Don’t blame lactate

I’ve been thinking about lactate and low carb lately, and haunted by guilt for not writing anything here in some while, I thought I’d share my thoughts.

If you’re even just remotely interested in exercise, chances are that you still know buildup of lactate should be avoided. Those with more exercise experience will have heard of the benefits of exercising at the lactate threshold, the exercise level where lactate production will exceed the rate of  removal, and lactate accumulates. Those with expert knowledge will perhaps pray for more lactate while exercising. It’s a funny thing really.

Lactate is produced when glucose is broken down. Glucose is first broken down to pyruvate, and lactate is then made from pyruvate via the enzyme lactate dehydrogenase (LDH). Lactate can be burned as energy and can also be turned back into glucose in the process called gluconeogenesis. The thing with lactate production is that we produce more at higher intensities of exercise. It is with dread that i remember the 800 meter competitions I competed in when I was younger. The last 100 m of those races was an exercise in willing my legs to move even though they felt like they would burst from pressure of lactate build up. Lactate has a poor reputation, but as it seems, it is quite undeserved.

Because lactate is produced from glucose, an athlete primarily fueling his body on carbohydrates will produce more lactate than one primarily fueled on fat.

In fact, lactate levels are notoriously lower after low carb, high fat diets and this is in one of the hallmarks of fat adaptation. Even 4 days of high fat dieting followed by a carb loading day will make you produce less lactate during exercise (and also burn proportionately more fat) (1).

In «The art and science of low carbohydrate performance», Volek and Phinney has this to say on the matter:

«An increased reliance on fat and a corresponding decrease in glycolysis during exercise is associated with less accumulation of lactate (a surrogate for hydrogen ion accumulation). As cellular lactate and hydrogen ion levels increase at higher intensities of exercise, there are several events that cause force production and work capacity to decrease. A key contributor in this process is the acidity (i.e., decreasing pH) associated with hydrogen ion buildup. Along with maximal oxygen consumption, lactate threshold (the exercise intensity where blood lactate begins to accumulate) is a major determinant of endurance performance. With the enhanced ability to oxidize lipid associated with keto-adaptation, there is less lactate production at any one workload, and thus an elevation in the threshold exercise intensity associated with increased acidity.»

As you see, reduced lactate production is used as an argument in favor of low carbohydrate dieting. But, this reasoning might be based on a shaky foundation. It rest on the assumption that more lactate is bad and that less is good. Also, acidity doesn’t seem to be the problem (2).

When we exercise, potassium ions (K+) leak out of the muscle cells and into the extracellular compartment causing the muscles be depolarized and losing their excitability. Muscles are sort of like batteries. There has to be a difference in electrical charge between the inside and the outside of the cell to make them contract. Loss of contractile force has often been blamed on lactic acid build up and the reduced pH that follows. 

Quite recently, a group of Danish researchers showed that rat muscles produced less force if potassium ion level in the incubation medium was high, but if lactic acid was added to the incubation, the muscles regained their force producing ability (3). Lactic acid acts on chloride channels in the muscles and prevents the muscles from becoming more depolarized (2). There is also an added effect on excitability by adding both lactic acid and adrenaline (4).

So it seems that lactate is in fact what keeps muscles from fatiguing when extracellular potassium is high and removing lactic acid would only cause us to fatigue earlier. We can no longer blame lactate.

But if this is true, as it seems to be, what then of the claims that low carb is beneficial because less lactate is produced?

Studies of low carbohydrate diets and endurance exercise performance indicate that lower carb may reduce the ability for high intensity sprints during endurance races (5). I wonder if this may in fact partly be explained by the reduced lactate output (of course it could simply be because fatty acids takes too darn long to oxidize). I asked Kristian Overgaard, one of the Danish researchers, and he answered:

«I would say that if a dietary intervention influences the glycolytic flux and production of lactic acid, this may affect muscle function through a number of different mechanisms – one of them being a reduction in excitability-protective effect of acidification, which our group has demonstrated in skeletal muscle. Whether this particular mechanism is important in explaining the reduced performance is speculative. But it is a possibility

Now, it was first believed that the effect of lactic acid on depolarization was due to the fact that it was an acid. For example, the Danish researchers exposed rat muscles, that were incubated in a high potassium ion solution, to CO2 and this caused an increased excitability. Because of this, my thinking was that increased levels of the ketone bodies beta-hydroxybutyrate and acetoacetate, might fulfill the same function as lactic acid, because they also are acids. But results from the Danish group suggested that the effect of lactic acid was on chloride channels and not a result of reduced pH. This does not however mean that ketone bodies may not exert some other positive influence, minimizing the proposed negative consequence of the reduced lactate output. 

