Attempting to define the "Damaged Metabolism"

Where reversing obesity is concerned, lots of excuse-making going on vis a vis the damaged metabolism.  Usually when someone challenges this to clarify what they mean, they are met with silence.  I've got four candidates based on various low carb theories and dieting truths.  So just some thoughts:  (OK a lot of thoughts - grin)

Insulin Resistance:

The original damaged metabolism, also referred to as a deranged metabolism.  The insulin resistant definitely have out of whack glucose (and fatty acid) metabolism.  As TWICHOO goes, carbs raise insulin leading to insulin resistance & hyperinsulinemia leading to fat accumulation as it is trapped in fat cells.  Leaving aside how one becomes IR, the state is indeed a deranged metabolism.  From Atkins-on, being IR has been blamed for an inability to lose weight, especially on standard CRD's.  Here's one area where LC truly shines!  It should probably be the first intervention for the morbidly obese insulin resistant person.  Yes, you read that correctly.  Why?  Because in free-living studies, it has been shown that LC diets work better for the short run producing more weight loss with less "effort" and experiencing less hunger.  But in controlled settings, it has been demonstrated that there's no magic for how LC works, it works by spontaneously reducing intake, and may even help increase NEAT though I'm not sure I've seen any study that measured significantly greater TDEE (the opposite actually).  Further, also in controlled studies where intake is controlled, it is calories and not the type of calories that produce weight loss.  Still further,  fasting insulin simply does not correlate with weight loss.  

While there may well be genetically pre-disposed "weight loss resistant" types, the fact remains that when compliance is verified, those who self-identify as resistant to weight loss, lose weight.  There is no evidence that IR and the ensuing hyperinsulinemia hamper weight loss.  To wit, I came across a study a while back that I blogged on:  Does Metabolic Syndrome hamper weight loss efforts?

Methods: A total of 107 women aged 49.1 ± 13.5 years old, with a body mass index (BMI) greater than 25 were studied. The subjects were prescribed a low-fat diet plus weight-reducing drugs when necessary.
Results: After 3 months, the subjects with metabolic syndrome lost more weight than those without (6.62% vs. 4.50%; P < 0.05). There was a positive correlation between the percentage of weight loss and the number of the components of metabolic syndrome present at baseline (Spearman ρ = 0.329; P < 0.01). Furthermore, patients in the quartile with the highest homeostasis model assessment index (HOMA-index) lost more weight than the remaining subjects (8.17% ± 3.34 vs. 5.59% ± 3.87; P < 0.05). These results were significant, even after adjustment for the medical treatment prescribed.
While it is possible the most "ill" were also given more weight-reducing drugs (though they controlled for this it may have contributed to the degree of the difference in weight loss), this still doesn't negate the fact that so-called "failed conventional means" of a low fat diet + (possible) meds produced superior results in those with the most damaged metabolisms where glucose/insulin are concerned.   

Leptin Resistance/Deficiency

Although there can be really no doubt that leptin is the dominant hormone regulating fat mass, studies using leptin to correct obesity have been limited in their success.  Leptin seems far more effective at preventing regain.  Human obesity associated with inherent leptin deficiency or signaling (the equivalents of db/db or ob/ob mice)  is rare.  And yet obesity is associated with elevated leptin levels indicating a degree of leptin resistance.  The whole "resistance" tag is getting increasingly murky if you ask me, because it implies decreased sensitivity to the action of a hormone when perhaps there are simply limits to how much a hormone can do.  Leptin stimulates fatty acid oxidation and raises metabolism, but it cannot completely compensate for chronic caloric excesses and can only upregulate one's metabolic rate so much.  Yet if fat cells continue to grow, they secrete more leptin that isn't usable.  It could be as simple as that.  Like pouring water (leptin) through a bucket with holes (receptors). Maybe the holes aren't clogged, they can only allow for 1 gallon per minute to drain through, pour in more than that and the water level in the bucket rises.  

The whole leptin discussion is confusing enough if one just looks at legitimate science.  After all it was discovered less than 20 years ago.  This is certainly not helped any by the low carb "experts".  Nora Gedgaudas comes close to plagiarizing Ron Rosedale whose theories on leptin spiking causing resistance are unsubstantiated by the literature.  Leptin Man himself -- Jack Kruse and his Leptin Reset protocol -- has yet to offer ANY rational for how the SAD causes LR or how his diet restores sensitivity.   Little if anything has been determined as to a dietary cause of leptin resistance, though triglycerides have been mentioned.  So what triglycerides?  Triglycerides are a generic term for the esterified form of fatty acids carried by various lipoproteins. Much to be done here, nothing to implicate either fat or carb per se.  So then we have what to do about this resistance if we've developed it.  Near as I can see, Jack is onto something hardly novel with his high protein breakfast.  I've linked to studies here before showing dietary protein seems to lower overnight leptin levels by increasing sensitivity (I'll try and come back to link to that).  But other than this, other speculations on leptin being the damaged component of one's metabolism -- from a dietary perspective -- are slim to none.  Certainly there is no evidence to substantiate some epic epigenetic switch whereby we can eat with abandon with leptin sensitivity and suddenly all hell breaks loose when we lose it.  

Leptin levels seem to be far more related -- again absent a genetic deficiency -- with the number and size of fat cells.  So there's quite a bit of evidence that the reduced-obese tend to be leptin deficient compared to those who have never become obese in the first place.  I suppose this contributes to a "damaged metabolism" of sorts, but it has nothing that I can find in the literature to do with the composition of one's diet, with the possible exception of protein.   I would like to see leptin replacement therapy and/or leptin sensitizers looked at more rigorously to assist those with maintenance.  BUT ... it seems that for the obese, any sort of "broken leptin metabolism" is not at the root of failure to lose weight.

