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Is there any Hope for Diabetes?

by Fred Hahn on July 6, 2011

Hope Warshaw R.D.

Hope Warshaw R.D.

Yes. Indeed there is. But it’s not exactly the kind of hope we want.

Hope Warshaw is a registered dietitian and diabetes educator who has gained a modicum of fame in the diabetic world. In fact, the great and powerful ADA endorses her work by virtue of the fact that they offer her articles on their website. As you’ll see in the video of her with Dr. Richard Bernstein later in this post, she’s pleasant enough and she appears to be sincere in her recommendations.

However, sincerity ain’t enough. And it sure doesn’t lower blood sugar.

In a recent egregious article in Diabetes Management, Hope made some very shocking comments regarding how diabetics should manage their diet.

In fact, her comments are so shocking that it’s high time that diabetics and the people who love them get super P.O.’d, email the magazine Editor-in-cheif and demand the scientific truth because what Hope is penning is almost criminal. What she writes, in my humble opinion, is tantamount to malpractice for an R.D.

As I see it, Hope (and others of her ilk), have some serious explaining to do. A diet for managing diabetes is more than a matter of personal food preferences as Hope suggests. We all already know we have the “right” to eat whatever we want and “deserve” to eat the foods we love. But these “rights” are totally beside the point. We are not all that different physiologically and in many ways we are virtually identical.

“Just the fact’s ma’am.” as Sgt. Friday said. That’s what diabetics need to know. Take a look at this statement:

Old Dogma: People with type 2 diabetes should follow a low carbohydrate diet.

New Reality: Nutrition recommendations for people with type 2 diabetes from the American Diabetes Association and other health authorities echo the recently unveiled U.S. 2010 Dietary Guidelines (1/31/11) for carbohydrate: about 45 to 65 percent of calories. (Americans currently eat about 45 to 50 percent of calories as carbohydrate–not a “high carb” intake.)

Old dogma? DOGMA??! It is not imagined, believed or an opinion that low carb diets work to control blood sugar – it is scientific fact. In fact, it is the only diet that can do so. Again, it’s not about what we like to eat, it’s about what manages the condition best.

And according to the USDA, the 2010 Dietary Guideline do not apply to diabetics or anyone with a health/medical condition. Shouldn’t Hope know this?

But hold the phone – she says that the ADA wants diabetics to derive 45% to 65% of their caloric intake as carbohydrate? I checked and this is not exactly what the ADA says but Hope sure is saying it. How can Hope support or rather, conjure up this wildly absurd recommendation? If followed, this recommendation will sure sell a lot of glucometers, insulin and Metformin!

O.K. Let me see if I have this straight. Fact: Diabetes is a condition of carbohydrate intolerance and if you’re a diabetic, your blood glucose level has to be monitored regularly to make sure that it is within a healthy range. (Even the Hope Warshaw’s of the world agree on this.) And carbs are the worst blood sugar offenders by far be they a glass of soda or be they a slice of 87 grain bread. All carbs turn to glucose.

O.K., now, a diabetic eats carbs and her blood sugar soars. She then is forced to take medicine to bring her blood sugar down or to keep it low before she eats the carbs in the first place – not the fat, not the protein – the carbs. So, given this scenario, the infinite wisdom of Hope is to recommend that diabetics derive 45%-65% of their calories from carbs.

I need a moment here. I think we all do.

Take that recommendation in my peeps. The ADA and Hope thinks it’s A.O.K for a diabetic to take in most of the calories they eat as carbs.

That’s like the AAFA telling people who are severely allergic to peanuts to eat more peanuts but have that EpiPen ready or to inject themselves with an EpiPen before they eat the peanuts. But make sure to eat lot’s of ‘em!

And hey, all you celiacs out there now hear this – you need to eat more bread! Don’t worry about your IBS or the other deadly conditions that gluten causes you. We got some good ol’ drugs to take care of all that!

The ADA food pyramid. Do you see the insulin sprinkled at the top like icing on the cake? Yummy!

The ADA food pyramid on the right. Do you see the insulin sprinkled at the top like icing on the cake? Yummy!

Hope goes on to say:

Countless research studies do not show long term (greater than six months to a year) benefit of low carb diets on blood glucose, weight control, or blood fats. People with type 2 diabetes, like the general public, should lighten up on added sugars and sweets (yes, they’re carbohydrate). They should eat sufficient amounts of fruits, vegetables, whole grains, and low fat dairy foods–all healthy sources of carbohydrate.

This is one wacky-worded paragraph.

OK – here’s where Hope is truly hopeless. Don’t you just love it when people say things like “Countless research studies…” Really – countless?” There are so many that the number is actually uncountable? That’s quite a lot. But why doesn’t she cite a few if there are so many? After all, she’s an R.D. and should hold herself to higher standards rather than blurt out false exaggerations.

