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Is leptin, not insulin, the real problem? -- Masterjohn's blog post

Answered on August 19, 2014
Created November 22, 2010 at 7:02 PM

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.

Ed71ab1c75c6a9bd217a599db0a3e117

(25477)

on March 04, 2011
at 02:31 PM

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.

Ed71ab1c75c6a9bd217a599db0a3e117

(25477)

on March 04, 2011
at 02:27 PM

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.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 05:59 PM

And yes, I think that's what the Jaminets are after. But then the question is why people like me thrive on 50-60g carbohydrate (the low end of their spectrum) and not higher, why people like you thrive on significantly less than that, and why other people are uncomfortable below 100g. There's always the out of "metabolic damage," but I doubt that is sufficient.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 05:53 PM

Of course then the question is just how much fat the body creates that way, how much energy is lost through that conversion. A lot of the sources, and interesting discussion, came up on this thread: http://paleohacks.com/questions/15588/de-novo-lipogenesis-and-gary-taubes Of course Eva and I made a bigger deal than we should have about the number of pounds that can add on gradually -- since that says nothing about how much of that fat your body is going to use for fuel; I mean: since you can *subtract* gradually also. It's just about getting more people out of the nightclub than in.

100fd85230060e754fc13394eee6d6f1

(18696)

on February 14, 2011
at 02:54 PM

Interesting point, Paul. I hadn't thought of that either. I guess the most efficient would be to eat *exactly* the amount of glucose you use, which I think is approximately what the Jaminets advocate.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 10:09 AM

I seem to be leaving all kinds of comments on long-gone threads recently, but it just occurred to me, Ambimorph, that maybe what JP was saying was something like what the Jaminets say: if you eat excess glucose (above around 150g) then your body will waste energy converting it to fat, so you may as well only eat the glucose that your body needs. OK, maybe JP wasn't saying that, but it is interesting. It's funny the way everyone makes a big deal out of the cost of gluconeogenesis and ketosis, but seems to forget that converting glucose to fat is also an energy-losing proposition for your body.

D88a6268af92c72494358d5ddd94f630

(70)

on November 27, 2010
at 09:05 AM

Thanks, will check this out. The Leptin Diet goes into great detail and explains the role of Leptin. Olly

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 26, 2010
at 10:18 PM

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: http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-iii-dietary.html ... Never heard of that first book, will have to take a look.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 24, 2010
at 01:25 AM

I agree on "it's just too early in the game ... to get attached to any one theory."

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 06:54 PM

You are correct that glycogenolysis is the main source of glucose, but with liver insulin resistance gluconeogenesis carries on all the time along with normal glycogen breakdown. This leads to high fasting blood sugar and higher blood sugar peaks after meals. Normally gluconeogenesis remains reduced while glycogen or food is available.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 06:53 PM

You are correct that glycogenolysis is the main source of glucose, but with liver insulin resistance gluconeogenesis carries on all the time along with normal glycogen breakdown. This leads to high fasting blood sugar and higher blood sugar peaks after meals. Normally gluconeogenesis remains reduced while glycogen or food is available. If you believe insulin resistance causes obesity you have probably been mislead by Gary Taubes, many people have.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 06:09 PM

@Matthew: On gluconeogenesis: that might be the case, nothing I said opposes that. But the point is that according to what I've learned glycogenolysis is the main thing -- i.e., using the *sugar* that is there in the liver to, uh, make sugar, instead of using protein. As for "also insulin resistance does not cause obesity" I'll assume you're teasing a little bit, since that's exactly what we've been talking about the whole time.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:52 PM

Even if I interpreted your statement in the most favourable light, it still would only say that LC is by definition eating less glucose than you burn. How does that change anything?

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:51 PM

Even if I interpreted your statement in the most favourable light, it still would only say that LC iby definition eating less glucose than you burn. How does that change anything?

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:48 PM

JP, you're saying all a LC diet does is ensure you consume <= what glucose you burn. I disagree. First of all, overweight people lose more weight on isocaloric diets with less carbohydrate, even when they are burning all the calories they ingest. Second, there is a qualitative metabolic difference in a low carb diet that is and is not ketogenic, and ketogenic diets are very powerfully therapeutic in a variety of ways.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 04:35 PM

Gluconeogenesis in the liver goes on unless insulin is present to reduce it. Insulin resistance in the liver means gluconeogenesis just carries on all the time. Also insulin resistance does not cause obesity.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 04:34 PM

Gluconeogenesis in the liver goes on unless insulin is present to reduce it. Insulin resistance in the liver means gluconeogenesis just carries on all the time. Also insulin resistance does not cause obesity.

