Showing posts with label Subcutaneous Fat (SCAT). Show all posts
Showing posts with label Subcutaneous Fat (SCAT). Show all posts

Sunday, April 24, 2011

Fatty Acid Trafficking

Here's an interesting recent study that LynMarie Daye of Adipo-Insights blog brought to my attention a while ago.  The link below is to the full text I'm sharing through GoogleDocs.

Downregulation of Adipose Tissue Fatty Acid Trafficking in Obesity, A Driver for Ectopic Fat Deposition?

Fats are continually being cycled in and out of our fat cells.  In the obese, circulating free fatty acids (or non-esterified fatty acids), NEFA, are often elevated.  These are often accompanied by deposition of fat in non-adipose tissues, aka ectopic fat deposition.  This ectopic fat is implicated in various impairments of cell function and even cell death (apoptosis) that result in insulin resistance, beta-cell dysfunction, etc.  This is often referred to as lipotoxicity.  

This study sought to determine if this lipotoxicity is due to excessive release of NEFA from adipose tissue or from impaired trapping by adipose tissue of the NEFA released from dietary fat.  This work is from Keith Frayn's group.  It might be worthwhile to read my blog post on Frayn's paper on adipose tissue as lipid buffer.
Read more »

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. 

Thursday, February 17, 2011

Elevated Free Fatty Acids: Detrimental?

As many of my readers know, I've been challenged lately on my beliefs on NEFA.  So I thought I would summarize my thinking on this in a post rather than having several comments scattered amongst a few threads.   I'm not going to be referencing my post here at this time (it's too time consuming to do so at the moment).  If/when I have the opportunity to do so in the future, I'll do a bumped update.  

These are my thoughts based on extensive research of the peer review literature on this topic, in almost all cases, considered review of full text articles including reading as many supporting citations in major reviews as possible.  Over the past year I have read at least a hundred such articles.

Elevated non-esterified or free fatty acids (NEFA/FFA) are a symptom associated with insulin resistance, Metabolic Syndrome (aka Syndrome X) and Type II diabetes.  The overwhelming evidence in the literature points to elevated NEFA being more than just associated with these conditions, but rather the initiating step in their development..   
Read more »

Friday, January 14, 2011

Insulin, Weight Loss & Water Weight

Reader kds posted a link to this Peter of Hyperlipid's blog post about the following study:  .Beneficial Effect of Diazoxide in Obese Hyperinsulinemic Adults

Basically, diazoxide is a compound that has been used to treat hypoglycemia and reduces insulin secretion.   Two groups of 12 obese hyperinsulinemic adults were treated with diazoxide or placebo for 8 weeks while each consuming the same Optifast diet.  Compared with the placebo group, DZ subjects had greater weight loss (9.5 ± 0.69% vs. 4.6 ± 0.61%, P < 0.001), greater decrease in body fat (P < 0.01), greater increase in fat-free mass to body fat ratio (P < 0.01), and greater attenuation of acute insulin response to glucose (P < 0.01).   This is pretty phenomenal and difficult to fathom -- almost twice the weight loss.  It was also reported that there was no significant change in resting energy expenditure (REE, RMR, BMR), and substrate use, as derived from indirect calorimetry, did not reveal any significant change in carbohydrate or fat metabolism in either group.  IOW, there was no stimulation of fatty acid oxidation accompanying the proposed decreased lipogenesis (presumably they're referring to esterification not de novo lipogenesis) and/or increased lipolysis (as evidenced by increases in FFA/NEFA levels).

Now, some may accuse me of rationalizing, but for all the claims I may disagree with, I have yet to see any of the "experts" -- even Taubes and Eades and the MA crowd -- imply that fatty acids can magically be "flushed" from the body without being "burnt" off (beta oxidation).  The only way out is for the LCFA to be broken down ultimately to CO2.  Therefore, there HAS to be an explanation here because insulin is not a magic molecule capable of creating or destroying matter.  If the diazoxide (DZ) didn't lead to increased fatty acid oxidation, and REE was unchanged, then likely futile cycling and uncoupling were not involved either -- these would cause increases in both FA oxidation and REE as they "blow off" or "waste" fatty acids.