And she virtually admits in this statement that she doesn’t know what macronutrient raises blood sugar. In other words, why isn’t she suggesting to diabetics – nay – shouting to them from on high – that they must keep their carb intake as low as possible and to make sure that the carbs they do eat come from vegetable sources? Why is she telling diabetics they should eat sufficient amount of carbs? For what purpose? Doesn’t she know of and hasn’t she read the National Institute of Health’s DRI report, specifically the section on carbs? Here it is:

Clinical Effects of Inadequate Carbohydrate Intake
The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed.

cereal

If you take a look-see at the comments section in the Diabetes Management mag article above, you’ll see that what Hope has to say about low carbing and what people who are actually low carbing have to say is quite different. And if you look closely, you’ll find nary a response from Hope. You also won’t find a single comment in support of Hope’s hogwash.

As I was writing this I read Nadia Al-Samarrie, the Editor-in-chief of Diabetes Management magazine’s article on her response to the responses. And what does she have to say? Hold on to your glucometers:

I am delighted that such a passionate, vocal group of low carbers follows Diabetes Health, but I take issue with their implication that Diabetes Health does not support low carb, and I disagree with their conviction that low carb is the one true path for people with diabetes.

It’s not a conviction, it’s scientific fact. Question Nadia – Will a low fat, high carb diet work to better blood sugar? Nope. A low protein, high carb diet? Nope. A low calorie diet? It might if the calories that are lowered come from carbs but who can stay on a low calorie diet? You’ll never take in enough micronutrients.

Or this one:

Despite the well documented merits of a low carb diet, the reality is that it’s not successful for everyone.

Wait a sec – does she mean that for some diabetics a low carb diet doesn’t keep their blood sugars more normal than a high carb diet? I think she does. If she didn’t, she’d be a lot clearer.

And anyway, it is physiologically impossible that this could be true for anyone who is diabetic. No diabetic would do better with more carbs rather than less carbs in their diet. It makes no difference whether they like the diet or not.

Shaw said: “Forget about likes and dislikes. They are of no consequence. Just do what must be done. This may not be happiness but it is greatness.”

“Personally,” Nadia says “I have not been successful on a low-carb diet, and that’s true of many other people with whom I am familiar. A low carb diet is difficult to stick to.”

Quitting smoking is difficult too if you’re a smoker. But if you’re a smoker, you’d better quit if you have emphysema. Same goes for alcohol if you’re an alcoholic. Again, it’s not about preference, it’s about the facts. And most diabetics are kept from knowing the facts.

What Nadia doesn’t know or can’t come to grips with, is she’s a sugar addict. She want’s her sugar and by gum (sugar free, right Hope?), she’s going to have hers.

Nadia goes on and on and on like this – it’s an interminable read. The illogic and “unscientificness” of it is enough to make your blood sugar boil.

Well, it’s one way to kill subscriptions.

But I suppose we do have to remember that magazines need to sell and to sell they need articles. I mean, can you imagine what would become of Diabetes Management magazine if every single article was a scientifically sound article with nary a sentence that misled? One shudders to think at the result.

Nadia and Hope – birds of a feather.

Take a look-see at this video of Hope and Richard Bernstein M.D. discussing the issue. (Sorry I couldn’t figure out how to embed the video here.)

After listening to what Dr. Bernstein is saying, and he’s stating facts, how can she hold the position she does? Has she ever read Dr. Bernstein’s book which is arguably the definitive text on the subject of diabetes? Might she be afraid of being sued by thousands of people who have followed her recommendations if she was to come clean and own up to the reality of diabetes management via a very low carb to no carb diet?

It seems to me that she should be more afraid to continue giving the advice she is. But it appears that Hope would rather your diabetic grandmother lose her feet before she loses face.

I say enough is enough. We’ve had it, haven’t we? I sure have. Aren’t you sick and tired of seeing commercials with false claims like Cheerios makes your heart healthy or the innuendo that oatmeal will cure your heart disease?

We need an outside judge or judges – a panel of new scientists to take us in a new direction – the right direction – which is away from dogma and opinion and instead towards known scientific nutritional realities. We need science. Science after all, is science.

Dr. Richard David Feinman, President of the Nutrition and Metabolism Society and Professor of Cell Biology at SUNY Downstate Medical Center suggests a new process:

“The previous Guidelines have not worked well. It is simply unreasonable to ask the DGAC to audit its own work. An external panel of scientists with no direct ties to nutritional policy would be able to do a more impartial evaluation of the data. This would be far better for everyone.”

I agree. Perhaps we’d see science rule the day and not dogma – true dogma.

Like Mark Twain said: “Be careful about reading health books. You may die of a misprint.”

I doubly agree. And I’ve written two of them!

So, considering all this, should Hope be the voice for diabetics who feel hopeless or should diabetics be Hopeless for there to be any chance of hope? I think you know the answer. At least I hope you do.