Mitochondrial Dysfunction

Where to begin.  There has been a lot of fuss over dysfunctional mitochondria -- impaired fatty acid oxidation in particular -- in the larger community over the past year or so.  Near as I can figure this traces back to a post series on satiety and hunger written by J Stanton of  At the risk of veering into gossip land a bit ... Eh, WTF, I'm going there!  When I first heard of J it was because of the series and folks like Beth of WeightMaven and Paul of Perfect Health linking to his site.  Gnolls?  Whassat??   Gnolls are the characters in a science fiction novel he wrote near as I can tell.  Do we learn any more about J and his background?  No.  So when one goes to his site and reads a "science" post, we are forewarned with the graphic up there.  Oh boy, I'm a'scared ... NOT!  Not SCIENCE!!  As a scientist, when someone warns me about the science or complexity of what they're about to present, I first go looking for some cred.  Not because that's the be all and end all, but it helps me calibrate my BS detector before proceeding, and when it goes off ....   And, so, I look at the FAQ and near as I can figure his "thang" is about reclaiming our evolutionary heritage which he relates in his book?  Anything about Stanton's background?  Nope.  So the guy's a paleo aficionado who advocates "eating like a predator" which presumably is a meat dominated diet.  Nothing else.  As serendipity would have it, one of Leptin Man's posts I read was on gnolls and Mg and IR.  So just in case this makes a difference to you, it appears J's day job is hair styling.  Not that there's anything wrong with that, but I become far more skeptical of his version of science as he presents it.  Much of his theories hinge on a few papers (here, go read from Part I if you must ;D )

For the sake of brevity, I'm going to skip the nitty gritty here and get to the punchline:  the "pre obese" and "post obese" have high RQ's while the obese actually have low RQ's.  A higher RQ favors carb burning over fats, a low RQ favors the opposite.  The closer to 1 the more carbs you are burning, the closer to 0.7 the more fats you are burning.  So this whole theory hinges on "pre obesity" suppressing fat burning, and "post obese not being good fat burners either thus leading to propensity to regain.  Impaired fat burning.  Dysfunctional mitochondria.  Fatty fat fat for you, and don't dare eat carbs!  Well, the paper this comes from seems to be a bit of an outlier.  That is, obese do not, in most studies, have lower RQ than lean per se.  However it is true that obesity + high fat diet will lower your RQ as your cells are essentially forced to burn fat.  I have many more thoughts on this for another day, but this dysfunction thing doesn't hold water.  Because:
  • If Stanton's paper is taken at face value, the obese burn fatty acids at higher rates and should be blowing through body fat
  • If the lower fatty acid oxidation by the mitochondria is due to a DEFECT in the fatty acid oxidation biochemistry/physiology itself, eating a higher fat diet (with or without carbs) would not fix it.
Peter/Hyperlipid picked up on this and ran with it, but frankly folks, once one admits to falsifying and fudging data, it's a long road back to credibility if that road ever ends.  Now J. Stanton recently put up another installment of his hunger/satiety series, and ... sigh ... he's slated to give a talk at AHS12 on the topic.  So address this I must, no matter how minor a player he seems to be.

There are some conditions that are genetic that are traced to mitochondrial defects.  These are rare and that rarity is the bottom line that should prevent us from wasting time searching down this rabbit hole to explain the obesity epidemic.  End of discussion ... but not for some with seemingly endless desire to poke at real obesity researchers and rationalize low carbing as the be all and end all.  But if common sense doesn't help you come to the realization that the dysfunction is the result of dietary abuses and excesses and not the cause of them, believe me when I tell you the scientific literature is full of studies looking at this, but almost totally absent of results demonstrating a mitochondrial dysfunction etiology of all metabolic ills.  Let me be clear, dysfunctional mitochondria pop up all over the place.  They are very real as are deranged metabolisms as a result.  And I have great pity for those who have the rare predisposition to such abnormalities, because your condition will probably be glossed over due to the vast majority not having it so the general population data make you scientifically non-existent in today's hyper obese environment.

Of one thing I'm pretty sure, if not certain.  Eating carbohydrate per se is not causing mitochondrial dysfunction and defective fat burning capacity in your mitochondria.  

Depressed Metabolic Rate

This one is actually the most "real" of the four.  Because the rise in "simple" obesity cannot be explained by either of the first two "damages".  Yes, transfats and fructose can be tied to IR, but the causal link just isn't there in the literature.  And yes, we can identify mitochondrial dysfunction in certain metabolic states, again, the causal link just isn't there either.  Indeed in both cases, as I've discussed, the causal link is opposite of the claims:  e.g. the "damage" is the result of the obesity/chronic caloric surplus and not the cause of it.  But having become obese and losing the weight vs. never becoming obese at all does "damage" one's metabolism.  And the more one cycles weight, and the more drastic the cycles, the greater that "damage" is likely to be.  Here are things we know to be almost absolute truths when generalizing to averages of populations: 
  • Resting metabolic rate (RMR aka basal BMR) is highly correlated with lean body mass in normal individuals.  
  • The obese have higher metabolic rates than the lean
  • Sustained caloric restriction can and often does elicit compensatory adaptations reducing RMR/BMR
  • Body weight loss almost always involves loss of both fat and lean mass
We also know to a reasonable degree of certainty, again generalizing to averages:
  • A reduced obese person weighing XX pounds likely has a lower RMR/BMR than a never-obese person weighing the same XX lbs
And for the individual, I'd bet on the following being true, although we can never know with certainty unless someone does a prospective study on a large population measuring this through the years:
  • A reduced obese person weighing XX pounds has a lower RMR/BMR than had they never become obese and had to lose a lot of weight in the first place.
  • A person who has cycled weight exacerbates the RMR/BMR lowering
This is compounded by aging, and for women, menopause.  While FAR from perfect, the caloric expenditure calculators out there almost invariable include gender, height & age in the "input" to estimate.   But, but, my 90 y.o. grandfather eats like a 20 y.o. and hasn't gained weight.  I don't care.  Does this fact change the reality that most of us "slow down" naturally as we age and/or go through hormonal upheaval?  No.  

