Low fat – we’re gonna need more nails

Low fat dieting for weight loss doesn’t work. That is, it works, just very very poorly. In fact it works just enough for confused obesity researchers to call the weight loss significant. Somewhere along the way, it was decided that a 5% loss of initial body weight is to be considered clinically significant [1]. So if you weigh 100kg and work your butt of (which is what you are not really doing) to get rid of 5kg, scientifically speaking that’s a success. When Bray, Bouchard and James wrote the Handbook of Obesity [2] they presented pretty compelling evidence that traditional weight loss does not work. They still continued recommending low fat for weight loss. The 2002 Cochrane meta-analysis titled “Advice on low-fat diets for obesity” by Pirozzo and coworkers [3] was recently withdrawn. The Cochrane organization claims the conclusions are out of date. What the metaanalysis showd was that

“…fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people.

And the authors concluded that both strategies produced a weight loss that was

“…so small as to be clinically insignificant.

This conclusion was reached by looking at the best studies available up till 2002. No new studies have provided evidence the conclusion of the meta-analysis was wrong, but it seems the Cochrane Collaboration could not live with such a politically incorrect conclusion.

In a new study, and a pretty damn large one at that, the researchers went out of their way to resurrect the dead, but sadly not buried lowfatforweightlossworksgoddamnit-hypothesis.

Enter the Look AHEAD Study. The study was a “…multicenter randomized clinical trial to examine the effects of a lifestyle intervention designed to achieve and maintain weight loss over the long term through decreased caloric intake and exercise.

Here’s how the authors view the study:

As perhaps the most extensive test of long-term multidisciplinary lifestyle intervention to date, the Look AHEAD (Action for Health in Diabetes) trial presents a unique opportunity to examine the long term viability of lifestyle intervention as a clinical and public health strategy for obesity and type 2 DM.

A total of 5,145 overweight/obese men and women with type 2 diabetes were randomly assigned to an intensive lifestyle intervention (ILI) or a usual care group, referred to as Diabetes Support and Education (DSE).

The ILI included diet modification and physical activity and was designed to induce at least a 7% weight loss at year 1 and to maintain this weight loss in subsequent years. The ILI participants were assigned a calorie goal (1200- 1800 kcal/d based on initial weight), with less than 30% of total calories from fat (<10% from saturated fat) and a minimum of 15% of total calories from protein.

The exercise goal was at least 175 minutes of physical activity per week, using activities similar in intensity to brisk walking. Behavioral strategies, including self monitoring, goal setting, and problem solving, were stressed. The ILI participants were seen weekly for the first 6 months and 3 times per month for the next 6 months, with a combination of group and individual contacts. During years 2 through 4, participants were seen individually at least once a month, contacted another time each month by telephone or e-mail, and offered a variety of ancillary group classes. At each session, participants were weighed, self-monitoring records were reviewed, and a new lesson was presented, following a standardized treatment protocol.

Bet you wonder what kind of marvelous results you can get from this intensive intervention. Bet you think all the participants in the ILI group came out of the study looking like Greek gods. I mean, 4 years of exercise, diet and pampering…

At the end of the 4 year period the participants in the ILI group, whose average baseline weight was 95kg in women and 109kg in men, reduced their weight by 4.7%. Actual weight loss was 4,9kg.

Here’s nice graph from the study 

This figure shows how 74% of the participants in the ILI group lost weight while 26% gained weight. Only 46% of the group lost more than 5% body weight: 


So there you have it. These are the grand effects of 4 years of intensive lifestyle changes. I’m not impressed.


Funny thing. If you read the abstracts, the article in which the main results were published [4] states that the average weight loss was 6,15%, yet in a more recent article addressing what factors correlated with long term success, the number is 4,7% [5]. It turns out that the number 6,15% is an average of the weight lost at 1, 2, 3 and 4 years which is not a very nice way to present data. I would say it’s a pretty poor way to present data. You have to read the entire article to find that “…the ILI group maintained a mean weight loss of 4.7% at year 4.


1. J. Stevens et al., «The Definition of Weight Maintenance,» Int J.Obes.(Lond) 30, no. 3 (2006): 391-399.

2. George A. Bray, Claude Bouchard, and W. P. T. James, Handbook of obesity, ed. George A. Bray, Claude Bouchard, and W. P. T. James. (New York: M. Dekker, 1997), xii, 1012.

3. S. Pirozzo et al., «Advice on Low-Fat Diets for Obesity,» Cochrane.Database.Syst.Rev., no. 2 (2002): CD003640.

4. R. R. Wing, «Long-Term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals With Type 2 Diabetes Mellitus: Four-Year Results of the Look AHEAD Trial,» Arch.Intern.Med. 170, no. 17 (2010): 1566-1575.

5. T. A. Wadden et al., «Four-Year Weight Losses in the Look AHEAD Study: Factors Associated With Long-Term Success,» Obesity.(Silver.Spring) 19, no. 10 (2011): 1987-1998.

The satiating effects of protein

«The mechanisms by which protein may affect satiety remain elusive.» 

Halton and Hu 2004 [1]

“Although the immediate satiating effect of dietary fat may be comparatively weak, there is no doubt that ingested fat does inhibit feeding.” 

Leonhardt 2004 [2]

LCHF opponents keep throwing out the same old argument, that fat is the least satiating macronutrient and that all that fat might thus make people hungry and unable to stay with the strategy. Eventually the low satiating effect of fat will cause people to gain weight. This is claimed despite the existence of several studies showing that people put on ad libitum high fat diets experience less hunger, lose weight and all over seem perfectly fine.