Anyway, these were my thoughts. Now they are yours. Have a nice day.

References

(1) Burke LM, Hawley JA, Angus DJ, Cox GR, Clark SA, Cummings NK et al. Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability. Med Sci Sports Exerc 2002; 34(1):83-91.

(2) de Paoli FV, Ortenblad N, Pedersen TH, Jorgensen R, Nielsen OB. Lactate per se improves the excitability of depolarized rat skeletal muscle by reducing the Cl- conductance. J Physiol 2010; 588(Pt 23):4785-4794.

(3) Overgaard K, Hojfeldt GW, Nielsen OB. Effects of acidification and increased extracellular potassium on dynamic muscle contractions in isolated rat muscles. J Physiol 2010; 588(Pt 24):5065-5076.

(4) de Paoli FV, Overgaard K, Pedersen TH, Nielsen OB. Additive protective effects of the addition of lactic acid and adrenaline on excitability and force in isolated rat skeletal muscle depressed by elevated extracellular K+. J Physiol 2007; 581(Pt 2):829-839.

(5) Havemann L, West SJ, Goedecke JH, Macdonald IA, St Clair GA, Noakes TD et al. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. J Appl Physiol 2006; 100(1):194-202.

Diet, weight loss and body composition changes

This is an unfortunately long post, and I apologize for it, but the reason is that I find all this so darn interesting.  Hope you do to.

A little while back I looked closer at some of the science behind diet, weight loss and body re-composition. I have heard people say on several occasions that a low carbohydrate diet will prevent loss of muscle mass and that all weight lost is fat. So I wanted to find out once and for all what really happens with our body when we lose weight. I’ll show you some of the data, and although these studies are not the only ones, I am confident that the studies presented here give a satisfactory accurateness

So there is much debate about what happens to our body composition when we lose weight and perhaps especially when we do it using a low carbohydrate diet. This quote is from Sachiko T. et al 2001. Dietary Protein and Weight Reduction: A Statement for Healthcare Professionals From the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association:

Some popular high-protein/low-carbohydrate diets limit carbohydrates to 10 to 20 g/d, which is one fifth of the minimum 100 g/d that is necessary to prevent loss of lean muscle tissue.

Clearly the AHA suggests that we will lose muscle tissue by going low carb. In my school we used the exercise physiology textbook from McArdle, Katch and Katch (2007) which said this:

…low carbohydrate diet sets the stage for a significant loss of lean tissue as the body recruits amino acids from muscle to maintain blood glucose via gluconeogenesis.

Once again, low carbohydrate dieting does not seem a good idea if we want to preserve muscle mass while we lose fat mass.

But the questions remains unanswered; how much muscle mass do we lose if we go low carb and can we do anything to prevent a potential loss of muscle tissue?

Let us look at some studies and see what they tell us.

Studies
This study from Bonnie Brehm and coworkers compared a low carbohydrate diet to a low fat diet:

All participants in the above study were women and they were obese. Dietary energy content was reduced in both diets and body composition was measured using Dual Energy X-ray Absorptiometry (DEXA). As you can see, weight loss was greater with low carb, but so was loss of lean body mass (LBM) and the percentage loss of LBM was not much different between diets. 
Here’s another study:
This was a crossover study where all the participants tried two different diets in random order. The results are given under:
As is usually the case in weight loss trials, the men lost more weight than the women. And once again low carb caused a greater weight loss, but also quite the loss of lean body mass. The women eating low fat seemed to lose the greatest percentage LBM, which is also a recurrent theme in weight loss trials. 
Next, here’s Kelly Meckling and coworkers:
One of the goals in this study was for the low fat group to reduce their calorie intake to the naturally reduced level of the low carbers. Weight loss did not differ between groups, but loss of LBM was significantly larger in the low carb group and over 25% of the LC weight loss was lean body mass. Body composition was measured using bioelectrical impedance analysis (BIA).
Next, as study from William Yancy and coworkers from 2004:
  