One problem I've encountered with all these studies, is that "post obese" can often mean as little as two months maintaining a significant weight loss.  I would love to see several years where RMR is measured along with weight.  As much as I hate anecdotes, I did seem to be able to eat more calories after about two years, so this "damage" while very real, is not necessarily permanent.  I have a post on this in the works with some thoughts on how to minimize it during weight loss and/or recover.

Onward ....

So ... where does all of this leave us?  Well, I've been around the LC internet community for just over 3 years now, read countless comments by others or directed at me in discussions, etc.  One thing is clear.  People are DESPERATE.  Not only to lose weight, but to divest themselves of ANY responsibility in their obesity.  Gary Taubes was *the savior* in that regard.  For over a decade he's convinced you that the guvmint and nutritionists and evil/bad scientists have been f'en with your health for the profit of Big Pharma and Agro and whatnot.  Look, any American who denies some role of lobbying and subsidies in all this is misguided IMO.  But the fact of the matter is that Americans didn't listen to the whole grain, low fat, LIMITED SWEETS ATOP THE PYRAMID, dogma as they guzzled down the sodas Lustig wants to use the force of that very same government to tax/regulate into oblivion.  Low fat dairy didn't make us fat either.  We -- Americans and other countries of relative affluence or citizens of far more countries with means -- are eating more and/or moving less.  This is neither brain surgery nor rocket science.  It's not *simple*, far from it, but "simple obesity", the stuff this epidemic is made of, is no mystery.  Dieting per se to combat it -- e.g. food restriction and cycling long periods of adherence with going off the diet -- is A contributing factor no doubt.  

If you are struggling beyond all struggling.  Cannot eat less than 3000 cal/day for example struggling.  There is something else going on, and perhaps you need to seek help elsewhere for your eating disorder.  I've hinted recently that I'll be addressing these soon.  And hopefully if there's something hormonal going on that is COMPLICATING (but likely not causing) matters, I wish you all the best in sorting that out without draining precious resources from your wallet.  But in my heart of hearts I see this damaged metabolism schtick put forth by various gurus as nothing more than another means of preying on desperate people for profit.  The beauty of it all for the profiteers is that when their magical plans don't work for you they can just blame it on you being irreparably damaged.  How sweet is that road to the bank?

Out of the blue last weekend my Dad started singing "I beg your pardon, I never promised you a rose garden, along with the sunshine, there's gotta be a little rain sometime.  Google the lyrics if you're a youngsta.  It's so relevent here.  Reality is the latter, which includes self responsibility.  The former is what books are selling.   But ya know what folks?  Running around in the rain half nekkid if a bit pudgy can be sheer delight!!


Kindke said…
CarbSane you didnt mention the Hepatic IR problem that Lustig pointed out in his recent paper. I guess you wasnt aware of it? TBH I only found out about it myself recently after a very kind person sent me the full text.

The short of it is, that people with "damaged metabolism's" have a problem in turning off hepatic glucose production in the face of an oral carbohydrate load. This leads to excessive postprandial hyperglycemia and hyperinsulemia/IR and all the other problems one gets on the obesity->T2DM road.

This also explains why one does well staying off the potatoes/starch, flooding your blood with generic glucose molecules will not be a good idea if you have trouble turning off hepatic glucose production.
Paul Jaminet said…
JS is a software engineer. He has an unusual personal hair style, but I don't believe he styles anyone else's hair.
Steven Hamley said…
I've done some research into mitochondrial dysfunction and leptin resistance here's what I found:

Mitochondrial disfunction (from lifestyle) is a contributing factor to many diseases (IR, T2D, Parkinsons, Alzheimers and obesity). Some studies said MD compromises fat metabolism, but unfortunately don't give a good explanation

Many leptin resistance reviews agree that LR is caused by SOCS3, PTP1B and endoplasmic reticulum stress. Mitochondrial dysfunction is strongly associated with and may cause ER stress. ER stress increases PTP1B. SOCS3 is elevated by IL-6 and lipopolysacchardide (Robb Wolf has been mentioning this lately).

Low carb diets (and other things) increase mitochondrial biogenesis, but carbs don't damage mitochondria. So that means they can't use that as an excuse. This to me might explain low carb flu, their success at weight loss and why Kitavins,etc are healthy.

Paleo is big on gut health and anti-inflammatory, which reduces LPS, IL-6 and SOCS3.

Of course, these aren't the only factors involved
ProudDaddy said…
Re RMR, and piggy-backing on recent comments on Suppversity, I too would like to see data after long-term weight maintenance. The study I commented on showed RMR increasing during the first weeks of maintenance. Further, this was RMR PER unit of lean body mass. However, as I understand it, lean body mass includes organs, fluids, and basically anything that is not fat -- not just muscle. Since weight loss, sans strength training, almost always involves loss of lean mass as well as fat, and since organ and serum, etc., are, it seems to me, unlikely to be the major source of this loss, I would like to see data on RMR per unit of muscle mass only. If muscle mass loss in the formerly obese is a higher ratio to total than lean body mass, then a reduced RMR might simply be due to reduced muscle.
A second point I would like to raise is why a metabolism that is measurably more efficient at rest could be deemed broken! It would seem to me that one should be happy about the reduced grocery bills this would imply -- provided one's hunger/homeostasis system is not broken. And therin lies the rub!
Galina L. said…
"Leptin seems far more effective at preventing regain. " - is it not enough to give it to the people who lost a lot of weight? It looks like maintaining could be trickier than the initial fat loss. I will never forget a commenter on GT blog BrightAngel who lost huge amount after bariatric surgery on something like 1200 cal a day, but in order to maintain she went much lower. Even from her writing it was obvious how snappy the lady was. Sorry, couldn't find more details from the Google besides the year 2010.

