Thursday, October 15, 2009

The thumb tack hypothesis

There are some interesting numbers in this paper from back in 2005. It's based around the well accepted fact that fat people move less than slim people. Apparently making heavy people move as much as thin people could easily result in 15kg of weight loss per year. That's pretty impressive for hiding the remote or putting drawing pins (thumbtacks?) on fat people's chairs.

The paper looked in great detail at the movement and energy expenditures of mildly obese people (BMI 33) or slim people (BMI 23). They found, as expected, that slim people move far more than fat people.

That's obvious from FIG 1. You really have to click to enlarge before it's readable:

From section A, top left chart, right hand pair of columns, you can see that thin people spent about 510 minutes up and walking.

Fat people were only up and moving for 370 minutes a day.

But now look at chart C, energy expended by activity, left hand pair of columns. The big red blocks on the tops of the columns are energy expended by being up and walking. Ignore the white extension, that's just the projection of what should (but won't) happen under the thumb tack hypothesis.

Thin people spent 800kcal per day on walking.

Fat people spent, guess what: 800kcal per day on walking.

Now, is that neat or is that neat? The lazy fatties were expending EXACTLY as many calories on being up and mobile as the slim people. This point seems to have escaped the authors' attention. Is this anti fat bias? Which group is laziest? Count those calories!

In fact, the only real difference between the groups is that obese people spent MORE calories overall per day and the excess is spent on basal metabolic rate. You cannot argue with a big body. It needs fuel. BMR is life. Obviously they have to eat more to do this.

The projection for 15 kg weight loss per year is based on making fat people mobile for as many minutes per day as thin people. But why should they do this? They are already spending as much energy as the thin person on spontaneous movement. They are spending MORE per day on BMR and an equal amount on odds and sods like the thermic effect of food. They eat more to make up for BMR and because their blood insulin levels steal a little food to store as fat.

Making them move more would simply need more calories. They would be hungrier.

The second phase of the experiment should have tested whether putting drawing pins on the chairs of fatties made them thin. The USA government is, after all, suggesting dance classes to replace TV viewing as the national pastime for its citizens. But I guess they really do know when they are on to a loser and decided not to test this.

Instead they looked at what happens when you make a fatty thin. Drop their weight down to BMI of 31 and look what happens. Well, nothing. A drop of 8kg from BMI 33 gets you down to BMI of 31, not 23. So we are not looking for a conversion from fat to thin, just a small increment, hopefully enough to show the trend. Here's FIG 2:

Weight loss means caloric deficit. BMR requires calories to sustain life so cannot be dropped much. The thermic effect of food etc expenditure makes little difference. If there are less calories spare during weight loss, what has to happen to movement? Look at chart A, right hand pair of columns. It drops from 390 minutes per day to 360 minutes per day, a drop of just under 10% in terms of time expended moving. Not statistically significant, but the trend is that weight loss by caloric restriction DECREASES spontaneous movement. This also was not noted by the authors, but would certainly have been predicted by Gary Taubes.

Get them down to BMI 23 and they would probably stay as still as practical for as long as practical. Then move to steal some food.

Over feeding makes you fat. It does it by increasing insulin levels. Do you then increase your spontaneous movement? The average extra free energy available during an increase of 4kg weight gain is small if insulin is packing most of those calories in to adipocytes, unless you are the outlier who upped their movement time by an hour a day (possibly the most insulin sensitive in the group?). The trend in spontaneous movement doesn't really show, but what hint there is is upward.

As Michael Eades has pointed out, he does see obese people who appear to be insulin sensitive, but they are uncommon. For most obese people the need is to lower insulin levels, then they won't need the thumb tacks on their chairs to either lose weight or become more mobile.

But thumb tacks on chairs is official policy. Without doing the trial.

Oh, I feel another paradox coming on!



Brad Reid said...

Peter, it is just really tough to lose weight via exercise because of our bodies' extreme operating efficiency.

You have likely seen this math.. the 912 MPG machine (us):

A 175 lb. man riding a bicycle at 15 mph on a flat surface burns .049 calories/lb./mile.

A gallon of gasoline has 31,000 calories.

So, a man could peddle a bike 912 miles on the equivalent of a gallon of gasoline.

Since we cannot safely consume/burn gasoline calories, 31,000 divided by 3500 calories/lb. of fat = 8.86 lbs. of bodyfat.

A human could peddle a bike 912 miles on 8.86 pounds of bodyfat.

