Fat and Insulin Sensitivity
Chris, from Westcountry CrossFit shot me a question about the recent PaleoDiet Newsletter. If you have not subscribed to the newsletter and/or read all the archives you are REALLY missing out! So, here is that most recent PDNL and Chriss’ question:
“Insulin resistance is thought to be an important contributing factor to the modern diseases of civilization such as metabolic syndrome, blood lipid disorders, hypertension, obesity and type II diabetes.1 Although genetics play a role in insulin resistance, the observation that obesity and diabetes are increasing at alarming rates worldwide suggests that there are vital environmental factors that also need to be considered.2
Although carbohydrates play an integral role in insulin resistance by elevating glucose levels, there is also strong evidence that the amount and quality of free fatty acids consumed contributes to insulin sensitivity.3 It has been shown in rats that under certain circumstances, free fatty acids are required for glucose-stimulated insulin resistance. Essentially, when rats are infused with a high level of glucose, in the absence of fatty acids, the insulin response is non-existent.4 In contrast, when this occurs in the presence of high levels of free fatty acids, glucose-stimulated insulin resistance is extremely elevated. It was shown in these studies on rats that the amount of saturation of the fatty acid was also correlated with insulin secretion.5 The more saturated the fat, the higher the insulin burst. Thus, in rats, it seems that free fatty acids are vit al to produce glucose-stimulated insulin resistance, and, of these, saturated fats have the most detrimental effects.
Whether this occurs in humans was investigated by Vessby et al. (2001), who established that the amount and quality of fat in the diet could also be important for the development of insulin resistance in our species. A group of 162 healthy subjects were given an isocaloric diet high in either saturated or monounsaturated fat for three months. As in rats, insulin resistance depended on the amount of fatty acids consumed and the saturation of those fatty acids. When the amount of energy gained from fat was greater than 37%, it was found that insulin sensitivity was impaired in both the saturated fat group (-7.8%) and the monounsaturated fat group (-3.3%). However, when the amount of energy coming from fat was less than 37%, a significant difference was found with saturated fat still decreasing insulin sensitivity (-12.5%) and monounsaturated fat increasing it (+8.8%). Within the context of this study, it would seem that insulin resistance can be improved on a diet c onsisting of less than 37% of energy from fat, with this fat coming predominantly from monounsaturated fatty acids.”
Does this have much relevance for those of us who are doing higher fat Zone variations or does the lowered carb intake mitigate this?
Hope everything is cool with you,
Great information from Prof. Cordain, great question from Chris. Here are my thoughts with jsut a little pre-amble upfront.
To the best of my Knowledge…
I want to throw out props to Prof. Cordain for staying un-emotional on this topic and simply citing the best evidence at hand. He has been lambasted by quite a number of people for his “moderate” stance on saturated fat in HG diets. It’s NOT that he is trying to be politically correct as some character assassins have suggested, it’s because THE FACTS (silly facts!) seem to indicate sat’d fat was a relatively modest percentage of fats consumed by HG’s. This may simply be a math incompetence for some folk! They Apparently do not understand that if sat’d fat makes up ~10-15% of the fat in grassfed critters (the lions share of that Steric acid…LDL neutral) that % remains FIXED regardless of whether folks are eating a 10% fat diet or a 80% fat diet. This appears to matter in the grand scheme of how the body responds to nutrients ingested, insulin, inflammation etc. I talked about this stuff a bunch in the Westonprice vs Paleo post, so I don’t want to get into that much more. I just wanted to take a moment and acknowledge the integrity that has gone into his work.
I find it interesting that Paleo nutrition has encompassed everything I’ve ever learned from other nutritional philosophies:
Macrobiotics-Once you get past the stupid attempt to make everyone eat brown rice and be vegetarian, the basic tenneant: Eat seasonally, and locally is perfectly supported by paleo nutrition. Even fermented foods are covered…offal anyone?