So ... where did the fatty acid mass go?
Read more »

Friday, October 29, 2010

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance

Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance

This is a very interesting article.  They looked at not only visceral vs. subQ abdominal fat, but differentiated between two types of abdominal SCAT (subcutaneous adipose tissue):  superficial vs. deep.

There is a well described fascial plane within the SAT of the abdomen (18, 28), with the superficial adipose layer possessing compact fascial septa (Camper’s fascia), whereas the deeper layer of adipose tissue has more loosely organized fascial septa (Scarpa’s fascia).  Fat lobules of the two sites also differ. The superficial layer is characterized by small tightly packed lobules, whereas those of the deeper layer are larger and distributed in an irregular manner (28). The thickness of the deep layer appears more variable among individuals and especially in relation to obesity (3). The presence of these fascial planes and differences in histology are well recognized with respect to liposuction, which generally is targeted toward the deep layer (15, 23).  Given the anatomical basis for considering the two layers of SAT in the abdomen different and the ability to delineate the fascial plane utilizing CT (22), the current study was undertaken to examine these adipose tissue depots from a metabolic perspective. The related purpose was to address current controversies regarding the importance of subcutaneous abdominal adipose tissue in relation to IR.
I doubt the screen shot below will show up well, but thought to include them anyway:


Summary of Body Composition:

  • Systemic FM (I'll use TotFM) was greater in the obese (obviously) and women compared to men in both groups.  
  • Thigh FM (I'll use TFM) and superficial abdominal SAT (I'll use SASAT) was also greater in the women
  • Deep abdominal SAT (I'll use DASAT) did not differ between genders
  • Obese had 2-3X as much DASAT and visceral adipose tissue (VAT) vs. lean
  • VAT was not significantly different between genders but trended towards greater VAT in males 
  • DASAT was significantly greater crossectional area than VAT in the obese
  • About 3/4's (mean ~76%) of the DASAT is located in the posterior (back), and this partitioning varied within a relatively small range (67-87%).  This distribution did not differ in obese v. lean or between genders.
  • Anterior and Posterior SASAT is more evenly distributed around the circumference of the abdomen,  being ~55% front /45% back.
  • The proportion of SASAT of all abdominal fat (I'll use TAFM)  was 45% v. 41% in lean women vs. obese women
  • The proportion of SASAT of all abdominal fat was only 28% in both lean and obese men
  • The proportion of DASAT of all abdominal fat did not differ significantly between genders but does appear to trend towards higher levels in men.
  • The difference in proportion of DASAT (compared to TAFM) was statistically significant for obese v. lean in both genders:  32% LW, 37% OW, 36% LM, 44% OM
  • VAT proportions were as follows:  23% LW, 36% OW, 20% LM, 27% OM.  This was stastically significant for obese v. lean but not for gender.
  • VAT was highly correlated with DASAT (r = 0.76),VAT was more modestly correlated with SASAT (r = 0.43).   Statistical Aside:  When two variables are tested for correlation, the closer r is to 1, the tighter the correlation so this is a rather "huge" difference between the two types of SAT and their correlations to VAT.  
Summary of Relationships between Types of Abdominal Adipose Tissue Depots and Metabolic Variables:
  • Glucose Rd (a measure of clearance rate) is negatively correlated with TotFM
  • Glucose Rd was not significantly correlated with SASAT or TFM
  • Glucose Rd was significantly negatively correlated with DASAT and VAT, the strength of this correlation (r) was similar between the two fat depots.
  • Combined DASAT & VAT (considered together) were even more strongly correlated (r = 0.68) with decreased glucose Rd than either fat depot considered separately
  • Both TotFM (this part is unclear, from the table I think it's TotFM, from the title of the section one might imply total truncal fat) and VAT accounted for 45% of the variance in insulin sensitivity.  Statistical aside:  This statement is related to the degree of correlation (r = correlation coefficient).  Let's use the common example of height and weight which are generally significantly correlated.  If you select an adult at random and measure their height, there will be considerable variability in the result.  If the r for the height weight correlation is 0.7 - made up number - then r^2 = 0.49 and we would say that 49% of the variability in weight is accounted for by its correlation to height. 
  • DASAT is independently associated with insulin sensitivity (r^2 = 0.51) when TotFM (again not sure if this was total truncal fat), VAT & DASAT are included in the model.
  • Controlling for either TotFM+VAT or TotFM+DASAT, SASAT was not associated with insulin sensitivity.
  • The strengths of association for various fat depots and insulin sensitivity were similar to those of glucose clearance and rank:  VAT, DASAT > TotFM, total abdominal SAT > SASAT
  • Correlations for glucose and insulin AUC (a measure of total exposure over a defined time period) were weaker.  But they were similar for VAT and DASAT and both greater than SASAT which seems to follow the correlation pattern of TFM
  • This pattern was repeated for fasting insulin where VAT and DASAT (r = 0.57 and 0.58 respectively) were significantly greater than for SASAT and TotFM (r = 0.26 and 0.27 respectively)
  • Other parameters are shown in the table below.  The pattern continues where SASAT "behaves" more similarly to TFM than do DASAT and VAT which behave similarly.

