Showing posts with label Metabolic Syndrome. Show all posts
Showing posts with label Metabolic Syndrome. Show all posts

Saturday, May 25, 2013

Why We Get (Sick) Fat (and Sick Livers) - Lessons from a Cafeteria Rat

Since we're talking about fructose and the liver of late, I thought I'd bump this post.  In this study groups of rats were fed one of four diets.  The "low fat" diet is better described as a high sucrose diet as 35% of the diet was sucrose.  This replaced 35% of the fat in the 45% "high fat" diet.  While the LF and HF rats gained a little more weight than the standard (also LF at 12%) chow rats, it is clear that the high fat has rather more negative metabolic effects.  I don't think the 35% sucrose diet was beneficial, rather the contrary, but that level of sucrose consumption, every single day for 10-15 weeks (which is a very long time for a human) is also hardly indicative of even SAD consumption.



Original Posting:  3/8/11

It seems fairly generally accepted that whatever the cause or progression, the so-called Metabolic Syndrome, Syndrome X and Type 2 Diabetes are associated with a dysregulation of adipose tissue metabolism, and fat tissue that is infiltrated with macrophages and secretes excessive amounts of inflammatory molecules called adipokines (e.g. TNF-α, IL-6).   A term has been coined, adisopathy, to describe this "sick fat".  

I've recently discussed the "Cafeteria Rat" study  as pertains weight gain in general.  But the other thing about this study is that it looked at the fat tissue with the different dietary interventions.  To recap, four groups of rats were fed ad libitum different diets:
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Saturday, April 13, 2013

Chronic Exposure to Free Fatty Acid Reduces Pancreatic β-Cell Insulin Content by Increasing Basal Insulin Secretion That Is Not Compensated For by a Corresponding Increase in Proinsulin Biosynthesis Translation

Coming next in the discussion of diabetes I am going to discuss insulin secretion in greater detail.  I was reminded of this post in the writing process.  So ... Bump!



Original Publish Date:  4/4/11

Chronic Exposure to Free Fatty Acid Reduces Pancreatic β-Cell Insulin Content by Increasing Basal Insulin Secretion That Is Not Compensated For by a Corresponding Increase in Proinsulin Biosynthesis Translation

JD McGarry contributing author.

{Please note:  Excerpts from the text will be edited somewhat to avoid "cluttering" references, statistical values, and some rounding of numbers.  Text will sometimes be presented in bullet form or with paragraph breaks to ease reading.  It is not my intent to plagiarize nor to alter the content.  If anyone feels I've altered the content in any meaningful way, do please let me know!}  Direct quotes will be indented.
FFA are an important physiological fuel for islets, and act as a supplemental nutrient secretagogue to potentiate insulin release acutely in the presence of glucose.
Translation:   β-cells run on fatty acids but this fuel also serves to stimulate insulin secretion.
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Tuesday, December 18, 2012

It's official. Jimmy Moore & Co. aren't interested in solving metabolic mysteries after all

UPDATE 9/14/13:  I am in the process of deciding exactly how to deal with one Dr. William L. Wilson, discoverer of the imaginary CARB Syndrome.    This appears to have been the only post of mine he links to in his unsolicited diagnosis of yours truly with this made up mental illness.   Further he offered treatment in the the form of his Carb-22 supplement.  

My purpose for this update is that some have -- rightfully, IMO -- taken him to task for making this bizarre diagnosis on the internet, of someone he has not only not met in person, but apparently knows very little accurate information about based on skimming a few blog posts.  After the fact he emailed me a link to the post, and posted one on another post on this blog.  He is busy answering many challenges to his post on his FB page at the moment.  

Rather than re-evaluate the prudence of his actions, he seems to be digging a hole.  One way he is doing that is claiming I am some public figure and it's fair game for everyone to diagnose me ... oh, and because in this post I essentially did the same thing with Jimmy Moore.  Now, this would not justify his actions, especially since as a licensed and practicing physician he is clearly subject to laws that I, a mere blogger, am not.   But let's clear a few things up anyway.

