I’ve received a number of questions about this recent paper, the official title being “Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport” but the popular media title usually running something like: “High fat diet causes diabetes.”
The only thing I’ve seen popularized more in the media, only to be subsequently proven wrong, would be a headline something to the effect: “End times are Neigh”. Granted, with the latter someone may well get that right and we will only see one example, but in the case of the former…well, this shit just won’t go away.
Today we will look at a number of concepts in this post to help folks wade through this mess in a more effective way. Right upfront let’s consider what goes into the “high fat” diet they are feeding the mice. From the paper:
Mice were provided either a standard diet (16.4% protein, 73._% carbohydrates and 10.5% fat with 4.07 kcal g−1; D12329, Research Diets) or a high-fat diet (16.4% protein, 25.5% carbohydrates and 58.0% fat with 5.56 kcal g−1; D12331, Research Diets).
In science we like to keep variables consistent, otherwise it’s not science, it’s voodoo. Now, we have some inherent problems when altering macronutrient ratios as we have three macros and if you tweak one, you generally tweak them all. What hormonal consequences might this have? More importantly, how much did the animals actually eat? We don’t know, the study design was not in a metabolic cage format so we don’t know if we have the confounder of a significant difference in total calorie intake between the two groups. Several other papers I reference later do provide information collected in a metabolic cage format, so it can and should be done. What we do see is an interesting bias on the part of the study authors. This from the introduction to the paper (which is repeated a dozen or so times throughout the paper):
A high-fat or Western-style diet leading to obesity is evidently a predisposing factor in disease susceptibility and onset5
5. Parillo, M. & Ricardi, G. Diet composition and the risk of type 2 diabetes: epidemiological and clinical evidence. Br. J. Nutr. 92, 7–19 (2004).
So, what is it? High fat diet, or a Westernized diet? We have examples of high fat cultures shifting away from traditional food sources and developing diabetes (Inuit) and we have low fat cultures transitioning to higher fat intake and developing diseases of civilization (Kitavans). I can also think of a few NON DIET situations that induce insulin resistance (we’ll talk about those later) but let’s take a look at what was actually fed to the mice. Please click on the links below and peruse the composition of the lab diets fed to the mice.
In both situations we have:
Casein-which has some known insulinogenic/proinflammatory properties.
Maltodextrin-likely corn derived and not much happening with regards to micronutrients.
Corn oil-Heavy in linoleic acid, which is known to promote liver pathology and insulin resistance, skinny on n-3’s other than alpha linolenic acid…not our best option for n-3’s, be we mice or men.
Coconut oil-Saturated fat, predominately in the form of lauric acid. Likely the best part of the chow.
As you will see later, the standard mouse chow (even high carb) is so unhealthy it’s oftentimes tough to keep the mice alive through a study.
Now, the high fat diet is designed to PROMOTE metabolic derangement and type 2 diabetes. It was designed for this purpose and it is well known that a high fat diet will induce type 2 diabetes in mice.
Oh, but wait! A high fat diet only induces type 2 diabetes in mice when substantial carbohydrate is present. A ketogenic diet does no such thing. In fact, a ketogenic diet in mice has demonstrated a number of benefits related to type 2 diabetes complications, neuro degeneration and other conditions.
It’s worth mentioning that when you read the methods section of that paper the researchers had to sacrifice the hi-carb diet (AIN-93M) mice early as the animals were dying from…the high carb diet! Or, was it the carbs? Perhaps it was the sugar, linoleic acid, casein…you know, all that shit the mice never evolved to eat…
Now we DO see impaired systemic insulin sensitivity in ketosis…is this a bad thing?
It is completely normal as limited glucose is spared for the brain during ketosis.
So, the hypothesis is clearly: “a HIGH FAT diet causes type 2 diabetes” yet when we dial the fat UP, type 2 diabetes…goes away. Fail, on many levels.
Here is what these folks have done:
1-Fed a diet known to cause insulin resistance to their mice (without tracking how much food either the control or HF mice ate. Sloppy science and sloppy reviewers…this was not even discussed in the limitations section).
2-Induced type 2 diabetes in said mice, and then performed various gene expression studies which indicate impaired glucose sensing in the pancreas (you can bet the same thing is occurring in the brain and liver, yet no mention of these alternate mechanisms is provided)
3-Looked at correlative genes in humans suffering from type 2 diabetes and found similar impairment.
4-Hung the cause of the insulin resistance on a high fat diet despite the fact a ketogenic diet (a REALLY high fat diet) does no such thing.
And somehow these folks get published!!
Now, I can induce insulin resistance via a number of non-dietary means, including sleep deprivation, sepsis and injury. Not surprisingly, when we look at some mechanisms the very same FOX2A gene the folks were looking at in the original paper that spawned this post is affected by sepsis. In this case it is hepatocytes (liver cells) and in the original paper the investigators were looking at pancreatic cells, but as insulin resistance tends to progress in a systemic fashion, and since we know the liver is a key player in this glucose regulations story…I’ll bet it’s the same story in both tissues.
That this paper was published, that these folks even ASKED the questions that they did and proceeded to attempt to answer them in the way they have is frankly shocking. It is also why the AHS11 was so damn important because we have a medical and research community that is just fracking lost. None are operating within an Evolutionary framework and this is the resultant tripe produced. At this point I’d go so far to say that it borders on malpractice or behavior necessitating litigation when researchers so epically drop the ball and the media subsequently grabs this stuff and runs with it.
That’s my finger wagging to the researchers and media, now I’m going to do a little finger wagging at some of y’all. One of the messages I received went like this:
“Robb, did you read this paper? What’s your opinion on it? I ate a high carb, grain based diet for years and was sick. Since I went paleo I’ve lost 65 lbs and what I suspect to be an autoimmune condition has gone away…but is there anything that this paper says that should concern me?”
I’m all for questioning our dearly held beliefs, and burning the house down when necessary, but I have a fair amount of faith in our personal experience. In the case of our eating and lifestyle habits it looks like something along this paleo/primal lifeway will make us Look, Feel & Perform better. Our biomarkers of health & disease go in a favorable direction.
DONE. Now it’s time to LIVE.
On the macro level we do not need much more than that and until the larger research community finally grasps the evolutionary biology perspective they will have limited offerings that are not outright dangerous to our health and wellbeing. This paper is a prime example.
Y’all do not need gurus, you need to tinker and go with your own experience. And do like Mark Sisson suggested and go play.