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

Friday, December 13, 2013

The NEAT part about Moving More

Random Bump!



Original publish date:  4/21/12

In writing up a post on metabolic rate and weight loss, I couldn't help but come across a ton of stuff I had in my draft bin and hard drive vis a vis exercise, lean body mass and metabolic rate.  This got me thinking about the usefulness of ELMM = Eat Less Move More as a strategy to flip the CICO balance along with other things we can do.  

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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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Sunday, September 2, 2012

The Hadza Hunter Gatherer Energy Expenditure Study

I've been asked by a few people to weigh in on a recent NYT article, Debunking the Hunter-Gatherer Workout, that discusses the following study (free full text):  Hunter-Gatherer Energetics and Human Obesity.  I didn't have a whole lot to say until I wrote this, and now it's rather long ... so I guess I did have quite a bit to say after all ;-)   But first, a little link love for Colby Vorland of nutsci.org who discussed this back in July:  Westerner energy expenditure compared to a hunter-gatherer population is equivalent.  In addition, Colby had discussed Energy expenditure and physical activity level are not higher in developing countries compared to industrialized.  I encourage reading both.

So from the NYT article:
We found that despite all this physical activity, the number of calories that the Hadza burned per day was indistinguishable from that of typical adults in Europe and the United States. We ran a number of statistical tests, accounting for body mass, lean body mass, age, sex and fat mass, and still found no difference in daily energy expenditure between the Hadza and their Western counterparts.
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Thursday, June 28, 2012

A Modest Proposal for Peer Review Research

With the advent of, and inexpensive nature of online sharing of information, I propose that all peer-review research should include (anonymous) raw data for each subject.  At the very least, there should be scatter plots presented for the individual data points for the main outcomes.

I frequently teach statistics, and one of the first things we discuss in that class is sort of the "first purpose" of it all.  Because before we can analyze data, first we must summarize and present the data in such a way that the "consumer" can readily glean information.  In one classic stats text -- Triola -- this part is given the acronym CVDOT.  C = Center, V = Variation, D = Distribution, O = Outliers and T = Time.  So we go through the various ways we can convey the center of a data set, it's variability, distribution, etc.  In most of the studies we discuss here, data is presented as a mean value +/- either the standard deviation or standard error (C +/- V in the acronym).  And further statistical analysis compares these means between groups for statistically significant differences.   If I have 20 subjects in a study, I can provide you with a table of all results sorted by subject number assigned randomly.  This tells you very little.  If all I do is sort the data ascending or descending, you can now readily pick out the range and "center" of the data.  Perhaps if data is of a more rounded nature, you might be able to pick out the most frequent or common values.  Outliers will jump off the page.  
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Monday, April 30, 2012

Rapid Weight Loss Tanks Metabolism? The TBL Study

Thanks to Yoni Freedhoff of Weighty Matters blog for providing me with the full text of this one.  Check out his take on the results.  Update 11/11/13:  Full text now available free HERE.
Context: An important goal during weight loss is to maximize fat loss while preserving metabolically active fat-free mass (FFM). Massive weight loss typically results in substantial loss of FFM potentially slowing metabolic rate.
Objective: Our objective was to determine whether a weight loss program consisting of diet restriction and vigorous exercise helped to preserve FFM and maintain resting metabolic rate (RMR).
Participants and Intervention: We measured body composition by dual-energy x-ray absorptiometry, RMR by indirect calorimetry, and total energy expenditure by doubly labeled water at baseline (n = 16), wk 6 (n = 11), and wk 30 (n = 16).
Results: At baseline, participants were severely obese (×± sd; body mass index 49.4 ± 9.4 kg/m2) with 49 ± 5% body fat. At wk 30, more than one third of initial body weight was lost (−38 ± 9%) and consisted of 17 ± 8% from FFM and 83 ± 8% from fat. RMR declined out of proportion to the decrease in body mass, demonstrating a substantial metabolic adaptation (−244 ± 231 and −504 ± 171 kcal/d at wk 6 and 30, respectively, P < 0.01). Energy expenditure attributed to physical activity increased by 10.2 ± 5.1 kcal/kg·d at wk 6 and 6.0 ± 4.1 kcal/kg·d at wk 30 (P < 0.001 vs. zero).
Conclusions: Despite relative preservation of FFM, exercise did not prevent dramatic slowing of resting metabolism out of proportion to weight loss. This metabolic adaptation may persist during weight maintenance and predispose to weight regain unless high levels of physical activity or caloric restriction are maintained.

