Paleo Diet and Paleolithic Diet Questions & Answers

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The idea that insulin resistance is a primary cause of Neolithic disease is a pretty popular one in Paleo/Primal circles. We also have Gary Taubes to thank for his exposition of the carbohydrate hypothesis that refined grains and sugars are the primary nutritional causes of obesity and the other Diseases of Civilization.

Now we have Chris Masterjohn suggesting that insulin may not be the primary problem, but rather leptin.

Saying that insulin causes insulin resistance is like saying that childhood mortality is caused by children.

And

a look at the genetic animal models of leptin and insulin resistance would suggest that leptin resistance has a much more prominent role in causing obesity and that insulin resistance without leptin resistance may not cause obesity at all.

Any thoughts on this post? Criticisms?

Are there any implications for the way we should be eating for better/optimal health? I'm particularly intrigued by this part:

Rather than a result of gluocose toxicity or fat toxicity or fructose toxicity, the development of insulin resistance may be a natural, protective, homeostatic response to energy overload.

Perhaps this is a step toward resolving the "is fruit/fructose bad for you" controversy in Paleo circles?

Thanks to Melissa for alerting me to Chris Masterjohn's excellent blog.

edited Nov 23 2010 at 3:22

asked Nov 22 2010 at 19:02

JJ
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Masterjohn's blinded by his own argument, leptin and insulin are just indicators of metabolic dysfunction. – Chris Nov 22 2010 at 20:29

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Here's the direct link to Masterjohn's post, everybody: blog.cholesterol-and-health.com/2010/11/… – Paul Nov 22 2010 at 20:49

Yikes. Sorry, I forgot to link the post! Thanks, Paul. – JJ Nov 23 2010 at 3:20

The problem I have with this is the following: If insulin is the problem (or 80% of it as Sisson says) - then I know what to do to control it - control my blood sugar, regulate carbs and protein to keep insulin lowish. If leptin is the problem, then what? I have no clue. As a T2 diabetic - it really helps me to focus on what I can control (blood sugar/insulin) - and it seems to be very effective for weight reduction. After all, untreated T1's are skinny and can't gain weight - why? Insulin is required to store fat. – Dave S. Nov 23 2010 at 9:32

I believe based upon the research generated by Amgen's new synthetic leptin drug that Masterjohn is spot on. The research on the hypothalamic signalling of leptin is critical piece of data in our evolving understanding of energy metabolism. – The Quilt Mar 4 2011 at 14:27

Paul · Accepted Answer · 2010-11-22 22:40:01Z UTC

I think it's helpful to point out that insulin resistance does not always lead to overweight. This seems to be a trend recently, and not necessarily a bad one. Right along with Masterjohn's recent post, there's Stephan's most recent post, "Glucose Tolerance in Non-industrial Cultures." The basic idea, and the lesson I think we should take from this, is that a lot of insulin resistance is a natural, good thing. We've talked about a related topic here on paleohacks (see my answer on a recent thread for the relevant links): what Peter calls "physiological insulin resistance." That's what happens when you habitually eat low-carbohydrate, and Stephan in fact uses it to account for a discrepancy in the data in his post. So, again, the basic idea is that insulin resistance can be a natural, good thing. Making this a little more detailed, we can say: a healthy human body (healthy from birth, Stephan stresses) can go into high-glucose mode and deal effectively with a lot of dietary carbohydrate, or a healthy human body can go into low-glucose mode and not deal effectively with a lot of carbohydrate. A few days, or maybe a week, is needed to transition between one and the other. (If you're living in a seasonal climate, or just one in which food sources vary gradually throughout the year, this is probably not such a big deal, because you make the transition and then you stay in the new mode for a while.)

Now, as to whether insulin resistance "causes" obesity or not, there is a sense in which, even if Masterjohn is entirely correct, insulin resistance is more of a "cause" than leptin resistance. This is a fine point in conceptual use, but I think it's important. If leptin resistance always leads to obesity (or prolonged leptin resistance, whatever), then the trouble is that leptin resistance just becomes tautologically identical with weight gain -- just like it doesn't really help to say that weight gain is caused by an excess in calories in over calories out. We all agree that that is the case; what's important is what causes that. So if leptin resistance is just the mechanism by which we get fat, then it doesn't do all that much good to talk about it as the cause. I'm exaggerating a little bit; it may not be the case that leptin resistance is as closely tied to obesity as, say, "lack of blood to the brain" is to "death". But the most important point is that it is more closely tied to it than insulin resistance is. So in fact because insulin resistance does not always lead to obesity, it can actually be considered as a real cause more so than leptin resistance can.

So the really helpful thing about what Masterjohn and Stephan are doing is pointing out that insulin resistance can be a cause of obesity, but it is not always the cause, or it is not always, when working alone, the cause of obesity.

(If you know that insulin resistance does not always lead to leptin resistance, and if you know -- separately -- that leptin resistance is just the mechanism by which we get fat, then this allows you to conclude that insulin resistance does not always, by itself, make you get fat.)

So what about the real meat of Jae's question? I think that in the end, if we still know that excess carbohydrate in general (regardless of kind, so even if it's not gluten or refined), in conjunction with other factors can lead to obesity, then what's the point in risking it? Why get 90% of your calories from sweet potatoes if you run the risk of obesity -- because it's not also the case that you have been ingesting, all your life, limited linoleic acid, no gluten, and no table sugar (to say nothing of vitamin D, etc.). It might also be the case that we'll uncover a culture somewhere else in the world, without any traces of the diseases of civilization, whose members drink soybean oil all day long, but have never touched gluten or sugar, and whose carbohydrate consumption is in the 5%-30% range.

