Google Giggles

Who'lda thunk anyone would find My Carb Sane-Asylum googling:

cute c57bl mouse

Set Point ~ Settling Point Part I: Just some thoughts

There's quite a bit of discussion going on over this topic in the comments HERE.

Archibald posted a link to Issues and Misconceptions About Obesity, the infamous Flatt paper.

Since this part was "hot" right now, I decided to blog on this, also because the issue has come up in other recent comments.

9. Conditions for body weight stability: “settling point” vs. “set point”

Although less obvious than the fact that energy intake must be equal to energy expenditure, weight stability also requires that the substrate mixture oxidized be equivalent, on average, to the composition of the nutrient mix consumed. When “substrate balance” is not achieved, changes in body composition occur, which in time are bound to elicit adjustments in food intake.  Weight maintenance thus tends to become established for a particular body composition in a given individual living under a particular set of circumstances. This corresponds to a “settling point”. Such a view accommodates the fact that circumstances cause weight stability to occur for various degrees of adiposity. Thus it seems to fit reality much better than the concept of a “set point” or “ponderostat” often invoked to explain weight stability. In fact, such a concept would seem to be utterly inconsistent with the rise in the preponderance of obesity, since set-points would have to be seen as preventing the impact of changing circumstances. It has sometimes been considered that “set-points” are reset for different conditions, but in effect this argument reduces the set-point phenomenon to a settling point.

The Damaged Metabolism Part I

This post is a bit of a "rush to publish" w/o any scientific literature or blog linking, etc.  I'll hopefully get to put the finishing touches on further installments addressing some studies (some James Krieger has discussed in posts on his blog and in comments here, and some others) and such.  

But the discussion came up again in the comments HERE , and I figured this might be as good a time as any to put at least a few general comments together.

Free Fatty Acids and Cytokines Induce Pancreatic ß-Cell Apoptosis by Different Mechanisms

Free Fatty Acids and Cytokines Induce Pancreatic ß-Cell Apoptosis by Different Mechanisms

(I've scrubbed the distracting reference numbers from some excerpts of the introduction and I'm also going to try to cite only the information pertinent to T2)

Hypercaloric diets containing large amounts of fat, also called the Western diet, contribute to a major extent to the increasing prevalence of obesity and type 2 diabetes mellitus (T2DM). T2DM is characterized by peripheral insulin resistance, pancreatic ß-cell dysfunction, and decreased ß-cell mass associated with increased rates of ß-cell apoptosis. Elevated levels of circulating free fatty acids (FFAs) contribute to the pathogenesis of T2DM. High concentrations of FFAs lead to both impairment of insulin action and ß-cell dysfunction.  Moreover, FFAs have been shown to cause ß -cell death, mainly by apoptosis. 

Of note, increased adiposity is associated not only with increased FFA release but also with adipocyte secretion of a variety of cytokines and cytokine-like adipokines, such as TNF -α, IL-6, leptin, resistin, and adiponectin. TNF-α has direct cytotoxic effects on pancreatic ß -cells, especially in combination with other cytokines.

I'm more than happy to discuss my weight ...

... but it really is besides the point.

I've finally fixed the picture issues over at my Who Is CarbSane page and it's been an interesting several weeks to read the musings about the internet about my weight, etc. based on my face shot.  I must be a cannonball, there's no way I can fit into the sizes I do, whatever ...

Join the Discussion On: Obesity and energy balance: is the tail wagging the dog?

Ripe for the weekend ... Has Gary Taubes been right all along? Is the whole tautology of the First Law of Thermodynamics whacked? Do we have this direction wrong?  Well, apparently quite a few have seen the paper I'll be sharing with you through Google Docs, and thought just that!  First, I'd like to thank Matt Metzgar for the PDF.  

OK, so what's this all about?  

Obesity and energy balance: is the tail wagging the dog?
JCK Wells and M Siervo .   European Journal of Clinical Nutrition (2011), 1–17.