So please, write, email, shout and stomp your feet. Don’t let Hope and her cronies continue to spout their misinformation. Do something about it. And do it now!

I've been involved in exercise ever since I became a member of The Charles Atlas Club when I was 10 years old. In 1998, I founded and established Serious Strength on the Upper West Side of NYC. My clients include kids, seniors (and everyone in between), top CEOs, celebrities, bestselling authors, journalists and TV personalities.
my book. my Gym.

in diabetes,Nutrition,weight loss/diet · 83 comments

{ 4 trackbacks }

Where Is The ‘Hope’ For Diabetics, Ms. Warshaw? « Liberation Wellness
July 6, 2011 at 8:23 PM
diabetes, health, ADA, – Slow Burn Fitness | imycanetu
July 9, 2011 at 9:29 AM
The Paleo Post has been updated « The Paleo Garden
August 14, 2011 at 11:59 AM
More Information on the Hope Warshaw/Diabetes Health Controversy
April 15, 2012 at 11:03 AM

{ 79 comments… read them below or add one }

Fred Hahn July 18, 2011 at 2:49 PM

I didn’t mean Shai’s personal opnion – I meant what her data shows. Ask her!

You did read this, right?

“Among the participants with diabetes, the proportion of glycated hemoglobin at 24 months decreased by 0.4±1.3% in the low-fat group, 0.5±1.1% in the Mediterranean-diet group, and 0.9±0.8% in the low-carbohydrate group. The changes were significant (P<0.05) only in the low-carbohydrate group (P=0.45 for the comparison among groups).”

You are trying really hard to find support to your belief that the Med diet did better for the diabetics. It’s just not true Evelyn. If you’re a diabetic, you want less carbs not more.

What you’re suggesting is that, given the same amount of calories and given the same type of carbs, a diabetic would do better eating 50% of her cals from carbs as opposed to 40% and that is simply not true.

Fred Hahn July 18, 2011 at 2:53 PM

A friends astute comment on the Shai paper:

“For diabetics, it wasn’t statistically singificant differences which is why Shai et al didn’t say the med group did better than the low-carb group, they say the med group and low-carb group fared better than the low-fat group. And in the sentence regarding the diabetics, they note that the med group did better than the low-fat group wrt fbg and insulin, they’re silent (in the results section) about the result of the low-carb group.

If you go look at the slide (Figure 4), you’ll see that for both the med group and low-carb group, they were very close with improvements – not statistically significant, thus the difference may be due to chance – however, compared to the low-fat group, it was significant. That’s what’s important here, not the “hard number” result since the difference between the two groups (med and LC) was not significant. Basically when you go to the next step – to clinical significance (which Shai et al does not get into) – there is really no difference between the two (statistically) for FBG and insulin…..BUT, the A1C is statistically significant in favor of the LC group – better than both the med and LF groups.

A1C is a better measure simply because it is measuring the daily BG average, that found between the FBG, excursions after eating and any lows throughout the day, for months – it is more important because it is a snapshot of the last three months, not a one-time FBG lab or one-time insulin lab…..its result is from the previous three months!”

Alex July 18, 2011 at 3:08 PM

@CarbSane: So we are back to the problem of taking a mean for all diabetic subjects at two years and comparing it to a mean for all subjects – both diabetic and non-diabetic – at baseline. Unless you can separate out the baseline diabetic readings from the non-diabetic readings and compare it to the two year diabetic readings – the results remain inconclusive.

What I mean by spurious FBG readings is that much depends on when you take them and what diet you follow when you take them. For instance there is a known anomaly called ‘dawn phenomenon’ – when you take a FBG first thing in the morning you can often get an uncharacteristically high reading. In my case, I would often get readings in excess of 6 mmol/L. However, an hour later (still fasted) this would drop to under 5 mmol/L. If I were to only take the first readings into account I would conclude that I was pre-diabetic or, at the very least, suffering from poor glycaemic control! My last HbA1c but me at 5.0%, which indicates an average blood glucose level (over the course of a day – fasted, post-prandial, etc.) of 4.5 mmol/L (81 mg/dL). I have also done a rolling blood glucose test over 16 hours and got that same result – which shows that HbA1c is a much better indicator of long-term and ongoing blood sugar control than one-off FBGs.

Fred Hahn July 18, 2011 at 3:19 PM

She just doesn’t want to come out and say she’s wrong about LC and diabetes. She’ll fight us to the death on this Alex.

And notice she avoided answering most of my questions one of which was, if you were advising a diabetic on how to eat, after teaching them about the different types of carbs and after convincing them to eat only real food sources of unprocessed carbs, would a diabetic do better on a diet of 50% carbs or 40% or even 10%? Evelyn is suggesting that a 50% diet of carbs is best just cuz the Shai paper shows this in her opinion.