Using a stored glycogen number of 200 grams here and there around the body would only operate the bike rider for a much shorter distance, then the fat burning would kick in.

Exercise's ineffectiveness for losing weight was highlighted on a PBS show not so long ago about exposing non-runners gradually to a running regimen culminating in a marathon... one pudgy female "oddly" stayed pudgy, and the researchers brought this fact up, that diet was a much more important input than exercise in weight loss.


Anna said...

My BMI at 22 is lower than the study participants and this rings true for me, too. My activity level, hunger intensity (or more often, lack of hunger), and eating levels are most definitely intertwined. Reading Taubes' book really clarified how my capacity for daily energy expenditure was reduced when I didn't eat enough. Problem was, the high fat/low carb food pattern kept my hunger so low many days that I sometimes didn't eat enough. Instead of losing weight or developing hunger to prompt eating, I found myself s-l-o-w-i-n-g down as the day went on. Now I try to make sure I eat before mid-afternoon, even if I'm not hungry.

Unknown said...

Hi Peter,

Been lurking for a your blog.

On this one I have to disagree with you a bit. That second graph showing no change in minutes of activity could just as well be an argument for the "lazy" hypothesis (I wouldn't call it lazy so much as movement preference though). The fact that even after weight loss or gain, people stuck to their standard movement pattern might just as easily show that people have a natural desire for a given quantity of movement that is unhampered by their weight.

I haven't seen enough research to prove things either way, but thought I'd play devil's advocate a bit here.


newbieinNoVa said...

Re your comment on insulin sensitivity and obesity, you may find this as fascinating as I did. I dug this up after viewing the video Dr. Eades posted on Twitter yesterday -- it's one of the studies Gardner showed on the subject of insulin resistance and sensitivity.

It doesn't seem that insulin sensitivity is that rare in obese folks.

Peter said...

Hi Brad,

Yes, that makes it about 2h cycling per Mars Bar...

Ian and ActBoldly, I suspect these might be related. People who are insulin sensitive gain weight easily on an insulin raising diet. It's when you can't gain weight any longer (by whatever mechanism) that you become diabetic... So body weight probably tells us very little about insulin sensitivity. In the weight loss group 8kg is actually quite a lot, although as a short communication there is essentially no information about time scale or technique for slimming or weight gain.

But whether you lower insulin by starvation or LC eating, both ultimately should allow access to fat stores. It's then a matter of how easily this occurs which determines how much energy is available for movement. So yes, it's hard to make any real conclusion from graph 2, especially as activity dropped in the weight loss group but not significantly so. Hard to comment on statistical vs biological significance here too. We'd probably need to go to Dr Eades posts on Keys' starvation experiments to pick up a time scale for activity loss on starvation, but there is a blue sky, bright sun, brilliant Autumn colours and I'm off work today so it's hill walking time!

What looks fascinating to me is that we seem to have an energy budget of about 800kcal for random movement when on free choice caloric intake....

Act, I've got a post brewing from Yudkin on subdividing slim volunteers in to those who found sucrose obesogenic and those who didn't. Prob insulin resistance related, before the obesity occurs. I think it was 50:50 but I'll check and post some time. The tendency, probably related to the metabolic flexibility concept, might even start in utero or before. Gasp, it might even be genetic!


Fred Hahn said...

And let us not forget that we have to subtract the amount of calories that would have been burned anyway doing nothing in particular.

So if you burn 500 calories dancing for an hour, you have to subtract the amount of calories you would have burned doing something else - even sitting still in a chair for that same time frame.

newbieinNoVa said...

One other comment. If you haven't watched the Gardner video (or don't have time to watch the whole thing) check out minutes 38-45 or so of the Gardner video (which is here:

He shows two other smallish studies on the question of LC vs LF and insulin sensitive/resistant as well as the data for his own larger study. In all three cases, IR folks do *much* better on LC compared to IS folks. Very interesting stuff!

Andrew S said...

What I remember from Taubes' GCBC was that obese people aren't moving less because they're lazy; they're moving less because they don't have energy. In the presence of insulin more activity won't burn fat, it will just lower their BMR or burn lean tissue, neither of which is desired. Thumb tacks won't burn fat, and until they do a study all they're doing is taking a correlation and assuming causation.

Peter said...

Fred, because the paper is so pared down you can't really see whether they accounted for all 24h of BMR in the BMR part of the column, if they did it should have accounted for those 500kcal, but the principle is the same, caloric output from movement was the same.