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Tuesday, April 24, 2012

Random Thoughts: Obesity, Weight loss, Metabolism, Diet & Exercise

In the interests of saving a bit of time and gathering thoughts, I thought I'd jot down some would-be comment replies in a blog post instead.  First, so we're all (newer readers especially) on the same page, I did no formal exercise during the active weight loss phase and long plateau from sometime summer 2007 through spring 2009.  This was not really by design, but more out of fear as the last time I low carbed I experienced the racing heart mostly when doing rather short periods of pilates and such.  So I kept meaning to up the activity level a bit but never really managed to get around to it.  In 2009 I did start doing concerted cardio -- walking and biking -- and later some more cardio-like exercise DVD's.  As for strength training, the only formal training I have done was that 100 pushups thing that was popular in 2010.  I got to 100 "girlie" pushups and was on my way with the regular ones when I pulled something in my side that made rolling over in bed painful!  So for me personally, regular exercise is a sporadic thing at best ... something I am trying to dedicate myself to just never seems to stick.  That said, I am very active.  Initially this was just doing the "parking far away at work" thing and such, but has progressed to deliberate short bouts of exercise like walking around the yard when I bring the garbage out, always running up stairs, just going up and down stairs for the heck of it, etc.etc.  Additionally, we go through a lot of wood with our fireplace to heat part of our home and I do pretty regular "workouts" transporting/stacking, chainsawing, etc. wood.  
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Friday, January 13, 2012

Irisin ~ Just the Pill for Low Carbers

There was an article in the NYT that was passed along to me the other day:

Exercise Hormone May Fight Obesity and Diabetes
A newly discovered hormone produced in response to exercise may be turning people’s white fat brown, a groundbreaking new study suggests, and in the process lessening their susceptibility to obesity, diabetes and other health problems.
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Wednesday, October 5, 2011

Fat Metabolism in Formerly Obese Women: Part II Resting Substrate Usage

Continuing the discussion from Part I

Fat metabolism in formerly obese women
Ranneries, et.al.  AJP-Endo, 1998.

In this part I wish to address the respiratory quotient, RQ.  The RQ is a measure of the relative amounts of energy derived from glucose oxidation vs. fatty acid oxidation.  

To recap the subjects of this study, when obese, the FO (formerly obese) subjects had body weights in excess of 120% normal weight.  They followed a conventional CRD to lose the weight and were weight stable for at least 2 months at 110% normal weight.  So weight losses were in excess of 10% bw and ranged from 15-20kg (33-44 lbs).    The FO & C groups were well matched as seen in Table 1.
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Friday, September 30, 2011

Mitochondria and High Fat Diets

Lots of buzz over mitochondria of late.  So I thought I'd share this find:

High-fat diets cause insulin resistance despite an increase in muscle mitochondria
It has been hypothesized that insulin resistance is mediated by a deficiency of mitochondria in skeletal muscle. In keeping with this hypothesis, high-fat diets that cause insulin resistance have been reported to result in a decrease in muscle mitochondria.    In contrast, we found that feeding rats high-fat diets that cause muscle insulin resistance results in a concomitant gradual increase in muscle mitochondria.
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Saturday, September 17, 2011

Insulin & Metabolic Rate ~ Am I Missing Anything?

