Insulin Wars IV: Todd Becker of Getting Stronger blog

Okey Dokey, I made a big boo boo and edited the original of this post to create another post in this series by changing the title.  Result?  The original disappeared.  Won't be doing that again!  Live and learn some more :-)  Anyway, luckily I had the post open in another browser window so I didn't lose it.  Phew!!  C&P'd the existing comments too.  Hope I didn't lose any!  Sorry if I did :-(

Friday, December 17, 2010

Insulin Wars IV: Todd Becker of Getting Stronger blog

I thought I would share some thoughts on some of the responses of LC "experts" to James Krieger's excellent series on insulin.  For any who missed them, here are the links  “Insulin…an Undeserved Bad Reputation”, Part 2,Part 3, Part 4Part 5.

Jimmy Moore asked an array of people in LC circles for their thoughts HERE

The subject of this installment is Todd Becker of Getting Stronger blog.

Becker repeats the same mantra several times in his rebuttal of James' piece.  Carbs --> IR & hyperinsulinemia --> shutting down fat burning and fat accumulation.  He repeatedly accuses James of ignoring this or that evidence while not providing any evidence for his statements of "fact".    So, here goes a mostly point-by-point rebuttal:
1. High-carb diets don’t lead to chronically high insulin levels
To support this contention, James makes the point that insulin is only elevated during and after meals, and not between meals. And since insulin levels come down between meals and during sleep, everything balances out. ... James’ characterization of the insulin response to meals underplays the fact that it can take 2-3 hours, or longer, after eating for insulin and glucose levels to return to baseline. So insulin levels won’t be at baseline for very long, except during sleep.
So?   This just demonstrates all the more that absolute insulin levels are less important to fat accumulation than the 24 hour or longer balance.  "Fat burning" NEVER stops, not even close, it is just down-regulated TEMPORARILY in response to dietary carb.  
And that’s only for individuals of normal weight who don’t snack. If you snack, those little blue “dips” in the first figure below totally disappear! For overweight people who have some degree of insulin resistance, it takes much more time for insulin levels to come down, and even the baseline level will be too high to lose much weight.
Consider this.  Losses on low carb diets are often most rapid during the early stages of the diet - a timeframe during which hyperinsulinemia has yet to be reversed.  They lose weight rapidly despite chronically elevated insulin.  
... So fat burning and ketosis just won’t happen. It doesn’t take much carbohydrate to keep the insulin up. Technically, one can lose weight with a high carb diet, but only if you eat fewer and smaller meals and space them out. And that is hard to do for many people, because elevated insulin can induce hunger...
I'll sound like a broken record here, but so does Becker ;-)  Fat burning is always happening.  And ketosis does also ... just not to the inefficient level of "spilling" to urine.   In any case, ketosis is not required for weight loss, even on low carb diets.  I've not seen evidence for that last statement.

This also undersells the real value of low carb diets — they do allow insulin levels to get low enough for lipolysis and ketosis to switch on. 
Here is the first instance where Becker mistakenly confuses lipolysis with "fat burning" aka lipid oxidation.  Broken record time again:  BOTH are "switched on" all the time, it is the rates that differ.  But while fat is mobilized (lipolysis to release FFA's from triglyceride stores) in response to energy need (substrate for beta-oxidation of fatty acids), the rates are not related in a causal fashion.  IOW, just because more fat is mobilized does not alter the rate of oxidation.  Neither does fat ingestion stimulate its own oxidation.  What happens to excess mobilized fat?  It either leads to chronically elevated circulating NEFA/FFA (bad!), or it is "recycled" back into triglyceride.

2. Protein stimulates insulin just as much as carbohydrate.

First of all, everyone concedes that protein induces an insulin response. In Protein Power, the Eadeses put this at about 50% the insulin response as from an equivalent mass of carbohydrate. But James seems to go beyond that and suggest that proteins can be just as insulinogenic or more so. However all his evidence for it is based on studies using mixtures of protein and carbohydrate, where significant levels of carbohydrate are present. ...
I don't really have the time right now to track down all the links, but if one searches Nuttall on PubMed, that research group has done a ton of work looking at insulin responses to carb/protein/alone/combo/fasting/fed, etc.  Insulin responses differ markedly between subjects and in the same subject vs. "dose" depending on context.  This argues against the whole insulin = fat accumulation per se.  But I would also point people to the following paper:  Insulin Responses to Foods.  Again, I don't have time to re-read James' articles, but if he didn't cite this, I'm citing it now!  