Weight loss with low carb was double that of low fat and this time loss of fat free mass (FFM) was actually quite larger in the low fat group. LBM is what is left if we remove fat mass and skeletal mass. Fat free mass is, not surprisingly, total mass minus fat mass. LBM and FFM are used interchangeably. 
It seems that loss of non-fat mass is common, regardless of diet, but we need to look at some more studies to get a clearer picture.
Here’s one from down under, from Manny Noakes:
This is a short study, but with 83 participants. The results are pretty similar, both when it comes to weight and LBM loss, but in both diets around 30% of the lost weight was LBM and that is rather much.
Another one from Australia. Here’s Jennifer Keogh and coworkers:
Both diets were 30% energy restricted and designed to be isocaloric. Once again there was a significant loss of fat free mass with both diet strategies.
Jeff Volek brought us this study in 2008:
An Atkins type diet was compared to a regular calorie restricted low fat diet in 40 men and women. Weight loss was greater with low carb, but so was loss of LBM. So far, there seems to be little truth to any claim that low carb preserves LBM.
This next one is another crossover study:
Alexandra Johnstone and coworkers showed us yet again that weight loss is greater with low carb, but that so is loss of FFM. Notice that this is a study of men only and so the percentage loss of FFM is much smaller than in studies of women.
One last study. Third one from Australia, this time by Grant D. Brinkworth:
118 people participated in this eight week study and were scanned with DEXA. Weight loss was greater with low carb and both groups lost about 20% FFM.
To summarize, loss of fat mass is greater with LC than LF diets. Loss of LBM is common on both LF and LC diets, but as we will see, not obligate. But there are some considerations to make first.
Considerations
First of all, any loss of water will usually be considered LBM and so if there is a difference in water loss between diets, this will affect loss of LBM/FFM. Carbohydrate restriction usually does cause a greater loss of body water, at least in the initial phase of the diet. Loss of glycogen with low carb will cause a parallel loss of water and so there is reason to expect a larger loss of LBM with low carb, and we need to remember that LBM is not a measure of muscle proteins.  
Contradictory findings
Although loss of LBM is clearly common on low carb diets, there are studies suggesting that such a loss can be avoided.
In a very small crossover study by Benoit et al from 1965 we can see the obvious advantage of low carb dieting compared to fasting:
Notice the difference in LBM loss. One likely advantage of carbohydrate restriction is that the combination of adequate protein intake and high ketone body production spares muscle proteins from being used to produce glucose. The Benoit study is small, but it suggests that loss of LBM is not a necessary consequence of low carb dieting.
And look at this one:
In this study of twelve men, LBM increased during the diet period, even though there was no change in the exercise pattern of the subjects. It is results like these, which sometimes appear, that suggests that it is possible to lose weight in a way that spares muscle tissue. In another very small study of very obese adolescents, similar results were found:
After eight weeks of a very low calorie ketogenic diet, lean body mass increased by almost 1,5kg while 15kg of fat was lost.
So I think it’s time to ask what the difference between these few studies where LBM increases (in spite of water loss) and the RCT’s where a low carbohydrate diet always leads to some LBM loss. But remember also that not all LBM is functional LBM. That is, we expect some loss of LBM and some LBM can be lost without negative consequences. We must remember to keep our feet on the ground, there is no problem with some loss of LBM with large losses of fat mass.
To make a long story short, there are some important factors we can manipulate in order to reduce loss of LBM. Being a man is perhaps the most effective. Men lose more fat and less LBM when they lose weight. It’s just the way it is. But both men and women can increase their protein intake. In many of the RCT’s in this post, average protein intake was low, often around 1g/kg body weight/day. The optimal intake is probably closer to 1.8g/kg/day (severely overweight people should use ideal body weight instead of actual body weight).
Several studies have found a correlation between protein intake and LBM loss. James Krieger wrote this in 2006:
  
And he concluded thusly:
In a very recent review article, Stuart Philips and Luc van Loon has this to say:
The thing with carbohydrate restriction is that is causes a greater fat loss and greater LBM loss than low fat strategies, but the end result is that low carb thus causes a greater reduction in body fat percentage and so the greater change in body composition. To optimize the results, protein intake should most likely be kept at >1,5g/kg/day. Here’s another quote from Phillips and van Loon:

There is also the matter of sodium and potassium that might play a part in the results. Potassium is an important intracellular ion in our muscles and adequate potassium is important for creating an anabolic environment. The trouble with ketosis or severe carbohydrate restriction is that it causes our kidneys to excrete sodium and unless that sodium is properly replaced the kidneys compensate by excreting potassium. In short, when optimal body composition changes is the goal, or optimal performance, salt intake is important and should be a good deal higher than the daily recommended intake.

