There's a much stronger correlation between serum myristic acid and liver fat than with serum palmitic acid. In the same way that I've observed that a heavy butter, but not a heavy beef fat intake, shoots my cholesterol levels to the moon, it seems that this evolutionarily novel fat also has a different effect on liver fat levels. This is a mark against butter, not saturated fat.

I don't see this being an argument for increased linoleic acid intake at all.

Interesting study, I'll be examining it for the next few days but here's some points I noticed:

Most biochemical markers of health were about the same in both groups at baseline (triglycerides, alanine aminotransferase, etc.) but some weren't. Weight was higher in the SFA group (and subsequently so was BMI, waste circumference, visceral fat, and total fat mass). Still, this difference was small, but it's an 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. So, this might suggest that the butter group had a slightly less healthy lifestyle.

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 and I'm not honestly sure but I think more context is needed to explain that variance.

As Travis pointed, this study used butter as the saturated fat source, which is important because it contains higher levels of the saturated fat myristic acid. 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 dietary changes in 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.

As someone else noted in their answer, the study was quite independent and doesn't note what food was being consumed (beyond sunflower oil in the PUFA group, butter in the SFA group, and scones in both). As Christopher Gagnon stated in his answer "Not many people put butter on salad". The study doesn't examine whether the PUFA group may have consumed healthier foods which could have affected the results.

Finally, sunflower oil and butter have differences beyond just their fatty acid compositions. Sunflower oil is rich in vitamin E (does Vit E improve symptoms of fatty liver disease? Some studies suggest it might). And, perhaps components in butter (like progesterone and IGF-1) negatively affected liver fat levels. I don't know, but you I'm suspicious that you can extrapolate the effects to just the fatty acids.

Edit:

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, CMast talks about how choline need is dependent on folate, b6, b12, and betaine intake (all of which lower choline need). In the SFA group, a lower intake of choline (and/or those choline sparing nutrients) and a greater need due to greater sat fat intake likely could have been responsible for greater liver fat accumulation.

I commented on a link to this study in another thread, but am glad you posted it as a question of its own, since it deserves further scrutiny.

I wouldn't make much of it without seeing more information about the diet of study participants. I'm not qualified to "debunk" a study, but I can come up with a couple questions:

1. The abstract says macronutrient ratios didn't change, but it didn't stipulate the actual ratios, nor if all participants had the same ratio.

2. They only studied "abdominally obese" people, 15% of whom had diabetes. Could metabolic derangement influence results--particulalry if they didn't control food choice? Did the group consuming SFA also include the diabetics? Alternatively, did the PUFA group include the diabetics, but they happened to be properly managing their conditions--including avoiding lots of refined carbs?

3. What did they eat? These studies rarely tell us what study participants actually consumed. The abstract mentions only butter. Everyone knows certain foods go well together, and to me it seems plainly obvious that the choice of a fat can naturally influence one to eat certain foods. I would think one less likely to spread olive oil on toast or pancakes. Not many people put butter on salad.

If they told participants who likely eat a SAD to limit their fat to SFA, it seems pretty likely to me that many would consume it with lots of refined and/or sugary carbs, so elevated lipids wouldn't surprise me.

I think the Vitamin E component of this study explains the differences :).

The study requested that the participants intake 15% of their energy as linoleic acid using the given food items. This is about 33 grams of fat. Per 100g of sunflower products, there is approximately 20 iu's of vitamin E. Enough to meet the RDA. The four main things this study found are the following:

1. Decrease in liver fat.
   • Vitamin E will do this, but seemingly only in the short term. Looking at this study, refer to figure 2. The effect of Vitamin E on all of this seems to be largely transient. Note how the ALT levels drop quickly in the Vitamin E group, and then level out. At the end of 96 weeks the Vitamin E did nothing. If this would of been a 10 week trial, the vitamin E would of been "effective."
2. Lowered cholesterol.
   • Vitamin E has not been shown to do this, but I'm pretty sure linoleic acid does actually do this. I don't think any of us really care here, as super low cholesterol isn't on our agenda, and I didn't even bother to look up a study. Just not interested in this part, haha.
3. Fasted insulin "tended" to be higher in SFA group rather than PUFA.
   • Vitamin E will help restore insulin sensitivity, or at least its been found in high-dose situations. Admittedly the dose in this study would of been 1/40 of the dose in this study, but given the overwhelming small decrease in fasted insulin in the PUFA diet, I don't think its a long shot that it was the Vitamin E's doing. In the compliant subjects data, its a mere fraction of a decrease, and as Mscott points out, it appears the SFA group was more insulin resistant from the get go.
   • Vitamin E helps insulin sensitivity in fructose-fed rats. Not exactly the best study to quote, but this seems rarely researched.
   • Here is another look in humans.
   • Note that the effect on insulin sensitivity seems mostly transient as well. This was only a 10 week study after all.
4. Plasma IL-1RA and TNF-R2 were lower during the PUFA diet than during the SFA diet.
   • Vitamin E Lowers IL-1
   • Additionally, here.

I think if this study would of gone on for another 10 or 20 weeks, there probably would not have been very many differences. If anything, I think we can learn from this study that whole foods or oils extracted merely through crushing like sunflower, coconut, olive, rather than some artificial chemically derived canola, corn, or soybean oil, still has better effects on the body.

I don't have much to back up this last statement, but I don't think the whole PUFA vs SFA thing is that big of a deal honestly. Or is omega-6/omega-3 ratios. I think as time goes on, we'll find that those foods which present us with a "damaging omega-6 ratio" are packaged together with things like Vitamin E and other anti-inflammatory agents that make up the difference.

http://co2factor.blogspot.com/2012/04/saturated-fat-versus-polyunsaturated.html

My philosophy:

Numbers can say anything we want them to say. In the end, we STILL don't really know what they MEAN. Is "fatty liver" bad? Is it transient? Did the butter cause inflammation, or was it something else in the person's life -- or is diabetes actually an inflammatory process in and of itself? In light of everything we DON'T know, I'm still leaning towards the following few basic rules.

1. Don't worry about numbers... weight on a scale, macronutrient/micronutrient ratios, cholesterol levels, etc.

2. Eat food prepared from scratch. As much as possible, have it be food that makes your essence/spirit/being sing.

3. Have that food come from ingredients you could make or grow at home, with the help of simple tools (yes, I actually have a hand-tool for obtaining nut and olive oils! You can find it here).

4. Follow your appetite. If you're not hungry, don't eat.

5. Make sure the plants and animals you eat grew in as close to THEIR natural state as is possible for you to afford.

6. Make your body work hard at least a little while every day -- then let it rest as completely as possible a while every day, too.

7. Let your mind be active, and challenge your beliefs at least once a day, then give yourself a break and just laugh over something completely senseless and silly, just because it feels good.

8. Treat the people around you with dignity, regardless of their eating habits, size, shape, or politics -- and make sure you let the people you truly cherish know that they're in your thoughts every day.

If I don't live a long and healthy life doing that -- then I guess I was meant to die young and I guess I'm not willing to waste a whole lot of time over-analyzing it.

It seems to be quite the opposite of what he writes here

http://wholehealthsource.blogspot.co.uk/2009/06/fatty-liver-reversal.html

Both cannot be right!

Much has been written here before about the fact that we don't know understand the mechanisms by which excessive omega 6 consumption causes disease. That it does not have a simple relation to inflammation (i.e., more LA = more AA-derived eicosaoids) as had previously been thought, has now been known for a few years.

I think it would be unwise to exonerate excessive consumption of linoleic acid on the basis of a few studies finding no correlation with poorly understand surrogate markers of disease. Such consumption is unnatural (i.e., unpaleo). There is decent evidence from human and animal trials that such consumption causes diseases, like cancer and heart disease. There is also contradictory evidence from other trials-- but these generally appear to be less well conducted.

I wonder what else they were eating. I am not an expert but I would guess that certain combinations are bad for health even if the food is individually neutral

This study doesn't mean anything to me, as I don't really eat butter, if it was coconut oil . vs. PUFA then Id take notice