From the Discussion:

The current study was undertaken to examine the novel hypothesis that superficial and deep depots of subcutaneous abdominal adiposity, defined anatomically by a fascial plane that divides the two depots and differing in histological characteristics (22), might also differ in regard to their association with insulin resistance.  The findings clearly indicate that strong differences do exist. Superficial SAT manifests a powerful relation to plasma leptin but a weak association with insulin resistance, and in these and other respects, it follows a pattern observed for thigh subcutaneous adipose tissue, a depot generally regarded as a weak determinant of insulin resistance. In contrast, the deep subcutaneous adipose tissue of the abdomen manifests a robust relation to IR and other key aspects that define the insulin resistance syndrome (e.g., blood pressure, fasting insulin, and lipids); moreover, it does so in a pattern nearly identical to that observed for visceral adiposity. Therefore, from the perspective of understanding body composition and insulin resistance, these results indicate that it is not accurate to ‘‘lump’’ these two differing adipose tissue depots into a single category, but instead it may be useful to ‘‘split’’ the depots in accord with the anatomic demarcation of the fascial plane (18).
From a personal standpoint, I find this somewhat reassuring as I'm pretty sure that my "central adiposity" is of the superficial variety.  Therefore the shift from its former location (thighs/butt) to the belly may well not have any negative health implications as the behavior of this fat is metabolically similar to that of the depots from where it shifted.  


Tuesday, October 19, 2010

Visceral fat and insulin resistance – causative or correlative?

Having been introduced to "the English guy" aka Keith Frayn, I've discovered a rather extensive, as well as diverse, body of work by this researcher.   I'm sure to be sharing more in the coming weeks.  

The association between abdominal fat accumulation and risk of chronic diseases, including type II diabetes and coronary heart disease, has long been recognized. Insulin resistance may be a key factor in this link. Many studies have pointed to an association between insulin resistance and intra-abdominal fat accumulation (visceral obesity). However there is no clear proof of a causal link between visceral fat accumulation and insulin resistance. In assessing the probability of a causal link, it is useful to consider potential mechanisms. One such potential causal link is the release of non-esterified fatty acids from visceral fat into the portal vein, so that they have direct effects on hepatic metabolism. Visceral fat has been shown in many studies to exhibit a high rate of lipolysis compared with subcutaneous fat depots. However, if the idea that visceral fat releases fatty acids into the portal vein at a high rate is examined critically, a number of difficulties appear.  Not least of these is the fact that continued high rates of lipolysis should lead to the disappearance of the visceral fat depot, unless these high rates of fat mobilization are matched by high rates of fat deposition. There is far less evidence for high rates of fat deposition in visceral adipose tissue, and some contrary evidence. Evidence for high rates of visceral lipolysis in vivo from studies involving catheterization of the portal vein is not strong. If this potential link is discounted, then other reasons for the relationship between visceral fat and insulin resistance must be considered.  One is that there is no direct causal link, but both co-correlate with some other variable. A possibility is that this other variable is subcutaneous abdominal fat, which usually outweighs intra-abdominal fat several-fold. Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. In conclusion, there is at present no proof of a causal link between visceral fat accumulation and insulin resistance, or the associated metabolic syndrome. The possibility of co-correlation with some other factor, such as subcutaneous abdominal fat accumulation, must not be forgotten.
Hmmmm.... Co-correlation.  