77732bf6bf2b8a360f523ef87c3b7523

(6157)

on November 23, 2010
at 02:56 PM

I agree on the N=me sentiment. I think advocating a low-ish carb, clean Paleo approach is going to work for most people, most of the time. But it's nice to be able to turn to the biochemistry in the cases that don't see significant improvement on this approach.

A968087cc1dd66d480749c02e4619ef4

(20436)

on November 23, 2010
at 09:32 AM

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.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 05:07 AM

Oh, right, Eva, thanks, it's good to point out the distinction. But I'm pretty sure that in the mouse experiments that Masterjohn was talking about, the insulin resistance the mice had was definitely "systemic" and, it would seem, not easily reversible -- but they were still skinny. That was what was noteworthy about it.

62ed65f3596aa2f62fa1d58a0c09f8c3

(20807)

on November 23, 2010
at 04:56 AM

Insulin resistance that is a useful and EASILY REVERSABLE condition to help preserve glucose in the blood is probably fine. As low as such a lowcarb diet is consistant, then blood glucose will not actually be super high at any particular time, just a tad high at fasting but not spiking all over the place after the low carb meals. The prob is when insulin resistance is a pathological difficult to reverse state that results in regular very high levels of blood glucose.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 04:17 AM

Excellent response, Paul.

D5db204527668aa712504995c0f8f96f

(551)

on November 23, 2010
at 04:14 AM

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.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 04:02 AM

Ha! Me an expert? That's a generous thing to say.

77732bf6bf2b8a360f523ef87c3b7523

(6157)

on November 23, 2010
at 03:25 AM

Your post was a little above my non-expert head, and thought-provoking. Thanks!

77732bf6bf2b8a360f523ef87c3b7523

(6157)

on November 23, 2010
at 03:20 AM

Yikes. Sorry, I forgot to link the post! Thanks, Paul.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 01:17 AM

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.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 22, 2010
at 09:12 PM

Good points, thanks!

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 22, 2010
at 08:49 PM

Here's the direct link to Masterjohn's post, everybody: http://blog.cholesterol-and-health.com/2010/11/is-insulin-resistance-really-making-us.html

1a8020e101199de55c1b3b726f342321

(1973)

on November 22, 2010
at 08:29 PM

Masterjohn's blinded by his own argument, leptin and insulin are just indicators of metabolic dysfunction.

A727956fa3f943057c4edb08ad9e864e

(4183)

on November 22, 2010
at 08:16 PM

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.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 22, 2010
at 08:11 PM

The fact that low carb diets help people is not evidence for insulin being the problem.

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4 Answers

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5
47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 22, 2010
at 10:40 PM

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.)

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 04:35 PM

Gluconeogenesis in the liver goes on unless insulin is present to reduce it. Insulin resistance in the liver means gluconeogenesis just carries on all the time. Also insulin resistance does not cause obesity.

77732bf6bf2b8a360f523ef87c3b7523

(6157)

on November 23, 2010
at 03:25 AM

Your post was a little above my non-expert head, and thought-provoking. Thanks!

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 06:09 PM

@Matthew: On gluconeogenesis: that might be the case, nothing I said opposes that. But the point is that according to what I've learned glycogenolysis is the main thing -- i.e., using the *sugar* that is there in the liver to, uh, make sugar, instead of using protein. As for "also insulin resistance does not cause obesity" I'll assume you're teasing a little bit, since that's exactly what we've been talking about the whole time.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 05:07 AM

Oh, right, Eva, thanks, it's good to point out the distinction. But I'm pretty sure that in the mouse experiments that Masterjohn was talking about, the insulin resistance the mice had was definitely "systemic" and, it would seem, not easily reversible -- but they were still skinny. That was what was noteworthy about it.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 06:53 PM

You are correct that glycogenolysis is the main source of glucose, but with liver insulin resistance gluconeogenesis carries on all the time along with normal glycogen breakdown. This leads to high fasting blood sugar and higher blood sugar peaks after meals. Normally gluconeogenesis remains reduced while glycogen or food is available. If you believe insulin resistance causes obesity you have probably been mislead by Gary Taubes, many people have.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 04:17 AM

Excellent response, Paul.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 06:54 PM

You are correct that glycogenolysis is the main source of glucose, but with liver insulin resistance gluconeogenesis carries on all the time along with normal glycogen breakdown. This leads to high fasting blood sugar and higher blood sugar peaks after meals. Normally gluconeogenesis remains reduced while glycogen or food is available.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 04:02 AM

Ha! Me an expert? That's a generous thing to say.