In his post he wrote:  
You might wonder how can I possibly diagnose someone with a disease who I have never personally met? Yes, to some extent I am speculating, but in medicine we often speculate about possible diseases in patients we have never seen when discussing cases with our colleagues in “curb side” consults. CarbSane even does this herself when she speculates that Jimmy Moore has Klinefelter’s syndrome and she doesn’t even have an MD behind her name. Over the years I have successfully treated thousands of patients who fit the CARB syndrome pattern and in my opinion CarbSane clearly falls into this category. After 35 years of clinical experience, my diagnostic skills are very sharp.
On FB he's written:
Out in the world physicians and every Tom, Dick and Harry speculate what might be wrong with public figures like CarbSane. Physicians do this all the time on TV and in the media. Even CarbSane does this when she speculates whether Jimmy Moore has a genetic condition.
You call my analysis of CarbSane “mean spirited”, yet she suggests that Jimmy Moore has Kleinfelter’s syndrome. Perhaps she was trying to give Jimmy information that would help him but I doubt it. Klinefelter’s syndrome is a genetic disorder you really can’t treat. If CarbSane really does have CARB syndrome, it is a reversible disorder that is quite easy to treat. If she doesn’t want to deal with it, that’s her choice and it’s fine with me. If she is interested in checking out, I have information that might be helpful to her.
There are more, perhaps I edit them in, perhaps not.  In any case, I can see how he thought that ... my wording is not always crystal clear, this is a blog after all, and I don't proof, edit and consolidate nearly as much as I would like to if I had infinite time.  But as it turns out, I did not.  Here are the exact words:

It has come up in comments here of late that Jimmy might have Klinefelter's syndrome which is one cause of hypogonadism.
Klinefelter's was raised by someone in comments  here (no I do not have the time nor desire to track a link down).  I also recall that I said at least once that I do not believe this to be the case.  A chromosomal condition like that is usually diagnosed early on.   However, there are many other causes of hypogonadism and he displays enough symptoms that if he were getting proper comprehensive care, this would at least have been addressed.    So let's be clear, I did *speculate* that this may be an issue for him, I did not diagnose him.

I did not wish to get Regina any more sneers aimed at her at the time so I didn't quote her post I linked to, but I will now.   Not to bring her any belated headaches, but because folks like Wilson are apparently too lazy to click through links and read the content that has stirred me to write what I do here.  I don't write this blog in a vacuum.  In this post, Regina wrote:
Since it is the endocrine system which largely controls our weight and hunger, it needs to function well for weight loss and maintenance. Yet, there are some endocrine issues which a diet alone cannot resolve - they are genetic - and Jimmy has, we've learned through his posts, hypogonadism.
Simply understood, that's where you, if male, have low testosterone, elevated LH and/or FSH, and often it leads to high serum ferritin (iron).

Jimmy has shared with readers that he has this condition - and it's something, that after reading up on it last night, one cannot change with diet alone. Now this isn't an excuse - but a reason that helps explain why Jimmy's appetite is such that he's driven to eat more than he requires. Those with hypogonadism are often insulin resistant, suffer abdominal obesity and gain weight easily.
Frankly, Regina stated this in far more definitive terms than I would have chosen.     Does he have hypogonadism?  I do not know.  But the point of the title of this post is that on some level, apparently, he does not care.   He is seemingly in a constant search for answers with blinders and very deep shades on in a darkened room.  He does not want to see.   For the time being the NuttyK was working for weight loss -- nevermind the worsening lipids, the stubborn UTI he had early on, the protein and crystals in his urine or anything else.  Mr. Healthy LC Diet was losing weight again.   