This article discusses essentially 5 types of "central adiposity", so I might suggest an alternate title of "Central fat and insulin resistance".
  • Intra-abdominal, aka Visceral Fat:  mesenteric and omental (pot-belly) in the front, and perirenal/retroperitoneal (as you see on my diagram these are different depots but described as the same in the article, so I take their intention to be non-subQ back fat).
  • Subcutaneous:  anterior (paunch) and posterior (love handles)
Here is a good diagram of where each of the various adipose depots are located:
Some excerpts:

A number of studies have been aimed at identifying which of these various abdominal depots is most closely associated with insulin resistance. This is problematic since the subcutaneous and intra-abdominal depots are themselves correlated ...
One approach used specifically to examine the contribution of the intraabdominal depots has been to select subjects with large or small amounts of intra-abdominal fat, but to match them for total body fat and for subcutaneous abdominal fat.... this approach seemed to show that intraabdominal fat accumulation is associated with insulin resistance ... [but in this] study the groups did also differ in subcutaneous abdominal fat (by 11% on average) ...  the complementary experiment, matching for intra-abdominal fat and comparing people with high and low amounts of subcutaneous abdominal fat, has not been done. 
Another approach is to study a large number of people and use correlation analysis.  Studies using this technique show that the closest correlation with insulin resistance is seen with the subcutaneous abdominal depots.   Interestingly, these studies seem to show that the posterior subcutaneous depot is more closely associated with insulin resistance than is the anterior depot ... perirenal depot in these studies is clearly not associated with insulin resistance.
There is, then, a clear association between abdominal obesity and insulin resistance. Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not, and more evidence on this point is needed. However the observation of a link between abdominal obesity and insulin resistance does not mean that the former causes the latter. It could mean that insulin resistance causes abdominal obesity, or that both abdominal obesity and insulin resistance co-correlate with some other factor. 


Here's a summary of the results/conclusions for each of the five fat types:

1.  Anterior SubQ (aka paunch, muffin top, belly roll, over the belt flop):  Associated with IR

2.  Posterior SubQ (aka love handles, haunches):  Associated with IR, stronger than ASQ

3.  Omental (aka beer belly, pot belly) & 4.  Mesenteric:   Associated with IR but the Portal Theory (that these depots release NEFA into the portal vein therefore have a direct effect on the liver is not born out by in vivo studies.  "Some studies suggest that the intra-abdominal or visceral depots show the closest link with insulin resistance, although others do not"

5.  Perirenal:  Not associated with IR

Sat Fat --> PUFA = Less SubQ Belly Fat?

Mostly a bookmarking post, but I found this interesting

Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity

For some reason I can't C&P the abstract.

They analyzed the results of 5 weeks on diets rich in sat fat vs. PUFA (described as spreads and oils, presumably high in omega 6 and probably some transfats :( ) on T2's, obese and non-obese subjects.  The study size was small, but I think most readers will be as surprised as I was by the results.

All of the PUFA groups had less subcutaneous belly fat at the end of the 5 weeks. This was statistically significant in the non-diabetics, both obese and non-obese.  Visceral fat either decreased or stayed the same. This was statistically significant for the diabetics, but not the non-diabetics.  

The PUFA group seemed to eat less, but total body weight didn't change.  Not sure what that's about.  Could be underreporting or a slower metabolism?  In any case, if this can reduce belly fat .....

Insulin sensitivity IMPROVED on the PUFA diet.  

This goes counter to that n=1 "study" by the journalist that altered her diet to consume O6's that has been making the LC rounds lately.  

Wednesday, August 18, 2010

Adiposopathy v. Obesity ~ I

I just came across the following article, and haven't quite digested the whole thing just yet.  Still, it is interesting so I thought I would share it here.  This post will be about the most curious topic in this paper, but I hope to revisit this in a series of future blog posts (hence the "I" in the title).  


Near as I can tell, the lead author, Harold Bays, is the doctor who coined the term "adiposopathy" or "sick fat".  