Protein, it is said, is the most satiating macronutrient. So the best dietary strategy is replacing fat with proteins and keeping carbs high.

My colleagues in dispute seem very eager to have me agree that protein is very satiating and that we at least should have this as common ground.

But my own experience urges me not to agree. If I reduce my fat intake and eat more protein, as I sometimes do, for example in periods of stress where I eat too much eggs and lean meat and forget about the fat, I feel horrible. My blood sugar drops and over time lethargy hits in. What’s more, I soon feel hungry and start craving fat/carb combos. Simply eating fat eases my symptoms. Eating carbohydrates would probably also ease my symptoms, but we all know that is no good long term solution.

So are proteins especially satiating?

Weigle et al [3] placed 19 subjects sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk.

Weigle is good for a laugh. Here’s from the introduction of the article

“Both low-fat diets (2– 4) and low-carbohydrate diets that are high in fat and protein have been shown to cause a decrease in ad libitum caloric intake and significant weight loss in humans. Thus, it appears that diets with fat contents at opposite extremes have the same therapeutic result, despite evidence that excessive dietary fat intake promotes obesity. This paradox could be explained if it is the high protein content rather than the lower carbohydrate content of low-carbohydrate diets that offsets the deleterious effect of high fat intakes and results in weight loss.” 

Quite the paradox there. Hope someone will resolve it someday. 

Weigle is often cited for showing that proteins are satiating. But measurements of hunger and fullness showed that even though hunger was reduced and fullness increased during the isocaloric diet, they returned to baseline with the ad libitum diet despite constant protein content. The reason the study is sited is because calorie intake dropped with higher protein. However, satiety and calorie intake did not seem to correlate. 
As in all similar studies, the high protein diet differed from the low protein diet in many aspects even though carbohydrate intake remained constant. Below is an example of what the two different diets might contain. 

So can we conclude that the hunger (temporarily) and body weight dropped because of the higher protein content? Of course not. That would be silly. It might be the proteins, but it might be any one of the other differing dietary factors.

Weigle and colleagues also wrote that

“It is likely that a reduction in dietary fat by 15% of total energy contributed to weight loss in the present study.”

This is a very strange thing to claim, as several studies where subjects are put on high fat diets reports significant weight loss and reduced hunger.

Weigle concluded thusly

“An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.” 

Skov et al [4] randomized 65 subjects to two ad libitum fat reduced (30%) diets for six months. One with 12% energy from protein and one with 25% from protein. Weight loss in the low protein group was 5.1kg and 8.9kg in the high protein group. By labeling the diet higher in protein a “high protein diet” our focus is drawn away from the fact that the high protein diet also had significantly less carbohydrates. This is a recurring problem; how should the diets be labeled? The labeling wouldn’t actually be problem if the researchers remembered to properly discuss the effects of reduced carbohydrate intake or reduced glycemic index. This, however, is often not done and when a diet labeled “high protein diet” is discussed the protein content usually get the major part of the attention.

Skov and his Danish research fellows later wrote that

“The mechanisms responsible for the larger weight loss caused by an HP diet may be attributed to a greater satiety and fullness, and also the thermogenic effect of protein.” 

But of course, they might be right. A number of studies have compared hunger and satiety in the hours following consumption of a single meal, and have come to the conclusion that a high-protein meal is more satiating. So to say that a high protein diet suppresses hunger might be a correct statement, but it’s still a bloody unfair statement. Because what matters is the long term effect on hunger, and what actually cause the decreased hunger. The studies looking at single meal effects are usually poorly controlled and there are many confounding factors. Also, the protein content of high protein meals is often very high, ranging from 40% to 75%, and most of the studies have very few participants.

One of these studies, from Stubbs et al [5] (60% protein), found that there was no difference in subsequent energy intake despite acutely reduced hunger following a high protein meal. This was one of the more well controlled single meal studies.

Thomas Holton [1] notes that

“There are, however, some methodological issues concerning this type of research. Satiety appears to be influenced by a wide variety of factors including palatability, food mass, energy density, fiber and glycemic index. When using real foods, it is difficult if not impossible to control for all of these influences at the same time while still delivering different amounts of protein.” 

Fat is often considered the least satiating macronutrient from these single meal studies. But it might not be that simple. Mark I Friedman found that hepatic ATP, or the energy availability of the liver, exerts a strong effect on feelings of hunger. What is important, is that there’s fuel available, be it glucose or fat. A theoretical satiating effect of proteins is their conversion to glucose by gluconeogenesis thus providing more fuel for the liver.

A quote from Friedman

“Hyperphagia associated with the development of obesity is accompanied by a metabolic state that fosters the deposition of fat in adipose tissue, the largest fuel storage compartment. This shift in fuel partitioning toward storage is independent of and occurs before the change in food intake in nearly every animal model studied. According to the model presented here, overeating results because fuels that would otherwise be oxidized to produce ATP in a detectable manner are redirected into fat stores.” [6] 

And what redirects fuel into fat stores? I’ll leave it to you to figure this one out yourself. The point is that according to Friedman’s work, a higher fat diet will reduce hunger by making both glucose and fat more available for oxidation.