In addition to minding our protein and salt intake, we can of course also do resistance exercise in order to increase lean mass retention or even increase lean mass while reducing fat mass. It is, not surprisingly, well documented that resistance exercise, as a part of weight loss, is very effective at reducing lean mass loss, regardless of diet. But in order for resistance exercise to yield optimal results, protein and salt intake must be optimized.  
Richard Wood and coworkers just published results from a study where overweight older men were put on two different diets with or without resistance exercise. Here are the results:
Even though the results favor both low carbohydrate dieting and resistance exercise, I must say that I was surprised at the amount of FFM loss in the low carbohydrate and resistance exercise group, even when considering that some is water loss. After 12 weeks I would have suspected FFM to have increased. But there are once again some factors to consider. First of all, the mean age of the participants were 60 years. This may have caused the results to be smaller than if younger men participated. Also the resistance exercise was not very heavy, it could have been a good deal heavier and it is likely that muscle hypertrophy would then have been greater.
Donald K. Layman and coworkers compared the effects of two different diets varying in protein and carbohydrate content, with or without resistance exercise. The graphs on the left are women and the ones on the right are men:

Clearly, both increasing protein/decreasing carbohydrate and resistance exercise improve body composition changes. The low carbohydrate diet in this study was not very low. Average carb intake during the intervention was 141g in LC and 126g in LC+RE. Protein intake was 110g and 102g respectively.

I’d like to compare the results of a study I conducted in 2010 with that of a study from Donnely from 1991:

These are two very different strategies. In our study the participant were told to be in dietary ketosis, but could eat as much as they liked. In Donnely’s study calories was severely restricted. Also in our study the participants exercised twice a week, whereas in Donnely’s they exercised four times per week (resistance exercise). They are both effective strategies both for losing weight and changing body composition, so it is up to us what we prefer. I for one would like to eat as much as I please and not have to exercise that much to get the results I want.

The conclusion
Loss of LBM with weight loss is common but not obligate. A low carbohydrate diet is no grantee for all weigh loss being fat. In order to achieve optimal body re-composition one should reduce carbohydrates, make sure to eat enough protein and salt, and do regular heavy resistance exercise. The results one can achieve are quite astonishing.

Carbs and cancer

This is not one of those “carbs cause cancer” posts. I though “Carbs and cancer” had a better ring to it than for example “Metabolism and cancer”, what with the alliteration and all. Still, it’s important to remember that although carbohydrate restriction is an effective treatment for cancer, this does not mean cancer is caused by consumption of carbs.

Our diet determines our health, even our risk of getting cancer and our risk of surviving it. Her are some reasons macronutrients matter:

The cause

– Humans who live on natural diets seem free of many cancers and also free of metabolic diseases [1]. Metabolic diseases such as obesity, diabetes, insulin resistance and heart disease, also coexist with cancer.

– A high body mass index increases the risk of most cancers [2].

– Cancer cells are normal cells that grow too fast and the cells need both energy and growth factors to grow at an increased pace. A logical theory of treatment would be to take away the energy and growth factors and starve the cancer cells.

– Hanahan and Weinberg suggested that six essential alterations in cell physiology could underlie malignant cell growth [3]. These six alterations were described as the hallmarks of nearly all cancers and included, 1) self-sufficiency in growth signals, 2) insensitivity to growth inhibitory signals, 3) evasion of programmed cell death (apoptosis), 4) limitless replicative potential, 5) sustained vascularity (angiogenesis), and 6) tissue invasion and metastasis.

Cancer cells crave glucose. Aerobic glycolysis, the breaking down of glucose in the presence of oxygen, but with high lactic acid production in the cytoplasm (the Warburg effect), is a metabolic hallmark of most tumors [3]. Almost all cancers express aerobic glycolysis, regardless of their tissue or cellular origin.

Enhanced glycolysis (the breakdown of glucose) is required for the rapid growth and survival of many tumor cells.

– People with type 2 diabetes are at increased risk of getting pancreatic, liver, colorectal, and bladder cancers, and non-Hodgkin lymphoma [4]. But if you have type 1 diabetes you have a reduced risk of lung cancer, Hodgkin’s lymphoma and prostate cancer.

Mitochondrial dysfunction is a key element in most cancers.

– One of the problems if you are insulin resistant is that the mitochondria are bombarded with energy and pushed to the max. This causes them to produce reactive oxygen species (ROS). Increased ROS production can impair genome stability, tumor suppressor gene function and control over cell proliferation [3].