Richard David Feinman July 19, 2011 at 10:44 AM

Just a note on the Shai paper:
Sometimes, in a large study, you paint a big picture, and then have to amplify details later. Sometimes that means putting out the results according to standards of the journal, the preferences of co-authors or sometimes (this never happens to me) you realize too late that there was a better way to present the data. The NEJM paper shows the results in terms of group statistics and this is sometimes misleading. I tried to give an example, on my blog, where it is totally misleading (http://wp.me/p16vK0-4l) although the post may be a little bit tedious. In any case, I have been in contact with Dr. Shai and she will be providing new information about the data that may make things clearer. I think the group statistics may have obscured the clearly beneficial effect of the low-carbohydrate arm which I think is Dr. Shai’s interpretation.
A couple of years ago, Dr. Shai and I were on a panel at the European Association for the Study of Diabetes. After my talk, somebody in the audience asked if a more moderate version of the low carb diet I had described, if more moderate version would be better. I said no, that if you have a moderate diet, you get moderate results. The moderator asked Dr. Shai about that and she agreed. A real low carbohydrate diet, she agreed, will give you the best results (for diabetes). Of course, we always describe it as the default diet, the one to try first. One size does not fit all but the science says that low-carb is your best bet.

Fred Hahn July 19, 2011 at 12:32 PM

Thank you Dr. Feinman for your input. I’m eager to hear more from Iris.

CarbSane July 19, 2011 at 12:37 PM

For now, we only have the group data from Shai. I look forward to the individual data. I am NOT saying a high (50% carb) diet is necessarily preferable for diabetics — talk about strawmen — and y’all are fixated on the 65 number from Warshaw forgetting that 45% one! And you are all also ignoring that the USDA carb breakdown is talking half the plate from fruit and veg and only 1/4 from grain (starch).

Fred, if Shai says the low carbers did better, but you say it wasn’t a proper low carb diet after all, where are we left?

Alex, a 10 pt difference might be spurious. A 30 point difference is harder to just explain away. The reality is, fasting insulin and FBG in diabetics are indicative of their degree of insulin resistance. Treating diabetes merely from a myopic view on glucose levels is misguided. Low carbers can ignore the NEFA (free fatty acids) all they like, but these circulating levels are every bit as much, if not more, responsible for the ultimate demise of the beta cells and metabolic dysfunction.

Lipotoxicity. Fred, you asked on my blog for me to provide the references. That’s the tab to start with. Then proceed to the Insulin Resistance one. I did answer your question BTW. Go read back. Now you answer mine. Why is your friend Dana taking two diabetes meds on the direction of a LC friendly doctor because of her elevated FBG if her HbA1c is normal if it’s all about the A1c anyway? Ask her. I’m very interested but she’s all mad at me for pointing out the obvious about the weights of prominent low carbers so I doubt she’d answer my question.

Fred Hahn July 19, 2011 at 1:06 PM

“For now, we only have the group data from Shai. I look forward to the individual data. I am NOT saying a high (50% carb) diet is necessarily preferable for diabetics — talk about strawmen — and y’all are fixated on the 65 number from Warshaw forgetting that 45% one!”

You were/are in favor of the Med diet over the LC diet, right? So where is the strawman? Warshaw said 45-65% carbs. THAT is what I am fixated on. 45% is FAR too high for a diabetic! I fail to see how you fail to see this. It’s weird Evelyn.

“And you are all also ignoring that the USDA carb breakdown is talking half the plate from fruit and veg and only 1/4 from grain (starch).”

That’s better than before, no question. Still…

“Fred, if Shai says the low carbers did better, but you say it wasn’t a proper low carb diet after all, where are we left?”

No I said it wasn’t an Atkins diet given how they described the LC arm. And a diet that 40% carbs is not what virtually all experts in LC consider LC.

“Alex, a 10 pt difference might be spurious. A 30 point difference is harder to just explain away. The reality is, fasting insulin and FBG in diabetics are indicative of their degree of insulin resistance. Treating diabetes merely from a myopic view on glucose levels is misguided.”

Alex was not ignoring it Evelyn. He was pointing out, and rightly so, the A1c is more important and that the difference in FI and FBG were not reported as stat significant. As the post from my friend above states:

“If you go look at the slide (Figure 4), you’ll see that for both the med group and low-carb group, they were very close with improvements – not statistically significant, thus the difference may be due to chance – however, compared to the low-fat group, it was significant. That’s what’s important here, not the “hard number” result since the difference between the two groups (med and LC) was not significant. Basically when you go to the next step – to clinical significance (which Shai et al does not get into) – there is really no difference between the two (statistically) for FBG and insulin…..BUT, the A1C is statistically significant in favor of the LC group – better than both the med and LF groups.”

“Low carbers can ignore the NEFA (free fatty acids) all they like, but these circulating levels are every bit as much, if not more, responsible for the ultimate demise of the beta cells and metabolic dysfunction.”

I don’t think this is correct Evelyn.

