There are many studies in which animals are fed refined high-fat diets to promote body fat gain under controlled conditions. Some of them compared different types of fats to one another. I've collected many of these over the years, and they are not consistent with one another. Some support the hypothesis that seed oils rich in linoleic acid cause more fat gain than other fats such as animal fats (2, 3, 4, 5), others show no difference (6, 7), and still others support the hypothesis that other fats cause more fat gain than seed oils (8, 9, 10). Perhaps unsurprisingly, studies in the latter category are most often cited. The only finding that is relatively consistent is that refined high-fat diets in which the fat comes mostly from omega-3 fatty acids (fish oil, flax oil, etc.) typically don't cause fat gain (11). However, these diets also cause a failure to thrive and pancreatic problems (11). Keep in mind these diets are the equivalent of getting 30-50% of your calories from fish or flax oil-- lower doses do not cause those problems.
Together, this broadly suggest to me that long-chain saturated, monounsaturated and omega-6 fatty acids are pretty much equivalent in their effects on body fatness in animals, and that differences observed in some studies are due to other factors such as the animals' flavor/texture preferences, minor constituents of the fats, the dietary background, or species/strain differences. In other words, seed oils are probably not inherently more fattening under controlled conditions than other types of fat.
Because of this, I think the idea that linoleic acid (the main fatty acid in most seed oils) interferes with thyroid function in a significant way is on shaky ground. There is some evidence from the rodent and cell culture literature that seed oils interfere with certain effects of thyroid hormone (12, 13, 14), however the overall physiological relevance of this is uncertain. Therefore, I've removed my old post, but kept the references (above) for those who are interested.
Another piece of evidence was the five year controlled human study in which volunteers ate a normal diet or a diet in which the animal fat was replaced by seed oils (15). Subjects in the seed oil group ended up weighing roughly 5% more than those in the normal diet group by about three years, although it wasn't designed to study the effects of dietary fat composition on weight change. There are a few problems with the study, including the fact that the investigators didn't measure body composition (so we don't know if the weight difference was in fat) and that many participants dropped out. It remains an interesting observation, but nothing to hang your hat on.
Now let's discuss the piece de resistance: the two studies that reported that feeding mice a diet with a poor omega-6:3 balance (excessive omega-6) caused a multi-generational obesity phenotype (16, 17). I was planning to discuss those studies in my AHS talk, so I revisited them to make sure they were solid. Unfortunately, I discovered serious flaws in both papers that fatally undermine the authors' conclusions. The short version is that neither study was properly controlled to come to the conclusion that omega-6:3 balance influenced fat gain. Both studies compared diets that differed in many ways, and that fact was not reported straightforwardly. In retrospect, I feel misled by these papers. I should have read them more carefully, and I apologize to my readers for that. As there is already too much misinformation on the internet, I've taken the post down.
So does this exonerate seed oils? Not necessarily. Our seed oil intake has increased dramatically in the last century, far exceeding that of our recent ancestors. Omega-3 intake has also increased, but the omega-6:3 ratio has nevertheless roughly doubled (18). As opposed to most other fatty acids, linoleic acid accumulates to a large degree in fat tissue (19, 20), and the amount depends on the proportion of linoleic acid in the diet. The linoleic acid content of body fat has increased tremendously in the US over the last 50 years, as shown in the following graph, based on a number of different studies, each of which is represented by an orange dot (21, 22, 23, 24, 25, 26, 27).
It's so linear that I can understand why someone might be suspicious of how I selected the studies, but I can assure you I included every relevant study I came across and was very surprised to see such a consistent trend. There are probably other studies out there, but the ones I found are sufficient to illustrate the change. I also included a study that looked at the linoleic acid content of chimpanzee fat, for reference (28). The caveat is that the paper doesn't specify if the chimp was captive or wild, so you can take it with a grain of salt. Linoleic acid in human breast milk has also increased quite a bit over the same time period (29).
I don't know what the consequences of this dramatic increase in the linoleic acid content of body fat and breast milk are, but it certainly gives me pause. We are truly living an uncontrolled experiment in the modern world. I think seed oils promote obesity because they're used to increase the reward/palatability value of processed food, but this would be equally applicable to animal fats and more saturated plant oils if they were used in the same foods. Do seed oils promote obesity by another mechanism as well? It's possible, but I'm not aware of any compelling evidence to support that idea at this point.
5 comments:
- fraz said...
-
Great post!
A true scientist is always open to revisiting previous hypotheses. Keep up the great work. - Ulyana Michailov said...
-
Fantastic that you put this all together, someone has to! Thank you :)
- M. said...
-
Hi Stephan,
What do you think about the idea that increased omega-6 consumption disrupts liver functions, which can contribute to fatty liver disease and eventually to metabolic syndrome? - Beth@WeightMaven said...
-
Well, I can't pass up the opportunity to bring up the endocannabinoid system and dietary PUFA. On the one hand, you certainly have obesity researchers interested in blocking ECS (if they can do so without horrible side effects) and on the other, you have at least one potential pathway where LA can be converted to anandamide (especially in those with chronically high insulin).
I've been wanting to check out the Kim paper (Endocannabinoid signaling and energy metabolism: a target for dietary intervention) that Emily Deans discussed here. Would love to hear your take on that. - Aravind said...
-
Hello Stephan,
Referring to the following post - http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-iii-dietary.html
Pulling out a few select quotes -
"Inflammation in the hypothalamus, with accompanying resistance to leptin signaling, has been reported in a number of animal studies of diet-induced obesity"
"Any time a disease involves inflammation, the first thing that comes to my mind is the balance between omega-6 and omega-3 fats. The modern Western diet is heavily weighted toward omega-6, which are the precursors to some very inflammatory substances (as well as a few that are anti-inflammatory). These substances are essential for health in the correct amounts, but they need to be balanced with omega-3 to prevent excessive and uncontrolled inflammatory responses. "
So is the mechanism : Seed oils --> distorted O3/O6 --> inflammation of hypothalamus --> leptin resistance --> obesity.
What say you?