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SORRY FOR THE INCONVENIENCE FOLKS

But marilynb aka mhb here has decided to share my link over at the LLVLC discussion board attributing the sharing to Matt.  Yes, he provided me with the PDF, and it's not "my" (or his) PDF, but I was sharing it through my Google Docs account via a link for my readers for the purpose of discussion.  I do not appreciate that being linked about without even properly acknowledging the source.  If you want to share and discuss, do it on your own account folks.   Some people are rather ... pathetic.

Anyway, anyone wanting the full text can email me and I'll be glad to provide it.  I'm going to have to rethink how to share full texts apparently.

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Baby Your Pancreas? Part II: Go all Jillian Michaels on your Liver?

This is more of a philosophical post/question that I'm putting out there.  Part I was more about the notion of the "tired pancreas" -- basically whether or not we need to "baby" our pancreas.  But now, let's presume that we do.  So we send it to the day spa by adopting a VLC diet.  What does this do?

Well initially, a VLC diet may do some favors for your liver.  Especially if you've been in a state of over-nutrition all along.  But after this initial respite, VLC now requires your liver to get on the exercise cycle to power the aromatherapy machine.  That silly analogy, of course, refers to the fact that the liver will be tasked with generating nearly all of the glucose your body needs to survive.  Gluconeogenesis (GNG) is a perfectly normal process, and essentially a nice recycle system for byproducts of less efficient metabolic pathways.  The human liver also seems capable of using GNG to provide all the glucose our bodies need.  But the question is, is this the optimal way to provide glucose to our cells - obligate or otherwise?

Is LC Morphing to HAES? Part II.1: What it is About Laura

At the time of posting, my installment in this series about Laura Dolson didn't catch much flack.   Of course later it was picked up on a bit, but in general I believe the lack of "backlash" on this one was that it spoke of an obvious truth -- and about someone who doesn't seem to have an active "internet personality" presence.   By that I mean Dolson blogs semiregularly over there w/o mentioning much about her personal weight issues.  Said weight issues one would have pretty much no idea about looking at her (likely Photo-shopped) face shot.  And let's read her bio, shall we?

Experience:

Laura has been developing health and education Web sites for over 10 years. She was a writer and cancer support provider at Mediconsult.com, and has taught health and nutrition classes at a junior high charter school in California. She has been focusing on low-carb and low-glycemic eating for over a decade -- investigating the emerging science related to low-carb eating, writing articles to help people change their diets, and developing healthy menus and recipes.

Baby your Pancreas? Part I: The Tired Pancreas

In the comments on a recent post on beta cell lipotoxicity, Ned Kock of Health Correlator blog posted gave a link to a post he made a while back entitled:  Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes.  This article deals with the concept of the "tired pancreas" in the development of diabetes.  It seems that (and hopefully he corrects me if I'm wrong here) Ned and I agree that this is not a likely explanation for diabetes.   Ned summarizes the progression of obesity induced T2 diabetes from Unger & Zhou, 2001.  It is worth mentioning that Unger is often summarily dismissed from the "scientific discussion roundtable" by low carbers because of the unfortunately titled "Gluttony and Sloth" paper, that, even more unfortunately also included a biblical verse.   Unger's hypothesis is very leptin-centric, but not at all incompatible with other lipotoxicity based theories.  Basically, lipotoxicity is the result of dysfunctional adipocytes leading to excessive "spill-over" of fatty acids into circulation and accumulation in ectopic tissues.   Unger & Zhou identify dysfunction in leptin secretion and/or signaling as the initiating factor in this process.  One thing that doesn't quite add up for me here is that I keep finding citations indicating leptin action increases free fatty acids which would seem counterintuitive.  In any case ...

Is LC Morphing to HAES? Part VIII: Can you be? Are You?

HAES = Health At Every Size

It is the brainchild of Dr. Linda Bacon.

Let’s face facts. We’ve lost the war on obesity. Fighting fat hasn’t made the fat go away. And being thinner, even if we knew how to successfully accomplish it, will not necessarily make us healthier or happier. The war on obesity has taken its toll. Extensive “collateral damage” has resulted: Food and body preoccupation, self-hatred, eating disorders, discrimination, poor health... Few of us are at peace with our bodies, whether because we’re fat or because we fear becoming fat.