“Lipotoxicity. Fred, you asked on my blog for me to provide the references. That’s the tab to start with. Then proceed to the Insulin Resistance one.”

I shall indeed.

“I did answer your question BTW. Go read back. Now you answer mine. Why is your friend Dana taking two diabetes meds on the direction of a LC friendly doctor because of her elevated FBG if her HbA1c is normal if it’s all about the A1c anyway? Ask her. I’m very interested but she’s all mad at me for pointing out the obvious about the weights of prominent low carbers so I doubt she’d answer my question.”

Maybe she shouldn’t be on those meds. I dunno. I don’t know where you are getting this info from BTW.

CarbSane July 19, 2011 at 3:12 PM

The info on Dana is from her own blog and podcasts. Maybe if she didn’t eat a 75% fat diet she wouldn’t need to be …. (I don’t know that for sure, but if we’re going to do broad dietetic “sweeps”, that would be my culprit)

Frayn, McGarry, Bierman, Boden v. Hahn. I’d say the NEFA issue is not as settled as you seem to think.

I don’t know who your friend is. Anonymity sucks ;-)

In the end, in Shai, LC was 40% carb, Med was 50%. Are you familiar with Gannon’s work?

Fred Hahn July 19, 2011 at 3:39 PM

“The info on Dana is from her own blog and podcasts. Maybe if she didn’t eat a 75% fat diet she wouldn’t need to be …. (I don’t know that for sure, but if we’re going to do broad dietetic “sweeps”, that would be my culprit)”

Oy vey. Eating a lot of fat does NOT damage beta cells. What “broad dietetic sweeps” are you referring to?

“Frayn, McGarry, Bierman, Boden v. Hahn. I’d say the NEFA issue is not as settled as you seem to think.”

Like I said I need to learn more about this. So why aren’t the Eskimos all diabetics? They’re just different, right? Like not human?

“I don’t know who your friend is. Anonymity sucks.”

Who the friend is doesn’t matter – what she is saying does.

In the end, in Shai, LC was 40% carb, Med was 50%.

In the end of what? Are you not getting what we are saying? Do you really look at studies with such tunnel vision or just this one? You are thinking about the Shai study very two dimensionally. You’re not trying to see how you might be wrong about your conclusions. That’s the mark of a good scientist. SO many people here from Alex, to Dr. Feinman, to my friend who is VERY astute, have presented very valid arguments in favor of the LC diet and you just wave them away.

We have presented our statements as to why we hold our positions and I think science sides with us. The differences in FI and FBG were NOT statistically significant between the LF and Med diets but the A1C WAS. And you’re forgetting that though the LC subjects ate less carbs they were instructed to increase the amount they ate. So over time, this affected FI and FBG more than the Med group – possibly. You have to accept the possibles.

“Are you familiar with Gannon’s work?”

Not especially – Mary Gannon?

Alex July 19, 2011 at 3:43 PM

@CarbSane: Re: Dana Carpender and her meds. According to her blog, her doctor – who diagnosed her with PCOS -has put her on a drug called Victoza because her fasting BG is high! She says:

“(For those of you who missed it, Dr. Andry explained that my fasting blood sugar is high because of the same high nighttime cortisol levels that screw up my sleep patterns — they also stimulate my liver to make too much sugar. Most of the day my blood sugar is fine, and my A1C levels have always been stone normal.)”

PCOS sufferers are often advised to moderate their carb intake BTW!

Fred Hahn July 19, 2011 at 3:51 PM

Well there you have it!

Fred Hahn July 19, 2011 at 4:49 PM

Evelyn – Please post the best paper you know of that indicates what you are saying WRT HF and beta cell damage. There is too much info on your site to find it. Just post a link to the citation please.

As far as I know this idea is nonsense. Where does Bowden say this?

Fred Hahn July 19, 2011 at 4:50 PM

IOW Evelyn, please show me the data. You made the claim.

Fred Hahn July 19, 2011 at 5:13 PM
Fred Hahn July 19, 2011 at 5:17 PM

If this is the paper, eating fat does not make you store fat in white tissue per se – but excess carbs along with fat sure will do a good job of that! Please tell me that you know this – that without carbohydrate storing fat in the fat cell is extremely difficult.

Alex July 19, 2011 at 6:06 PM

That paper seems to cite other studies which DO NOT say what is claimed and ultimately do not appear to support that paper’s findings. For example:

“SFAs exhibit a particularly strong effect to induce WAT inflammation (25)”

Yet the study cited in support of this statement, (25) Kien CL, Bunn JY, Ugrasbul F : Increasing dietary palmitic acid decreases fat oxidation and daily energy expenditure, does not appear to say this at all – as even the title indicates!
Full text: http://www.ajcn.org/content/82/2/320.long

Another example:

“Accelerated β-oxidation of SFAs causes excess electron flux in the mitochondrial respiratory chain, resulting in increased production of reactive oxygen species (ROS), which was reported to cause insulin resistance and an inflammatory response in adipocytes (31).”