As I see it, a fat guy bench pressing 50kg 20 times is no lazier than a skinny guy bench pressing 10kg 100 times, even if the fat guy does it in just a few minutes then sits around in the gym looking fat and lazy while the skinny guy does his hundred reps! They both shifted 1000kg through a fixed distance...

Act, I got to listen yesterday. He's sensible, sounds like a scientist in his ability to discard a hypothesis, soy and isoflavones are apparently out of favour as the mystic elixir of the East nowadays. Nice to know. Must be hard to accept Atkins being correct if you are a vegetarian. Now he just has to go through fibre, cholesterol and palmitic acid re education. Unfortunately there is only so much time for re education in a career!

I would suspect everyone does well on LC as it mimics starvation and anyone who cannot cope with starvation starved many generations ago. Only the insulin sensitive cope with low fat high complex carbs (a la Kitavans). I suspect it is a happy chance that LC side steps insulin resistance, although this may be intrinsic to what insulin resistance is. Personally I doubt very much that LC "cures" pathological insulin resistance. It's just the correct metabolic fuel choice for when pathological insulin resistance (which I think might be mitochondrial) is present because it mimics the physiological insulin resistance of starvation/carbohydrate restriction..... If it didn't, medicine and pathology would be very different!


newbieinNoVa said...

Peter, I think a big issue re LF and LC is long-term compliance. Carbs are hard to give up. Gardner's study showed that folks who started on Atkins really wound up closer to the Zone at 6 months (30% carb). So it's probably important to know who really benefits from LC and what level is necessary/beneficial from a long-term standpoint.

I agree we don't know enough to guess whether LC "cures" IR. But you certainly are unlikely to move towards IS if a higher carb diet is the major contributor towards IR.

Then there's the question of specific foods in the diet. Right now, I'm intrigued by the theory Stephan Guyenet blogs about re wheat and sugar (and lectins!).

I also am curious about the role of dieting and aspartame. But it's hard to see how either of these play a major role given the rise in childhood obesity and diabetes, where neither dieting nor aspartame are much a factor. Wheat and sugar make much more sense since they are a huge part of kids' diets.

Stephan thinks that once you're IR, all carbs are probably problematic, but I think that's something that would be interesting to study. And I plan on doing a study of one some day myself :).


Fred Hahn said...

I think a lot of folks wind up eating more carbs when on an Atkins diet because they are not educated about how caustic sugar is to the body, specifically its contributuin to cardiac inflammation.

If they knew this, I doubt you'd see as much of a trend towards a 30% carb intake.

Anna said...

I'll piggy-back onto Fred's comment with the observation that the glycemic index has also given people a false-sense of which carbs to eat or not eat. I can't tell you how many people say to me (including one of my parents who I now know is diabetic and probably has been for years), "but it's a low-glycemic carb" as they offer me some sort of starchy side dish or high-fructose sweetener like agave syrup.

The glycemic index baloney is sold extremely well to people are looking for a way to continue to indulge in "safe carbs", but they don't get it that low-glycemic or not, it still too many carbs and will raise BG too high, too long, or both (or in the case of high fructose agave syrup, will lead to a fatty liver). Most of them don't realize the tests that made up the GI/GL load don't really apply to people with glucose regulation issues because the test subjects were young, healthy, and still had intact glucose regulation.

My idea of low glycemic carbs I can enjoy is off-the-chart low - romaine lettuce, not whole grains!

Peter said...

Anna and Fred,

Personally I'd like to see as much money spend preaching the minimisation of glycaemic load as is currently spent preaching minimising fat intake. Do that for 30 years and then see who could avoid sticking to Atkins! A time when your friends and relatives take one look at your plate of wholemeal low fat lasagna and gasp in horror, while adding cream to their high fat ice cream and berries after their steak. Then see about compliance!


Peter said...

Beth, wheat and sugar are what was shipped to HGs well before margarine was thought of (I think). As glucose seems to me to be pretty non toxic it then comes down to fructose and lectins. Nothing to argue with there. I don't like PUFA but I think you can break a human with fructose and it is very hard to unbreak them. Linoleic acid certainly makes it worse.

Oh, and in the words of the Red Hot Chili Peppers, "Life is not a read through". We only get one shot. Hmm, I must be getting old!


Anonymous said...

>>That's obvious from FIG 1. You really have to click to enlarge before it's readable.