Food Combining- Eat starches away from protein. Eat fruits alone. Paleo humans did just this. Does one need to adhere perfectly to this model? Of course not, but it is interesting that this mirrors paleo cooking more than not. Read the book !Kung San: Men Women and Work in a Foraging Society a great example of this. Also, Cordain covered this topic in a recent PDNL.
To put all this in perspectiveve, lets consider the seasonal variability in not only our ancestors foods (plant and animal) but also the food available to the critters they ate. Looking at the critters, we see a peak in bodyfatness AND saturated fat content in the late fall. This analysis by Cordain is pretty clear on that topic. We also tend to see our greatest amounts and diversity in carbohydrate rich foods in the late summer and fall. I think it is clear by this point that not only are carbs a significant issue in insulin resistance and subsequent fatness, this whole process is greatly worsened when fat and carbs (particularly fructose) are consumed together. Subsequent periods headed towards the ketogenic with very little vegetation and mainly protein and fat consumed. The !Kung and other HG’s show this pattern of seasonal increases and decreases in body fat. This is well documented in the !kung who live in equatorial Africa! Despite this there are periods of the year when total calorie intake is upwards of 90% from animal sources. As one migrates further north this punctuation in food availability becomes more dramatic. This due to greatly reduced plant sources, both in total and on a seasonal basis.
So, the take-home in all that is that we (actually everything alive) tends to run in cycles and our nutrient intake is reflective of this. Part of our modern conundrum is we have both fat and carbs a plenty. The carbs being from autoimmune promoting grains, which also have the nasty effect of disrupting insulin sensitivity.
Now, related to the literature Prof. Cordain is siting, it would appear a certain level of fat intake, particularly sat’d fat, may confer benefit with regards to insulin sensitivity. The Inuit who have traditionally consumed a high fat diet, far in excess of the 37% Prof. Cordain sites, with nothing to report besides good health. It is interesting to note however, the more cold an environment, typically the LESS saturated the fat in an animal. This fat distribution is even reflective within the bodies of animals with more polly0unsaturated fats in the extremities. Why? This improves membrane fluidity of cells. Saturated fat is solid at higher temperatures than mono’s (like olive oil) and polly’s (like fish oil). Think about the demands of reindeer legs and whale flippers that are exposed to sub-zero temperatures. Too much sat’d fat and those tissues simply quit functioning.
That is all some historical perspective and some evolutionary biology. What does practical implementation show us? Folks I’ve worked with (myself included) who are following an athlete’s zone diet, or CLC paleo diet show remarkably good blood lipids. Low insulin, blood glucose, and triglycerides to name a few. By the nature of how most folks pull off these approaches to eating, they end up with a moderate amount of sat’d fat, high mono’s and ample poly’s in the form of fish oil.
I think tinkering with PWO nutrition and intermittent fasting really improves all this. We are further improving insulin sensitivity AND minimizing the problematic state of carbs and fat released into the bloodstream together. This is another shortcoming of the Zone as commonly practiced and it likely answers why I can tolerate more carbs if taken away from all fat sources…less insulin release.
All this considered, a high Sat’d fat intake is NOT a death sentence in and of itself! The kitava studies show this pretty clearly. Prof. Cordain has made the point Sat’d fat is but one of many factors in CVD, with hyper insulinism being the main issue.
At the end of the day the basic paleo/zone prescription is still sound. If we could get a group of folks to do a controlled trial on this we would have a solid data-set on which to hang our collective hats. As it stands, we just need to make the best inferences we can from the data at hand, supplemented with our own empirical findings.
This concludes my 2 days of lolly-gagging from the book. I need to get cracking on chapter 3. I am also on the road the next 4 weeks straight…oh God help me! I will do my damndest to get to questions, I will liklely just be able to update the Road Forager posts. I can do that from my iphone (ask me about the Light Saber app sometime!!!!). I will be soooo fracking glad when that damn book is finished! I greatly prefer working on shit like this vs the organisation that goes into a project like the book. Hey, I still do not have a title…any pithy ideas?