Back last September I got all riled up over "All The Stupid Stuff in My Face from the Grant Whores." The main impetus for the post at the time was the many ridiculous articles in the media claiming that saturated fat is making us fat by stimulating appetite in the brain.
While the new articles were indeed ridiculous, they were all sourcing this study that I also cited (full text):
…This finding was specific for palmitic acid, as the monounsaturated fatty acid, oleic acid, neither increased membrane localization of PKC-θ nor induced insulin resistance. Finally, arcuate-specific knockdown of PKC-θ attenuated diet-induced obesity and improved insulin signaling. These results suggest that many of the deleterious effects of high-fat diets, specifically those enriched with palmitic acid, are CNS mediated via PKC-θ activation, resulting in reduced insulin activity.
Hmm. Well, of course, I’m by no means an expert on any of this at all. I’m just a guy who has racked up 60 pounds of weight loss primarily by means of a very high fat diet, particularly saturated fat. It just strikes me as odd that a natural, whole, real food — animal fat, coconut fat — gets singled out for suspicion when I’d guess that for average americans, a good 70% of their caloric intake comes from various "foods" that didn’t exist for 99.99% of our evolution. Hell, I think millions of Americans are getting 25% of their energy and more just from sugar drinks.
And yet the focus is always on the meat, not the bread it’s wrapped in, or the frankenfat mayo it’s slathered in, or the plastic "cheese" lying atop it. But was that the real aim of this research, or is that just how the media played it?
…As I was saying, my focus was on the stupidity of the news articles but I directed the real ire towards the researchers. Well, one of them came across that post and wasn’t amused. But before I deal with that specifically, it tuned out that Dr. Stephan Guyenet, whom we know so well over here, did a fairly comprehensive review of that study just two days after I published my driveby piece. Now, having corresponded in email with Stephan dozens of times since shortly after he began blogging, not to mention his blogging itself, it’s safe to say, at least from my perspective, that he was rather impressed with the study that gave rise to all those stupid news articles.
We’ve been having an interesting discussion in the comments about a recently published paper by Dr. Stephen C. Benoit and colleagues (free full text). They showed that a butter-rich diet causes weight gain and insulin resistance in rats, compared to a low-fat diet or a diet based on olive oil. They published a thorough description of the diets’ compositions, which is very much appreciated!
They went on to show that infusing palmitic acid (a 16-carbon saturated fat) directly into the brain of rats also caused insulin resistance relative to oleic acid (an 18-carbon monounsaturated fat, like in olive oil).
He then goes on to explain in some detail the interesting connection between insulin and palmitic acid (saturated fat), concluding that, in essence, what these researchers showed actually made perfect sense in an evolutionary context. Here’s what I think might be the bottom line so far as this rodent study is concerned.
One of the most interesting things about this study is the butter group that the investigators fed the same number of calories as the low-fat group (this is called pair-feeding). This group did not become overweight, and did not experience elevated fasting insulin and blood glucose relative to the low-fat group*. This shows clearly that the adverse effects of the butter diet were primarily due to the fact that rodents overeat when fed a high-fat diet.
That asterisk points to a footnote.
* The pair-fed butter group did show a lowered sensitivity to insulin, but given its normal weight, normal fasting insulin, and normal blood sugar, it really cannot be said to exhibit metabolic dysfunction in my opinion. Human "metabolic syndrome" involves overweight and elevated fasting insulin, which these rats did not have. Furthermore, the investigators did not show that the insulin sensitivity of the pair-fed butter group was different than a pair-fed olive oil group (they didn’t make that comparison), so the finding doesn’t implicate saturated fat specifically. Insulin sensitivity is determined in part by carbohydrate intake. This is normal. The more carbohydrate the body has to dispose of, the better it gets at handling it. On a high-fat diet, you don’t need much insulin sensitivity to keep blood glucose in the normal range, because you aren’t ingesting much glucose. On the other hand, in high-fat (low carbohydrate) diet trials on insulin-resistant people, insulin sensitivity often improves, however this is not the case in healthy insulin-sensitive people.
But you really should go read Stephan’s whole post to get a fair grasp of what has been shown.
…If I’m not mistaken, it’s pretty well known anecdotally amongst many of us fatties and former fatties that high-fat, low-carb diets promote insulin resistance and the effect many find (including myself) when losing lots of fat is elevated blood glucose, especially in the morning (Dawn Phenomenon). UK Veterinarian Peter Dobromylskyj at Hyperlipid generally refers to all of this as Physiological Insulin Resistance and has been blogging about it for at least two years by my count. You can click here for about three pages worth of posts. I particularly like this quote from this post:
I like palmitic acid. It causes insulin resistance. Thank goodness.