I would but I'm too fat to make the effort.

Anonymous said...

Not ever being obese, I've found from personal experience that while insulin is important in controlling weight, still, total calories determines weight gain/loss. For instance, I tried a diet of 90% butter, while eating more than I needed, and so I gained weight.

Off topic, Peter I've noticed your remark on the limits of blogging software, and also that you reference lots of PubMed studies. So I thought it might be helpful to make a Blogger gadget that goes into your sidebar. It pulls all the PubMed links you've used in your blog, gets the citation's title, and groups it by blog post. Links navigate to the original post or citation. A small demo is here. Thanks for reading.

Anonymous said...

forgot to add it can be searched in "add a gadget" as "pubmed citations"

Fred Hahn said...

No carb said:

"Not ever being obese, I've found from personal experience that while insulin is important in controlling weight, still, total calories determines weight gain/loss. For instance, I tried a diet of 90% butter, while eating more than I needed, and so I gained weight."

I have to say I find it VERY difficult to believe that you ate a diet of 90% butter for any length of time. Sorry to be a doubting Thomas but this seems highly doubtful.

Butter has sugar. Perhaps you should have tried ghee?

Calories do NOT determine weight gain - type I diabetics cannot gain weight without insulin no matter how much they eat. Insulin is required to put on fat. The human body is an open system. The types of calories matter. A MA exists however slight when carbohydrate is low and protein fat is high.

There are no calorie receptors in the body.

Anonymous said...

"Calories do NOT determine weight gain - type I diabetics cannot gain weight without insulin no matter how much they eat. Insulin is required to put on fat."

Yeah, except you always have a base level of insulin in your system, as a non-diabetic, even when you're not eating protein or carbs.

Bris said...
This comment has been removed by the author.
Bris said...

"Type I diabetics cannot gain weight without insulin no matter how much they eat. Insulin is required to put on fat."

Wrong. Before insulin was discovered in the 1920s Type 1 diabetics (who don't produce any insulin) were placed on zero-carbohydrate meat-based diets. They gained weight on these diets.

Low carb diets cause weight loss via reduced calorie intake due to reduced appetite. The body cannot tolerate high amounts of protein (over 5g/kg bodyweight). Fat intake >80% causes diarrhoea.

Carbohydrate intake has no effect on appetite. People gain weigh on high carb diets simply because they consume excess calories.

"There are no calorie receptors in the body."

Humans instinctively match daily calorie intake with energy expenditure to within ~0.2% regardless of diet. This is why it usually takes decades to become severely overweight.

Bris said...

JB said:

"Peter, it is just really tough to lose weight via exercise because of our bodies' extreme operating efficiency."

There is nothing efficient about the human body's energy use. A world class road cyclist can only produce 0.5 hp for one hour. 80% of our energy output is in the form of heat.

The only reason why exercise is "ineffective" is that very few people ever do anywhere near enough to lose weight. Jogging for 30 minutes a day is only going to burn 1kg of fat in a month.

Elite athletes are often forced to gorge themselves constantly to maintain their weight.

Our HG ancestors would have been burning at least 1000Cal a day in physical activity over their BMR. This is equivalent to burning 50kg of fat per year.

Loren Cordain has stated that "adequate" exercise for a male is 'running 15 miles wearing a 25lb backpack every day.'

Fred Hahn said...

"Loren Cordain has stated that "adequate" exercise for a male is 'running 15 miles wearing a 25lb backpack every day."

This amount of exercise is absurd. Humans are not designed - no animal for that matter is designed - for an amount of exercise and punishment.

Maintaining a normal body weight is all about eating real food. Exercise should be for maintaining and/or increasing lean tissue.

Fred Hahn said...

"Wrong. Before insulin was discovered in the 1920s Type 1 diabetics (who don't produce any insulin) were placed on zero-carbohydrate meat-based diets. They gained weight on these diets."

Reference please. I think you are missing the point howevere Bris. I am sure that these diabetics you mention were given insulin. But the fact remains, no insulinm no fat storage. That is not debatable.

All the body knows is fat, carbs and protein. You will NOT necessarily get loose stools eating an 80% fat diet. If so it will be temporary. But 80% is an arbitrary number you made up. Most paelo-eating folks stick to a 60-70% fat diet, 20-30% protein 10-20%carb eating plan.

"Humans instinctively match daily calorie intake with energy expenditure to within ~0.2% regardless of diet. This is why it usually takes decades to become severely overweight."

