Attempting to define the "Damaged Metabolism"
Where 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?
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 Gnolls.org. 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 )
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 Gnolls.org. 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.
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 ....
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!!
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!!
1 comments:
KindkeApr 19, 2012 01:13 PM
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.
Reply
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.