So, to sum it up, it appears to me now that:
- The researchers in that study did decent science, and
- It was hijacked by the media in order to write the typical sensational crap.
So once Dr. Benoit posted those comments I linked to above, he also sent me an email essentially reiterating the same points. I replied and promised to look into it and he was kind enough to provide me with the following.
Let me make a few points about the blog.
1. The links you posted were to news stories, not to the actual paper. If you review and reconsider, I would encourage you to take a look at the article. It’s free (because of NIH support) here.
2. The paper was not about ice cream, burgers or even whether saturated fats are “bad.” Debbie knew that the molecular mechanism is well-understood. Fats cause peripheral insulin resistance by activating an enzyme called PKC. Active PKC serine phosphorylates insulin receptor substrates. When this happens, the insulin receptor cannot phosphorylate their tyrosine residues and they remain inactive. In muscle, this means that GLUT4 is not translocated to cell membranes and blood glucose goes up. (The effect in the periphery is well documented and if you are ever in Cincinnati and want to stop by the lab and actually see it work for yourself in the lab, let me know and I will be happy to arrange a demo. If you like, you can even be the “subject” and see how your own insulin sensitivity changes. Labs here do this work all the time in people.). Because we study insulin signaling in brain, she wanted to know if a similar process happened there. It does. The end result is a blunted hypothalamic output of insulin’s effects on appetite and also on the vagus-mediated CNS control of liver glucose production.
3. The work in that paper took 4 years and a lot of sweat and tears from many people. We didn’t set out to prove that fats were “bad” – we set out to see if a well-known process in muscle also occurs in the brain. This is important for obesity and also cognitive disorders. Those papers are also on PubMed.
4. JCI is a top-tier journal. When papers are published there, universities like to send out press releases. Both UC and UTSW did so. Our internal people interviewed us first and did their level best to “dumb down” the science to something digestible and “cute” for a press release… like “ice cream goes to your brain”. You’ll see that almost all the reports are based on the press release, NOT the actual paper. This is almost always the case for these studies. We didn’t feed mice ice cream and we didn’t claim that people shouldn’t eat fats or animal products. We found how certain molecules affect the activity of an enzyme in the brain. It was the process of translating that information for the press…. And then what the PRESS/MEDIA did with it that is the problem. I have all but stopped these things. I rarely talk to them. But Debbie is new to UTSW and they pressured her to talk to as many media outlets as possible, I know that she was not comfortable with the outcome of several reports/interviews because the media/film crew edited 30-60 minutes of discussion into a 1-3 min “cute” clip.
5. Both Debbie and I are aware that the real culprit is simple/processed carbohydrate (e.g., high fructose corn syrup, etc). Good luck on EVER getting that out of the American diet. We are not attempting to say that fat or meat is bad. In fact, the obesity research group at UC was one of the first to publish a clinical trial on the Atkins diet (here and here) and I am part of a new study (in review) showing that Atkins is actually better than the AHA diet for insulin sensitivity and increasing adiponectin levels, a hormone that improves insulin signaling. I can tell you that when they first tried to publish this work they were denied by major journals because the editors didn’t believe it. Eventually it was and is now established fact. I can only remain hopeful that the “process” of science will continue and will continue to correct itself as it has for over 100 years. We both believe that the combination of fat and carbs is what is causing the obesity epidemic eliminating one or the other will improve the situation, but like I said for many reasons it is not possible to eliminate the carbs, especially simple sugars.
6. I rarely respond to these because there simply isn’t time. It’s not that I don’t care or think that I am better than anyone, I just don’t have time to write on blogs… one could easily spend the whole day and of course enjoy the lively debate, but at the end of the day it doesn’t help my lab move forward so my practice is to avoid if possible.
There was more, but much of it was of a personal nature about one of the other researchers that I don’t think is appropriate to publish.
In the end it’s pretty clear to me that I was wrong to target them. I do have two disagreements with Dr. Benoit.
- In all of his communications he has emphasized the level, intensity and length of the work. I’m not an adherent to the Labor Theory of Value. I’m now satisfied that their work is sound, and so it has value. But it matters not to me whether it took 5 minutes or 10 years to produce.
- I firmly believe that there is room and justification for the sorts of vitriol I spew, human beings or not. But I recognize that I spewed at the wrong folks this time and I regret that. Thankfully, there are plenty who actually deserve it. I will probably do better in the future to primarily direct public hangings to news media unless I’m particularly familiar with a piece of research.
I am grateful for Dr. Benoit for taking the time to contact me. Now that I’m aware of the greater context, the last thing I’d want is for that post hanging out there unchecked. I will be updating it with a link to this post.