I am less desperate now than 5 years ago. At least some people were helped , and probably nothing works for everyone.
Lesley Scott said…
" It looks like maintaining could be trickier than the initial fat loss." True - so, so true. I've been able to, but in many ways it's been more of a struggle than the weight loss part.
You forgot another reason I've been researching a lot lately:

Damaged hypothalamus (resulting in increased urge to eat and/or reduced RMR) from:

- high sugar foods
- high fat foods
- fast food and boxed food that are scientifically made to produce unnaturally high reward
- enormous-sized meals
- failure to "exercise" the hypothalamus by cutting it off from the body's natural environment (using climate control, too much clothing and always perfect-temp showers)
- drugs (both pharmceuticals and illegal)
- other unnaturally overstimulating and addictive things in our modern world (gambling, video games, or even pornography)

All of these have a tendency to degrade the hypothalamus over time due to their overstimulatory effects. This can cause bodyfat setpoint to go out of whack. I've found that meditation and breathing combined with taking out or cutting down on all the overstimulating elements really helped me attain and retain my weight loss.
CarbSane said…
Hi Galina! I'm not sure what you mean by "is it not enough to give it to the people who lost a lot of weight?" I'd like to see leptin therapy for those who've lost a lot of weight go mainstream. If it helps even a small percentage, it's worthwhile IMO ... after all if it helps just 5% that would double long term success rates!

As to Bright Angel, I file stories like that in my BS file. Metabolisms slow, sure, but I've yet to see a resting metabolic rate under 1000 cal/day in any study. I have a post in the works about metabolic rate.
Kindke, why is eating glucose so bad for you if your liver has to make it whenever you don't get enough? Does anyone in the LC community address this contradiction?

Seems like carbs are exactly what the liver needs in order to stop having to make glucose.
bentleyj74 said…
Your muscle mass is a less significant contributor to your rmr than you'd expect. Even bone tissue is lean mass and some of that lost mass involves organs returning to a more reasonable size after having been enlarged to accommodate obesity. You can somewhat influence this [by using resistance training] to favor fat loss over muscle loss but these margins are small. At the end of the day it probably doesn't matter. Muscle burns a ridiculously small amount of calories compared to the rest of the lean mass in the body.
Tomas said…
I also would tend to think that formerly obese people would have still more fat and less muscle than never obese in general. Hopefully I understand your view correctly :)
If that is the case, then I guess it may be more appropriate to measure RMR in lean mass only. I haven't done the numbers, but from the top of my head is seems reasonable :)
Nigel Kinbrum said…
Jason Sandeman made this exact point in a reply to Richard Nikoley.
"Even more weird – now that I have introduced the starches into the diet – I have actually got better control now. I thought my insulin needs would go up – but they haven’t. They’ve gone down." To which I replied:-

"How about this for an explanation? You now have a well-controlled glucose input to your circulation via diet, which has suppressed the poorly-controlled glucose input to your circulation via hepatic glucose production."

The above situation applies to people who don't have Hepatic IR. The best way to avoid Hepatic IR is to Eat Less by whatever means you can. The portal vein goes to the liver, so the liver gets first dibs at glucose, fructose & galactose from dietary carbohydrates.

The liver naturally empties itself by producing glucose to fuel the brain. Stop putting stuff into the liver faster than it can come out!
Kindke said…
Hyperglycemia is toxic, just ask the diabetics who have had limb amputations for thier feedback........

Eating glucose is fine and dandy aslong as your Liver is working properly. I.E. its suppose to suppress glucose production when you eat carbs. thats NORMAL.

However as Lustig suggests most if not all of us that are on the obesity->T2DM->MetSyn highway have selective hepatic IR, whereby the liver DOES NOT properly suppress glucose production when we eat a potato.

The shitty part is that the lipogenesis pathway in the liver goes on as normal, which i think is a pretty damn good explanation why fatty liver always accompanies MetSyn. There is alot of evidence that fatty liver is infact just an effect of hepatic IR, and not the CAUSE.
Keenan said…
Can you link to the full text?
Keenan said…
Some of lustig's reasons for frucose being bad would actually help in diabetes imo. Up to 10 ounces of sugar a day was used to cure diabetes in the late 1800s and if you check out some of my blog post I explain why fructose can help the "metabolic syndrome"
Maybe this is where portion control comes in. Eat (or drink) too many calories at one meal, every day for a lifetime, and you get hepatic IR. With restaurant meal sizes getting bigger (calorically speaking) every year over the last 3 decades, it's no wonder we'd be damaged by now. And people have been gradually eating out more during that time as well.