Reference please. Is the loss of lean tissue as the years roll on figured into this 'equation?'

"Low carb diets cause weight loss via reduced calorie intake due to reduced appetite."

Since it is true that some people can indeed take in more calories than their BMR and not gain fat and since some can do the opposite, your statement is false. I probably don't need to reference the research in the book 'Good Calories Bad Calories' for support, right?

And remember, weight loss and fat loss are very different.

"The body cannot tolerate high amounts of protein (over 5g/kg bodyweight)."

Even if this is true (which I don't believe it is - reference please) so what? Who's going to eat that much protein? Even hardcore bodybuilders don't eat this much.

Bris - obesity is a disorder of excess fat accumulation casued by a disruption in the hormonal mechanisms of the human body caused by excessive insulin production (among other things).

You don't look at a 6'6", 10 year old boy and say - "Hey look - he's really eating too much and he's lazy!" Hormones are out of control. You don't watch a pregnant woman who is bawling over her choice of ice cream at Ben and Jerry's and say "She's a nutjob." Hormones are raging.

Hormones, not total calories are the deeper picture. We need to be looking more deeply into the obesity issue especially for children.

Brad Reid said...


Some time ago, I think it was Arthur DeVany who posited the idea from his research that a paleolithic man might have had a "2X" or "3X" lifestyle meaning that he/she burned, through the rigors of a tough, demanding life, two or three times base calories needs. So, if 1,500 calories was the bogey, then 3,000 to 4,500 owing to their heightened activities.

My guess is if this is accurate, it ensures that using stored bodyfat as the source for a lot of those calories on many days was essential between successful hunts.

Yes, to lots of calories ending up as heat...we are warm blooded and regulate such matters. Where heat signals wasted energy in some systems, maybe less so for systems depending on it?

For me, the idea that a man weighing 175 lbs. can ride a bike from Dallas, to Houston, back to Dallas, and back to Houston... on 8 or 9 lbs. of bodyfat... it is still pretty impressive.

Other than a personal general belief that about 2/3s or more of one's food should be fat calories of the right sorts, then carbs and protein, it seems to me that the real goal is to optimize, via insulin and other factors, the ability to get excess sugar out of the blood where it is harmful, then to be able to get energy out of stored fat, when blood sugar is too low.


Dr. B G said...

Actually the human body's efficiency adapts to demand -- more demand (high intensity short duration v. low intensity long duration) changes the genetic expression of different receptors in the muscles and hormones. Different muscles fibers are favored dep on the demand (fast twitch v. slow twitch) and the mitochondrial quantity change accordingly as well.

This has been shown in studies... as well as the many who follow Paleo type ancestral exercises! Personally noticed I eat less and have more energy -- could it be I have better hormones and better insulin and better efficiency? Yes -- it is all modifiable. Hormones and demand...

Matt Stone said...

Good post. I can't believe that those fatties are moving that much. I'd be lucky if I moved 37 minutes a day. 370?

There are a couple of fallacies in the post though, one is that BMR can't change much. The range of BMR is -50% on the downside, meaning you can go from burning 3,000 at stable weight to burning 1,500 on stable weight.

On the topside, you can increase BMR by 100%, meaning you can maintain weight on 6,000 vs. a normal 3,000.

It's a biological fundamental that very few are hip to, but that studies such as Ancel Keys' starvation study and Ethan Sims overfeeding has shown very conclusively.

Overfeeding also does not raise insulin levels, but actually decreases insulin resistance and leptin resistance and lowers insulin levels, which is why overfeeding leads to massive decreases in hunger and rapid weight loss when overfeeding stops. It's a mirror to the effects of underfeeding.

Overfeeding can actually be quite metabolically healing, and builds tremendous digestive strength.

Matt Stone said...

The insulin component is so true though, and it takes such a tiny fraction of calories to be diverted into fat storage compared to that burned to create a steady increase in total body fat.

For example, the energy found in a single peanut being stored in body fat on a daily basis is enough to make a person gain the typical 40 pounds between ages 20 and 60. It's not something we could ever consciously regulate.

Anonymous said...

and the mitochondrial quantity change accordingly as well.

Do you have studies on humans as opposed to rats showing this?

Dr. B G said...

J Am Coll Cardiol. 1997 Apr;29(5):1067-73.

Effects of endurance training on mitochondrial ultrastructure and fiber type distribution in skeletal muscle of patients with stable chronic heart failure. Hambrecht R, et al.