As my regular readers are well aware, I've read a ton of peer review research on insulin and its action.  I also have a pretty freakish memory for certain things, so if I'd come across even an aside from a reputable source, I would have remembered it.  

So, I have yet to come across any information that insulin directly alters metabolism.  By that I mean the basal metabolic rate to keep you live and not-so-kickin -- BMR/RMR/REE.  As close as it comes is that insulin stimulates glycolysis (oxidation of glucose for energy), but it also suppresses fatty acid metabolism so that would seem to be a wash to me -- substrate switch but no impact on total rate of fuel burning.  I'm also not talking about minor differences in the TEF for carbs vs. other macros as this does not appear to be related to hormones per se.  

I'm talking whether insulin has any known action like that of leptin that specifically increases or decreases metabolic rate.  Have I missed anything?

Thanks in advance!

Monday, August 29, 2011

Fat Metabolism in Formerly Obese Women: Part I Resting Metabolic Rate

Wow!  Many recent events and blog posts about the web have hit a lot of my deja vu "memory nerves".  This has had me going to the draft bin looking for what it is I'm reminded of.  This one was sparked by being linked to a series discussing hunger and satiety over at gnolls.org.  I'm going to link you to Part IV as that is where the paper I'm discussing in this post/series is cited, but J. Stanton  has links to other installments.  

So, most of this current post has been in my hopper since February!  But this article/study has actually been "on my plate" longer still, as the PDF was downloaded to my HD back in June 2010 after reading James Krieger's  piece on the ease of regain.   I'm going to break this up into three parts:  
  • Part I dealing just with resting energy expenditure and its contribution to our overall "metabolic rates".  

  • Part II will deal with the resting metabolism in terms of contributions of fat and carbohydrate

  • Part III will address expenditure and substrate usage during and after exercise.  




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Friday, April 22, 2011

Exercise v. Diet for Weight Loss

In recent months, mainly sparked by Mr. Exercise Only Makes You Hungry's appearance on the Dr. Oz show, there seems to have been some renewed interest in the LC community in the role of exercise for weight loss.  Most studies show little effect of exercise only, but, as the authors of this study I'm about to share state,  "these conclusions are drawn from studies in which individual energy intake and expenditure were not rigorously controlled or accurately measured" .  When it has been controlled, the calorie deficits created through exercise alone were not sufficient to produce significant weight loss.


This study was done in weight stable (6+ months prior to study) obese (BMI >27) men with waist circumferences over 100 cm (~39").    The men were sedentary, non-smokers, non-light drinkers, and had normal lipids and glucose tolerance.

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Wednesday, December 29, 2010

Metabolism v. Fat Burning

I was reading Alcohol Revisited on Low Carb by Dana Carpender and something she said jumped out at me:
No doubt, however, that alcohol can be fattening, not only because of the calories it contains, but because it slows metabolism - to quote a medical journal article I read, "Alcohol profoundly inhibits lipolysis." In English this means that alcohol slows fat-burning to a crawl. Like carbs, your body burns alcohol preferentially. Don't expect to burn any fat until you've burned through all your alcohol calories. 
First of all, Carpender makes the all-to-common mistake of equating lipolysis with actual fat-burning.  As I summarized in Lip-ocabulary , lipolysis is the breaking apart of triglycerides to glycerol and free fatty acids.   This occurs constantly in our bodies, inside the fat cells by hormone sensitive lipase (HSL) to release FFA's continually as part of the triglyceride/free fatty acid cycle, and in the capillary beds by lipoprotein lipase (LPL).  To further complicate the matter, lipolysis is not stimulated systemically in the same manner.  LPL can be activated in fat tissue so as to release FFA's temporarily so that they can be taken up into the adipose tissue, while it is reduced in muscles that don't need the fuel at the moment.  In any case, we continually recycle up to 60% of FFA back into triglycerides (storage form) both in fat cells and peripheral tissues.   Bottom line, lipolysis rates are not necessarily predictive of ß-oxidation - e.g. "fat burning".
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Monday, June 7, 2010

Skipping Breakfast

This is not an LC study -- indeed one could describe it as just the opposite -- but it is interesting nonetheless

Deleterious effects of omitting breakfast on insulin sensitivity and fasting lipid profiles in healthy lean women

10 healthy lean young women participated in this cross-over study (they serve as their own control and get each treatment).