Maybe calories should be counted after all: not over a day but at each sitting. Caloric drinks and highly refined foods come back into the spotlight now, though for a different reason that just raised insulin.
ProudDaddy said…
Re fatty liver as result, not cause, of MetSyn: I too would be interested in the studies. I can't remember -- on a very low calorie diet which improves first, hepatic and pancreatic triglycerides or IR?
ProudDaddy said…
@Bentley: Do you have a reference for the relative contribution of muscle to RMR? I would really appreciate it.
@Tomas: If we assume bentleyj74 is correct, then we would still seem to have the fact that the WATER content of the body, a significant part of lean body mass as I understand it, does not, I would assume, contibute to RMR?
How 'bout we compare RMR per unit of DRY non-fat body mass in the formerly- vs. never-obese? If they are significantly different, then I'll stop bugging Carbsane about strength training -- until the next time:-)
bentleyj74 said…
Reduced rmr is also due to just being SMALLER. I agree it shouldn't be regarded as a bad thing. Your rmr is what it is. You can bump it a tiny bit behaviorally but there again homeostasis is going to be a force to be reckoned with no matter what. There's a flawed societal perception that small lean people have high metabolisms when in fact virtually every overweight person of similar size to me has a rmr above mine by several hundred cals. They can even LOSE weight eating higher calories than it takes for me to GAIN weight. Until they are smaller that is. It's a non issue until the amount you require to sustain your mass FEELS uncomfortable. If things are functioning smoothly it shouldn't.
As I'm reluctant to attribute the rise in obesity (both in severity and demography), especially among children, to a massive failure of personal responsibility, I'm intrigued by this line of thinking.

Two things you didn't mention are environmental toxins and the brain/gut connection. Kurt Harris recently seems to be noodling thru the microbiome as source of DOCs which presumably also includes obesity.
bentleyj74 said…
@Bentley: Do you have a reference for the relative contribution of muscle to RMR? I would really appreciate it.

Yep, I do. I'll dig it up for you some time today :)
ProudDaddy said…
If one doesn't like the applicability of the laws of thermodynamics, then how about conservation of mass? I am fairly confident that the dry weight of my body cannot increase more than the dry weight of the food I ingest, a situation some of these excessive weight gain claims would suggest. If my Social Security checks were a bit bigger, I'd be willing to fund a session in a metabolic chamber for JM so that we all can get back to the science of the diabesity problem:-)
Nigel Kinbrum said…
Approximately how many minutes of programme do you get between ad-breaks and how long are ad-breaks in the US?

In the UK, we get about 13 minutes of programme between ad-breaks and ad-breaks are about 2 minutes long.

I believe that ads are highly effective at increasing demand for Crap-In-A-Bag and that advertising has drastically increased in volume and cunning over the years. This is why I only watch TV on-line with ad-blocking.
CarbSane said…
Thanks Paul! Perhaps Jack was just being cute then. FWIW, I'm not impressed by Stanton's writings but I think I'll attend his AHS12 talk (unless he's pitted against my list of must sees that you're on). Eh, at least I'll see this unusual hairstyle ;-)
Tsimblist said…
@ProudDaddy: I did a quick Google and came up with this:
"It is fascinating to note that the combined energy expenditure of the heart, lungs, kidneys, brain and liver represent approximately 80% of the TDEE (Elia 1992)."

And this one has a nice chart:
CarbSane said…
Thanks for your input here Steve! Feel free to link to that great blog post of yours on this (my browser is loading new pages very slowly or I'd go look). This reminds me I have a paper somewhere that looked at mitochondrial biogenesis and it had no relation to metabolic rate or glucose transport if memory serves. Gotta look for that!
CarbSane said…
I've found a fair bit of info that higher RMR increases mortality risk. In animals, longevity is associated with lower RMR. So we're back to the whole quality v. quantity of life. As we age we lose LBM anyway, I'd rather keep it even if it's metabolically expensive to do so. I think the point of wanting a higher metabolism PDaddy is that then one can eat a bit more. Especially for us women, that can often mean a pretty pitiful amount of food to avoid regaining. It is not unusual to see women my age report maintaining on 1200 cal/day which just isn't a heckuvalot of food in the real world. By that I mean it's hard to be any sort of social being when you have to abstain all the time.
Galina L. said…
It looks like you may appreciate Thai-chi and Que-gong. I doing a lot of it lately, even paying for private weekly lessons first time in my life (I am on a stringy side). It feels like the perfect combination of concentration on briefing and movement, and it all creates some meditation effect as well.
This comment has been removed by the author.
Agreed, Nige.

I stay the hell away from TV for this very reason. Not just to avoid the stuff the ads sell, but to avoid the ridiculous stimulatory effect they have on the brain. Have you noticed how overly loud and colorful they are?

They are like a freaking video game and hallucinate me if I see them in a bar or at someone's house. I tell you it's really something if you're not used to it. Imagine how silent and peaceful the world was before TV. Now we don't even notice it on while we're in a restaurant drinking or at home having dinner.
Sue said…
So would eating 20% less of your TDEE be best for weight loss - wont slow metabolism too much? But regardless you will always have a decrease in metabolism when your weight decreases and this is nothing to be concerned about? I have yo-yo dieted quite a bit and after reading that post on SuppVersity kind of feel that it's hopeless but don't want to give up.
Nigel, it varies by network, but it's in that ballpark. And yes, the whole cues thing is huge. I've joked that alcohol is my gateway drug to overeating, but for many people what primes them is just everyday stress. But my contention is that there are strategies that can help protect folks here that is more than eat less, move more (e.g. whole foods diet, proper exercise, good sleep, stress mgmt etc).
CarbSane said…
@Beth: I'm musing here less about causes of obesity, but this notion that the obese have somehow "broken" their metabolisms beyond repair and this keeps them from losing weight and/or maintaining losses. If you have info on environmental toxins altering metabolic rate I'd be very interested.

Here's my thinking of obesity & diseases these days. Most diseases are due to deranged hormones and signaling and out of whack circulating metabolite levels. To the degree that obesity correlates with disease rates it is to the extent that impaired fat cell function adds to the problem. Dunno if that makes sense, but I think the "A" causes "B" (disease) causes "C" (obesity) doesn't hold up to scrutiny in many cases. It's probably more that "C" can be a factor that causes "A" that causes "B".