– The glycolytic enzyme «glyceraldehyde-3-phosphate dehydrogenase» potential is upregulated in many common tumors. GAPDH is also a transcription activator and link the metabolic state to gene transcription.

– The integrity of the nuclear genome is largely dependent on the functionality and energy production of the mitochondria.

– Impaired mitochondrial function can also induce abnormalities in tumor suppressor genes and oncogenes.

– Some viruses are associated with certain cancers. Several of these viruses are known to affect the mitochondria.

– While the mutator phenotype of cancer can be linked to impaired mitochondrial function, normal mitochondrial function can suppress tumorigenesis. We can suppress cells capability of causing tumors by fusing cytoplasm from normal cells without a nucleus with tumor cells. This suggests that normal mitochondria can suppress the tumorigenic phenotype [3].

– The function of a tumor suppressor gene called p53 is linked to cellular respiration. Damage to the respiration will gradually reduce p53 function.

– The study of cancer and metabolism involves such fancy words as «the Warburg effect» and «von Hippel-Lindau,» so there’s got to be something to it 🙂

If cancer is a disease of energy metabolism, then a rational approach to cancer management can be found in therapies that target energy metabolism. 
The cure

– Growth and progression of cancers of the mammary, brain, colon, pancreas, lung, and prostate has been reduced following energy restriction.

– Due to accumulated genetic mutations, cancer cells lack metabolic flexibility, so shifting the metabolism makes sense.

– Many tumors have abnormalities in the genes and enzymes needed to metabolize ketone bodies for energy so ketogenic diets are especially potent.

– It is well established that dietary energy restriction protects against cancer in many animal models, but…

– Freedland and coworkers transplanted prostate cancer cells into mice. The mice were then divided into one ketogenic group, one low fat group and one western diet. After 51 days the tumor volume in the low carb mice was 33% smaller than the other two groups, despite similar energy intake [5].

– Zhou and coworkers put mice with malignant brain cancer on a ketogenic diet meant for epilepsy and showed that the diet decreased the intracerebral growth by 65% compared to mice on control diet [6].

– LJ Martin and coworkers randomized women to a low fat diet or a control group, hoping to affect the risk of breast cancer. They did. But not how they wanted. Over an average of 10 years low fat eating led to 118 invasive breast cancers while the control had 102. Carbohydrate intake was found to correlate with cancer risk [7].

– A group of Japanese researchers [8] hypothesized that the increase in colorectal cancer in Japan could be due to increased fat intake. So they told 373 people with previous cancer to restrict their fat energy ratio to 18-22%. After 4 years the researchers were surprised to find that fat restriction had increased the risk of cancer recurrence.

– A group of Italian researchers found direct relations between dietary GI and GL and risk of renal cell carcinoma [9].

– In 1995, two pediatric patients with malignant Astrocytoma tumors were put on a 60% MCT diet to induce ketosis. PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects One patient exhibited significant clinical improvements in mood and new skill development during the study- continued the diet and remained free of cancer progression [10].

– An Italian case control study from 1996 found that the risk of breast cancer decreased with increasing total fat intake and that the risk increased with increasing intake of available carbohydrates [11].

Eugene Fine at Albert Einstein College of Medicine of Yeshiva University, have been using a 1 month Atkins diet in cancer patients, hoping to see a reduction in tumor size. Results have not been published yet.

Stephen J. Freedland at Duke Univeristy is currently testing the hypothesis that an Atkins diet will prevent or at least minimize the metabolic consequences of androgen deprivation therapy in prostate cancer treatment.

The University of Würzburg Hospital has recommended a low carb, ketogenic diet for cancer patients since 2007

– Other studies are testing ketogenic diets in relation to cancer treatment. There’s much interesting knowledge to come

 

Impaired mitochondrial energy metabolism seems to underlie the origin of most cancers. To improve mitochondrial function: avoid toxic foods, read the Perfect Health Diet, avoid foods that induce inflammation, make sure to produce ketones now and then and remember to exercise. 

References

1. Lindeberg S: Food and western disease: health and nutrition from an evolutionary perspective. Chichester: Wiley-Blackwell; 2010.

2. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M: Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 2008, 371: 569-578.

