http://www.ncbi.nlm.nih.gov/pubmed/18993165
http://www.ncbi.nlm.nih.gov/pubmed/16896723
http://www.ncbi.nlm.nih.gov/pubmed/11165454
So many things completely prevent endothelial dysfunction is response to a high SFA meal! It’s incredible that some people can read the literature and be convinced that the big important thing is getting those evil SFAs out of the diet. For anyone eating and living in a healthy way there is basically no effect, our bodies can handle SFAs just fine, they just need some nutrients and exercise.
I would kind of like to see a study like “A high linoleic acid diet increases oxidative stress in vivo and affects nitric oxide metabolism in humans.” except with adequate n-3s and sufficient vitamin E for both groups (though vitamin E is significantly higher in the n-6 group). I still suspect that the N-6 group would do worse but that’s to be determined, I also think the next step in the whole long-term clinical trial scene is to do something like that where N-6 replacing SFA with increasesd n-3 is compared with SFA replacing n-6 with increased n-3 also.
So much uncertainty, but for now I’m avoiding a high intake of polyunsaturated oils, especially when fried, and eating a nutritious diet that improves lipid metabolism. I see this as pretty fool-proof 😀
Oh man, it’ll take me some time to click through all the papers you posted!
In the end, I agree with your final sentence. I think everyone will be best served by eating a nutritious diet devoid of processed foods (and thus devoid of the piles of O6 that is all to prevalent in the modern diet!). For the majority of people, that simple advice can go a really long way!
@ Stabby, “I also think the next step in the whole long-term clinical trial scene is to do something like that where N-6 replacing SFA with increasesd n-3 is compared with SFA replacing n-6 with increased n-3 also.”
this has occurred to me too; this would be replicating the Kitavan diet pattern, or the Pacific Island diet Paul Jaminet talks about, or many traditional diets where fish and dairy are cheap supplemental foods.
Oh yeah I forgot that this is essentially the Kitavans. Well we know it’s compatible with few heart attacks then 😀
@ VP, I believe this study was really designed to test the superiority of a Mediterranean diet meal over a standard one. And possibly some overseeing elderly HOD type wrote the abstract and put a more old-fashioned spin on it.
I think that is often the case, that senior authors who are forced to sign off on papers by young researchers that they don’t agree or don’t see the point of and put their own views in the abstract.
Bottom line – did they isolate the variable that’s singled out in the abstract, or make a reasonable attempt to do so? No.
Interesting that this was an Israeli study. The Israeli paradox isn’t about a diet high in saturated fat:
http://www.ncbi.nlm.nih.gov/pubmed/8960090
http://www.ncbi.nlm.nih.gov/pubmed/17923822
http://ajcn.nutrition.org/content/77/2/521.full
From the latter:
Prior to the introduction of solvent-extracted vegetable oils and soy- rand corn-based animal husbandry over approximately the past 70 y, no population had been exposed to the current intakes of linoleic acid. We may well be experiencing the “linoleic acid paradox,” in which a supposedly healthy fatty acid (ie, one that lowers total cholesterol) is associated with increasing rates of cancer and inflammatory and cardiovascular diseases during these same decades. Compounding and confounding this paradox are low intakes of α-linolenic acid and other n−3 (fish) oils.
Thanks George- you’ve given me quite the collection of papers to check out! Generally speaking- I’m just frustrated that 2 very different meals were boiled down to “The main difference between the two meals in the current study was in their fatty acid composition.”
I think the Israeli Paradox is very interesting (though I don’t think it’s a paradox, as I am not under any impression that an excess of PUFA is good for anyone). I’m not sure what the actual experiment set out to show (it just doesn’t make sense in the context of other experiences they referenced). If they really wanted to look at the effects of the FA content of a single meal (as they claim) they could have easily made a shake that was standardized with only variation in FA composition instead of 2 such different meals…. I’m guessing it’s what they have on offer in their hospital caf! (Neither represents a mediterranean style meal by my standards).
Maybe the whole thing was done to settle an argument that had started in their staff cafeteria; “Nuts and pasta is the healthier option!” “Nah, there’s nothing wrong with sausage and chips!”
So they made up some cover story to apply for funding. “We’ll be testing the inflammatory effect of saturated fats, actually”.
Ha! I think you nailed it!