Health at Every Size is the new peace movement.Very simply, it acknowledges that good health can best be realized independent from considerations of size. It supports people—of all sizes—in addressing health directly by adopting healthy behaviors.

Internet Impersonation Insanity

http://livinlavidalowcarb.com/blog/low-carb-conversations-podcast-episode-19-tony-kenck-and-kim-bosold-decry-the-war-on-fats/11384#comment-73690

Someone named "Evelyn" was having a little fun with Jimmy Moore.  Not me!

β-Cell lipotoxicity in the pathogenesis of non-insulin-dependent diabetes mellitus of obese rats: Impairment in adipocyte-β-cell relationships

β-Cell lipotoxicity in the pathogenesis of non-insulin-dependent diabetes mellitus of obese rats: Impairment in adipocyte-β-cell relationships

Yes, this is a rat study, but it seems applicable in light of the recent Diabetes "Crash Diet" Cure and the reductions in pancreatic fat seen in the study.  The study and the pancreatic fat issue were discussed here.  Summary:  11 diabetics followed a 600 cal/day diet for 8 weeks and regained normal insulin secretion and glycemic control.  The restored glucose induced insulin secretion (GSIS) was attributed to reduction in pancreatic fat content.

The investigators in the current study had this to say in the introduction:

Dr. Eades on Starvation Diets

When the recent news broke that a Crash Diet (600 cal/day) cured diabetes, discussed HERE,  HERE,  HERE, there was the inevitable evoking of the Minnesota Starvation Experiment in the low carb circles.   A while back, I addressed the MSE in a post entitled Starvation Diets shortly after I had blogged on a study in which one part involved putting three obese women on a 1500 cal/day liquid reducing diet.

The point of that last blog post was that  in the 1970's, the average intake of American women was 1550 cals.   Now folks, keep in mind that averages mean that some women ate less and some ate more.   Dr. Michael Dansinger -- he of the famous diet comparison study and consultant on The Biggest Loser -- told Jimmy during his interview with him that they generally cut the contestants' intake in half on that show.  I don't have time to go back and listen, and the exact numbers aren't really all that important, but the women generally start out eating around 3000 cal/day, so their reducing diet is 1500 cal/day.  Lots of low carbers sneer at TBL as, of course, being the wrong way to lose weight, they could just go low carb and achieve the same results by eating more.  

Is LC Morphing to HAES? Part VII: It's Real HAES-pocrisy Jimmy!

*** WARNING ***

This turned out to be a long post.  There's no science in it, it's mostly about personalities and such. This is directed towards anyone looking towards anyone in the LLVLC and "friends" community and such for advice or even a bit of inspiration.  If that's not you, I suggest just moving on and waiting for me to return to more science based blogging. It's coming back, I promise.  But if it is you, this is a must read if you're interested in knowing the full story behind the real Jiiiiiiimyeeeee Mooooooooore!

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Forgotten Atkins Quotes

There are at least two bona fide dietary approaches for the overweight individual -- restricting calories and restricting carbohydrates.  Both approaches, in my opinion, are meritorious and generally beneficial to most persons who are overweight, and both represent a decided improvement over the use of amphetamines or other medications, useless gadgets or doing nothing at all.

Statement of Robert C. Atkins, MD to the

Senate Select Committee on Nutrition and Human Needs

April 12, 1973

Join the discussion on: LF Diet & CVD Risk in the WHI Trial

There were actually two different papers from the Women's Health Initiative low fat diet trial brought up in the comments of another post.  It seems this one engendered more discussion and I mixed up who cited which paper.  So I started this thread.  