3. Seyfried TN, Shelton LM: Cancer as a metabolic disease. Nutr Metab (Lond) 2010, 7: 7.

4. Tabares-Seisdedos R, Dumont N, Baudot A, Valderas JM, Climent J, Valencia A, Crespo-Facorro B, Vieta E, Gomez-Beneyto M, Martinez S, Rubenstein JL: No paradox, no progress: inverse cancer comorbidity in people with other complex diseases. Lancet Oncol 2011, 12: 604-608.

5. Freedland SJ, Mavropoulos J, Wang A, Darshan M, Demark-Wahnefried W, Aronson WJ, Cohen P, Hwang D, Peterson B, Fields T, Pizzo SV, Isaacs WB: Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate 2008, 68: 11-19.

6. Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, Seyfried TN: The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutr Metab (Lond) 2007, 4: 5.

7. Martin LJ, Li Q, Melnichouk O, Greenberg C, Minkin S, Hislop G, Boyd NF: A randomized trial of dietary intervention for breast cancer prevention. Cancer Res 2011, 71: 123-133.

8. Nakamura T, Ishikawa H, Takeyama I, Kawano A, Ishiguro S, Otani T, Okuda T, Murakami Y, Sakai T, Matsuura N: Excessive fat restriction might promote the recurrence of colorectal tumors. Nutr Cancer 2010, 62: 154-163.

9. Galeone C, Pelucchi C, Maso LD, Negri E, Talamini R, Montella M, Ramazzotti V, Bellocco R, Franceschi S, La Vecchia C: Glycemic index, glycemic load and renal cell carcinoma risk. Ann Oncol 2009, 20: 1881-1885.

10. Nebeling LC, Miraldi F, Shurin SB, Lerner E: Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports. J Am Coll Nutr 1995, 14: 202-208.

11. Franceschi S, Favero A, Decarli A, Negri E, La Vecchia C, Ferraroni M, Russo A, Salvini S, Amadori D, Conti E, Montella M, Giacosa A: Intake of macronutrients and risk of breast cancer. Lancet 1996, 347: 1351-1356.

http://www.time.com/time/health/article/0,8599,1662484,00.html

Fat people are liars

Obviously! Obesity is a remarkably simple problem to solve. Eat less and move more. When energy expenditure exceeds energy intake, you lose weight. Many people claim to have tried eating less and exercising more and claim that it does not work. As this would be a violation of the laws of thermodynamics it is quite unlikely.

Not only do overweight people claim to break the fundamental laws of nature they also constantly lie about how much they actually eat.

Elaine Prewitt and coworkers examined the effect of a 37%-fat (HF) diet for 4 weeks followed by a 20%-fat diet (LF) for 20 weeks on body composition and weight in 18 premenopausal women with body mass index (BMI) of 18-44. They found that

Despite adjustments in energy intake to maintain weight throughout the study, by the end of the LF period, energy intake had increased significantly in comparison with the HF diet (119% of the HF intake, P < 0.0001). 

The authors knew what kind of people they were dealing with and wrote

We have no means of assessing the degree of food waste by subjects when meals were taken out but there was no reason to attribute the magnitude of energy increase we observed to overreporting of dietary infractions. By contrast, one would expect the subjects, particularly obese subjects, to underreport extra foods eaten.

W. Daniel Schmidt and coworkers exercised overweight women. All study groups were put on an energy restricted diet. The control group only dieted without changing exercise routines, but somehow they didn’t lose any weight. The authors write:

The fact that the control subjects in our study did not lose weight is perplexing and conflicts with other research that generally supports weight loss with caloric restriction [17, 18]. One explanation may be that subjects simply underreported the amount of calories consumed, thus making this an issue of noncompliance. 

Not only are fat people liars, but fat people on low fat diets are the worst. James Krieger, everyone’s favorite researcher, suggests that:

…subjects on low-fat diets systematically underreport energy intake compared with subjects on low carbohydrate diets.

In support of his theory he cites a study where weight loss from a low fat diet did not turn out as predicted.

Fat people on low fat diets are not only the worst liars around, they are also not very smart. Kelly A. Meckling and coworkers compared a low fat diet to a low carbohydrate diet in overweight men and women. They write:

Energy restriction alone predicted a weight loss of 5.5. and 6.9 kg, respectively, in the LF and LC groups, which was close to the observed values of 6.8 and 7 kg for the same groups. Slight differences, particularly for LF subjects might be explained by underreporting of habitual diets, as the subjects became better able to estimate their intakes and keep better food records as the trial proceeded. 

Those put i a low carb group obviously nailed the food reporting task right away, even before they actually were put on the diet, and missed the predicted weight loss by a mere 100 grams.