Daniel H. Bessesen [7] also believes that what separates obesity prone and those prone to leanness are differences in the trafficking of fat. He writes

“It may be that a preferential delivery of dietary fat to metabolically active tissues including liver and skeletal muscle allows more accurate sensing of dietary fat in a manner that promotes more accurate coupling between dietary fat intake and oxidation. Conversely, preferential delivery of dietary fat to adipose tissue may impair nutrient sensing and promote weight gain.” 

On low carb ketogenic diets, hunger is often drastically reduced within a matter of a few days after initiation of carb restriction. With fasting or starvation we see a drop in hunger with increased ketone body concentration. This satiating effect is often attributed to the ketone bodies themselves, in particular beta-hydroxybutyrate, but according to Friedman’s theory it could just as likely be caused by the increased internal energy availability that occurs when lipolysis and fat oxidation (with a subsequent increased ketone body production) are increased. 

Some studies also suggest that you will experience a stronger hunger if you eat some food as mostly carbs, than if you eat no food at all. 
The belief that high protein diets are especially satiating seem similar to the belief that high fat diets are fattening. Of course they might be, but as I said, it would be a bloody unfair statement. In animal studies high fat diets often do cause obesity, but normally only in the presence of a substantial amount of carbohydrates (or crazy amounts of frankenfats). The term “high fat diet” does not imply minimal carbohydrates. High protein diets might decrease hunger, but higher protein diets are usually lower in carbohydrates, sugars and have a lower glycemic index. Attributing the decreased hunger to the proteins might be just as much off target as attributing weight gain to fat.

Halton and Hu illustrates this point when they term many low carb study diets, high protein, low carb diets. Like the much sited study by Samaha et al [8]. In this study the low carb diet was a 1630kcal, 22% protein, 41% fat and 37% carbohydrate diet. Protein intake was well below 1g per kilo body weight. It produced a greater weight loss than a 1576kcal, 16% protein, 51% carbohydrate and 33%fat diet. The results can hardly be attributed to the proteins alone. Holtan and Hu, in their review of high protein diets and satiety, forget to discuss the potential long term satiating effects of increased fat intake.

Monika Leonhardt [2] seem more open and writes

“Fat seems to be less satiating than carbohydrate and might therefore lead to passive overconsumption [4]. Yet, in rodents, the efficacy of a high-fat diet to induce hyperphagia appears to be related to the energy and carbohydrate content of the diet. Therefore, overeating of high-fat diets is presumably not due to the high fat content alone. This assumption is in line with recent studies in humans showing that a high-fat, low-carbohydrate diet reduced rather than increased voluntary energy intake.” 

Leonhardt continues to suggest that overeating on a high fat diet might be, amongst others, due to

“the high energy density of such diets in combination with their carbohydrate content” 

“the usually low postprandial oxidation of ingested fat in the presence of carbohydrates.”

That protein exerts some acute satiating effect compared to carbohydrate and fat is hardly a good point. It is an interesting observation, but not an argument in favor of high protein diets. People put on high fat low carbohydrate diets also feel their hunger disappear and shed weight without caloric restriction. The high protein diets seem to stem from the cognitive dissonance of the upholders of the traditional dietary dogma. First fat was fattening, now it seems carbs are equally so. What they are left with are diets low in both fat and carbohydrates, diets that do not consider any of the important roles of the vast variety of fatty acids available to the body. I’ll eat my hat the day some anthropologist can show me a traditional human population thriving on a high protein, low fat, low carbohydrate diet. Fat matters.


1. Halton TL, Hu FB: The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr 2004, 23: 373-385.

2. Leonhardt M, Langhans W: Fatty acid oxidation and control of food intake. Physiol Behav 2004, 83: 645-651.

3. Weigle DS, Breen PA, Matthys CC, Callahan HS, Meeuws KE, Burden VR, Purnell JQ: A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr 2005, 82: 41-48.

4. Skov AR, Toubro S, Ronn B, Holm L, Astrup A: Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int J Obes Relat Metab Disord 1999, 23: 528-536.

5. Stubbs RJ, van Wyk MC, Johnstone AM, Harbron CG: Breakfasts high in protein, fat or carbohydrate: effect on within-day appetite and energy balance. Eur J Clin Nutr 1996, 50: 409-417.

6. Friedman MI: Control of energy intake by energy metabolism. Am J Clin Nutr 1995, 62: 1096S-1100S.

7. Bessesen DH: Update on obesity. J Clin Endocrinol Metab 2008, 93: 2027-2034.

8. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L: A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003, 348: 2074-2081.

Physical activity and weight loss

Physical activity is a poor strategy for weight loss. Still, all around the world, clinicians and health personnel are chasing fat people around, getting them to move, move and move even more. When, in the end it becomes clear that moving more doesn’t affect weight, the blame is often put on the overweight. They must be doing it wrong, they’re too lazy between exercise bouts and they are obviously stuffing themselves.

Jakicic et al recently conducted a trial where participants were divided into three physical exercise groups differing in activity doses. With no dietary change recommendations they wanted to show the 18 month effects of either 150 min PA/week, 300 min PA/week or a self help group provided a self help intervention to increase PA.

278 overweight subjects were included. The PA interventions included behavioral interventions, individual exercise and some group sessions. The self help group were given a manual and a monthly newsletter, seemingly to inspire change.

So how much weight do you lose if you exercise 150 min/week for 18 months? 0,7kg!

Then what about 300 min/week? 0,8kg!

Being given newsletters and a pamphlet results in 0,5kg weight loss. 