Since this is a new concept, I'll briefly describe what I'm doing here and let y'all have at it!  I am embedding a discussion topic from the Meeting Rooms in this blog post (this time I'll shut off comments, if you want to give some input/feedback on this concept in general, add your thoughts to the comments on the inaugural post).   All are welcome to join and I hope you will!  I have some thoughts on this one, too, but will probably lurk and wait until hopefully a few folks have added their says.  I realize some made comments already on another thread regarding this.  If I haven't done so already by the time you read this, I will copy them to the discussion.   Hat tip to Lucas Tafur for bringing this topic up.

Let's discuss!

Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.

Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML, Wassertheil-Smoller S, Kuller LH, LaCroix AZ, Langer RD, Lasser NL, Lewis CE, Limacher MC, Margolis KL, Mysiw WJ, Ockene JK, Parker LM, Perri MG, Phillips L, Prentice RL, Robbins J, Rossouw JE, Sarto GE, Schatz IJ, Snetselaar LG, Stevens VJ, Tinker LF, Trevisan M, Vitolins MZ, Anderson GL, Assaf AR, Bassford T, Beresford SA, Black HR, Brunner RL, Brzyski RG, Caan B, Chlebowski RT, Gass M, Granek I, Greenland P, Hays J, Heber D, Heiss G, Hendrix SL, Hubbell FA, Johnson KC, Kotchen JM.

JAMA. 2006 Feb 8;295(6):655-66.

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Join the discussion on: Effects of LF Diet on glucose, insulin and IR in the WHI Trial

This seemed like a good paper to discuss in our next installment of the discussion of scientific literature.  Since this is a new concept, I'll briefly describe what I'm doing here and let y'all have at it!  I am embedding a discussion topic from the Meeting Rooms in this blog post (this time I'll shut off comments, if you want to give some input/feedback on this concept in general, add your thoughts to the comments on the inaugural post).  This time the PDF is being shared through Google docs so everyone can have access to the full text.  All are welcome to join and I hope you will!  I have some thoughts on this one, but will probably lurk and wait until hopefully a few folks have added their says.  I realize some made comments already on another thread regarding this.  If it's not too much trouble perhaps you can C&P them into the discussion here.   Hat tip to O'Primitivo for bringing this up.

Let's discuss!

Effects of LF Diet on glucose, insulin and IR in the WHI Trial

James M Shikany, Karen L Margolis, Mary Pettinger, Rebecca D Jackson, Marian C Limacher, Simin Liu, Lawrence S Phillips, and Lesley F Tinker.   Am J Clin Nutr 2011;94:75–85.

Effects of FFA and Ketone Levels on Basal Insulin Secretion

From Guenther Boden's group at Temple  

Acute Lowering of Plasma Fatty Acids Lowers Basal Insulin Secretion in Diabetic and Nondiabetic Subjects

In this study, these researchers used nicotinic acid (NA, aka niacin) to lower fasting/basal free fatty acid (FFA aka NEFA) levels and looked at basal/fasting insulin secretion rates (ISR's).   They also measured beta-hydroxybutyrate (they use β-OHB abbreviation in the manuscript), otherwise known as ketones.   The NA was administered orally every 30 min for the four hour duration of the test for subjects in the fasted state.   They essentially compared two groups of diabetics with non-diabetic controls.  Euglycemic clamps were used in one group of diabetics and controls -- blood glucose held constant at normal levels -- mean glucose 5.3 and 5.1 mmol/l  respectively.  They also tested a group of diabetics at elevated fasting glucose with an isoglycemic clamp -- again blood glucose held constant but this time at 10 mmol/l.  To rule out any direct effect of NA on insulin, a control was done with a lipid infusion to prevent FFA levels from changing and it was determined that NA did not alter insulin.  I've summarized the data in the table below:

The Nutrition and Metabolism Society's Ad Campaign Smear of Hope Warshaw

The web went ablaze this past week or so over the ADA's Hope Warshaw, who penned a piece for Diabetes Health.  Judging from the reaction some might think is was akin to Mein Kamf  or something.  I mean the hypocrisy of those in the extended LLVLC community is just too much to bear at times.  What did Hope Warshaw write that was so inflammatory?  It's a short piece, but it boils down to this:

• Apparently Warshaw makes the claim that low carb is "old dogma" in diabetes circles, and
• Warshaw advocates eating a slightly higher carb (45%-65%) diet that by virtue of macronutrient ratios will result in a lower fat intake compared to the current (45%) average carb consumption.  
• Advocacy of earlier pharmaceutical intervention upon diagnosis.
• Cognition that weight loss is most effective in the first months or years following diagnosis and basically that we should be proactive with "prediabetes" screenings and diagnoses.