Childhood obesity is no secret to me either. Kids have always loved junk and will tend to overeat it. But when I was growing up I ate in my home or food prepared at home (boxed lunch) probably 90% of the time. There were not many opportunities to get food outside the home. We had no breakfast served in my grammar school, vending machines? I don't recall there being any, and we had a very small kitchen off an auditorium that served as a cafeteria. Not much was served for lunch, most of us brought our own, and most of the time I walked home to eat and back to school. I did not personally know (as in friends with, carpool with, etc.) a single person that didn't have two parents. Some of the moms worked, my own part time from about the time I was in the 4th grade. Bottom line, my parents controlled the types and amounts of food I ate (except for when I was at granny's and had access to Frosted Flakes and scooter pies -- but I had two breakfasts those days and Mom was always puzzled how I didn't eat much if anything come lunch). Nowadays kids are making those choices for themselves outside of the home and often even in the home. Processed food is engineered food. No way I would even drink a small coke daily let alone several (Lustig's crusade). Heck, Mom diluted my juice. If I drank anything else it was water or tea (maybe a T honey in a whole pot if any sweetener). Kids somehow have more money in their pockets these days and junk is cheap and there are no adults around telling them not to eat it. They're not buying "healthy whole grains".

I also think BMI is fatally flawed for assessing obesity in growing children. A kid that gets protein from their McD's but too many calories likely builds more lean mass and gains more weight just as in that Bray study. I want to see evidence of this epidemic of obese 6 month olds. So far all I've seen is Lustig make that claim and everyone repeats it. IS there one?
CarbSane said…
Oh man o man was I brutalized for saying just that in my podcast with Jimmy! I said you can't gain more than a pound of fat mass eating a pound of cookies and specifically said this excludes water weight. Oh how many people think I'm a total nut for believing that! Insulin has magical properties indeed ... the lack of it causes common sense resistance.
Galina L. said…
I wonder, how much weight a person should loose in order to benefit from the leptine injections? Or probably the level of leptine indicates the arriving on a weight loss plateau. What if it explains almost every weight-loss stall?
Sanjeev said…
> evidence of this epidemic of obese 6 month olds


like the alleged epidemic of infant diabetes that was predicted 20 years ago and for which I recall mounting warnings and alarm, that never materialized, I've yet to see this proven.

Anyone else see the 60 minutes piece with Lustig? They couldn't find ONE credible voice of reason for that piece? The oncology researcher who eats no sugar anymore because of blood sugar effects but says nothing about rice and potatoes.

The neurologist was the only one there I found at all reasonable.
CarbSane said…
Hi Sue, As I mentioned to Galina I have a post in the works about metabolic rate and impact of calorie restriction, etc. I found so much new stuff I'd like to add that I'll probably have to break it up into parts. It turns out that not everyone even compensates even with dramatic caloric restriction (PSMF) and rebound is highly variable when weight stabilized at a reduced weight. Another thing, however, is that some sort of calorie cycling to achieve a total caloric deficit may well help prevent this. I'm thinking that 2 day a week VLC 500 cal diet vs. sustained caloric deficit Med diet study I blogged on a while back. If I'm not mistaken, WW points work over a week or there's some sort of "saving points,earning points" thing there for higher calorie days here and there. I wish having RMR measured were more accessible, it would give us more information to be realistic about all of this. But say you maintain at 1800 cal/day, then 500*28 = 14,000 cals = 4 lbs stored lipid in a month. That gives you 2-3 free days to eat at 1800. There's nothing to say that fasting a full 24 hours once a week (takes care of almost half of your target calorie deficit if it works for you!) is a bad approach -- provided you're not a compensator who can't stop eating the rest of the time. But by doing that, one would only have to cut back to 1300 cal/day 3 or 4 of the other days of the week. Or cut back to 1550 all days, or cut to 1000 one day and splurge on 2100 another. This seems to work for many, whether physiologically or psychologically.
ProudDaddy said…
@Tsimblist: Thanks for the references. I did some calculations on the 1989 Elliot study results and must reluctantly conclude that loss of muscle was a very small part of the problem.
@bentleyj74: Thanks to Tsimblist, you're off the hook. Thanks, anyway!
I'm left with two questions:
1. How much does the RMR return during long-term maintenance?
and 2. How else can I bug Evelyn about strength training?

As for 1., it looks like Evelyn will soon be posting some well-researched data,
and as for 2., HEDEN, 2011!!!
ProudDaddy said…
@Evelyn: I believe that Adel is a physicist, so I think all three of us may have found complete common ground on the law of conservation of mass. Of course, JM might have some sort of nuclear reaction going on...cold fusion?
Gwen said…
Oh Evelyn, so often on some of these blogs I want to make a nice long comment about how adult and children's eating habits have changed over the last few decades, but I just never do. Until today!

I'm 51 and I remember that as a child there wasn't a fast food place on every corner. It was a HUGE treat when my parents would take us out for a McDonald's. My mother worked full time and every great once in a while, she would bring home a couple of bags of White Castle hamburgers (I'm from Ohio) or a bucket of Kentucky Fried Chicken after work on a Friday night. Oh my! That was a big deal. Otherwise, it was only homecooked meals and packed school lunches. My mother also never bought sodas or fruit juices. We drank milk at meals. I remember one Halloween when I was out trick or treating, I passed some other trick or treating friends who passed the word that Marcy's parents were handing out cans of Pepsi. Marcy's dad worked for the distributor. I hightailed it to their house because a can of Pepsi was an awesome treat. LOL! And, of course, Gunther is right - portion size has changed dramatically. Look up the size of a bottle of Coca-Cola 40-50 years ago or the size of a McDonald's Coke and hamburger.