To be fair, these are intention to treat analyses, and so the results show the effect of being told to exercise rather than actually doing the exercise. Still, reported increased caloric expenditure per week was 442kcal for self help, 348kcal for 150 min/week and 832kcal for 300 min/week.

The authors did a secondary analysis where participants were grouped based on whether there was weight gain, weight loss, or weight stability. This analysis showed that a small weigh loss is possible and managed to obscure cause and effect completely. Luckily the authors are aware of this and writes:

Despite these findings, concluding that PA alone can result in the magnitude of weight loss observed in WT-LOSS within the retrospective secondary analysis may be misleading. There is some indication that participants classified as WT-LOSS, who lost 7.4% of their body weight compared to baseline (Table 3 and Figure 2) also made significant changes in their eating behavior as measured by the EBI questionnaire (Table 3), despite the lack of an intervention promoting a reduction in energy intake. 

And how do they conclude?

In summary, the mean change in body weight resulting from an intervention that promotes 150–300 min/week of moderate- intensity PA with no reduction in energy intake is 3% of their initial body weight in this study, with these subjects categorized retrospectively as WT-LOSS for secondary analysis. Individuals categorized as WT-LOSS for these secondary analyses do appear to be more compliant with initially increasing PA by 245 min/ week and maintaining an increase of at least 161 min/week at the conclusion of this 18-month study. 

In somewhat simpler terms, physical activity can produce a small weight loss and if you don’t lose any weight you’re not doing it right.

The setpoint hypothesis revisited

The homeostasis 

(hō’mē-ō-stā’sĭs): The ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes.

Humans are warm blooded and the enzymes that make us, require a certain temperature to operate optimally. The water and ion concentration of cells must remain at a certain level to allow for normal cellular processes to occur. Homeostatic processes make us able to adapt to environmental changes. Feedback mechanisms are responsible for maintaining particular levels of processes. Most processes allow for some variation, but if pushed too far in one direction the process may break down.

Body temperature is maintained by thermoreceptors communicating with our hypothalamus, by sweating, vasoconstriction and dilation, hairs standing on end, shivering, shifts in metabolism and other. All of these factors work in unison and affect each other and by doing so maintain our body temperature at around a rough mean.

During energy restriction we get hungry, our thyroid hormone levels decrease, non essential processes like that of reproduction is down regulated, and energy expenditure goes down. It is difficult to make people gain weight by overfeeding and it is difficult to make people lose weight by underfeeding. The feeding always affects energy expenditure. Thus body weight or some level of cellular mass is required for survival and the body is self regulating to make sure sufficient tissue mass is present for survival and eventually reproduction.

None of this justifies the use of the term “setpoint” in body weight regulation.

The set point 

“Again, this supports the idea that the body has a body fat mass ‘set point’ that it attempts to defend against changes in either direction. It’s one of many systems in the body that attempt to maintain homeostasis.” 

Stephan Guyenet 

Although I have much respect for Stephan Guyenet and appreciate his very fine blog, I don’t understand his focus on the body fat setpoint. I don’t understand anyones focus on body fat setpoint for that matter. I’ve never felt comfortable using the “setpoint” word when it comes to body weight regulation. It makes me think of a glowing red number etched into my hypothalamus. “15 kg fat” NO MORE, NO LESS. It does not feel very “organic” to have a set point and I’m pretty sure I am organic. But of course, no one is claiming there is a number etched in my brain.

When it comes to the body fat setpoint, I rather like the lake comparison. A lake can for those less informed seem to have a set point of water level. Despite rather large fluctuations in temperature, evaporation and water going into and out of the lake, the lake maintains it water level because the factors mostly responsible for the level influence each other. This does not mean that it is difficult to change the level, nor does it mean the lake «attempts to defend against change.» Build a damn dam and the water level will go up. Drain it, and the level goes down. It’s not very hard, you just have to push the right buttons.

If our fat mass changes through life and in various situations and in fact is not that difficult to change, then why the hell say it’s a set point? It’s obviously not very set, is it? Most of the time we are gaining and losing fat at pretty much equal speeds, although with constant variations around the mean. The fact that the fat storing and fat using process does not spiral out of control either way, that most of us don’t get very lean or very obese, would mean that there is a control mechanism, a feedback loop or a set point. But all the body’s processes are regulated. We are self regulated and all processes work best around a given mean determined by the nature of the very process and the processes it affects or is affected by.

A homeostatic process must have a level to operate on. It’s the way the world works. The level can usually be changed by modifying the factors that make the process.

Stephan Guyenet claims that one criterion for the cause of modern fat gain is that it “…has to cause leptin resistance or otherwise disturb the setpoint.”

What I don’t understand is, why can’t we say disturb the “regulation of body weight”, “the metabolism” or “the process.” Why “disturb the setpoint”?

The language

“..the body doesn’t want to lose weight. It’s extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.” 

Stephan Guyenet 

Whenever body fat setpoint is discussed it seems the body is at war with one of its processes. Why turn it into fight? Obviously it is not that difficult to “fight the fat mass set point”. I’ve asked people who’ve lost weight who said it was easy. What’s more is that they have stayed lean with ease. The setpoint hypothesis was invented mostly because people didn’t lose weight by eating low fat and that they often regained lost weight. Now, I could try to change the water level of a lake by drinking the water through a straw, and when failing I could conclude that the water level is “extremely difficult to fight”, but it wouldn’t be a very good conclusion.