62ed65f3596aa2f62fa1d58a0c09f8c3

(20807)

on November 23, 2010
at 04:56 AM

Insulin resistance that is a useful and EASILY REVERSABLE condition to help preserve glucose in the blood is probably fine. As low as such a lowcarb diet is consistant, then blood glucose will not actually be super high at any particular time, just a tad high at fasting but not spiking all over the place after the low carb meals. The prob is when insulin resistance is a pathological difficult to reverse state that results in regular very high levels of blood glucose.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 23, 2010
at 04:34 PM

Gluconeogenesis in the liver goes on unless insulin is present to reduce it. Insulin resistance in the liver means gluconeogenesis just carries on all the time. Also insulin resistance does not cause obesity.

3
100fd85230060e754fc13394eee6d6f1

(18696)

on November 22, 2010
at 08:00 PM

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.

D5db204527668aa712504995c0f8f96f

(551)

on November 23, 2010
at 04:14 AM

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.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:51 PM

Even if I interpreted your statement in the most favourable light, it still would only say that LC iby definition eating less glucose than you burn. How does that change anything?

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:48 PM

JP, you're saying all a LC diet does is ensure you consume <= what glucose you burn. I disagree. First of all, overweight people lose more weight on isocaloric diets with less carbohydrate, even when they are burning all the calories they ingest. Second, there is a qualitative metabolic difference in a low carb diet that is and is not ketogenic, and ketogenic diets are very powerfully therapeutic in a variety of ways.

0bc6cbb653cdc5e82400f6da920f11eb

(19235)

on November 22, 2010
at 08:11 PM

The fact that low carb diets help people is not evidence for insulin being the problem.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 23, 2010
at 05:52 PM

Even if I interpreted your statement in the most favourable light, it still would only say that LC is by definition eating less glucose than you burn. How does that change anything?

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 23, 2010
at 01:17 AM

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.

A727956fa3f943057c4edb08ad9e864e

(4183)

on November 22, 2010
at 08:16 PM

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.

100fd85230060e754fc13394eee6d6f1

(18696)

on November 22, 2010
at 09:12 PM

Good points, thanks!

100fd85230060e754fc13394eee6d6f1

(18696)

on February 14, 2011
at 02:54 PM

Interesting point, Paul. I hadn't thought of that either. I guess the most efficient would be to eat *exactly* the amount of glucose you use, which I think is approximately what the Jaminets advocate.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 05:53 PM

Of course then the question is just how much fat the body creates that way, how much energy is lost through that conversion. A lot of the sources, and interesting discussion, came up on this thread: http://paleohacks.com/questions/15588/de-novo-lipogenesis-and-gary-taubes Of course Eva and I made a bigger deal than we should have about the number of pounds that can add on gradually -- since that says nothing about how much of that fat your body is going to use for fuel; I mean: since you can *subtract* gradually also. It's just about getting more people out of the nightclub than in.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 05:59 PM

And yes, I think that's what the Jaminets are after. But then the question is why people like me thrive on 50-60g carbohydrate (the low end of their spectrum) and not higher, why people like you thrive on significantly less than that, and why other people are uncomfortable below 100g. There's always the out of "metabolic damage," but I doubt that is sufficient.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on February 14, 2011
at 10:09 AM

I seem to be leaving all kinds of comments on long-gone threads recently, but it just occurred to me, Ambimorph, that maybe what JP was saying was something like what the Jaminets say: if you eat excess glucose (above around 150g) then your body will waste energy converting it to fat, so you may as well only eat the glucose that your body needs. OK, maybe JP wasn't saying that, but it is interesting. It's funny the way everyone makes a big deal out of the cost of gluconeogenesis and ketosis, but seems to forget that converting glucose to fat is also an energy-losing proposition for your body.

2
62ed65f3596aa2f62fa1d58a0c09f8c3

(20807)

on November 23, 2010
at 05:04 AM

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.

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 24, 2010
at 01:25 AM

I agree on "it's just too early in the game ... to get attached to any one theory."

77732bf6bf2b8a360f523ef87c3b7523

(6157)

on November 23, 2010
at 02:56 PM

I agree on the N=me sentiment. I think advocating a low-ish carb, clean Paleo approach is going to work for most people, most of the time. But it's nice to be able to turn to the biochemistry in the cases that don't see significant improvement on this approach.

0
D88a6268af92c72494358d5ddd94f630

on November 26, 2010
at 11:45 AM

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):

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

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

D88a6268af92c72494358d5ddd94f630

(70)

on November 27, 2010
at 09:05 AM

Thanks, will check this out. The Leptin Diet goes into great detail and explains the role of Leptin. Olly

47a42b6be94caf700fce9509e38bb6a4

(9647)

on November 26, 2010
at 10:18 PM

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: http://wholehealthsource.blogspot.com/2010/01/body-fat-setpoint-part-iii-dietary.html ... Never heard of that first book, will have to take a look.

Ed71ab1c75c6a9bd217a599db0a3e117

(25477)

on March 04, 2011
at 02:31 PM

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.

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