Again, if you check the cited study, (31) Lin Y, Berg AH, Iyengar P, Lam TK, Giacca
A, Combs TP, Rajala MW, Du X, Rollman B, Li W, Hawkins M, Barzilai N, Rhodes CJ,
Fantus IG, Brownlee M, Scherer PE : The hyperglycemia-induced inflammatory response in adipocytes : the role of reactive oxygen species, the title makes it clear that they are discussing high blood sugar (hyperglycaemia) causing an inflammatory response in adipocytes due to increased ROS!
Full text: http://www.jbc.org/content/280/6/4617.long

Fred Hahn July 20, 2011 at 8:26 AM

On page 89 of that paper, they seem to be confusing dietary saturated fat and plasma saturated fats.

Among dietary fat constituents, saturated fat, which contains saturated fatty acids (SFA), is drawing particular attention these days, since a strong
correlation between SFA intake and the metabolic syndrome, which exhibits insulin resistance, has been reported (21-23). Foods that contain a high
level of SFA are dairy products, fatty meats, palm oil, coconut oil and some processed foods (24). Although overconsumption of FFAs generally leads
to chronic low-grade inflammation in WAT, as described above, SFAs exhibit a particularly strong effect to induce WAT inflammation (25).”

This is wrong and ridiculous. The paper itself is kinda crummy.

CarbSane July 20, 2011 at 12:59 PM

Alex, PCOS is related to insulin resistance. Fifteen years eating high fat low carb and Dana has IR. Go figure …

Read the paper(s) linked to in these blog posts:
http://carbsanity.blogspot.com/2010/10/insulin-resistance-taubes-v-frayn.html
http://carbsanity.blogspot.com/2011/05/myth-of-starving-cells_09.html
http://carbsanity.blogspot.com/2011/04/fatty-acid-trafficking.html
http://carbsanity.blogspot.com/2011/07/diabetes-crash-cure-pancreatic-fat.html

There’s lots more. Elevated NEFA leads to ectopic fat accumulation that impairs cell function and/or kills the cells. The beta cells are particularly vulnerable. Frayn has discussed the problem with postprandial elevations in NEFA — in folks who fail to properly trap the fatty acids released from chylomicrons. This is the connection of dietary fat to fatty acids. If y’all believe the insulin hypothesis, an LC diet would only serve to exacerbate this situation by adding even more fat with less efficient trapping.

I suspect if they were easier to measure and we could give diabetics NEFA-meters, we’d see a shift in treatments. Lower NEFA, improve IR. LC is excellent early on for managing hyperglycemia, but at maintenance it likely is exacerbating the underlying pathology. This isn’t a new idea, it’s been around for a long time from Bierman and McGarry (https://docs.google.com/viewer?a=v&pid=explorer&chrome=true&srcid=0Bz4TDaehOqMKYWM2ZDBiZTItNTIwNC0) and later Frayn and Boden.

Any google scholar search on beta cell lipotoxicity will net you a shitload of hits.
http://scholar.google.com/scholar?q=beta+cell+lipotoxicity&um=1&ie=UTF-8&sa=N&hl=en&tab=ws

0MzUyLWFiZDItMmM2NWUxYTEyYzQ1&authkey=CIDehrkE&hl=en

Alex July 20, 2011 at 2:55 PM

@CarbSane: What has NEFA got to do with dietary fats? NEFA stands for non-esterified fatty acids and they are the fatty acids released from adipocytes via the action of HSL (hormone sensitive lipase) not the fatty acids liberated from the fats we eat. The lipids liberated from adipocytes may be toxic for any number of reasons not at all related to the fats we eat. Body fat is a ‘sink’ for environmental toxins that the liver cannot cope with all at once. Also, if the majority of the fatty acids released are of the polyunsaturated variety – because we eat a ‘heart-healthy’ diet of mainly polyunsaturated fats – they are more easily prone to oxidation (unlike saturated fatty acids), which is a likely source of toxicity.

You seem to be getting your facts mixed up and ascribing problems with one thing to others that are not directly related and applicable – a bit like the researchers who blamed dietary saturated fats for our ills but were actually using hydrogenated oils (trans fats) in their studies!

Also, the fatty acids stored as triglycerides in adipocytes could just as easily come from the glucose liberated from the carbs we eat as they can directly from the fats we eat.

Excess fatty acids in the blood (hyperlipidemia) is not unique to people eating high fat diets – in fact, you are more likely to find people eating excessive dietary carbohydrates will have hyperlipidemia and adopting a low carb (thus high fat) diet will reduce hyperlipidemia.

Alex July 20, 2011 at 3:00 PM

PCOS features the symptom of insulin resistance but you cannot therefore deduce that a high fat diet produced the insulin resistance that then directly led to PCOS! That’s a bit like saying, that just because a primary symptom of the common cold is rhinitis and rhinitis is also a feature of the pollen allergy ‘hay fever’, that you can catch a cold from smelling too many flowers!