I believe firmly that our language is a great obstacle for scientific progress. The main reason is that it is very hard to imagine things that cannot be put into preexisting words. Also our minds operate within the boundaries of our language and language will limit the things we can imagine. I think quantum physics is a good example of an area in which the language simply is not sufficient. The electrons can be in several places in the same time. Some things are both particles and waves. Matter consists mostly of empty space and so on. On top of it all, once words are set, once something is described in a particular way, it usually stays that way.

In Guyenets posts about the body fat setpoint, the word setpoint is often given with quotation marks, like in the above quote. I can only assume that this means that the word setpoint is not an accurate description of what he is talking about, that it is not actually a set point, but that it is used for the lack of a better word.

Guyenet also writes extensively about leptin. Leptin is an interesting protein, but it is just one of those signaling molecules involved in the homeostatic regulation. Of course weight will change if we or nature messes with leptin, its receptors in the hypothalamus or any other involved part. But the existence of leptin does not justify the use of the setpoint term.

Body fat mass can be quite easy to change so why the hell do we need the setpoint? I feel the word contributes nothing to our understanding and if anything just complicates the matter more than necessary. How about adding a muscle mass setpoint and a bone mass setpoint? How about a hair growing speed setpoint or a saliva setpoint? Does it help our understanding?

I do not think the use of the word setpoint is neutral. It affects out thinking and I am afraid its existence is a net negative contributor to the science of body weight.

On the website of one of the leading obesity clinics in Norway we are told that the clinic bases its work on the setpoint theory. They call it theory, but talk about it as an undeniable fact. This is a problem because the hypothesis rests on the assumption that weight loss is inherently difficult and that the body (in the words of Guynet) “will fight” that weight loss. It is not a very positive attitude. Remember that the setpoint hypothesis saw light of day partly because losing weight through traditional (eating less) methods did not give the expected (based on thermodynamics) results and that people constantly regained lost weight. The clinic thus operates on the assumption that it may take years of hard work to change the setpoint downwards and that it takes a very short time to change the setpoint upward (that the body «gets used» to a new higher level of fat mass).

What if the obesity clinic, instead of basing its treatment on setpoint theory (forcing overweight people to starve and doing insane amounts of exercise), said that weight loss does not have to be difficult and lasting weight loss is possible? What if they read some real science, pushed the right buttons and stopped torturing people? The studies are out there. It really does not have to be difficult. The metabolism must be altered, mostly through changing the hormonal milieu and reducing inflammation thus achieving a homeostatic regulation at a lower amount of body fat mass. And there is little evidence it has to take years to do so.

The conclusion

«When something seems ‘the most obvious thing in the world’ it means that any attempt to understand the world has been given up.» 

 Bertolt Brecht 

If the point of this rambling is lost on you, let me try to sum it up.

The body fat “setpoint” is just a word used to describe a level of a self regulating biological process.

To call a certain mean level of a homeostatic regulation a set point is unproblematic. As far as I can see, this is how Stephan Guyenet uses the term. But when medical professionals use the setpoint hypothesis to argue that body weight loss by nature is difficult and near impossible, we have a problem. The continued use of the expression seems to affect both medical professionals and researchers in a negative way, because it closes their mind for other possibilities, among them that weight loss from a physiological point of view is easy if you just push the right buttons. That we do not always know what these buttons are does not mean weight loss must be difficult, only that we are ignorant. Many aspects of metabolic regulation are under our control. Most important of all is that the level of homeostatic regulation of body fat called the setpoint, seems to be determined by what we eat.

Kurt Harris, the messiah, the hype and the throwing of scales

I think Kurt Harris is a smart man and makes some very good points now and then, not to mention his reading list resembles my own. But reading his blog recently I keep thinking of Monty Pythons Life of Brian. For those less versed in the film (shame on you!), Brian is mistaken for the messiah and tries his best to convince a rapidly growing crowd that he’s not. But whatever he does, it is taken as a sign and further confirmation that he is the messiah and he can do nothing wrong.

Dr. Harris stopped blogging for a while, which somehow seemed to increase his blogging status. He disabled his comments section and I bet that also increased his standing. In a recent post he talks about the important fact that people are focusing too much on stupid details and forgetting about true science, the bigger picture and how to relax and enjoy life. According to Harris in the “do no harm” post: “I’ve had more laudatory emails and fresh donations (Thank you all!) as a result of this post than any I’ve written in a long time.

Kurt is the new Brian. “Therapy versus Life,” has an important message and despite how obvious it is, it needs to be repeated. Worrying about the lectins in the beans you just ate or whether or not you should add an extra t-spoon of coconut oil to your daily diet will only take down a road you really don’t want to go. It will not make you live longer or happier!

Sure, a good diet can make life better, you might lose weight and be more toned. But life’s there to be lived. I advocate a diet mostly free of modern foods and I am really interested in finding answers about what foods affect the body in what way and what exercise is the most effective and so on. But I’m constantly working hard not to lose my head (and perhaps overcompensating a bit) and under no circumstance am I willing to give up beans with my bacon, beer or ice-cream or sugar (yeah that’s right, glucose AND fructose) in my daily cup of earl gray tea. Oh, and I’ve been exercising regularly once a week for about the last six months. Why? Because it doesn’t matter.

I’m not saying it’s easy to be happy. I’m saying we will definitely not get any happier by focusing on minor and insignificant details relating to diet or exercise.