....The real question is what happens after the meal and between meals, and once the body gets inundated with carbohydrate over many years, raising basal insulin levels and leading to insulin resistance and a hypoglycemic response....
I've presented a lot of evidence to dispel this notion on this blog.  Post-prandial insulin responses to an energy balanced diet, even a modestly hypercaloric one, do not lead to insulin resistance no matter how many times Becker and like thinkers repeat the assertion.  It is the result of eating a  chronic hypercaloric diet and overstuffing the fat cells that leads to IR, etc.  Some may well be predisposed to develop IR, but it is not using one's pancreas that causes resistance to the hormone.   Hypoglycemia?  Here I thought in the metabolically "messed up" the glucose concentrations never come back down to even baseline.  Can't have it both ways!!

This can only be answered by studying how obese, insulin resistant or hypoglycemic individuals response to high carb meals. Normal individuals aren’t the ones with the problem! ...
Well, I can sort of agree with this when discussing how best to address the already obese.  But we're talking about blaming carbohydrates and insulin for MAKING us fat, or did I miss that part in Taubes' various books and lectures?  . Given that there hasn't been some mass mutation in the human race in the past few decades,  almost all of us started out *normal* so how did we become the ones with the problem??

..... James also denies that protein has any counteracting effect due to glucagon. He cites some studies showing that glucagon does not lead to lipolysis (fat burning). ... In a real physiological situation, the glucagon levels increase towards the end of the protein meal, as insulin is headed down. This helps the body to free up glucose from glycogen and fatty acids from fat tissue, in order to prevent a hypoglycemic response. But with low carb dieting and fasting, glucagon can remain high while insulin gets very low. ...

Here is the second time Becker erroneously equates lipolysis with fat burning.  I'll take this opportunity to make two important points:

1.  Not even all lipolysis is the same!  LPL acts in capillary beds to convert trigs to FFA's for transport into cells while HSL acts inside the cells (mostly adipocytes in my understanding) to actually "mobilize fat" out of remote storage to circulation.  

2.  It is undesirable to have increased HSL activity to "mobilize fat" without an increased need for the energy substrate.  Lipid consumption does not stimulate its own oxidation.  Lipase activity does not correlate with fatty acid oxidation.

3. Insulin suppresses, doesn’t stimulate appetite

... James cites studies in which insulin was directly injected (“central administration”) into the hypothalamus — the brain’s appetite center — and this caused suppression of appetite. ... Under these highly artificial conditions, there was appetite suppression. ...That is typical of most hormones and enzymes — they have different effects at different levels and locations in the body.

However, one should really look at how insulin acts on the body during the course of normal eating behavior. ... However, when eating high carbohydrate meals like doughnuts or orange juice, there is often both a blood sugar spike and an insulin spike that leads to a rebound effect with glucose dipping below normal baseline, giving rise to raveous hunger, tiredness, crankiness, and hypoglycemic symptoms. And this is even worse if you are insulin resistant, where the high insulin levels continue longer then needed, leading to intensified hunger. ...
Again, hypoglycemia is actually not seen in many people, especially the insulin resistant who experience some impairment in insulin-mediated glucose disposal.  And again, protein is the most satiating of macronutrients and it stimulates insulin.   But Becker does make a good point about not extrapolating the effects of exogenous administration of a hormone at concentrations in excess of normal endogenous levels to "real life".  If only some science writers heeded this admonition. 
4. The body can store fat even when it has low insulin levels.