Fred Hahn July 20, 2011 at 3:34 PM

First of all PCOS is PCOS. IR is IR. PCOS is not caused by someone’s diet, it is a genotype in women.While it is true that many women with PCOS also have IR, some don’t. If Dana was to eat a typical American diet, she’d have full blown diabetes. So her low carb diet is keeping her from that and from having worse IR.

“There’s lots more. Elevated NEFA leads to ectopic fat accumulation that impairs cell function and/or kills the cells.”

Only in the presence of high carbohydrate intake!

“If y’all believe the insulin hypothesis, an LC diet would only serve to exacerbate this situation by adding even more fat with less efficient trapping.”

“Insulin hypothesis” – LOL. This statement is false. LC diets lead to LOWER triglyceride levels, not higher.

CarbSane July 21, 2011 at 11:11 AM

There’s clearly no point in continuing participation further here. In Dana’s case, she has developed elevated fasting glucose over the years which is an indication of hepatic IR (there are different types of insulin resistance, or perhaps a better way to say that is that different tissues become IR for different reasons). Her doctor, rather than looking at her diet, went immediately to the medications, and when med #1 didn’t work, along came med #2. Is this not what you (Fred) and others are accusing Hope of? There’s not much difference between saying “keep eating your carbs and just take your insulin” and “keep eating your fat and just take your insulin sensitizers”. Food for thought though I doubt anyone here would think on that.

Alex, I’m well aware that dietary fat does not equal NEFA, but the Fatty Acid Trafficking post (Frayn) is probably the best one to see where it can be a culprit.

Have a nice day folks!

Fred Hahn July 21, 2011 at 12:11 PM

“There’s clearly no point in continuing participation further here.”

Agreed since you are not taking in and understanding what we are saying.

“In Dana’s case, she has developed elevated fasting glucose over the years which is an indication of hepatic IR (there are different types of insulin resistance, or perhaps a better way to say that is that different tissues become IR for different reasons). Her doctor, rather than looking at her diet, went immediately to the medications, and when med #1 didn’t work, along came med #2. Is this not what you (Fred) and others are accusing Hope of?”

No it’s not! Dana has PCOS. Can you not put two and two together here? Hope advises diabetics to take in a minimum of 45% of calories as carbs which includes grains and starches. Then she advises diabetics to take meds if they need them (which ALL will need to if they eat a minimum of 45% carbs) INSTEAD of telling them to eat LESS carbs!

Do you not get this? You think eating too few carbs CAUSES or leads to IR and that is complete nonsense. No paper supports this. It is completely metabolically illogical.

“There’s not much difference between saying “keep eating your carbs and just take your insulin” and “keep eating your fat and just take your insulin sensitizers”.

Oy vey. What you don’t get it that you really don’t understand how it works and worse you don’t want to.

“Food for thought though I doubt anyone here would think on that.”

We ALL have thought on it a lot and explained why you are incorrect – completely incorrect – on this issue.

“Alex, I’m well aware that dietary fat does not equal NEFA, but the Fatty Acid Trafficking post (Frayn) is probably the best one to see where it can be a culprit.”

Please explain how this can be sans dietary carbohydrate. Show me where in any paper you can find that this is taken into account.

Have a nice day folks!

Alex July 22, 2011 at 6:12 AM

CarbSane said: “Alex, I’m well aware that dietary fat does not equal NEFA, but the Fatty Acid Trafficking post (Frayn) is probably the best one to see where it can be a culprit.”

Fred responded: “Please explain how this can be sans dietary carbohydrate. Show me where in any paper you can find that this is taken into account.”

Precisely. The Frayn study you reference clearly states that the test meals were ‘standard meals’. In the absence of any details on the exact make up of these meals (that I can find in the full text of the study), we are forced to assume a pretty ‘standard’ macronutrient ratio of >=50% carbohydrate, =protein>carbohydrate>fat. This does not indicate energy substrate preference.

Of any of the first three, supply dictates rate of oxidation/clearance. However, with fat, it is not enough to supply more fat in order to increase oxidation rate; you have to limit the others also – specifically carbohydrates. This is why any study showing a negative outcome to increased dietary fat intake almost invariably included a high carbohydrate intake also. In studies where dietary fat is increased at the expense of dietary carbohydrate, there is usually a positive outcome or, at the least, a benign or neutral effect.

With regard to NEFA and ‘fatty acid trafficking’ there does not seem to be any account made of re-esterification of fatty acids or ‘futile cycling’, in which there is a LOSS of energy.