She also wrote:  
If nothing else, Jimmy is a prolific blogger - he's got websites, podcasts, YouTube videos, a forum, twitter and facebook - and this leaves us with a lot of information to ponder about his weight maintenance, gains and losses.
Yes he is.  And for those that don't know, I have a freakish memory and I remember a lot.  Especially numbers, images, dates, phrases, etc.etc.etc.  I see, hear and write a lot.  This reinforces it.  This may come off as obsession when it is not.  Jimmy used to blog daily about what he ate along with notes.  Routinely discuss struggles and ask for advice.  As he became more dogmatic and those offering advice kept giving him advice he didn't want to hear, he got mighty testy at times.  I vividly recall him asking for thoughts on a topic and when someone responded with their thoughts they were rudely shot down with a "nobody asked you".   I used to be one of those people who tried to help him.   Others remember me.  I remember them.  Eventually, Jimmy just started censoring any "advice" he didn't like ... and the pot shot posts at his "nasty" critics started insinuating all manner of bad behavior.  NEVER. HAPPENED.   

Regina, one last time (in response to Jimmy's comment in a post to which she was responding to:  "Was it the keto-adaptation or the calorie-cutting that has worked in producing the weight loss success I’ve seen? If you ask me, I say WHO CARES?!"):
Well, I care - not only about Jimmy as a person and friend, but also for those within the low-carb community, who despite doing everything seemingly right, fail to lose weight or gain and will do anything - even something extreme - to lose the weight.
So then, what has been going on?

What context might explain Jimmy's weight gains and losses?

And more importantly, why are those important considerations for anyone ready to jump on board the nutritional ketosis bandwagon and do what Jimmy's doing?
When Jimmy embarked on this extreme nutritional ketosis experiment seemingly everyone jumped on board.  I know not everyone, but enough.  Even a 100 lb perfectly healthy woman did.  Thankfully she had the common sense to stop before she harmed herself.   Three years ago now Jimmy went on an eggfast.  The following year on his lead a woman engaged in one.  Face went tingly, passed out.  Stuff like that.  I have highlighted here how SO many are stuck or weigh more than they ever did.   How so many see their insulin sensitivity worsen, their body composition and fat distribution change unfavorably.  For crying out loud one low carber had to cut her hair because too much was falling out  -- and still she advocates for the "healthy" diet.  There's more at stake than just money, but wasting money is enough of a bad thing, no?

I do NOT mock their looks or weight.  I do NOT attack them personally.  I DO think it is pertinent information that an advocate for a diet be honest in their delivery.  If a diet is not working for you, you really have a lot of nerve promoting it to anyone.  Period.  That Jimmy Moore is too mired in dogma to alter his diet ... Well, many have tried.  I may not have the friends Regina has in the LC community, but I do not want to see people potentially harm their health taking advice from charlatans ... even if many of those people don't particularly like me.

I provide my readers with the science here.  I'll occasionally share *my opinion* and clearly state it as such for people to consider as they see fit.   I think that on the whole Cholesterol Clarity will do far more harm than good and that it deserved at least one honest appraisal on its merits.   Jimmy Moore can't even be honest with himself any more what is going on with his health and it is evident throughout the book and the quotes he chose so selectively to entwine with his biased narrative.  






Original Publish Date:  12/18/12

I would like to give props and offer my support, though she probably doesn't really want it, to Regina Wilshire of Weight of the Evidence blog.  By the time I had found the LC community in 2009, her blogging had apparently tapered off and I had not really come across much bearing her name other than the occasional picture.  Oh ... and the post on Jimmy's now defunct and deleted menus blog identifying her as a "heavy low carber".  It was that post that caused me to mention her in a post of my own (2011) addressing the topic, hence due to Jimmy's inclusion of her in his post, her name got included in mine.   I also named a few of her low carbing friends, and the rest, as they say, is history.  I hope in retrospect, some of these folks are able to see that I meant no harm or ill will in merely highlighting what I did.  It's pretty obvious, to everyone except the low carbers it seems, that on the whole advocates of the lifestyle are more overweight or obese than advocates of other lifestyles.
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Saturday, September 29, 2012

Dysregulation of Glucose Handling: Underlying Defect, Permanent Damage or Fixable Milieu?