Everyone knows low fat fatties are the worst. Thermodynamics applied to food and the body is very simple, yet predicted weight loss are often not achieved by low fat fatties.

Writes Jennifer B Keogh and colleagues (when a low carb group lost more weight than a low fat group in their study):

Greater weight loss with a low-carbohydrate diet than with a conventional low-fat diet has been reported previously (2– 4, 57). Subjects in these studies reported similar energy intakes despite differences in weight loss, which suggests that the conventional diet group underreported their intake (3, 4, 57).

A group of Dutch researchers set out to test the extent of underreporting in 30 obese men. Their conclusion:

Total underreporting by the obese men was explained by underrecording and undereating. The obese men selectively underreported fat intake.

Not only did these men lie about how much they were eating, they didn’t even eat as much as they should have. They underrate. Those bastards!

If by chance you are wondering if the methods of the Dutch researchers were bulletproof, they weren’t. Still…

It is possible that overweight people under report more than lean people. But people seem to think that the under reporting somehow is the reason they are fat. They don’t know how much they eat and so they stuff themselves and grow fat. It is also possible that low fat diets does not work very well and that the human body is more metabolically complex than the simple energy calculations used predict.

But if overweight people do really under report more than «normal» weight people, are they then fat because they under report and lie, or are they perhaps under reporting because they are fat and afraid of being stigmatized as gluttonous and desperately trying to keep some of their dignity?

What if…

And then, one Thursday, nearly two thousand years after one man had been nailed to a tree for saying how great it would be to be nice to people for a change, a girl sitting on her own in a small cafe in Rickmansworth suddenly realized what it was that had been going wrong all this time, and she finally knew how the world could be made a good and happy place. This time it was right, it would work, and no one would have to get nailed to anything. Sadly, however, before she could get to a phone to tell anyone about it, a terrible stupid catastrophe occurred, and the idea was lost forever.” 

Douglas Adams 

What if there was one way to lose weight that was the correct way. One way that would always work. In the name of moderation, let’s say a method that works 90% of the time – there will always be the odd case of Prader-Willi or some strange genetic disorder that screws up the perfect statistics. So let’s say 90% and round it up.

So, a way to lose weight that always works. Let us also say that this method already exists and that it has been around for ages, and although many know about it few know it is the right one.

Let us also imagine that there are two main foundations to the method. One is the reduction of inflammation, in which the intake of easily digestible carbohydrates and the intake of omega 6 fatty acids amongst other factors play important roles. The other foundation is the increase of lipolysis (getting the body to burn its own excessively stored energy instead of asking for external energy), because weight loss and fat burning are two parts of the same. In increasing lipolysis the reduction of insulin and glucose levels are of paramount importance. Doing so requires the reduction of easily digestible carbohydrates.

Now let us say that this method i.e. eating mostly animal products, supplementing with vegetables and taking in copious amounts of non omega 6 fats and no refined carbohydrates, always works. But we don’t know it, because too few of us are looking at the details, and to many are focusing on the entire weight loss “package.”

In weight loss studies the participants lose weight by utilizing different approaches, but no approach ever has a 100% success rate. All participant may lose some weight, but some lose more than others and some often nothing at all. But no matter the method, lost weight often returns quickly. These results have led many researchers to think weight loss in it self is futile. It has led some to reason it is all due to lack of willpower.

But might the results fool us?

Imagine you start following the Atkins diet. You lose lots of weight during the first weeks. But then you start feeling unwell. You get tired, light headed and you get headaches and your stamina is not what it used to be.

So you decide to increase your intake of carbohydrates. The symptoms disappear and in a short while the lost weight has returned. From that moment on you proclaim that you have tried everything from Ornish to Atkins, but nothing worked for you.

But let’s say one of the many weight loss regimes you tried actually was the right one. That “this time it was right, it would work” but “a terrible stupid catastrophe occurred, and the idea was lost forever.”

You forgot to put salt on your food.

Salt is important when you restrict your carbohydrate intake and you often have to increase your salt intake with carbohydrate restriction, not decrease it as many does.

Such a simple, stupid little thing could separate success and failure. It could deprive you of the chance to finally get it right.

There are many less significant factors that can easily mess thing up despite us having the foundational principles right and thus make the whole strategy seem futile. Salt is one, stress another. Too little sunlight or even to little carbohydrates are yet others.

Imagine that the right way is already here, but we are blinded by our search for quick fixes, inability to deduct or simply our lack of knowledge.

