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Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Friday, December 17, 2010

Insulin Wars V: Dr. Richard Feinman

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 2Part 3, Part 4Part 5.

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

The subject of this installment is Dr. Richard Feinman, infamous to me for his mangling of thermodynamics. 


In any case, Feinman focuses on the relationship between insulin its suppression of hormone sensitive lipase, HSL, the enzyme responsible for lipolysis in our fat cells and release of free fatty acids (NEFA/FFA).  This one really caught my eye because he evokes the following study by Hernandez et.al. that I have previously come across, demonstrating a similar effect of low-carb diets releasing NEFA that I blogged on HERE discussing the following study:  Acute exposure to long-chain fatty acids impairs α2-adrenergic receptor-mediated antilipolysis in human adipose tissue.
Carbohydrate is the major stimulus for insulin secretion and carbohydrate restriction will lower insulin secretion and, as he says, the reduction in insulin will relieve the inhibition of hormone sensitive lipase so that fat will be mobilized and there will be an increase in fatty acids due to fat breakdown.
Feinman joins a long list of LC advocates focusing on only one "side" of the Fatty Acid/Triglyceride cycle.  Yes, low insulin levels do lead to "fat breakdown", but the released FFA's have not left our bodies.  Now either they are taken up by cells and ultimately "burnt" (oxidized), or they are "recycled" back into triglycerides, either taken back up by our adipose tissue or stored in lipid droplets in ectopic (non-adipose) tissues.  Lipolysis is not fat burning.
So here is an example where chronic insulin is reduced from Hernandez, et al. comparing low carbohydrate diets (“high fat” in their paper) and high carbohydrate diets in healthy obese adults. The figure clearly shows the decrease in insulin and corresponding increase in circulating fatty acids. Notice how the release of fatty acids is exactly out of phase with the insulin. The meal comes at a low point in the insulin levels and as the insulin starts to go up, free fatty acids starts to go down as the breakdown of fat is inhibited by insulin.
Unfortunately the full text of that paper is not available for us to see the figure he's referring to, but I've highlighted before that NEFA is still released following a large carby/fatty meal.  Nobody is arguing against insulin's suppressive role in this phenomenon.

This is from Eckel’s lab and the title of the paper is “Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet” which is not accurate; it is really the failure to suppress the response to dietary fat.
Oh, I don't know about that.  Let's look at the abstract:
Objective: The purpose of this study was to compare the effect of a low-carbohydrate diet (≤20 g/d) with a high-carbohydrate diet (55% of total energy intake) on fasting and hourly metabolic variables during active weight loss.
Design: Healthy, obese adults (n = 32; 22 women, 10 men) were randomly assigned to receive either a carbohydrate-restricted diet [High Fat; mean ± SD body mass index (BMI; in kg/m2): 35.8 ± 2.9] or a calorie-restricted, low-fat diet (High Carb; BMI: 36.7 ± 4.6) for 6 wk. A 24-h in-patient feeding study was performed at baseline and after 6 wk. Glucose, insulin, free fatty acids (FFAs), and triglycerides were measured hourly during meals, at regimented times. Remnant lipoprotein cholesterol was measured every 4 h.
Results: Patients lost a similar amount of weight in both groups (P = 0.57). There was an absence of any diet treatment effect between groups on fasting triglycerides or on remnant lipoprotein cholesterol, which was the main outcome. Fasting insulin decreased (P = 0.03), and both fasting (P = 0.040) and 24-h FFAs (P < 0.0001) increased within the High Fat group. Twenty-four-hour insulin decreased (P < 0.05 for both groups). Fasting LDL cholesterol decreased in the High Carb group only (P= 0.003). In both groups, the differences in fasting and 24-h FFAs at 6 wk were significantly correlated with the change in LDL cholesterol (fasting FFA: r = 0.41, P= 0.02; 24-h FFA: r = 0.52, P = 0.002).
Conclusions: Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs. 
Fasting and 24-h FFA levels are regulated by the Triglyceride/FFA cycle and release from adipose tissue.  Dietary fat is transported in bundled triglyceride form (chylomicrons), it contributes very little to 24-h FFA exposure and not at all to fasting levels.  So I would say the authors properly entitled their research paper.  Feinman continues:
This is not surprising given that there is much more fat in the low carbohydrate diet and the additional release of free fatty acids is a good thing on a weight loss diet. It means that you are losing fat.
Umm no and no.  I've blogged extensively regarding the deleterious effects of elevated NEFA.  Indeed, elevated fasting FFA levels is one of the factors considered in characterizing the metabolic syndrome and diabetes.  Excessive circulating NEFA is as deleterious as hyperglycemia if not more.  This paper shows that low carbohydrate diets, as I've feared, exacerbates this prong of MetS and diabetes during weight loss.  Greater release of FFA's is not a good thing unless accompanied by increased oxidation of said FFA's.  You are only "losing fat" if the FFA's are subsequently oxidized, otherwise you're just inducing insulin resistance, ectopic lipid accumulation, etc.  It also can't be ignored, as Feinman does, that despite greater lipolysis and release of FFA's, the two groups lost a similar amount of weight.
The paper is also written as if this were a new effect rather than his particular eisegesis of a phenomenon that is in all the textbooks. So, there is no question that a low carbohydrate diet reduces insulin and lipolysis is increased.
Actually I've not seen weight loss comparison studies that compare the two dietary effects on NEFA levels.  24-h insulin decreased in both groups.