How many times have you heard some version of the following?
  • Sure starches are OK for 20-something CrossFitters
  • My body just can't tolerate carbohydrates
  • If I hadn't damaged my metabolism, maybe I could eat carbs now, but I can't
  • I used up my carb allotment as a kid so I can't eat them now (I blew out my pancreas)
  • Type II diabetes is a disease of carbohydrate intolerance
The list could go on.
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Sunday, March 11, 2012

Is Low Fat & High Fructose Causing Metabolic Syndrome?

Via Twitter, Beth from Weight Maven blog asked me if I read That Paleo Guy and a recent paper he blogged on.  The answers would be no and no, but I have now ;-)    The title of the study is:  Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?
 
The following stuck out at me from the conclusion of the paper:
In conclusion, we would urge medical practitioners to encourage individuals exhibiting MetS to strongly limit the consumption of dietary fructose [75] and other high-glycemic-index carbohydrates, and to stop discouraging them from consuming foods rich in cholesterol [76].
Now I don't know what medical practitioners are out there pushing fructose on people, but the recommendations to consume fruit are a far far cry from endorsing the consumption of sugar sweetened beverages and lots of juice.   I do think it's a crime that fruit juices are considered the equivalent of a piece of fruit to many nutritionists, but that aside, it is darned near impossible to eat 50g of fructose per day eating just whole fruits, let alone the 100g and upwards amounts in liquid form often used in studies.  There have also been scant few isocaloric studies done with fructose. 

In any case, as I read the study, I couldn't help getting "flashbacks" of sorts of the "Cafeteria Rat" study I blogged about over a year ago.  There is so much to that study that, yes, was in rats, but so are a heckuvalot of studies on MetSyn.   I'll be bumping the three posts directly referencing the study, and in a few days I'll publish the rest of this post that is in the hopper.  Here are the links anyway:




The last one deals with the effects that were seen on the liver, fat tissue and pancreatic cells and is probably most pertinent to a discussion of the fructose/low cholesterol hypothesis. 

Sunday, December 11, 2011

The Latest LC Beats Other Diets Study

I'm hesitant to discuss this one, because we don't even have an abstract of a published paper.  But since it's going to be bantied about the LC web anyway, I might as well comment on what information we have.

Here's the press release from the conference at which it was presented:


Here's an article that provides some additional info:  Cutting carbs just 2 days a week can spur weight loss

Piecing together the information provided together it appears that they compared weight loss and changes in biomarkers for breast cancer risk in women over a four month period.  The diet details are sketchy, but it seems they compared the following diets:

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Saturday, November 19, 2011

Gary Debunks Taubes ~ It's the Fructose Stupid!

The Marquee:  
Gary Debunks Taubes ~ It's the Fructose Stupid!
Starring Gary Taubes
Special guest appearance by Stephan Guyenet

The Scene:
Curtain rises
Gary Taubes, clad in grey corduroy pajamas and bunny slippers is in the basement of his home, that he has fastidiously transformed into an exact replica of the lecture hall where he infamously confronted Stephan Guyenet, PhD.  At the lectern stands a life-sized voodoo doll bearing a striking resemblence to Stephan.  While poking imaginary pins into the doll ...
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Thursday, October 27, 2011

Glucose Assessments, Safe Starches and Interpretations

Before I serve up any more leptinade here at the Asylum, I wanted to share some broader thoughts on the analyses and implications of various measures of blood glucose levels as relates to normal and non-T1 diabetics.