OBJECTIVES: The present study was designed to evaluate the effects of an ambulatory training program in patients with chronic heart failure (CHF) on the ultrastructural morphology of mitochondria and fiber type distribution of skeletal muscle and its relation to peripheral perfusion.
BACKGROUND: Recent studies in patients with CHF have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise.
METHODS; Patients were prospectively randomized to either a training group (n = 9; mean [+/- SD] left ventricular ejection fraction [LVEF] 26 +/- 10) participating in an ambulatory training program or to a physically inactive control group (n = 9; LVEF 28 +/- 10%). At baseline and after 6 months, patients underwent symptom-limited bicycle exercise testing with measurement of central and peripheral hemodynamic variables as well as percutaneous needle biopsies of the vastus lateralis muscle. The mitochondrial ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry; cytochrome c oxidase activity was visualized by histochemistry and subsequently quantitated by morphometry. The fiber type distribution was determined by adenosine triphosphatase staining.
RESULTS: After 6 months of exercise training there was a significant increase of 41% in the surface density of cytochrome c oxidase-positive mitochondria (SVMOcox+) (p < 0.05 vs. control) and of 43% in the surface density of mitochondrial cristae (SVMC) (p < 0.05 vs. control). Furthermore, exercise training induced a 92% increase in the surface density of the mitochondrial inner border membrane (p < 0.05 vs. control). In contrast, the total number of cytochrome c oxidase-positive mitochondria remained essentially unchanged. Exercise-induced improvement in peak oxygen uptake was closely linked to changes in SVMOcox+ (p < 0.01, r = 0.66). After exercise training, changes in submaximal femoral venous lactate levels were not related to changes in submaximal leg blood flow (r = -0.4), but were inversely related to changes in the volume density of mitochondria (p = 0.01; r = -0.6) as well as to changes in SVMC (p < 0.05; r = -0.5). After exercise training there was a "reshift" from type II to type I fibers (p < 0.05 vs. control). CONCLUSIONS: Patients with CHF who engage in regular physical exercise show enhanced oxidative enzyme activity in the working skeletal muscle and a concomitant reshift to type I fibers. These exercise-induced changes in oxidative capacity appear to be unrelated to changes in peripheral perfusion.

PMID: 9120161

Dr. B G said...

It's been known since the 1970s... but recently... you have to use 'em or your lose 'em! There are physiological reasons to 'taper' prior to a half-marathon or other events. The intramyofibrillar mitochondria only increase in quantity preferentially toward the END of training, non-linearly. Dr. Fluck has interesting thoughts (*haa). A high fat diet can prime the mitochondria... but not raise the mitochondria. Got use it.

The effect of concurrent endurance and strength training on quantitative estimates of subsarcolemmal and intermyofibrillar mitochondria.
Chilibeck PD, Syrotuik DG, Bell GJ.

Int J Sports Med. 2002 Jan;23(1):33-9.


Med Sci Sports Exerc. 2003 Jan;35(1):95-104. Links
Plasticity of skeletal muscle mitochondria: structure and function.Hoppeler H, Fluck M.
Department of Anatomy, University of Bern, Switzerland.

Mitochondria in skeletal muscle tissue can undergo rapid and characteristic changes as a consequence of manipulations of muscle use and environmental conditions. Endurance exercise training leads to increases of mitochondrial volume of up to 50% in training interventions of a few weeks in previously untrained subjects. Additionally, a shift of substrate metabolism toward a higher reliance on lipids is observed, structurally reflected as a doubling of the intramyocellular lipid content. A similar increase in intramyocellular lipids without an increase in mitochondrial volume is observed as a consequence of a high-fat diet. Strength training has a major impact on muscle myofibrillar volume, however the mitochondrial compartment appears relatively unchanged. Bedrest and microgravity conditions lead to losses of both myofibrillar and mitochondrial volume, likely as a consequence of the decrease in metabolic and mechanical stress on muscle tissue. Permanent severe hypoxia leads to a loss of muscle mass and muscle oxidative capacity; however, hypoxia signaling events are triggered, which lead to distinct reprogramming phenomena of the transcriptome of the muscle cells. The molecular mechanisms that orchestrate the plasticity of skeletal muscle mitochondria are just beginning to unfold. The present data indicate that transcriptional events largely contribute to increases in mitochondrial mass in human skeletal muscle with endurance training. Expression of mitochondrial proteins from the nuclear and mitochondrial genomes is coordinated and involves the nuclear-encoded transcription factors NRF-1 and TFAM. Transcription of genes encoding the mitochondrial proteins involved in beta oxidation can be regulated separately from the genes of the Krebs cycle and the respiratory chain. Transcription factors AP-1 and PPARalpha/gamma and the protein kinase AMPK are signaling molecules that transduce the metabolic and mechanical factors sensed during endurance training into the complex transcriptional adaptations of mitochondrial proteins.