In any case, it has become clear to me that insulin plays a protective role by preventing excessive release of fatty acids from their proper storage depots, as stated in my above linked study.   

15 comments:

kds said...

---Yes, low insulin levels do lead to "fat breakdown", but the released FFA's have not left our bodies. Now either they are taken up by cells and ultimately "burnt" (oxidized), or they are "recycled" back into triglycerides, either taken back up by our adipose tissue or stored in lipid droplets in ectopic (non-adipose) tissues. Lipolysis is not fat burning.---

Indeed, it is true that lipolysis is not synonymous with fat burning, but it does appear that in the fed state FAs are more likely to be committed by CPTI to beta oxidation (rather than formation of TAGs by G3P-AT) in the absence of insulin.

http://tiny.cc/e28oo

CarbSane said...

Interesting link there kds. Firstly it's important to recognize we're talking liver cells here and the recycling of fatty acids to VLDL. So it would seem that when insulin is higher (fed state) more would be packaged up, when insulin is lower (fasted state) more would go to be burnt as fuel.

Still, the total rate of oxidation is dictated by metabolic need. If low carb induced reductions in insulin and increases in lipolysis lead to net increases in lipid oxidation above that of oxidation + glycolysis in a higher carb state, this should be reflected in changes in TDEE or RMR/BMR. In this study that I blogged on here you can look at the fasting insulin levels for four groups that were on LC or LF diet and exercised or not, and there was no change in RMR.

Fred Hahn said...

One thing you didn't mention was the decrease in HDL in the low fat subjects.

Also, Eckel et al did not differentiate the LDL particles. It is known that LC diets shift the particles from small dense to large buoyant. The total increase in LDL is not an issue if the type of LDL particles are altered for the better.

Eckel's conclusion then is misleading:

"In conclusion, our data indicate that a high-fat diet, instead of a calorie- and fat-restricted diet, increased LDL-cholesterol concentrations over 6 wk, and that this effect related at least in part to the lack of suppression of both fasting FFA and FFA measured hourly for 24 h. Despite this adverse effect,"

It is not an adverse effect if the LDL particles shifted away from the small dense. And since he did not mention the decline in HDL in the low fat group when a lower HDL level is in and of itself a negative finding, one is left to wonder about a possible bias.

Fred Hahn said...

And where is your support for this statement:

"Excessive circulating NEFA is as deleterious as hyperglycemia if not more."