Treatments:
EB = eat breakfast { cereal with low fat milk :-(  }
OB = omit breakfast  -- this group received the same meal eaten by the breakfast group later in the day.

The women selected were regular breakfast eaters prior to the study.

Essentially both groups ate ad libitum from similar foods for the remainder of the day and recorded intake.

Measurements were made of REE, TEF, EI, fasting and postprandrial insulin & glucose, and fasting lipid and uric acid levels.

Other abbreviations used:
EI = energy intake
REE = resting energy expenditure
TEF = thermal effect of food


DISCUSSION:

The aim of this study was to compare the effects of OB and EB on EI, REE, and indexes of carbohydrate and lipid metabolism and plasma uric acid concentrations. We found that, in healthy lean women, OB led to a higher plasma total and LDL-cholesterol concentrations and lower postprandial insulin sensitivity than did EB. Mean reported total EI was significantly lower during the EB period than during the OB period.  

... The mean reported EI was significantly lower in the EB period than in the OB period. This is at variance with previous studies that reported either no difference (2, 3, 9, 10) or even lower EIs (3, 10) in persons who omitted breakfast than in those who ate breakfast, despite a lower BMI in the latter group (3, 10). We did not find any differences in macronutrient composition between the EB and OB groups, which was inconsistent with the previous studies (11, 12). However, this inconsistency is likely to reflect the fact that we ensured breakfast cereal was consumed in both intervention periods; the difference was the time of its consumption. Underreporting of EIs, especially for snacks (37), might lead to errors in data interpretation and also to inconsistent results. We also had underreporting in this study, but the similar degree of underreporting between the habitual diet and the EB period, as well as the crossover design, suggests that the higher total intake in the OB period is a reliable observation even if the absolute intake is not.
... The current study did not find any difference in fasting REE and TEF between the EB and OB periods. It is suggested that, if OB has any effect on EE, a longer intervention is needed for that effect to emerge. ... Further long-term studies are required to explore the effect of breakfast consumption on EI, EE, and, finally, body weight.
...The current study reports no significant difference in fasting blood glucose and glucose profile after the test meal. These results were expected because, during short-term interventions in healthy subjects, blood glucose is likely to remain constant, and any compensation would occur via changes in insulin secretion. Furthermore, no significant differences appeared in baseline insulin concentrations or HOMA-IR values over the course of the experiment. The peak postprandial insulin response tended to be lower after the EB period than after the OB period, and the AUC of insulin profile after the test meal showed a significantly higher response after the OB period than after the EB period. Overall, we suggest that OB may reduce postprandial but not fasting insulin sensitivity in lean people. 
... Regarding the changes in plasma lipids, the present study indicates that plasma total and LDL-cholesterol concentrations increased after the OB period more than they did after the EB period. Fasting plasma HDL-cholesterol and triacylglycerol concentrations, however, showed no significant differences between the EB and OB periods. The effect of EB in reducing lipid concentration was in agreement with the findings of previous studies (11, 12, 18). However, the mechanism proposed in the previous studies, in which a lower fat intake was associated with EB, cannot explain our results, because we did not find any significant difference in total fat intake.
Insulin stimulates hydroxy methyl glutaryl-Co-A reductase, one of the rate-limiting enzymes in cholesterol synthesis. Lower total and LDL-cholesterol concentrations after the EB period might be due to a lower insulin stimulation of hydroxyl methyl glutaryl-Co-A reductase.