Again, James is technically right on this point. He points out that glucose can passively diffuse into cells and be fixed into triglycerides (fat) even without the action of insulin. While that’s true, it happens at less than 20% of the rate that occurs when insulin is present! And it only happens when glucose levels are very high, whereas in the presence of insulin, even trace levels of glucose will be stored as glycogen or fat.
There's nothing wrong with glucose being stored as glycogen, and my readers know well by now that trace glucose of all things is not stored as fat.   I suggest Becker needs to read Jequier and Hellerstein.
It is also true that dietary fat can be stored as adipose tissue without the action of insulin. There is another enzyme, Acylation Stimulating Protein (ASP) which allows fatty acids to be taken up into fat cells, even when insulin levels are low and no carbohydrate is present. However, this is a highly reversible process, and the fat comes out of storage as easily as it goes into storage — whereas with insulin levels elevated even slightly above baseline, the release of fatty acids from adipose tissue is totally inhibited! So this is night and day. The only way to stay fat on a high fat diet is to continuously eat high amounts of fat with no break in the action. As soon as your meal is over, or you exercise, the fat starts coming off. Whereas with hi carbohydrate diets and high insulin, it probably takes 3-5 hours minimum to even get started with fat burning
This is so very wrong on so many levels.  As Taubes even discusses in GCBC, there's a continuous cycling of fats into and out of fat tissue in both the fasted and fed states.   Insulin regulates the release of fatty acids by its suppressive action on HSL but it never stops it completely.   Indeed excessive release of fatty acids from fat stores resulting in elevated circulating NEFA precedes the development of peripheral insulin resistance and hypERglycemia.  But Becker gets ASP (not an enzyme as was pointed out in the comments of another post) all wrong.  If one were to read around the LC web, they would think that ASP were some novel and controversial protein whose action is not well characterized.  However this is not the case, it has been well characterized, shown to stimulate glucose transport on its own, and is described as the main regulator of fat storage (esterification) in the scientific literature.  Insulin can amplify ASP, but chylomicrons from dietary fat stimulate its action to a several-fold greater degree.  In any case, in this post, the cited study demonstrated what actually happens after eating a large high fat, high carb meal.  During the first hour or two when insulin is elevated, there is a net release of fatty acids from fat tissue, while later on, when ASP is stimulated, there is net storage of fatty acids.  This is diametrically opposed to Becker's assertions.   ASP's function seems to be to clear fats from the bloodstream whenever and however they get elevated.  The obese also have elevated fasting ASP levels, and dietary fat is the most potent ASP stimulator.  By Becker's logic (and Taubes' and others who believe the "carbs drive insulin drives fat accumulation" canard) it is fats that make us fat because fat drives ASP drives fat accumulation.  If carbs lead to hyperinsulinemia, then fats lead to hyperASPemia.  Note:  I'm not saying this is the case, just that it would follow by applying insulin theory to the protein that would be a hormone were it not produced "on site" most responsible for fat deposition.  Seems to me the elevated NEFA chronically stimulates both ASP and insulin production in an effort to keep excesses where they are meant to be stored and protect the body from lipotoxicity.

5. Insulin resistance causes high basal insulin levels, not the other way around

... My own view is that he is right about this second effect (IR causes hyperinsulinemia) , but he is wrong to deny the first effect (hyperinsulinemia is one cause of insulin resistance). It is just a fact that a high carbohydrate diet, eaten over many years, keeps insulin levels high, reducing fat burning and leading to fat accumulation. I think James’ studies focussing on single meals overlook the long term effects. ...
It is simply NOT a fact.  I'm getting annoyed as I keep reading the same things about "fat burning".  Cue record (or is that the MP3 player these days?):  We alway burn some fat.  Apparently hyperinsulinemia can be self-perpetuating, and may well be why LC diets work well initially for  the insulin resistant (a subject for a future blog post), but it doesn't develop just from using one's pancreas.  Now if one is eating high carb foods morning noon and night in excess, yes, they will have a higher insulin AUC throughout the day, but they will also be stuffing their fat cells setting in motion the adisopathy that leads to IR and hyperinsulinemia. 