PMID: 12544642

Unknown said...

Well, thanks, but I'm looking for evidence on high-fat diets increasing the number/density of mitochondria without added exercise.

That's what's being claimed, so that's what needs to be proven. Or is the claim pulled out of thin air?

Fred Hahn said...

In this study:

"The effect of strength training on estimates of mitochondrial density and distribution throughout muscle Fibres"

Philip D. Chilibeck á Daniel G. Syrotuik á Gordon J. Bell
Eur J Appl Physiol (1999) 80: 604±609

If you calculate the numbers properly you'll see that though mitochondrial density decreased as a result of myofibular hypertrophy the total volume of mitochondria increased significanlty.

Also, endurance training can lead to skeletal muscle loss which can be seen under the micrscope as an increase in mitochondrial density but which is not positive.

Peter said...

OK, back on blog for a while!

No carb and Fred, I think there are subtle differences between the type one diabetic and the no carber/all fatter. These are thoughts, not evidence based.

The first is that we always have some glucose reserve, even if it is only in protein. If we manage to eat hypercaloric amounts of fat but cannot store it there will be an oversupply of fatty acids. If the liver has enough fatty acids it will become physiologically insulin resistant and secrete a little glucose. This glucose will provoke an insulin rise. It only takes a little insulin to store fat. When nothing is broken this is how I see it should work. I can't see that total waste of excess fat calories is what would happen.

In the type one diabetic there would be no compensatory secretion of insulin and glucose would rise while free fatty acids continued to cause glucose rejection. Without the supplementary insulin, glucose and fatty acids would rise until we get the classic diabetic ketoacidosis.

What probably determines outcome is the residual ability of a type 1 diabetic pancreas to muster enough insulin to respond to the physiological signaling through hepatic glucose secretion in response to FFAs making it ignore insulin's signal to hold on to glycogen. However carb restricted type 1 diabetics were, pre insulin, they did usually die in the medium term unless they had some residual pancreatic function left.

Bris, I'd agree with Fred, Cordain has said some unbelievably stupid things on occasions. This smells like one of them!

JB, I think we store all fat as adipose tissue all the time. Even from meal to meal fat moves from the gut to adipose tissue, even if it's only for a few hours. Otherwise LC/high fat eaters would be massively hypertriglyceridaemic from chylomicrons. It gets packed away. The beauty of LC is that it gets unpacked just as easily, without hunger...

Matt, I think the above is how I see the physiology, but again it's not hard data. People rarely measure what you want them to!


As I see it the number is relatively unimportant compared to the activity. When I started following this after your initial query what came out was that mitochondria are not organelles, they are more like living entities in their own right and they are a heterogenous bunch. Some are powerhouses and some are duds and there is s sort of sex to share DNA to minimse the number of duds. That might be why there is so little emphasis on numbers in most studies. Dr BG's links and Fred's comments are both very perceptive in this respect.

To query the assertion that high fat diets increase mitochondrial numbers in humans is excellent as a regulator of unsubstantiated statements. Let's say they do in mice. But I personally would be amazed if mice mitochondria responded differently to human mitochondria. I've even got time for C. elegans mitochondria being pretty much the same as human ones...


With appologies, this is probably (even more) full of typos (than usual)!

Ken said...

Moving Too Little or Eating Too Much? .
How much physical activity do we really need?

mathman said...

Peter -

What is the main problem with protein? I wanted to know why eating close to a gram per pound of LBM would be bad. Is it the insulin?

Fred Hahn said...

"What is the main problem with protein? I wanted to know why eating close to a gram per pound of LBM would be bad. Is it the insulin?"

It isn't bad and if you are weight lifting it should be more in the realm of 1.2gms per pound of lean body mass.

Eating this much protein is not bad so long as your carbs are low. Glucagon 'offsets' so to speak or rather takes care of the rise in insulin from higher protein intakes. This is best described in books by Drs. Eades and by Taubes.