I've bolded selected results from the study.  I find it interesting that timing of eating seems to influence insulin sensitivity but not really sure if this has any relevance at all to low carb dietary approaches.  Jimmy Moore over at Livin La Vida Low Carb stated that there was almost unanimous opposition to intermittent fasting to treat hyperinsulinemia, and I wonder if this might be one of the reasons.

I also find interesting the energy intake -- it was significantly lower for the breakfast eaters.  As stated in the excerpt above, the researchers controlled for the cereal intake by giving the OB group the same breakfast meal later in the day.  This is actually somewhat counter to my personal experience in that on days I eat early in the day (even a good LC egg meal) I often find myself hungrier during the day.

I wonder if the results of this study do provide some rationale to eating carbs earlier in the day if you're going to eat them.  At least in this study, those eating a carby breakfast ate less overall and had better insulin sensitivity.  More importantly, there appears to be less of an insulin spike if one starts their metabolic engine earlier in the day.  Things that make you go hmmmmm...

Sunday, June 6, 2010

Brown Fat and the MYTH of Diet-Induced Thermogenesis

Brown Fat and the Myth of Diet-Induced Thermogenesis


INTRODUCTION:  The concept that brown adipose tissue (BAT) is a thermogenic tissue initially came from morphological changes in the tissue when animals were exposed to the cold (Smith and Horwitz, 1969). The physiological basis for the enormous capacity of BAT for heat production during cold exposure awaited the ingenious application of radiolabeled microspheres to measure blood flow in BAT and other tissues (Foster and Frydman, 1978). That production of heat occurred by uncoupling mitochondria was firmly established with the elegant experiments of Nicholls on physiology of BAT mitochondria and Ricquier’s identification of a unique cold-inducible protein in the mitochondria of BAT (Nicholls and Locke, 1984). The presence of large amounts of differentiated BAT in human neonates and species like sheep that require active thermogenesis at birth to protect the newborn from cold exposure on a snow-covered pasture in spring argues that BAT evolved primarily to function as a thermogenic system to protect body temperature (Casteilla et al., 1989).
What is a matter for debate is whether BAT thermogenesis burns off excess calories in a state of positive energy balance o maintain energy homeostasis as a major physiological function.  This concept emerged from experiments in the 1970s when Rothwell and Stock observed that rats fed a cafeteria diet (composed of junk foods high in fats and sugars) gained less weight than expected from caloric intake, and they proposed that excess unaccounted calories were being burned off by the induction of BAT thermogenesis (Rothwell and Stock, 1979).  Accordingly, BAT thermogenesis was proposed as a mechanism not only for protecting body temperature, but also to protect against obesity and the development of insulin resistance.  The data for diet-induced thermogenesis dovetailed with evidence that cold sensitivity and obesity phenotypes in ob/ob mice were associated with defective BAT nonshivering thermogenesis (Trayhurn et al., 1977). This idea that obesity was caused by a defective BAT set in motion a major effort by clinicians to find obese individuals with a slow metabolism. Prentice has commented on the depth of frustration experienced by clinicians when they failed to find obese humans with slow metabolism (Prentice and Jebb, 2004). Prentice blamed research investigating energy expenditure in the ob/ob mouse for this fruitless phase of obesity research in humans, concluding that the fundamental phenotypes of obesity and body weight regulation in ob/ob mice and humans were different. It is now well established that energy expenditure increases as a function of body mass in humans, and accordingly severe obesity is associated with an increase in energy expenditure (Leibel et al., 1995). Moreover, in the interim it became clear that ob/ob mice have neither reduced energy expenditure nor defective BAT per se. Energy expenditure in ob/ob mice was underestimated from the erroneous calculation of energy expenditure in studies comparing lean and obese mice, a problem that persists with a frustratingly high frequency to this day (Butler and Kozak, 2010).  Perceived defects in brown fat did not come from intrinsic defects in Ucp1 induction, but from secondary problems related to excessive white fat in morbidly obese ob/ob mice and regulatory problems arising from downregulation of b1- and b3-adrenergic receptors in ob/ob mice and other models of obesity that attenuate induction of Ucp1 and lipolysis (Robidoux et al., 2004). That none of the phenotypes of energy balance in ob/ob mice are due to modulation of Ucp1 expression was established with experiments showing that phenotypes of energy balance including food intake, adiposity, and oxygen consumption do not vary between ob/ob and Lep / .Ucp / mice under basal and leptin-stimulated conditions (Ukropec et al., 2006). Accordingly, the basic phenotypes relating to energy expenditure and obesity in mouse and human models of leptin null mutations are in agreement (Farooqi et al., 1999), and the data do not implicate BAT.