And can you explain why if high fat diets lead to IR, as Dr. Eckel and a bunch of other low carb naysayers purport, why does the research on high fat diets like Atkins, conducted by Dr. Jeff Volek, Dr. Feinman, Dr. Westman, Dr. Shai, and many others all show increases in insulin sensitivity, fat/weight loss, lower triglycerides, higher HDL etc.?

Where is the evidence that LC/HF diets are deleterious to health? Where is the hard data? You can't just say it's unhealthy, you have to show it.

Sanjeev said...

> And can you explain why if high fat diets lead to IR, as Dr. Eckel
> and a bunch of other low carb naysayers purport

If I read you right Fred you think CarbSane is anti low carb.

She is NOT ... she claims low carb diets are an effective tool for body fat loss.

> And can you explain why if high fat diets lead to IR, as Dr. Eckel
> and a bunch of other low carb naysayers purport

Some low carb promoters claim it too ...

CarbSane and Petro of the Hyperlipid blog. It was @ Petro's Hyperlipid I first learned palmitic acid by itself directly produces a type of insulin resistance

Leo said...

And can you explain why if high fat diets lead to IR, as Dr. Eckel and a bunch of other low carb naysayers purport, why does the research on high fat diets like Atkins, conducted by Dr. Jeff Volek, Dr. Feinman, Dr. Westman, Dr. Shai, and many others all show increases in insulin sensitivity, fat/weight loss, lower triglycerides, higher HDL etc.?

Because they lost weight and any diet, adequate in protein, that causes weight loss show the same positive effects.

CarbSane said...

@Fred: Please check out:http://carbsanity.blogspot.com/search/label/NEFA/FFA

Anyone who actually reads this blog instead of skimming knows that this is a personal issue for me and I started my research to make SURE this diet is healthy.

Stay tuned in the next week or so I've got a summary blog on IR that will include thoughts on LC and IR with and without weight loss.

Fred Hahn said...

No I was not suggesting that Carbsane was anti-low carb. Sorry if it came across like that.

But often statements are made here that are half-truths and exaggerations not to mention a tad mean spirited and accusatory when it isn't called for.

"CarbSane and Petro of the Hyperlipid blog. It was @ Petro's Hyperlipid I first learned palmitic acid by itself directly produces a type of insulin resistance."

Where is the evidence for this? If someone could point me in the direction of experiments that show this I'd be grateful.

"Because they lost weight and any diet, adequate in protein, that causes weight loss show the same positive effects."

This is not necessarily the case. And low carb always shows better effects than low fat.

http://bit.ly/dZ1rXm

And bear in mind that when you restrict calories
in a diet study, you restrict carbs from baseline. Often the reduction in carbs is quite marked from what the subjects were eating before. This is often overlooked and under appreciated by researchers when summarizing. Almost all low fat, low calorie diets are low carb compared to what the subjects were eating before.


"Anyone who actually reads this blog instead of skimming knows that this is a personal issue for me and I started my research to make SURE this diet is healthy."

Well we can't read everything Carbsane. Skimming is sometimes the best we can do when there are hundreds of good blogs to read. I'll read your post and report back.

But let me ask you this, why do you assume that a LC diet is unhealthy? All of the trials have shown otherwise. It's almost as if you are looking to find reasons to believe that it is unhealthy.

Fred Hahn said...

This link doesn't lead to a blog post on NEFA.

http://carbsanity.blogspot.com/search/label/NEFA/FFA

CarbSane said...

Well Fred, if you can't be bothered to read the blog, then don't bother commenting on its content and don't harrass my readers when they make a statement like Sanjeev did about palmitic acid. One does not have to read that often here to know that NEFA are a major research focus of mine.

For some reason the / in the url prevents that link from working. That's the NEFA/FFA label down the right hand side of my blog containing 42 entries at the moment. Or you could do more specific search using the search box to narrow things down.