Paleo is fad (fad = a temporary fashion; a craze, interest or activity that (some) people follow enthusiastically, but lasts for a short period of time). Sure it’s a good idea to not eat modern foods, but we must not start suggesting that a food is bad because it is modern. And we must not forget that a paleo diet is not actually a defined diet, but rather a some general guidelines based on not so strong evidence about what our ancestors ate.

Paleo is likely a fad because humans are crazy about inventing new words, labeling everything and grouping things together. The world is to complex not to make subgroups of everything and we’re so bloody good at it. Don’t get me wrong, I actually like the word paleo, but I bet a new craze will take over; the paleo group feel will dilute and hopefully integrate more into standard dietary advice.

But what about the throwing of scales? Talking to more and more people trying to lose weight just further convinces me that weighing is an obstacle for success. The first thing you should do if you want to lose weight is to chuck the old measuring tool in the trash. As I said, humans get to caught up in details and especially numbers on a scale. Have patience, in time you’ll know if you are losing fat. You were clothes, don’t you? Your clothes are the only reference you need. If you can’t get in or out of them, you’ve gained weight. Oh, and perhaps some getting to know your body and how you actually feel might help to.

And as for me? I feel an overpowering urge to tackle the “set-point” hypothesis issue. Something smells fishy about the standard theory which Harris and Guyenet, amongst others, find the most fitting.

What is the best exercise for fat loss? Part V – the conclusion

I wondered what the best exercise for fat loss was. I honestly didn’t know the answer, but now feel I have acquired a more thorough understanding. As a scientist I ask questions I want answered and work to find the answers. However, all this digging in the details and nerding about does not mean fat loss should be a primary motivation for exercising. On the contrary, if the only reason that you exercise is to try to lose weight and everything else about exercising is a pain in the ass, I would recommend you to stop exercising. No matter your external motivation for exercising, be it health in general, weight loss, muscle strength or flexibility, if you want exercise to be a positive part of your life you need to find an exercise form that gives you something more, that is motivated by internal factors, preferably that you enjoy the actual exercising. If you want to lose weight and you know high intensity strength based exercise is the most effective exercise, but you would rather swim because you really like swimming, than the choice is simple. Swim!

That being said, for the sake of curiosity, let’s see what the best exercise for fat loss is.

There is not enough data to say much about what exercise form is more efficient, whether running is better than cycling for example or a step machine better than elliptical trainer. There are just too many other variables. There is however enough data to make a calculated guess about aerobic versus resistance exercise, and about exercise amount and intensity.

Just wanted to illustrate the expected effects of exercising without dieting. The below table gives a few examples of just how much weight and fat you can expect to lose. Results are not god, and tend to become poorer in time in the longer lasting trials. Many of the results are non significant. What this tells us is that diet matters. A lot. 

It seems that resistance exercise is or can be just as effective as aerobic exercise in improving body composition. Resistance exercise usually cause some fat loss while also increasing muscle mass. Aerobic exercise usually causes larger loss of fat, but also larger loss of muscle. High intensity aerobic exercise causes less lean mass loss than low intensity.

The best exercise for fat loss should:

– be of medium to high intensity (frequently bring you above lactate threshold)

– include resistance exercises

– be interval based (30 min of sprint intervals is most likely better than 60 min jogging)

– not be performed every day (rest is important and more is not better than the right amount)

– exercise the whole body

– be combined with a high protein low glycemic diet for maximal improvement in body composition.

That’s it, as far as I can tell. Feel free to disagree. Tomorrow I’m off to the Norwegian Directorate of Health and the unveiling of the new national dietary guidelines. The snack there is crap (usually fruit), but hopefully there’s coffee and plenty of it.

What is the best exercise for fat loss? Part IV

The bias
I have this theory. In the last post I concluded that there is sufficient data for recommending high intensity exercise in favor of low intensity for fat loss. Admittedly, the data in support of this is not strong. It is there, but I would not bet my life on it yet.

I might be a bit biased in favor of high intensity because of my theory that seems rigidly stuck in my brain. From the world of resistance exercise, we know that you can use a number of strategies to build muscles. Some use slow movements with relatively low resistance where the muscles are activated for a long time. Others use quick movements with high loads allowing for a greater workload to be performed in a shorter amount of time. Some simply cut blood flow to the working muscles which also will make them grow. The bottom line is that the one important factor when it comes to muscle hypertrophy seems to be the amount of physiologic stress placed on the working muscles during exercise. So you can stress a muscle or muscle group by making it work for a long time like in static strength training or you can do the standard high load high repetition fast movement exercise. You can even do pure eccentric exercises rather than the usual concentric/eccentric. All of this and pretty much everything in between will cause muscle growth. It is the total workload, the time multiplied by load, that matters.

The concept is very similar to the energy hypothesis that claims it is the amount of energy spent during exercise that determines fat loss, rather than intensity or time by itself. The difference is that the hypertrophy theory is supported by science whereas the energy hypothesis is not.

Although hypertrophy can be achieved in many ways, there is a limit to the equation, workload = time x load. It is not only the amount of work done that determines muscle growth. Running, for example will not build significant amounts of muscle even if some of the muscles involved perform a great workload. The reason is that somewhere in the area between multiple repetition resistance exercise and endurance exercise the stimulus changes and thus the physiological adaptations.

Most people are aware of this and know that walking or running is a poor strategy for building muscles.