The Common Measures:

1.  Fasting Blood Glucose (FBG):  Usually after at least a 10 hr or 12 hr fast.  The implication of this is that it is a measure of basal glucose levels.   Probably more than any other parameter, this one is subject to any manner of fluctuations and can vary 10-20 points mg/dL or more from just one aberration in eating the day before.  Also the degree of activity and length of time since awakening can dramatically alter FBG as can one's stress levels, medications (even an aspirin) and sleep patterns.  This is not going to make as much of a difference with an untreated frank diabetic as their overactive glucose production by the liver likely dominates.  But for the non-diabetic, it is easy to have a "bad day" exceeding prediabetic thresholds.  
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Wednesday, October 26, 2011

Some Spiked Leptinade with My Science Krispies Please!

Well, Jimmy Moore is out with another installment of his crusade against "safe starches".  Yeah, I know, I know.  He's all about learning and helping people get to the truth, moving the debate forward constructively, and above all else protecting people from potentially bad advice such as that a major staple macronutrient for 99.99% of the human population for at least the past 10 millenia and more can actually be "safe".  Sorry, but I call things as I see them, baaayybee!   

It's another long piece, and I just can't stomach reading much of Jimmy's self-delusions anymore.  But I am interested in this whole notion that somehow we're all somewhere on a diabetic spectrum and our carb-induced post-prandial glucose spikes are lining our rat poison sprinkled paths to an early grave.  The post includes a long response by Dr. Ron Rosedale, pastor at the Church of the Not-Too-Late-in-the-Day Spiked Leptinade Drinkers.  

I'm going to address a few of the cited studies and Rosedale's basic claims.  (I'll be breaking this up in parts).  
The crux of the ‘safe starches’ argument is that no harm will come of this and it is, in fact, healthy. It is acknowledged that blood glucose will elevate after eating ‘safe starches’, but will generally stay below 140 mg/dl that Jaminet says is perfectly safe. Is it?? The science writing (below) is on the wall and the answer is…clearly no.
It is important to realize that this answer is no; there is no safe intake of sugar, nor a threshold level of blood sugar below which no harm will come, and I will shortly devote a fair amount of time to show this.

Now it would have been nice for Rosedale to include links to his science ... you know, just to make it a bit easier for the curious to go check out the studies in their entirety.  But by not doing so only those pesky blogger types like moi will likely bother. 
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Wednesday, August 31, 2011

Revisiting the Fatty Diets & Diabetes Study ~ How to Make Mickey Fat or Fattier


In her piece over at MDA on the How Fatty Diets Cause Diabetes, Denise Minger spent a bit of time discussing the strain of mouse used in the study.  That being the not-uncute fella you see pictured here:  A C57BL/6J mouse.   Denise describes these mice as:  "uber-susceptible to obesity, high blood sugar, insulin resistance, leptin resistance, and all that other fun stuff plaguing modern humans."  This didn't really square with my memory from when I blogged on a study involving this critter.  Took me a few minutes to remember what that blog was ... Of Mice and (Wo)Men.  That post dealt with a calorie restriction study using this same mouse.  In looking for info on this mouse, I had come across this paper:  The High-Fat Diet–Fed Mouse.  Since I was mostly looking for info on lifespan and such at the time, the subtitle didn't "hit me", that being:  A Model for Studying Mechanisms and Treatment of Impaired Glucose Tolerance and Type 2 Diabetes.  The paper describes this mouse's propensity towards obesity (and IGT and T2 diabetes) when fed a high fat (58%) diet vs. a standard low fat (11%) chow.  However, in the calorie restriction study, these mice did not become obese on standard chow (11%F, 69%C, 20%P, Teklad Global 2016).  Therefore I think it would be more fair to say that they are susceptible to diet-induced obesity (DIO), but not obesity per se on a more appropriate diet.
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Sunday, August 28, 2011

Where do triglycerides come from? Part III

If you haven't done so already, you may want to read Part I and Part II first.  Part II, especially, discusses the sources of fatty acids for VLDL triglycerides manufactured by the liver and two secretory pathways - an immediate one and a delayed one.  In this part I'll discuss the results of that study:



This group uses different radioactive tracers to identify the source the fatty acids in VLDL-triglycerides.  This study differed from the study in Part I in that it looked at prolonged triglyceride levels - fasting and postprandial - rather than just fasting.  For one week prior to the study all subjects were provided a standard diet (outpatient basis) of 50% carb, 35% fat, 15% protein*, at weight maintaining levels.  I would note that this would mean the obese study groups were likely ingesting significantly more than the lean controls.  The study diet followed for 5 weeks essentially replaced 20% of fat energy with carbohydrate energy for approximately 70% carb, 15% fat, 15% protein*.    It was noted that caloric content was similar, simple sugars were the same as a percentage, but absolute simple sugar intake was almost 40% more on the high carb diet.  The high carb diet also contained 50% more fiber and almost 90% less cholesterol.
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Tuesday, August 23, 2011

How Fatty Diets Cause Diabetes

How Fatty Diets Cause Diabetes

This was the provocative title of the Science Daily piece that made a minor splash across the LC web recently.  Perhaps overshadowed by the AHS drama and fallout, but nonetheless picked up on by a number of people.  The article begins with:
Newly diagnosed type 2 diabetics tend to have one thing in common: obesity. Exactly how diet and obesity trigger diabetes has long been the subject of intense scientific research. A new study led by Jamey D. Marth, Ph.D., director of the Center for Nanomedicine, a collaboration between the University of California, Santa Barbara and Sanford-Burnham Medical Research Institute (Sanford-Burnham), has revealed a pathway that links high-fat diets to a sequence of molecular events responsible for the onset and severity of diabetes.
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Sunday, August 14, 2011

Glucose and NEFA: From Dysfunctional Metabolism to Toxicity

This post started out as a comment in response to Paul Jaminet's mention of a post on this blog in his Around the Web post yesterday.  It got rather long so I decided to move it here.  In the interest of more rapid publication, I'm not going to be doing a whole lot of referencing in my discussion here, but if you're interested in a particular statement please indicate so in the comments section and I'll try to track down the reference(s) I have in mind.  Paul writes:
Every once in a while someone writes to ask me if they should fear a high-fat diet because of CarbSane’s writings on lipotoxicity. I reply that lipotoxicity only appears after metabolic syndrome has developed and, while it may drive the transition from obesity to diabetes, it is not a cause of obesity, and not a danger to people who don’t have metabolic syndrome. Also, the implications for diet are not obvious, since carb intake suppresses NEFA clearance from the blood and enhances glucotoxicity. The literature commonly speaks of “glucolipotoxicity” to describe this compounded toxicity problem. CarbSane hasn’t always been clear on these points, so it’s good to see an excellent post from her covering the basics.
Thanks for the shout out Paul!

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Saturday, May 28, 2011

Elevated Free Fatty Acids Further Impair Glucose Tolerance in IGT but not NGT

High concentrations of nonesterified fatty acids (NEFA) are a risk factor for developing type 2 diabetes in Pima Indians. In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians.
The subjects were 151 Pima - 107 with normal glucose tolerance (NGT) and 44 with impaired glucose tolerance (IGT) at the outset of the study.  At the outset none of the subjects had been diagnosed with frank diabetes.  These subjects were part of a study on pathogenesis of diabetes in the Pima and returned for annual visits to have various tests performed.  Of note, offspring of diabetic mothers were excluded from the analysis, thus the NGT group did not include this "at risk" group. 
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Monday, May 9, 2011

The Myth of Starving Cells

On the heels of my last post discussing Tom Naughton's novel theory on obesity and blood glucose regulation, I'm reminded again of the whole "fatty acids are locked away in the fat cells" - what I'll call the Starving Cells  Myth - of obesity.  Dr. Eades is weighing in on his blog on Taubes' Why We Get Fat and reiterates once again the fallacy that is the locked away fat.  Here's how he puts it:

... A non-obese person eats, uses the energy from the food and stores the rest. During the time between meals and during sleep, the non-obese person draws on the stored fat to provide energy. When the fat cell mass decreases to a certain critical point, the body signals the brain that the fat cells need a refill, so the brain initiates the hunger response. The non-obese person eats, uses some energy for immediate needs, fills the fat cells with the rest, uses the stored energy as needed, and then the cycle repeats.
It doesn’t work that way in the obese. Obese people eat, use the energy required for immediate needs and store the rest. But–and this is the extremely important ‘but’– during the time between meals and during sleep, obese people can’t access their fat stores because their baseline insulin is too high. When they can’t get to their stored fat, the lack of access to energy sets in motion all the same biochemical signals in the obese person that get sent in the non-obese, who have depleted the energy storage in their fat cells. And these signals are converted by their brains into the drive to feed, i.e., intense hunger. They have to eat to provide for their immediate energy needs because, thanks to chronically elevated insulin levels, they can’t get into to their own stored fat, even though it’s there waiting in massive quantities.
Now this all sounds perfectly reasonable, which is probably why so many just accept this as truth coming from an expert and all.   

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Sunday, May 8, 2011

Q: What's worse than an education in Human Metabolism from a journalist?

A:  An education in Human Metabolism from a comedian.

Blogger stats are interesting things at times.  It's curious to see where people find this place from.  Following my Insulin Wars series, I was rather shocked to see the Tom Naughton, aka Fat Head, installment shoot up my most read posts list, where it remained for a very long time.  As that series went, that particular post was no big deal.   I had quite a lot of traffic coming from Tom's blog.  What this tells me is that a LOT of people are getting their information from a comedian!  This guy actually has a lecture DVD out now.

This isn't good folks!!

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Tuesday, March 22, 2011

Insulin Resistance ~ Taubes v. McGarry ~ Speaking of Banting ...


This post is fast fowarding to the final contribution to the field by JD McGarry.  I'll back track and be posting works in between in coming weeks.  According to this tribute to McGarry, he was quite ill by this point, and indeed he was unable to deliver the lecture, but was present at its delivery.  It is unfortunate that Taubes has misrepresented McGarry's work, because as I read more and more about this man and from this man, he really was a scientist in the vein of bucking conventional wisdom ... something that should have perked Taubes' interest.


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Friday, March 4, 2011

Monday, February 21, 2011

Adipose Tissue Characteristics in Obese Teens & Insulin Resistance


Yes ... I'm going to be on a bit of a bookmarking post spree here :-)

This study looked at fat cell size and proliferation in obese teens and compared this to IR and fatty liver.  This study seems to be consistent with the whole "critical threshold" or "normal fat capacity" theories on why some obese are relatively "metabolically healthy" while others are not.  I've not, however, had a chance to read thoroughly.

Conclusions:  A reduced lipo-/adipogenic capacity, fraction, and estimated number of large subcutaneous adipocytes may contribute to the abnormal distribution of abdominal fat and hepatic steatosis, as well as to insulin resistance in obese adolescents.

Thinking out loud:  It seems more and more to me these days that abdominal fat - visceral in particular - is our short term buffer as Frayn describes the behavior of fat tissue in the postprandial period (recently fed state).  Overages go into our subcutaneous "overflow tank".  If we have insufficient capacity in that tank, our fat gets "sick".  

Subcutaneous and Visceral Adipose Tissue: Their Relation to the Metabolic Syndrome

Subcutaneous and Visceral Adipose Tissue: Their Relation to the Metabolic Syndrome

Another bookmarking post of sorts.

One interesting statement:

... in a review of 23 published studies of intervention strategies to promote loss of visceral adipose tissue... (32) concluded that individuals with greater visceral fat mass, either through an increase in body weight or the propensity to store fat in the visceral depot, lose more visceral fat when adjusted to the loss of body fat, regardless of the intervention applied (caloric restriction, pharmacological therapy, or exercise) because the visceral adipocyte has a higher lipolytic rate also in the steady state. 
For me, this makes my body fat distribution change all the more confusing, except that it does seem I'm talking more subQ belly fat than visceral in my case.