Adiposopathy is pathologic adipose tissue dysfunction that may be initiated and/or exacerbated by fat accumulation (adiposity) in genetically susceptible patients [1••].  Adipocytes are metabolically active and adipose tissue is an important endocrine organ (Table 1) [2••]. Abnormalities of adipocyte factors contribute to dysmetabolism (Fig. 1), and adiposopathy [1••,3•] promotes some of the most common metabolic diseases encountered in clinical practice, including type 2 diabetes mellitus (T2DM), hypertension, and dyslipidemia.


This is a summary paper focusing on the fact that it is dysfunction of the adipose tissue rather than the amount of adipose tissue that is responsible for Metabolic Syndrome.  Thus explaining your "metabolically obese thin people" and "metabolically normal obese people", etc.   The focus, as the title implies, is MetS treatments that target the fat cell dysfunction rather than simply the person's fat mass.  

Sick fat appears to be related to adipocyte hypertrophy -- an enlarged fat cell:
It has been known since the 1970s that adipocyte hypertrophy increases the lipid/protein ratio of the adipocyte (through a relative consistency in protein content coupled with increased fat content) [13], decreases the responsiveness of adipose tissue to insulin [14], and increases the risk of metabolic diseases such as T2DM [15] and dyslipidemia, even if adipocyte hypertrophy is found in only slightly overweight individuals [16]. In fact, adipocyte hypertrophy is more closely linked to metabolic abnormalities, such as insulin resistance, than is an increase in total body fat [17].
An increase in fat cell size represents a failure of adipose tissue to adequately proliferate and differentiate [18] (as found with obesity and T2DM [19]) and, therefore, a failure to inadequately accommodate a further increase in energy influx [20]. Adipocyte hypertrophy may indicate a resistance or inability to store triglycerides beyond some maximal amount [21]. 
(This is consistent with the Critical Visceral Fat Theory I blogged on previously.)


For this post, I want to focus on the discussion of one of the pharmaceutical treatments:  PPAR-gamma agonists.  (Here's a LINK to general information on these drugs --  thiazolidinediones or “glitazones.” -- Actos and Avandia).  I'm not promoting pharmaceutical therapy, and Avandia has seen a lot of negative press of late, but nonetheless I find the mechanism of action of these drugs to be interesting.

These compounds appear to "cure" sick fat by stimulating the proliferation of new, small, young adipocytes and/or promote the death (apoptosis) of dysfunctional hypertrophied large fat cells.  Since SCAT has a greater ability to differentiate, and VAT cells are more metabolically active, this seems to have differential effects on the two types of adipose tissue.  These drugs tend to cause fat mass gain in SCAT, and loss in VAT, but appear to be most effective in the patients who are fatter to begin with and who gain more fat.  Yes, you read that right.  

From an adipose tissue metabolism standpoint, PPARγ agents have been shown to reduce free fatty acids [23••,91], increase adiponectin [92–94], and reduce leptin [93] (although not consistently so [95]), with unconfirmed effects upon resistin [95,96], IL-6 [97], and tumor necrosis factor-α [95,97]. Thus, it appears that many of the favorable effects of PPARγ agents upon glucose metabolism and adipocyte function may be most related to improvements in free fatty acid metabolism

I've seen diabetics list these meds in their treatment regimes and yet be on weight loss regimes.  In some ways this seems counter productive.  One way to try to cure sick fat is to try to reverse the dysfunction by emptying out the cells.  Another, it appears, would be to replace sick adipocytes with healthy ones.  While weight gain may be the last thing a person wants, I know I probably would resist it were I diabetic, it is interesting to consider.  



Monday, August 9, 2010

Can low carb cause central adiposity?

This is mostly a post of a personal nature, but I thought I would put it here on the science side of things because I'll try to tie observations and anecdotes in with some scientific backing/references.

Personal background for my interest in this:  

As a child I had a rather boyish body until around age 12 or so.  At that age my shape (butt and thighs) started coming out (not fat though), but I was a rather late bloomer.  I didn't gain my "puberty weight" until I was 16 or so -- perhaps 20 lbs -- again mostly in my butt/thighs.  Anyone remember Tracey Gold from Growing Pains?  That would be pretty close (pre-anorexia) to my shape.  I lost the weight then yo-yo'd most of my 20's on various diet plans (none of which were low carb).  Although cycling as high as the 200-210 range and as low as 145 during that time, my general body type did not change.  I would always gain or lose weight mostly in my butt/thighs only getting the back and belly bulges at top weights.  My midriff was always  one of my better assets at the bottom of weight swings.  Probably TMI, but my breast size pretty much went up and down about 1.5 cupsize with weight/size.  In 1997 my weight hit up against an all time high and I was wearing 16's.  Well dressed at my high weight I was Delta Burke-ish.