Oh the horror!  String her up now!!

Internet Insanity

Oh life's fun sometimes.  You make a comment or two around the net and it wakes up the sleeping crazies out there.  I have found the all out character assault on Hope Warshaw by the LC internet lynch mob to be reprehensible and I will have something to say about that later today.  I had a lot of time on my hands yesterday spent in waiting rooms  ... I got a little carried away ;-)  

But there was something about Fred Hahn's contentions in his lovely hit piece that really hit a nerve.

Quote 1:  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.

 Quote 2:  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. 

Join a discussion on: Saturated fatty acids and insulin resistance

Hi gang!  I'm going to try something a little different here with my blog.  Mirrorball had the idea to start a Scientific Discussion Group of sorts over at the Meeting Rooms, but we're not getting much in the way of takers.    So I thought I'd try a few things.

The first is this post per se, because I know far more people read feeds, etc., to see if we can't snag a few more interested takers for such a thing.

The second is that the really cool thing about my discussion board system is that I can embed a topic right here in this blog post for everyone to talk amongst themselves without going anywhere, yet this thread will be over in the Scientific Discussion sub-forum at the Meeting Rooms.  This should also give those who have trouble logging into blogger the ability to join in as well.  The default is a flat style display, but this should also allow for greater ease in following discussions that have, at times, become very difficult to follow in the comments here.  With the discussion you can view things in list and threaded form to navigate a reply thread and reply inline.  You can even reply by email if you select the "Email replies" option.  How cool is that!

Diabetes ~ A Disease by any other Name?

A HUGE bit of prefacing here ... If you're anxious to skip that and get to the subject matter, use your browser's search function to find **** to blow right on by.  

In the coming days (perhaps weeks, hopefully not months but who knows ... life's busy these days),  I'll have more to say regarding Diabetes 101's Jenny Ruhl's interview with Jimmy Moore.  Cliff Notes version is that I'm glad I listened to the whole thing because although I found myself shaking my head at times in the  beginning, later in the interview I found myself nodding more in agreement.  A huge hats off to Jenny for her amazing composure and articulation.  Wow, you would think she did this sort of thing every day!

See? I Told You So!!

I've got to say, I about fell off my chair reading the following comment from Stephan Guyenet over at Whole Health Source blog as it flittered through my feed reader.  In response to a comment by Thomas, basically asking if insulin surges or calories ultimately govern weight loss/gain, Stephan had this to say:

Yes, the excess calorie consumption is the key. Insulin spikes do not increase food intake unless they cause hypoglycemia. In fact, insulin is kind of like leptin's kid brother: it acts in the brain to constrain fat mass.

Also, insulin is co-secreted with amylin, which also constrains fat mass by increasing satiation and possibly leptin sensitivity.

All this postprandial insulin spikes = fat gain stuff is nonsense as far as I can tell. I still haven't seen a shred of convincing evidence to support it, and in fact, the evidence I've seen mostly supports the opposite hypothesis, that insulin spikes oppose fat gain. The idea that postprandial insulin causes fat gain is contradicted by the most basic empirical facts in both human and animal studies. As I said before, I don't know a single person who studies metabolism/endocrinology professionally who takes that idea seriously-- it is confined to the popular press and internet blogs/forums.

Been saying this and backing it up with citations galore for over a year now.  I'm excited to see others finally setting the record straight publicly.  First Stephan comes out as a not-so-closet potato eater.  Now he's forthrightly rejected Taubes' insulin hypothesis.  What next?  Dancing with the Stars?   Or perhaps the next institution of higher learning inclined to invite Gary Taubes to lecture their medical students might be better served inviting someone else.