But there is no denying that a high carbohydrate diet is one major cause of both fat gain and insulin resistance — perhaps THE major cause.
Really?  Has Becker yet provided evidence for this statement?  No.
 In short, insulin resistance and high insulin levels reinforce each other. This is a “viscous circle” in which the pieces are both cause and effect of each other. James Kreiger wants to deny that half of this causal story is possible. (High carbohydrates causing insulin resistance). I don’t know how he can deny that in the face of very clear epidemiological evidence, that populations eating high levels of carbohydrates become obese.
Huh?  As stated before, once one is hyperinsulinemic, there's evidence that the elevated insulin does exert a self-perpetuating effect and sets up a vicious cycle.  On that point I'm in agreement with Becker.  But, there is no evidence that a strong post-prandial insulin response leads to insulin resistance.  The only populations becoming obese eating high levels of carbs are not doing so in the absence of eating high levels of fats and overall calories.   Repeating the same misinformation does not make it fact.   
Certainly, it is worse if there are high levels of fructose and little fiber in the diet. But even eating a lot of pasta and potatoes (which have little fructose) makes you fat.The examples that people give of populations which stay lean on a “high carbohydrate” diet (Kitavans, Okinawans) can be explained because the total amount of calories is much less, the people are more active, and there is enough time between meals fasting that allows insulin levels to plummet.
So ... their insulin is at normal levels because they don't OVEREAT carbs (or food in general) and they are LESS SEDENTARY.  Hmmmmmm.....  And here I thought overeating and sedentary behavior had nothing to do with fat accumulation, only insulin possesses that magical power. 
Stephan Guyenet’s articles on the Kitavans indicate that their insulin levels are half those of the Swedes! So this only reinforces the importance of keeping insulin levels low!
No, it reinforces the fact that carbohydrate consumption per se and the accompanying post-prandial insulin does not lead to elevated basal insulin levels, the cessation of fat burning and obesity.   Their insulin levels are low because they are insulin sensitive and produce insulin in response to an energy balanced diet.  This is likely due to the fact that carb consumption is not in the context of high fat and calorie levels, and they are more active.  Go figure!

Edited to add a parting thought:   lipid oxidation rates are higher in the obese and total NEFA delivery to consuming tissues and NEFA/tissue mass ratio is greater in the obese  and yet these same folks tend to be hyperinsulinemic.  This would seem to pretty much counter the whole insulin stops fat burning "chant".


Matthew said...
Nice post. "The examples that people give of populations which stay lean on a “high carbohydrate” diet (Kitavans, Okinawans) can be explained because the total amount of calories is much less, the people are more active, and there is enough time between meals fasting that allows insulin levels to plummet." That quote is quite amusing :) An additional point from this quote "In a real physiological situation, the glucagon levels increase towards the end of the protein meal, as insulin is headed down. This helps the body to free up glucose from glycogen and fatty acids from fat tissue..." I have seen this argument before that while protein raises insulin the glucagon helps release fat at the same time. However this quote is from my copy of Frayn's Metabolic Regulation: "Glucagon has a potent effect in isolated fat cells in the laboratory, but appears not to affect fat mobilization in humans in vivo" It does not say anymore than this on the subject. I do enjoy reading your blog. Matthew
Mario Renato said...
Carbsane, "It is the result of eating a chronic hypercaloric diet and overstuffing the fat cells that leads to IR, etc." I allways wondered if a long term, chronic, hypercaloric diet is enough to cause IR and diabetes. Or if we have to add some environmental endocrine disruptors, like PCBs, bisphenol-A, pesticides, phthalates, etc, etc, to the equation.
CarbSane said...
@Matthew, welcome to the Asylum and thanks! So ... someone else out there has Frayn's book :) Yes, that quote was amusing and part of the typical logical gymnastics engaged in attempts to explain away the monster elephant in the room. I think glucagon's role in any of this has been diminished as more research has been done. Clearly carbs and protein both stimulate insulin but differing metabolic pathways.


CarbSane said…
@Mario, it seems that T2 diabetes has been associated with obesity since either have been around and long before we were exposed to various toxins. It would be interesting to see if the rates of T2 in normal weight adults has increased. I don't have time at the moment to properly consider those links and comment on them specifically. But my gut says we need no additional toxins for IR to develop, but they may well contribute to the more rapid progression than diet alone.
Mario Iwakura said…

"it seems that T2 diabetes has been associated with obesity since either have been around and long before we were exposed to various toxins."

I'm really not sure about that! At least one historical toxin seems associated to diabetes: lead.
Mario Iwakura said…
And possibly others industrial heavy metals, like zinc, arsenic, cadmium, mercury and nickel:
Sanjeev said…
4. The body can store fat even when it has low insulin levels.
Again, James is technically right on this point.
Wouldn't it be awesome if Taubes could do 1/10th as well?