It was then I discovered Atkins and, coupled with a very active job, I lost 40 lbs in a few months getting down to size 8 jeans.  This was the beginning of my body shape transformation.  I lost proportionally more weight in my thighs this time, but not in my waist.  This time tummy weight either remained or perhaps even shifted.  When I went off LC I regained weight rapidly and blew right on through my former upper limit.  I gained it everywhere, but most prominently in the belly like I never had before.  One more cycle of loss and regain a few years later and let's just say that my belly stuck out considerably more than my 40/42D+'s!!  You know, all my life I had difficulty finding clothing that fit at any weight -- my waist was disproportionately small compared to my thighs.  Pants that fit my thighs gapped at the waist.  And when I was heavier, it got worse as larger sizes, especially true plus sizes, tended to just get bigger in the waist.   But since that first low carb weight LOSS, pants have fit me better at every size.  Sometimes I even had extra room in the seat!

This body type was not only foreign to me, but in the past I could always write my weight off as not particularly unhealthy b/c I carried most of it well below the waist.  Now, I carried it around the middle and upper arms and less so proportionally in legs and backside.  Today, after losing the weight I fit (even too big) pants I wore 15 years ago when I weighed some 40 lbs less.  My chest size has gone down from the 40-42 mark to a 36, but I still must shop the "full cut" lines for D cups.  Fifteen years ago when I wore the aforementioned pants I was a 34C in a regular cut.

So, why am I telling you all this info?  Because this is one of my root causes for concern over the healthfulness of LC eating.  Today, the largest remaining fat "depots" are my belly, breasts, and upper arms (although that seems to be more skin).  I wonder over the hormonal implications of having larger breasts when I'm now officially menopausal.  And I worry over my central "obesity" although somewhat comforted that it appears to still be sub-Q vs. visceral.  I don't know if I'm some sort of odd-ball in this regard, but even if so, is this seemingly permanent shift in my fat distribution dangerous, benign or even beneficial?  

In this regard, I've looked to some of the women in the low carb community.  How are they looking after years of low carbing?  I was not encouraged.  Back in early 2009 I came across some pictures of Laura Dolson, Dr. Mary Vernon and Dana Carpender.  All overweight or downright obese.  Although I've never seen the pictures, in their recent book,  MD Eades developed a belly despite low carbing requiring a 6 Week "Cure".  A cruise through various LC forums and blogs will unearth numerous success stories with either stalling out 20+ lbs north of goal and/or weight regain.

Recently I came across some more recent pics of Dana from Jimmy Moore's 2010 Low Carb Cruise, and thought to myself that these were comforting.  I chanced by her blog, read back a bit, and noted that she's now at a low weight for herself and wearing size 10/12's.  Her book was about a 40 lb weight loss on low carb, but she's blogged over the years about weight fluctuations.  In any case, I was flabbergasted when she posted some gymsuit pictures of herself on her new blog:  My Total Gym Transformation.  Kudos to Dana for her honesty in posting these.  But yikes!  If this is the result of 15 years of "fighting the low fat lie" and eating low carb, am I the only one for whom the side pics registered cause for concern?

And then I look at Jimmy Moore.  Obviously not a woman, but a long term low carber who has been steadily gaining weight (and having only short-term success to date at losing it) for almost 3 years now.  One can look at pictures from Jan 2010 here and here.  Now it is difficult w/o seeing pics of his original weight loss progression, but when I look at the before/afters, on his various websites, at over 400 lbs Jimmy seemed to distribute his weight fairly well around his body.  Sure, he had a belly, but in this pic of Jimmy +30 from low weight at 260 lbs, despite remaining rather consistently low carb, one can see where he's gaining ... and the 2010 pics seem to indicate most of it is going to the worst place from a health perspective.