Anonymous said...

whether or not this sounds doubtful, the fact of the matter is, for a period of about 3-4 weeks (until I was certain this diet was putting on weight), I consumed 4-6 sticks of butter / 1-1.5 lbs of beef tallow (tissue and oil); meat was held at 1-1.5 lbs beef chuck.

perhaps 90% was too high an estimate, so let's break down the numbers:

typical day:
beef chuck 16oz, 86g protein, 429 fat kcal, 798 kcal
4 sticks butter 0.27g carbs, 367g fat, 3241 fat kcal

(429+3241)/(798+3241) = 0.9086

If it was beef tallow, I consumed both the tissue and the oil, so let's estimate 1 lb fat = 3500 kcal,that's about 3500-5250.

I'm 150lb, 5-9, low-active. I probably didn't need all those calories.

That's what happens when I'm told that fat can't make fat.

I see this was asked here in the comments.

Anonymous said...

hate to do this, but since I realized the nutrition links aren't working, I put the images of the nutrition facts here.

mathman said...

I would love to hear Peter's thoughts or anyone else following a Jan K.-type of diet. I have been hearing more and more that the carbs and fats are interchangable for optimal health so long as protein remains low-why?

Also, from a longevity standpoint is more mitochondria better? This seems like the "stoking the fire" analogy which speeds cell processes and creates more oxidative damage.

LeenaS said...

As for your latter question, the mitocondria count. According to Nick Lane more is better; much better.

More means smaller work load for each mitochondria. Which means less leaking electrons and better control on the general quality of the thousands of mitochondia units in each and every cell.

And as for Dr. Lane, he seems to be getting quite a bit of respect on his wievs, and not just articles in Science:
Very interesting work indeed (thanks peter for this!)


Jocelyn said...


Fat does put on fat in certain amounts, thank god. Fat needs to put on fat, or else we'd have died out a long time ago. We seem to all accept that our ancestors had to tap into those stores of bottom-fat on a regular basis, how is this possible (or anything other than deadly) unless we are quickly able to restore those stores of bottom-fat?? In-fact, putting on fat from fat is the only conclusion to draw if you think eating fat is an adaption in humans.

other person:
carbs or fat calories, which is going to give you a powerhouse of fat soluble vitamins? what does bread give you?

Fred Hahn said...

Mathman said:

"I would love to hear Peter's thoughts or anyone else following a Jan K.-type of diet. I have been hearing more and more that the carbs and fats are interchangable for optimal health so long as protein remains low-why?"

I don't know what Jan K. is but research pretty much shows that if protein intake is optimal, you can swap fat for carbs for weight loss, not for optimal health.

Yes we can indeed get fatter eating only fat and protein in excess of our caloric needs. However, I doubt one could become obese eating like this.

gunther gatherer said...

Fred Hahn

JK is Jan Kwasniewski and his diet is the Optimal Diet. Peter talks about it in the "Food" and "What I Eat" blog categories. Basically it is an 80% animal fat diet. If you follow Peter's additional recommendations, you also take out grains, add omega 3 and tweak a few other things.


I've been on OD for 2 years. Besides losing the weight I wanted to lose almost effortlessly (6 months with no hunger), I have also seen a resolution of many symptoms of immune system breakdown, such as stoppage of hair loss, disappearance of chills and low body temp, resolution of Reynauds, and off-blog, Peter and I have discussed whether a recent kidney stone incident I had was actually the OD SHRINKING the kidney stones in my kidneys over the last 2 years so that they could finally pass down the ureter. In other words, the OD didn't cause the stones, it finally got the small enough to get rid of.

Of course, we'll never know if that's the case, but I really haven't slept as well or had as much energy before I started the plan.

Full disclosure: Not selling anything and have never even met Jan Kwasniewski or Peter personally!

Hope that helps.

Peter said...

Gunther (and Bamboo),

Thanks for the comment, pain free I hope!

With Bamboo's comment on the Praise the Lard post I think it is timely to run through the biochemistry we discussed as a post. Might get some time tomorrow but after that it's 3 12 hour dayshifts coming up so...


mathman said...

thanks everyone for the input but only Fred has actually addressed the protein issue. I understand the value of high fat, and already eat this way. My query is the scientific understanding as to why too much protein is damaging (personally vested since I eat a lot of meat)? I always try to choose fatty cuts but I still eat over 100g of protein a day.
LeenaS- Thanks, that makes sense.