We also did not have some sort of packaged "snack" available. Nowadays it's so typical to have some "goldfish" crackers or Cheerios available in the car or stroller for children to snack on. It seems to me that if you eat a proper meal there is no need for a snack and that's the way my husband and I are raising our son.

The other thing that you've all noticed is the growth of food as some sort of entertainment. Aren't there scads of shows related to food and cooking? Again, growing up I could watch Julia Child or The Galloping Gourmet on PBS and that's it. And why is it necessary to have a well known chef write a monthly column including a recipe in an interior decorating magazine? Yet open up any home design magazine and that's just what you'll find. All the time we're surrounded by food! It just seems that we have too much of something, but I'm not sure what. Is it so much food and easily accessed? Too much money? Too much time? Or something else?

We have a single mother to a 13 year old boy as one of our neighbors. Both are obese. How often do we wave a greeting as they are coming home from work/school carrying their dinner - bags of fast food. Often my husband and son will be out playing and the 13 year old will join them. One time after the boy left, my son asked my husband, "why is XXX always chewing something?" My husband and I chuckled over that question but the truth is, the boy always has something in his pocket (candy) to eat but my son never notices it - just the constant chewing.

Well, I think I've satisfied this long-term itch I've had to say these things :) . Thanks for letting me!
Tonus said…
"How else can I bug Evelyn about strength training?"

Just ask Fred Hahn to show up. ;)
I'm completely with you on the "broken beyond repair" issue (hello, my fasting insulin was 24 in late 2009 and I'm eating 100g of starch and managing to lose weight ;).

But I guess what I'm trying to get at is that the reason folks flock to the gurus is that most have not found "eat less, move more" an effective strategy for weight loss or weight loss maintenance. There is something more to it, and I don't think it's just emotional disorders.
ProudDaddy said…
@gunther: I think you have stated the correct location for the problem in most of us. It would be helpful, it seems, to be able to determine what the "damage" is. E.g., are we talking dead neurons, fewer leptin or whatever receptors, a blood-brain barrier problem, receptors filled with an incorrect signalling substance, etc., etc.? IMHO, only when we know the precise "damage" can we then search for mechanisms, and then search for causes like the ones you describe.
Oh, and here's NHANES data on obesity in the 2-5 age group.

And here's quick retrospective study on infant obesity:

"The prevalence of infant obesity was 16%. ... Infant obesity strongly predicted obesity at age 24 months. Risk factors included excessive intrapartum weight gain or being born large for gestational age. Clinicians diagnosed obesity in only a minority of children. Primary care providers need to diagnose obesity in infants and work to develop effective interventions."

Epigenetics anyone?
Galina L. said…
I lost significant amount of weight(approximately 50 lb) two times in my life through diet and exercise. First time at 27 and second at 38. I also have been exercising all my life and eat almost exclusively the food I cooked. After 45 something got changed and LCarb diet was the only working thing left. It could be multiple reasons - approaching menopause, several weight-losses in my past, under-active thyroid. Should I consider myself to be broken? I have to limit the amount of food I eat and exercise a discipline if I don't want to bounce back. People with a perfect metabolism don't have to do so.
bentleyj74 said…
"The prevalence of infant obesity was 16%. ... Infant obesity strongly predicted obesity at age 24 months. Risk factors included excessive intrapartum weight gain or being born large for gestational age. Clinicians diagnosed obesity in only a minority of children. Primary care providers need to diagnose obesity in infants and work to develop effective interventions."

Epigenetics anyone?

I wouldn't rule it out as a contributor but it's not the most obvious answer.
Kindke said…
Cliff which full text?

BTW the fructose thing, its funny actually, I tolerate fruit and honey FAR FAR better than I tolerate potatoes. I wish I could eat potatoes and not gain weight, baked potatoes with cheese is one of my favourite meals :)
Well, the obvious answer is Lustig's "baby milkshakes" (modern formula). Are the infants at fault for eating too much and moving too little?
bentleyj74 said…
"There is something more to it, and I don't think it's just emotional disorders."

I don't think it's an either/or ...what is emotion? Physiological feedback. Reward pathways, distress, coping mechanisms...the list could go on forever. Anything emotional is also physical.
bentleyj74 said…
Parents know the easiest way to shut a crying baby up...stick a full bottle in it's mouth hungry or not. I've seen parents continue to insist on a feeding even though the child was turning away and gagging until they finally complied on downing the last few ounces. I think it's possible to have childrens satiety signaling disrupted so early they have no concept of "normal" function.
bentleyj74 said…
"It is not unusual to see women my age report maintaining on 1200 cal/day which just isn't a heckuvalot of food in the real world."