My theory is that the whole «exercise intensity and fat loss» issue is of a similar nature, that to a certain degree, it is the amount of work performed that matters the most. Both low and high intensity exercise cause fat loss, but somewhere in the declining intensity area the stimulus becomes different and fat loss is reduced. Shopping, gardening and other everyday activities with low intensity, but often of long duration seem poor strategies for weight loss. Likely, we are working to close to the body’s comfort zone to make it adapt. Or put in better words, the body does not adapt to these activities because it doesn’t need to, it already has.

This means that high or low intensity might not matter that much, as long as the tissues are exposed to new stimuli, forcing them to adapt. However, this is not to say that high intensity is not better than low, the question is how much better.

As with muscle hypertrophy, if the goal is to maximize all factors, then high intensity, high workloads and variation in stimuli is important. I believe it is the same with exercise intensity and fat loss. This might explain some of the variation in results found in different trials.

The losing of fat and not muscles
Loss of muscle mass is common with weight loss, independent of dietary approach. Some diets seem to lead to better muscle mass retention and some exercise forms will prevent muscle loss. But we must make sure not to assume that all muscle loss is a negative thing. The size of our muscles will determine our appearances while their function is what will affect our health.

In school I was taught that one important factor for skeletal muscle hypertrophy was positive energy balance. You had to take in more than you expended. This however, turned out to be wrong. The muscles might need a readily supply of fuel, but they couldn’t care less if the energy comes from glycogen and fat stores or from food. Thus it is theoretically possible to lose fat mass while increasing muscle mass.

Fleck and Kraemer [1] concludes that in untrained individuals doing regular resistance exercise you can expect a 2kg increased muscle mass in 14 weeks. That’s about 0.06kg per exercise session. If we consider the women only trials the number is about 0.04kg per session.

Resistance exercise builds muscles when we’re not dieting, but does this hold true when we are simultaneously losing fat mass? Short answer, yes. We can. But, you would not come to that conclusion if you put together a meta-analysis of decent trials. The reason is that in several studies fat loss is significant while muscle growth is not. However, when the mean is zero change, the individual data will show that many did increase their lean mass while losing fat.

I know this is a statistical quagmire, but part of my conclusion will still be based on individual results rather than the reported means. The reason is that when several people in a resistance exercise study build muscle, it is very likely that the exercise is to blame. This is not a strategy I would use when for example looking at weight loss results from low fat diet studies that show a mean zero improvement. If finding that half the participant lost weight and the other half did not, it would not be smart to claim that low fat diets works. There are a great many things that lead us to lose weight, although it almost always involves some reduction in dietary carbs. But as I said, when people gain muscle in a resistance exercise trial, the gain is extremely likely to come from the resistance exercise.

There is another issue as well. Many body composition studies are done with DEXA (dual energy x-ray absorptiometry). Because adipose tissue mass is considered 85% lipid and 15% water, and because DEXA measurement of fat free mass includes this adipose tissue water, a loss of adipose tissue without loss of fat free mass suggests favorable changes in muscle mass.

When I did a small study in 2009 I found that in eight women who did regular resistance exercise in combination with a ketogenic diet, four of them increased lean body mass, while four reduced it. The study was not large enough to indicate what factors were responsible for the lack of muscle mass gain in the other four. I guess anything from dietary protein (amino acids), thyroid issues to stress might contribute [2]. 

Figure 2 from Jabekk et al 2009. Lc+Ex= Low carb + resistance exercise. Ex=resistance exercise.
Shadid and Jensen [3] compared 20 weeks of pioglitazone with exercise and diet. Diet and exercise resulted in 11.8kg mean weight loss. The group was instructed in a 500kcal deficit diet and in an exercise program starting with 15min of aerobic exercise three times per week at 50% of each individual’s heart rate reserve. This was gradually increased to 45min aerobic exercise four times a week at 60–70% of heart rate reserve. The surprising find in the study was that the intervention caused a mean 9.5kg fat loss and a non significant 0.5kg reduction in fat free mass, which is an unusually small reduction.

Barbara A. Gower et al [4] also got surprisingly good results from a traditional very low energy diet in overweight women. Mean fat mass lost was 11.2kg. White women in the trial lost a non significant 0,77kg lean mass while the African American women lost 1.53kg (non significant) lean mass.

In both the above trials, several individuals managed to increase their lean mass while reducing fat mass. This was even done without any reported resistance exercise. Most if not all of the participants in the trials were insulin resistant, which if improved, I suspect can cause muscle growth by itself.

Gary Hunter [5] who coauthored the Gower trial found that in women who lost 12kg of weight, resistance exercise conserved lean mass. The women were randomized to diet only, diet and resistance exercise or diet and aerobic exercise.

Figure 1 from Hunter et al 2008. FFM=fat free mass. AA=african-american. EA=european-american
In a study from 1988 Douglas L. Ballor et al [6] concluded similarly to Hunter and stated that “In conclusion, data from this study indicate that weight training added to a caloric restriction program results in maintenance of LBW [Lean Body Weight] and regional increases in muscle area. When diet plus weight-training exercise is compared with exercise without caloric restriction, there is no difference in the rate of strength gain or magnitude of upper-arm muscle area increase.» 
From Ballor et al 1988. C=control. DO=diet only. DPE=diet plus exercise. EO=Exercise only. 
It might seem counterintuitive, but finding that endurance exercise increases lean mass or attenuate lean mass loss is quite common. Janssen et al [7] found that aerobic and resistance exercise did equally well in preserving muscle mass with dieting in premenopausal obese women. This finding reflected their previous (1999) trial with both men and women, which also found preservation of lean mass with both resistance and aerobic exercise.

