A few months ago a study titled “Effects of n−6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial” was published in the American Journal of Clinical Nutrition. This study compared the effects of polyunsaturated fat, in the form of sunflower oil, with saturated fat, in the form of butter on various markers of health. The results of this study seem to indicate that saturated fat produces higher insulin, higher levels of inflammatory mediators, a worse lipid profile, and greater accumulation of liver fat. Ouch.
Still, I think there are some problems with this study that weakens it as evidence that saturated fat is bad and polyunsaturated vegetable oils are good.
Here are some of the qualms and questions I had about this study:
1. Before the trial began, most biochemical markers of health were about the same in both groups (triglycerides, alanine aminotransferase, etc.) but some weren’t. Weight in the SFA group was higher by about 11 pounds (and subsequently so was BMI, waste circumference, visceral fat, and total fat mass). Still, this difference was small, but it’s worth noting. As calculated using a homeostasis model assessment-estimate for insulin resistance (HOMA-IR), the SFA group was higher than the PUFA group (2.0 vs. 2.6) and the SFA group was right on the line for what is often considered the clinical cutoff for insulin resistance. This might suggest that the butter group had a less healthy lifestyle.
2. Plasma levels of high molecular weight adiponectin were quite different in the PUFA vs. SFA groups (2.62 vs. 3.56). Many people might consider this in the favor of the SFA group, but let me raise some points about this. Adiponectin is a protein which studies show appears to reduce inflammation and improve insulin sensitivity. However, adiponectin is also inversely associated with body fat levels, yet both groups were almost equally fat, so why were the saturated fat group’s adiponectin levels higher? There could be more to this paradox and I’m looking into it.
3. This study used butter as the saturated fat source, which is important because it contains uniquely higher levels of the saturated fat myristic acid compared to other saturated fat sources like beef fat. Myristic acid may have unique effects on health compared to the other saturated fatty acids and the study even had graphs which seemed to support this: 1: The graphs illustrate the correlation the researchers found between liver fat and changes in blood levels of myristic acid (14:0 on the left) and palmitic (16:0) on the right. The correlation is much stronger with myristic and fairly weak (especially after removing outliers) for palmitic. There are many different kinds of saturated fat and some have been clearly shown to be healthier than others.
4. Importantly, the study was fairly independent and doesn’t note what foods were being consumed (beyond sunflower oil in the PUFA group, butter in the SFA group, and scones in both). To quote another commenter discussing this study: “Not many people put butter on salad”. Actually, I’ve been known to put butter on my salad, but I don’t think I’m reflective of the average person. Basically, the study doesn’t examine whether the PUFA group may have consumed healthier foods with their sunflower oil which could have affected the results. More on this in number 8.
5. Sunflower oil and butter have differences beyond just their fatty acid compositions. Sunflower oil is rich in vitamin E. Unsurprisingly, studies show vitamin E might decreases liver fat levels and lower insulin, two effects seen in the PUFA group. Also, perhaps components in butter (like dairy hormones) negatively affected liver fat and insulin sensitivity. I’m suspicious that you can extrapolate the effects to just the fatty acids.
6. This study’s duration was 10 weeks. Some people have claimed that the ill effects of linoleic acid rich fats like sunflower oil take longer to manifest. It would have been interesting to see a study like this carried out longer. There is some evidence that saturated fat’s effect on LDL cholesterol is transient; it may increase at first and then decrease later.
7. Triglycerides and lathosterol levels in the blood decreased on the PUFA diet and increased on the SFA diet. However, triglycerides were fairly insignificantly changed, could easily have been due to standard error, and with a P-value of .19, this study proves very little about serum triglyceride levels. Lathosterol I could care less about, honestly. It’s interesting, but I don’t consider it worth worrying about.
8. Finally, I wonder how choline may have played into the results of this study. Chris Masterjohn has written a bit about choline, including this awesome post on how choline deficiency is probably the main driver of a fatty liver. Choline deficiency could have significantly influenced the results and we don’t even know what the choline intake in either group was (choline receives no mention in this study). Masterjohn also points out in his article that “saturated fats increase the choline requirement a bit more than PUFAs do”, citing this study. Finally, in this related post, Masterjohn talks about how choline need is dependent on folate, b6, b12, and betaine intake (all of which lower choline need). In the SFA group, if a lower intake of choline (and/or those choline sparing nutrients) was coupled with a greater choline need due to greater sat fat intake, this likely could have been responsible for greater liver fat accumulation.