In over- and under-feeding studies we see that the amount of the caloric excess/deficit does not accurately or linearly predict the amount of fat gain or loss. Over-fat and obese people invariably have higher energy expenditures than their lean counterparts (certainly not lower – as is often assumed by the ‘gluttony & sloth’ charge made against them). Much of this is down to an increase of basal metabolism and is one of the homoeostatic mechanisms the body has to maintain a balance between energy coming in and going out – thus preserving the body composition status quo. In fact, there are some who say we should look at substrate storage balance, rather than caloric balance, as the prime determinant of how the metabolism and body composition of an individual is balanced, i.e., body-fat ‘set-point’.

From an evolutionary perspective, we have to accept that food was not always instantly available on a daily basis as it is in today’s modern world. So, during periods without sufficient food, it was necessary to survival (the ability to obtain food when available – whether by hunting or gathering) that we did not lose much in the way of skeletal muscle. On the other hand, when food was abundantly available, it would also be counter-productive to accumulate too much body fat as that would also negatively affect out physical capabilities when it came to hunting/gathering or fighting/fleeing predators and other threats.

So it makes sense that the body would maintain a body tissue balance (within certain tolerances) irrespective of food availability or our rate of food ingestion and physical activity. These ‘set-points’ are vigorously defended and very slow to change in either direction. Obesity does not happen overnight but creeps up on people over years of even modest overindulgence (and that is just as likely type and quality of food rather than just sheer calories!). People trying to gain lean mass will attest to the effort and time required to achieve even modest changes and the speed with which those changes revert if that effort is not maintained!

So the ability to simply cycle excess fatty acids through the body via repeated lipolysis (into NEFA) and re-esterification, thus expending excess energy, makes evolutionary sense and explains why under- and over-feeding do not automatically predict a degree of weight loss/gain that is equal to the difference in calories in/out! The same is true of amino acids – they can be converted to glucose with no net gain in energy.

It should also be apparent that the substrate hierarchy indicates the degree of toxic potential if allowed to remain in the blood stream in excess quantities: alcohol being the most toxic, followed by amino acids, glucose and, finally/least toxic, fatty acids.

With regard to insulin resistance, dietary fat – in isolation – has no effect on insulin secretion. It can have an incretin effect – that is to say it can prime the beta cells of the pancreas to increase the secretion of insulin when carbohydrates are consumed but it is still the carbohydrate and NOT the fact that elicits the insulin response – eating dietary fat, while limiting the carbohydrate will still keep serum insulin at low basal levels.

Secondly it has been shown that palmitic acid (one of the saturated fatty acids) will result in a degree of transitory, physiological peripheral insulin resistance – usually in muscle tissue. Again, this is for sound evolutionary reasons. In a diet of predominantly meat protein and fat and very little carbohydrate, you want to optimise the use of fatty
acids and ketones as an energy substrate in tissues that are capable of using them freely while preserving all available glucose for use by tissues and cells that can only use glucose in anaerobic glycolytic respiration. However, there is no compelling evidence that this effect will lead to long-term or permanent insulin resistance. Studies that highlight this effect usually use isolated palmitic acid, while most food sources of saturated fat are, at most, only 50% saturated (most of the rest being monounsaturated with a small remainder that is polyunsaturated) of that, only a modest percentage will be palmitic acid.

All of these factors have to be taken into account when ascribing dietary causes to obesity and disease!

Alex July 22, 2011 at 6:18 AM

Oops! It seems the latter part of the third paragraph and first part of the fourth paragraph of my response above got mangled in some unintentional editing! It should read:

In the absence of any details on the exact make up of these meals (that I can find in the full text of the study), we are forced to assume a pretty ’standard’ macronutrient ratio of >=50% carbohydrate, =protein>carbohydrate>fat. This does not indicate energy substrate preference.

Fred Hahn July 22, 2011 at 6:56 AM

Well said Alex – and you’re hired. ;)

Q: What do you do for a living? Are you in the health field or just a nutritional brainiac? You sure do seem to have a handle on this issue – far more than I do. I could not have given that speech!

Alex July 22, 2011 at 7:22 AM

Thanks, Fred! I’m recently out of work – again! I have ‘recreational’ nutritional qualifications but I am not a professional nutritionist or dietician (and, to be honest, I would not want to be, given the prevailing ‘nutritional wisdom’ that is required for a professionally recognised qualification!). I try to read and keep up to date with the nutritional research on an ongoing basis and always try to be both critical and logical about what I read before accepting it at face value.

BTW, my correction seems to have suffered the same editorial fate – so it doesn’t seem to make sense – I don’t know why!

Alex July 29, 2011 at 2:44 PM

Just an additional point re PCOS, insulin resistance and a primal diet. Here is an account from a reader of Mark’s Daily Apple recounting her struggle with PCOS and how a primal diet – high in fats and low in carbs (especially from grains) cured her and allowed her to come off her meds:
http://www.marksdailyapple.com/i-didn%e2%80%99t-just-%e2%80%9cmanage%e2%80%9d-my-condition-i-beat-it-and-wiped-the-floor-with-it/

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