I'm sure there are several things on palmitic acid and insulin resistance here too. Or you might start here: http://scholar.google.com/scholar?q=palmitic+acid+insulin+resistance&hl=en&as_sdt=0&as_vis=1&oi=scholart

Re: But often statements are made here that are half-truths and exaggerations not to mention a tad mean spirited and accusatory when it isn't called for.

Yeah and we don't know anyone else who's a tad mean spirited and accusatory or writes screeds full of KNOWN half-truths and exaggerations now do we?

Fred Hahn said...

"Well Fred, if you can't be bothered to read the blog, then don't bother commenting on its content"

I do read the blog just not every single post. Relax.

"and don't harrass my readers when they make a statement like Sanjeev did about palmitic acid."

Harass?? I said "Where is the evidence for this? If someone could point me in the direction of experiments that show this I'd be grateful." How is this harassing someone? You are reading harassment into it - why?

"One does not have to read that often here to know that NEFA are a major research focus of mine."

OK, so, then could you please point me in the direction of a post you've written that supports your statement "Excessive circulating NEFA is as deleterious as hyperglycemia if not more." I am genuinely curious to read about this.

"For some reason the / in the url prevents that link from working. That's the NEFA/FFA label down the right hand side of my blog containing 42 entries at the moment. Or you could do more specific search using the search box to narrow things down."

Well I'll try to find it.

"I'm sure there are several things on palmitic acid and insulin resistance here too. Or you might start here: http://scholar.google.com/scholar?q=palmitic+acid+insulin+resistance&hl=en&as_sdt=0&as_vis=1&oi=scholart"

OK. Thanks.

"Re: But often statements are made here that are half-truths and exaggerations not to mention a tad mean spirited and accusatory when it isn't called for."

"Yeah and we don't know anyone else who's a tad mean spirited and accusatory or writes screeds full of KNOWN half-truths and exaggerations now do we?"

Touche. But mean-spirited and accusatory only when called for in self defense.

As for half truths and exaggerations, like what?

CarbSane said...

You haven't posted here in like 6 months, so I don't think it's good form to come back with a bunch of "what's your evidence" demands for comments on the blog.

On the NEFA front, a couple you may want to start with:
http://carbsanity.blogspot.com/2010/07/up-for-debate-diabetes-mellitus-or.html
http://carbsanity.blogspot.com/2010/07/up-for-debate-diabetes-mellitus-or.html (this one includes palmitate)

CarbSane said...

Sorry ... 2nd link same as first. Don't have the time to track the other one down again. If you're genuinely interested I think you'll find a ton of info at my NEFA/FFA label.

revelo said...

I'm surprised Fred hasn't sprung his famous "the burden of proof is on the claimant" line on you. He uses that a lot elsewhere. Reminds me of those Scientology types. Point out to them some of the corrupt practices of Scientology, and they respond "but where's your evidence for these accusations, you don't have any proof".

The strongest argument, IMO, against the whole primal living/slow burn/low-carb theory is precisely what these practices do to the mind. I believe Fred Hahn is partially right. If you want to lose weight and gain muscle, then low-carb and slow-burn probably work faster than anything else. Unfortunately, the price you pay is to end up like Fred Hahn. Yoga and high-carb is a much better choice. Slower yes, but at least you preserve your sanity.

Sanjeev said...

> I'm surprised Fred hasn't sprung his famous "the
> burden of proof is on the claimant" line on you.

He did. Several times.

HEY FREDdy baby: I'm still waiting on your responses to my questions. About your utter, total, absolute cluelessness on biology.

The same FRED behaviour repeated ad nauseum - demand answers immediately of others and never directly, substantively answer questions put to you. Ignore, answer a different question, try to distract the discussion ... never answer the question.

And I was mistaken about you FRED, my apologies: You're not more predictable than a box of rocks. A box could break & the rocks spill out.

In fact, you're more predictable than a single large rock in a stable geological region.

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