CONCLUSIONS:  Would it matter to our concepts of energy balance if there was no diet-induced thermogenesis? Probably not, since as I have argued from the phenotypes of several genetic models of thermogenesis, no compelling case can be made for diet-driven thermogenesis. Expenditure of energy to balance food intake would come principally from physical activity and maintenance of body temperature in individuals in harmony with their environment; this would exclude most modern humans.  The realization this past year that significant levels of BAT continue to exist in adult humans has opened the door to research that will aim to determine how this remarkable thermogenic system may be associated with the obesity epidemic and to discover new ways to utilize the potential to expand and activate BAT thermogenesis to prevent or reduce obesity in individuals. Similar excitement about the potential contribution of variation in BAT to slow metabolism and increased susceptibility to obesity occurred 30 years ago. The effort that flowed from this excitement and energy faded because we failed to understand that the function of BAT in mammals is to maintain body temperature in the face of a cold environment and not to maintain a normal body weight free of insulin resistance in the face of an obesogenic environment.

BOTTOM LINE?  The  title of this review says it all.  Those proposing a metabolic advantage for LC diets involving futile cycling of fat have no leg to stand on for that aspect.

Sunday, April 25, 2010

Effects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women

Effects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women

My Summary:

Subjects:  23 Obese (44 +/- 4% BF), Healthy, Premenopausal Women (Range 21-47, late 30's on average) 

Compared:  Two diets -- one low fat LF , one low carb LC,  and Two exercise states -- one aerobic EX, one no exercise  NX -- Four groups were compared LF/NX, LF/EX, LC/NX, LC/EX.

Study Length:  12 Weeks of weight loss, preceded by 5 weeks maintenance (MI), and followed by 6 weeks maintenance (MII).

Diets - Carb/Protein/Fat:  Maintenance - 45/20/35 ; LC - 25/25/50 ; LF - 60/25/15  It is worth noting that the LC vs. LF comparison kept protein constant.  The caloric content of the reducing diets was individualized to each participant to be ~75% of measured RMR.

Exercise:   3X/week, 45 minutes = 15 min on each of three different cardio machines, 60-65% VO2max

Measured:  Changes in body composition, Resting Metabolic Rate (RMR), thermic effect of a meal (TEM aka TEF), and total daily energy expenditure (TDEE).

Results:

  • LC lost a bit more weight than LF:  10.6 kg ± 2.0 vs  8.1 ± 3.0 kg   (P 0.037)  
  • Diet composition did not significantly influence body composition or energy expenditure changes
  • RMR was reduced similarly for both diets:  0.54 MJ/d (~130 calories)
  • TEM/TEF did not differ between the two diets
  • Exercise resulted in greater loss of fat mass 8.8 ± 2.1 kg vs. 6.1 ± 2.3 kg  (P = 0.008) 
  • Exercise maintained TDEE better +0.07 ± 1.23  vs. -1.46 ± 1.04  (P 0.004) due directly to exercise, and  +0.75 ± 1.06 for the exercisers vs -0.61 ± 1.03 MJ/d  (P = 0.006) for the non-exercisers not solely attributed to the exercise sessions.   I'm not sure these are additive, but +0.82 MJ vs -2.07 MJ between the two.  This is a swing of almost 3 MJ or ~ 700 calories!!