Contrary to Janssen et al, Geliebter et al [8] and Bryner et al [9] did find that resistance exercise was more effective in improving lean mass with weight loss than aerobic exercise.

The combination of resistance training with aerobic training has been shown to be superior for body weight and fat loss and to result in greater lean body mass compared to aerobic exercise alone in several randomized controlled trials.

Park et al [10] for example, found that aerobic exercise reduced fat percentage by 9.2 while combining it with resistance exercise reduced fat percentage by 10.3. Lean mass increased by 0.9kg with aerobic exercise and by 5.6kg with combined exercise. This trial did not use a dietary intervention and the subjects had a mean BMI of 25. But it is an interesting example of how the exercise did not cause a weight change but still caused a significant body composition change.

Using a combination of high protein diet and resistance exercise Wycherley et al [11] demonstrated an 11.4kg fat mass reduction in 16 weeks. The reduction was accompanied by a 2.4kg reduction in fat free mass. The body composition results are impressive, but as I said we rarely if ever find a significant mean fat loss in combination with significant mean fat free mass gain.

Saving the best for last, Kevin David Ballard and colleagues is responsible for a meeting abstract from 2008 titled “Effects of diets restricted in fat and carbohydrate with and without resistance training on body composition and cardiovascular risk.” Ballard reports results from the Department of Kinesiology at University of Connecticut were heavyweights like Jeff Volek and William Kraemer reside. They report having examined the effects of carbohydrate restricted (CRD) and low fat diets (LFD) alone and in combination with resistance training (RT) in 47 overweight men.

The results state that “Reductions in body mass, fat mass, percent body fat and abdominal fat were greater in the CRD than the LFD (p<0.001).” and that “Gains in lean body mass were demonstrated in the RT groups only (p=0.004).” Their conclusion: “Resistance exercise is an effective strategy to combat diet induced losses of lean body mass.

On the matter of resistance exercise and fat-free mass Donnely and ACSM [12] concludes thusly: “…most studies combining resistance training with energy restriction report improved lean body mass compared to dieting alone.” They continue; “In summary, resistance training does not seem to be effective for weight reduction in the order of 3% of initial weight and does not add to weight loss when combined with diet restriction. Resistance training increases fat-free mass when used alone or in combination with weight loss from diet restriction. Resistance training may increase loss of fat mass when combined with aerobic exercise compared to resistance training alone.

Petra Stiegler and Adam Cunliffe [13] did a very good job addressing the evidence for the effect of exercise and diet on anthropometric variables. They conclude that: “…it becomes clear that a combination of modest caloric restriction combined with endurance exercise or endurance and physical training of different modes is preferable over dietary modification alone to induce favorable changes in body composition accompany ing weight loss.

The Conclusion 
It is possible to increase lean mass while losing fat mass. There are many factors at play but a high animal protein diet and resistance exercise is the best strategy we know of. Resistance exercise is very effective at increasing lean body mass, and it seems that this effect remains even if people are dieting and the effect is observed in both low and high carbohydrate diets. The addition of endurance exercise to diet and resistance exercise seems to slightly increase fat mass loss, but has little effect on lean mass.

The references

1. Fleck SJ, Kraemer WJ: Designing resistance training programs. Champaign, IL: Human Kinetics; 2004.

2. Jabekk PT, Moe IA, Meen HD, Tomten SE, Hostmark AT: Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat. Nutr Metab (Lond) 2010, 7: 17.

3. Shadid S, Jensen MD: Effects of pioglitazone versus diet and exercise on metabolic health and fat distribution in upper body obesity. Diabetes Care 2003, 26: 3148-3152.

4. Gower BA, Weinsier RL, Jordan JM, Hunter GR, Desmond R: Effects of weight loss on changes in insulin sensitivity and lipid concentrations in premenopausal African American and white women. Am J Clin Nutr 2002, 76: 923-927.

5. Hunter GR, Byrne NM, Sirikul B, Fernandez JR, Zuckerman PA, Darnell BE, Gower BA: Resistance training conserves fat-free mass and resting energy expenditure following weight loss. Obesity (Silver Spring) 2008, 16: 1045-1051.

6. Ballor DL, Katch VL, Becque MD, Marks CR: Resistance weight training during caloric restriction enhances lean body weight maintenance. Am J Clin Nutr 1988, 47: 19-25.

7. Janssen I, Fortier A, Hudson R, Ross R: Effects of an energy-restrictive diet with or without exercise on abdominal fat, intermuscular fat, and metabolic risk factors in obese women. Diabetes Care 2002, 25: 431-438.

8. Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA: Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr 1997, 66: 557-563.

9. Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R: Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body mass and resting metabolic rate. J Am Coll Nutr 1999, 18: 115-121.

10. Park SK, Park JH, Kwon YC, Kim HS, Yoon MS, Park HT: The effect of combined aerobic and resistance exercise training on abdominal fat in obese middle-aged women. J Physiol Anthropol Appl Human Sci 2003, 22: 129-135.

11. Wycherley TP, Noakes M, Clifton PM, Cleanthous X, Keogh JB, Brinkworth GD: A high-protein diet with resistance exercise training improves weight loss and body composition in overweight and obese patients with type 2 diabetes. Diabetes Care 2010, 33: 969-976.

12. Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK: American College of Sports Medicine Position Stand. Appropriate physical activity intervention strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc 2009, 41: 459-471.

13. Stiegler P, Cunliffe A: The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss. Sports Med 2006, 36: 239-262.

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