No, it isn't. In a world of muffins and pizza 1200 just isn't going very far at all. It's a heck of a lot of broccoli and apples though.
Unknown said…
So far, that's my experience as well Kindke. A little honey in my coffee is invisible in my blood glucose--as is the heavy cream added with it. Cream and fruit is also fine. A sweet potato, though, has to be a reasonable portion for me to stay under 140 at 1 hour post-prandial. I must also admit that a huge feast of fruit will also spike my bg but it's gone within 90 minutes.
Unknown said…
I like reading J Stanton's articles. For me they resonate without specifically causing me to eat/not eat any particular food or meal.
Unknown said…
My metabolism is probably unique in medical history. As some background, I have been testing my blood sugar level every ten minutes for eighteen hours a day for the past 43 years. During this period I have consumed well over 14,000 calories per day on every single day of the year, yet I have not gained a single pound. However, you must also take into account that on a daily basis I have introduced ice cubes into a part of my anatomy that I shall not mention. The fundamental truth I have discovered is that combining the introduction of the ice cubes with the spiking of the glucose, I can eat astonishing quantities of food of any and all types without ever gaining weight. I hope to expand on my experiences in my new blog very soon.
garymar said…
Gwen, I'm 58 and I remember a time when McDonald's was the place for teenagers to hang out. They bought some food and then made out (kissing, in the American idiom) in their cars. It was a drive-in! It was also a huge teen meeting place on the weekends. This was before the Big Mac, and the kids called the hamburgers "gut bombs". They knew it wasn't the best food in the world. It was a huge treat when my older teenage brother would drive me there for a burger, fries, and shake.
Sue said…
Depending on choice of food you can feel quite full on 1200.
Sue said…
Thankds Evelyn, look forward to post(s) on metabolic rate. I like the idea of caloric cycling.
Galina L. said…
It is why I appreciate IF. With no snacks, one of meals is a small one, second meal I eat to satiety. Since my "personal preferences" are more modest that JM's, it works to control my total food intake.
Keenan said…
The full text to lustigs paper.

Fruit in the right context needs barely any insulin to be metabolized due to the nutrients like potassium. This is why studies done with any type of refined diet on sugar are BS.
ProudDaddy said…
I too anxiously await your posts on metabolic rate. I hope you'll include some tnoughts on how a "damaged" metabolism, a more "efficient" metabolism, becomes the problem; i.e., why our homeostasis regulators don't just adjust to the reduced need.
bentleyj74 said…
"Depending on choice of food you can feel quite full on 1200."

Left index finger on nose, right index finger pointed at Sue.
Woodey said…
After reading Slow Burn by Hahn I'm not sold on his 30 minutes a week is all one needs to be fit line. Having spent a part of my teens and all of my 20s immersed in the gym talking to trainers, bodybuilders, and reading books on the subject I found his point of view to be very contradictory.

Bottom line from every athlete I ever worked out with or got trained by said the more you put into your workouts the better the results. Now they also said that the weightlifting was just one piece of the pie. Nutrition, sleep schedule and workout schedule (making sure you rest the muscles and not overdo it)where just as important if not more so....oh and also a thing called genetics played a part as well. We were very envious of the Asian weightlifters because of their tendency to be naturally lean and not have the extra fat most of us had to struggle to keep off. Man they looked ripped even in the off season.

The other rule of thumb was you keep your workouts around the 60-90 minute mark and never longer than 2hrs, excess weightlifting was counter-productive to progress.

The 30 minutes a week thing strikes me as catering to the couch potato and in reality isn't going to do squat for a person really trying to make a dent in their fitness.

Squatting till you couldn't walk very well or felt nauseous > than two min of slow burn leg workouts.
CarbSane said…
Enjoyed your little "rant" Gwen! And Gary, below, I too recall hanging out at BK as a teenager to meet cute guys from a neighboring high school! I've told this story many times but heck once more can't hurt. I live in the neighborhood where I grew up and if it weren't for Halloween and ~8:30 am when I get boxed into my street from the long line of kidlet carrying cars, you'd think there were no kids in the neighborhood. When I was a kid we were out riding bikes, playing touch football, SPUD, etc. all times of day or night when we weren't in school and the only time I got driven to school was in bad weather or running late. It's like the scene out of Fat Head which makes me not "get" Naughton even more as he blames the government and grains for obesity.
CarbSane said…
@Gunther: Do you feel this damage is permanent? I'm thinking possibly or even probably in terms of homeostasis but it's hard to separate habit from signaling in intelligent beings, eh?
CarbSane said…
I got MAJORLY sidetracked doing my Adipose Tissue Growth series (yes I'll get back to it - grin) doing a post on fat in late term gestation and infancy. Babies born small for gestational age gain fat very rapidly and are at risk for obesity. Probably over a year ago I came across a study that babies of obese mothers drink more formula. Then there's the faulty use of BMI or even weight as a measure b/c formulas that are higher in protein by only a couple percent or two predispose towards "obesity" but it seems more reasonable that they build more lean mass during rapid growth. Same goes for the studies in kids that show no benefit of activity using BMI. I've seen lots of "obese" children that look rather normal to me. I guess the reason I ask is that while I see more obese grade school age kids these days than I recall from my classmates, I'm not seeing more pudgy babies. I was a pudgy baby who had access to sugary goodies at Granny's house where I spent several mornings a week until I went to kindergarten. I grew into a lean kid, one might call me scrawny but for the fact that I was a little muscular even then. I used to baby sit for the entire neighborhood and have saw tons of infants up close and personal doing that and saw lots of pudgy babies in the late 70's early 80's.

Childhood obesity is real, but in some ways overblown too. In my generation there was such a thing as growing out of one's baby fat. I've watched friends', relatives' and neighbors' kids do just that more often than not. Which is not to say we shouldn't pay attention to true obesity in children, just that I think many are prematurely being labeled and are likely more harmed by the humiliation and intervention when they'll grow out of it. We see these stories on the news all too often.
Hi CS. I think if you're coming from a lifetime of obesity and yo-yoing, you'll have to do much more meticulous maintenance of your behavior than someone who never had this problem. But can you reach really low BF even if your hypothalamus was damaged, and not feel deprived or starved? Yes, you can. And it doesn't feel like a struggle.

But maintenance is the key, and I do find that over time (and it's only been a few months of this new approach), I have markedly less urges to eat more than necessary and/or to binge. I also have more spontaneous urges to move and play and do sports, something I always had to force myself to do before. I take this as a sign of healing.

The more I read about the brain, the more I see what an amazingly adaptable and renewable organ it is. This should give us hope.