Some of the tabulated hormone & blood glucose findings:  (You can click to enlarge)


Interestingly, the LF/NX group had the same fasting insulin as the LC/EX group during the reducing phase., the LC/NX group had the highest fasting insulin.  I don't think these were statistically significant (especially because it looks like some samples were lost), but this counters the general belief that low carb diets necessarily impact fasting insulin levels.  One can see that fasting insulin decreased in all groups probably attributed to weight loss in general.

From the Discussion:

More important than total weight losses, however, are the relative changes in FFM and FM. Exercise training was a major determinant of the changes in body composition, with FM comprising 89.4% of the weight loss in the Ex group, compared with only 71.3% in the Nx group.
Exercise led to more FAT loss irrespective of diet.

The increased fat loss in the Ex group indicates a greater energy deficit, but this cannot be attributed to the energy costs of the exercise sessions alone because the diet prescriptions for the Ex subjects were increased to compensate for the energy expended during the exercise sessions. The rationale for this compensation was to avoid a greater energy deficit in the Ex subjects relative to the Nx group, because changes in FFM (6) and RMR (30, 35) have been shown to depend on the degree of energy restriction.  
So they held the calorie deficit constant for the caloric expenditure associated with the exercise session itself.  But interestingly:  
.
The increased fat loss in the Ex group cannot be attributed to maintenance of RMR, because in this study aerobic exercise failed to have a protective effect on RMR. ... In the present study, RMR, which comprised 58 ± 6% of the subjects’ daily energy expenditure, demonstrated the commonly observed decrease during the reducing diet in all treatment groups.
RMR was also measured during MII after the subjects consumed an isoenergetic diet for 4 wk. RMR values increased relative to energy restriction levels, but remained significantly depressed during MII.  
That second quote is depressing and probably is what causes relapses and regain.  I contend that a goodly portion of the adult obesity epidemic (especially in women) is probably due to dieting in the first place.  Repeated bouts of caloric restriction depress RMR (and thus TDEE), and there's a "hangover" effect that is not attributable just to reduced caloric needs to maintain a lower mass.

A unique feature of this study is that we measured free-living TDEE. Aerobic exercise played an important role in maintaining TDEE during weight reduction. The lack of a significant change in TDEE in the Ex group (+ 1.2 ± 12.2%) is in sharp contrast with the decrease of 12.3 ± 8.8% observed in the Nx group during low-energy feeding. The major effect of Ex on TDEE during weight reduction was its effect on physical activity. Because the change in TDEE is equal to the sum of the changes in RMR, TEM/TEF, and physical activity, and because the changes in RMR and TEM/TEF were comparable in the Ex and Nx groups, we were able to deduce that the significant TDEE difference between groups was attributable to a difference in physical activity (Figure 3). Although compensatory reductions in spontaneous physical activity are classic responses to undernutrition and must also be considered as part of the energy balance picture during energy restriction (43), the addition of aerobic exercise during the reducing diet proved to be an effective method for preventing this decrease. In contrast with the Nx group, the Ex group increased their physical activity by 0.75 ± 1.06 MJ/d, offsetting the decreases in RMR and TEM/TEF, yielding virtually no change in TDEE.   Note:  0.1 MJ (mega joule) is roughly equal to 25 food calories.
What this says to me is that ELMM IS the most effective method to lose weight after all.  I gotta say, my personal journey included rapid weight loss without formal exercise, but I'm a more active person by nature.  As weight was lost, I did become more physically active (taking stairs, parking further away from destination, etc.) so I think I probably staved off some of the TDEE reductions.  But this can be highly individual as the large variation in the mean (>140%) meant that for some of the exercisers, TDEE was not maintained and/or was still reduced.  Still, your chances seem better when including moderate aerobic exercise into the mix.