Now I've hesitated making this post as I don't want to be seen as picking on or criticizing these nice folks, but if we can't scrutinize LC "celebs" and look to them for long term prospects, who can we look to?  In the end my thinking is that they "put it out there" so I'm not out of line commenting here in my little ol' blog.

Considering all of the information I've gathered on the etiology of insulin resistance, I think the above may well be two examples of how long term low carbing can increase insulin resistance and perhaps body fat distribution that may be influenced by whatever few carbs one might consume.  I also consider that the extreme carnivore wing of the LC community tends to be the only ones that get truly lean.  My thoughts on this are that they are probably very insulin resistant but it doesn't lead to overt problems because they eat essentially no carbs so their body's inability to handle them normally is not challenged.  It is also very difficult to overconsume on meats, especially when dairy is omitted or extremely limited.

From a recently referenced article:


VAT may influence central SCAT
Mauriege et al found that adrenoreceptor sensitivity was increased in SCAT cells of individuals who have a higher VAT accumulation compared to those with a low VAT deposition [112]. SCAT adipocytes from women with visceral obesity exhibit higher lipolysis rates in vitro than those obtained from women with little VAT [113]. Mauriege et al also demonstrated that among men with high levels of VAT, SCAT adipocytes are more sensitive to β-adrenergic lipolysis which may further exacerbate an impaired insulin action, a potentially important factor in the etiology of metabolic syndrome associated with visceral obesity [112]. Moreover, an increased truncal SCAT mass and an increased amount of VAT mass can independently predict insulin resistance [114]. Together, these findings support that VAT may enhance central SCAT lipolysis and accelerate release of peripheral FFAs.
So the fact that at least a goodly portion of my trunk fat appears to be SCAT, this may indicate excess VAT. The measurements in the Eades recent book offer me little insight into the matter.  Another way to read this is that the trunk fat is an indicator of a degree of IR independent of whether or not my VAT is out of whack.
Later in this same article estrogen is discussed:
Estrogen
Estrogen promotes the accumulation of peripheral gluteo-femoral SCAT, which may be protective [131]. The abundant presence of peripheral fat mass in generally obese women is associated with increased plasma adiponectin, and the loss of estrogen with menopause is associated with an increase in central fat [132]. This accounts for the progression in many overweight women after menopause from a predominantly pear-shape or "gynoid" habitus to the apple or "android" shape. Contrary to popular belief, menopause does not seem to independently cause a gain in total body weight; the increases in BMI that often accompany menopause are usually consistent with normal aging [133]. However, even without weight gain, body fat distribution changes; postmenopausal obese women tend to accumulate abdominal fat along with deterioration of risk factors, even if total body weight and BMI do not change during menopause transition.
After menopause, when ovarian function declines, adipocytes become the primary source of endogenous estrogens [134], and compared to "gynoid" or pear-shaped women, those with central obesity (apple- or "android-" shaped) have lower plasma SHBG and higher estradiol [125,135]. This suggests regional differences in the enzymatic conversion of steroid hormones in VAT versus SCAT [125,136-138]. In ovarian hormone-deficient women, SCAT adipocyte size, lipoprotein lipase (LPL) activity, and basal lipolysis were not found to be significantly greater compared to regularly cycling premenopausal women. However, in the ovarian hormone-deficient women, omental (VAT) adipocyte size was significantly higher, and the omental/SCAT LPL activity ratio and VAT lipolysis were also significantly higher [139]. 
Perhaps my belly is now the inevitable result of my "change of life".  But I am a bit young to have gone through all of this.   I wonder sometimes if LC didn't perhaps accelerate this by influencing estrogen rather than vice versa?  I suppose I'll never know.  But it is worth repeating that the first shift in fat distribution occurred in my early 30's during weight LOSS through low carb.

I would appreciate any input from other (particularly female) low carbers if they have experienced similar as well as any thoughts on whether or not I should be concerned by this as much as I am.





Critical Visceral Adipose Tissue Theory


I found this article almost a year ago, posted it on an LC discussion board, and was mostly greeted with silence so I had sort of forgotten about it.  In any case, I was reminded of the article while recently reading LynMarie's latest post on her blog:  Fat Fails First?  (Incidentally, that post corresponds well with my own recent offering on the topic:  The Progression of Insulin Resistance ).  

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