Does this sound familiar? It should. Tolerated is not optimal. Kurt Harris was "so bored with the Kitavans" a long time ago. I think we can still be bored with them. Until we see a really good reason to eat a very high proportion of our calories from carbohydrate, I don't see that all this makes a difference.

Most importantly, the insights of Taubes (or whoever can claim them first) remain. Weight gain and weight loss are still not about consciously manipulating one's input and output of calories (because those are not independent variables, etc.). They are still about altering what's going on with the hormones in your body. This is confirmed by a great set of posts by Stephan from some time back: the "Body Fat Setpoint" series. (Here's the first one; look at the archive from January 2010 for the rest.) Stephan gives us a leptin-centric account of fat gain and fat loss -- but much of it accords with what Taubes has to teach us. Everybody wins.

One more note: I think Masterjohn makes a little mistake in his post. He says that when the liver becomes insulin resistant it will continue to produce glucose from gluconeogenesis, and keep sending glucose out into the blood. That may be the case, but why the complexity? Why does everyone like talking about gluconeogenesis so much? Whatever happened to good old-fashioned glycogenolysis? Breaking down the glycogen that is already there in the liver is surely the first option for the liver; gluconeogenesis comes after, for obvious reasons (because you have to burn protein). I would guess that Masterjohn is used to talking about the situation in an LC or VLC body, where gluconeogenesis is much more common. I think it's a small oversight. (Correct me if I'm missing something.)

Ambimorph · Answer 2 · 2010-11-22 20:08:17Z UTC

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I agree the discovery of the role of insulin has been so exciting that people have gotten simplistic about what it can and can't explain, but that doesn't mean it isn't a big part of the problem. After all, countless people have lost weight and regained health through a low carb diet. That there is a minority for whom it hasn't solved their problems, doesn't make it not a primary cause. It's just not the whole story.

edited Nov 22 2010 at 20:08

answered Nov 22 2010 at 20:00

Ambimorph
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The fact that low carb diets help people is not evidence for insulin being the problem. – Matt Nov 22 2010 at 20:11

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Low carb does help control blood sugar though, which can mitigate the effects of established insulin resistance. But AFAIK, the weight loss from low carb is more likely to do which reduced triglycerides allowing more leptin to get to the hypothalmus, reducing appetite, so it does always come back to leptin. – sarah-ann Nov 22 2010 at 20:16

Good points, thanks! – Ambimorph Nov 22 2010 at 21:12

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The fact that low-carb diets help people makes it likely that insulin is at least part of the problem. It just doesn't guarantee that insulin is the only problem. So, basically: the fact that low-carb diets help people is evidence for insulin being the problem. – Paul Nov 23 2010 at 1:17

Low carbs diets only work because most people don't burn enough of the glucose (or compounds that are transformed into glucose) and glycogen. In other words, if you ain't going to burn all that ''sugar'', the best strategy is to reduce the amount you eat from nutrition (instead of activity). (well, unless you have metabolic problems). No need to really make it more complicated. – JP Nov 23 2010 at 4:14

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Eva · Answer 3 · 2010-11-23 05:04:34Z UTC

I think there are likely multiple influences that push in the same direction, from nutrient deficiences in a marjority of the population, to grain oil, grain, and sugar consumption, to lack of vitamin D, to stress, to potential chemical biological changes that such treatment creates in the body. I do watch the science with interest, but there is much we don't know yet about the chemical processes in the body. I suspect insulin and ghrelin are involved, but which, if any of them, are more at the crux of the problem remains to be seen. I think it's just too early in the game for me to get attached to any one theory. The important thing for me is I know that paleo does work and makes me feel healthier and more alive. So that is the most important science for me, ie the science of N=me. Beyond that as to why it works chemically, will probably continue to be a source of ongoing curiosity and amazement for quite some time.

Olly HT · Answer 4 · 2010-11-26 11:45:03Z UTC

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I would definitely recommend reading the following books to get a great insight into Leptin and Insulin and many other causative factors of the obesity (syndrome x conditions):

The Leptin Diet, Byron J Richards
Lights Out, T S Wilry, Bent Formby

Leptin is the master hormone and regulates the production of insulin and all other hormones.

answered Nov 26 2010 at 11:45

Olly HT
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	That last statement in your answer is not uncontroversial. I kind of usually assume it, but I've seen some good debate about this. Check out the comments to Stephan's series on the body fat setpoint for great discussion of this and some good links, etc. Especially the third installment: wholehealthsource.blogspot.com/2010/01/… ... Never heard of that first book, will have to take a look. – Paul Nov 26 2010 at 22:18
	Thanks, will check this out. The Leptin Diet goes into great detail and explains the role of Leptin. Olly – Olly HT Nov 27 2010 at 9:05
	The leterature is defintitely pointing towards leptin being more important at the hypothalmic level. Leptin seems to more of acontrol switch of the hypothalamus than insulin. Insulin in the brain acts locally and not as a modifier of synaptic signalling. – The Quilt Mar 4 2011 at 14:31

Is leptin, not insulin, the real problem? — Masterjohn’s blog post

4 Answers