Understanding

This is a philosophical post of sorts that's been knocking around in my head for a while.  I've briefly defined here before the type of intellectual bullying that goes on that I've always referred to in my real life as baffling with bullshit.  A more detailed example can be found in this blog post.  Today I want to talk about another tactic prevalent in the works and writings of pseudoscience journalists and bloggers.  It's the use of the concept of whether or not someone understands something, basically taking advantage of the general lack of knowledge in the population as a whole to make them feel stupid.  This, too, is a form of intellectual bullying folks, there's no doubt about it.  I'm sure there's some fancy Latin phrase for all of this, but I just want to point out how it is used against folks in debate and encourage would be victims to stick up for themselves and not fall for it!

Diabetes "Crash" Cures: VLCal vs. VLCarb

As I was looking at the results from the VLCal diet that "cured" diabetes, I was reminded of the discussion of "curing" vs. remission of diabetes over at Dr. Davis' Heart Scan blog.   At the time I couldn't recall the thread in which it had occurred but just now stumbled across it.   The post was entitled The Westman Diet.   Westman being Dr. Eric Westman of Duke University whom most of my readers are probably rather familiar with.

In that post Davis cites the following study:

The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus

    mnjjjjjjjjjjjjjj  <- low carb house carnivore input 

Clinical Data Unit Converter

Reading an American website in the UK?  Or reading a European study in the US?  It's a PITA!  If you're looking to put values into the system you're used to, here's about the best list I've ever come across.

Clinical Data Unit Converter

I found this looking to convert insulin from µU/mL to pmol/L.  The conversion factor is 6.945.  

So:  10 µU/mL = 10 * 6.945 = 69.45 pmol/L

Going the other way just divide.  

So 100 pmol/L = 100 / 6.945 = 14.4 µU/mL

It's Not Personal Jimmy

I've received a number of back channel communications -- most from well meaning friends -- regarding my recent calling out of the low carb community in posts like the "Is LC Morphing into HAES" series.   I've also eavesdropped on several discussions about me (from before my interview with Jimmy on through after that blog post series unveiled) where folks really "don't get me".

At this point I want all of my readers to realize that, yes, there is a personal component to my relationship with, and opinion of, Jimmy Moore.  We had exchanged an email/PM or few regarding discussions on his forum as well as my commenting several times on his menus blog regarding his weight struggles over time since I joined up on his forum a little over two years ago.  This was all before the LC Chief of Police  (Fred Hahn) found my blog entry on glyceroneogenesis that violated the LC Profanity Code.  Where were my three seashells when I needed them?

The Diabetes "Crash" Cure Revisited

I think there were some issues brought up in the comments of my original offering on this topic to warrant a followup post.

OnePointFive made the following remarks (excerpts) I'd like to address:

I thought that the trial was interesting and that'more research is needed' but with so few subjects and only a 12 week follow up (in the paper) didn't justify the 'cure' headlines.

I agree, I think the word *cure* subsequently splashed across headlines is a bit of an overstatement.  Even in the short follow-up period, 3/11 had their diabetes return.   So even though all were theoretically "cured" at 2 months, this was not permanent once they reverted to a normal diet.   Since the average gain was just over 3kg or almost 7 lbs, it would be interesting to see the individual data, and if the three who reverted back were the ones who gained the most due to returning more full bore to their former habits.  My gut says probably!  

The Diabetes "Crash" Cure & Pancreatic Fat

I'm a little late to the party weighing in on the recent "hot news" on a crash diet curing diabetes.  But weigh in I must.  If you don't know what I'm referring to, here's the study:

Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol 

That was heralded in media reports like this one:  Low-calorie diet offers hope of cure for type 2 diabetes

It just so happened that I had a journal article open in my browser dealing with pancreatic fat content and diabetes when I received an email about this from a reader.  So I sort of had this topic on my mind and was probably more receptive to what the study found vis a vis this factor than others might have been.