When I first learned of carbohydrate restriction it all sounded so easy. I thought everybody could lose weight if only they were taught the basic principles – the foundations. I’ve changed my mind now. Not getting professional help could be what keeps you from finally getting to the truth.

The great tragedy of it all is that most weight loss strategies will be unsuccessful most of the time and you will not know if your unsuccessful attempts are because the basic principles are wrong or if you got them right, but a minor detail was out of whack.

High fat diets and endurance exercise performance

«When first thrown wholly upon a diet of reindeer meat, it seems inadequate to properly nourish the system, and there is an apparent weakness and inability to perform severe exertive fatiguing journeys. But this soon passes away in the course of two or three weeks.«

The above excerpt is from the journal of Lt. Frederick Schwatka who covered over 3000 miles on foot over ice, snow and tundra, along with 17 other expedition members and 44 dogs, returning to Hudson’s Bay in March of 1880. Once the initial provisions were depleted, the expedition’s only source of food was hunting and fishing.

Many people go low carb/high fat for better health and vitality and at the same time exercise quite a lot. There is little to indicate that recreational physical activity performance is impaired by low carbohydrate feeding. However, the case for low carb/high fat diets for competition exercise is somewhat different.

There are highly skilled sportsmen who admit to following a low carbohydrate lifestyle who still perform world class.

In the recent 2010 Winter Olympics, Swedish biathlon performer Bjørn Ferry won the gold medal in12.5km pursuit. Ferry proclaimed following the gold medal that he would celebrate with some champagne and cream. He is known for following a low carb diet strategy.

Fellow countryman and triathlon world champion Jonas Colting, was quoted in Swedish Runners World saying the carbohydrate supremacy is a brainwashing scheme that would have made George Orwell proud. He also explained that;

Not until the mid 90’s when I came in contact with foreign influences and new findings did I make changes that so far have produced four European and World Championship medals and two victories in the Ultraman World Championship.

Colting follows the “train low-race high” principle where high carbohydrate intake is reserved for the immediate time around competition.

There are many athletes who follow a more or less strict low carb dietary regimen with great success. However the scientific data to support this strategy is actually poor and close to non-existing.

During the 80s and 90s and up until a few years ago there was a big interest in examining diets with different macronutrient composition as a means to enhance exercise performance. High fat diet (HFD) studies seem to have been especially popular during the nineties up until about 4 years ago, when the interest subsided. The declined interest came after several reviews concluded that high fat diets did not enhance performance and sometimes even caused a decreased performance and suboptimal adaptations to exercise. The foundation for these conclusions was poor. The fact is that there is a lack of well controlled longitudinal studies to conclude either way.

The theory 
In theory the performance enhancing effect of high fat diets is simple. Our body is fueled by two sources: food and stored energy. During exercise food is not an option so the required energy must be supplied by energy stores. These stores are either carbohydrate stored as glycogen in liver and muscles or fat stored in fat tissue and muscles. The amount of energy stored as glycogen isn’t really that much and after a brief bout of exercise the stores are emptied. The normal muscle glycogen stores of well trained athletes are generally sufficient to fuel activities up to 60–90 min.

If we eat carbohydrate rich diets the body will get most of its energy from glycogen during exercise. If we on the other hand eat high fat the body will get a greater proportion of its needed fuel from fat.

Moreover, the point of fatigue during exercise closely correlates with the reduction of glycogen stores beneath a certain point. If however we can make the body use fat as the primary energy source during exercise, glycogen can be spared and performance increased. The energy stored as fat also does not get depleted and so is not a limiting factor.

The amount of glycogen stored in muscles are often estimated to be 300-900g and the amount in the liver about 80-100g.

Although glycogen obviously is a short term energy source, the reliance on glycogen and carbohydrate for fuel is the norm in most forms of exercise. When exercise duration increases athletes simply keep consuming carbs during exercise and competition to keep glycogen stores from depleting.

Many of us who have been involved in sports for some time are familiar with the concept of carbohydrate loading. It has been a part of sports literature from 1939. The concept stems from the1920 data of Krogh and Lindhard, who build themselves a homemade chamber where they were able to measure how different diets caused different respiratory exchange ratio (RER).

The carb for sports supremacy came about following a 1939 study by Christensen and Hansen who did a crossover study with a low carb diet, a moderate carb diet and a high carb diet, each for a period of 1week. After each diet, time to exhaustion was measured on an ergometer bike. Compared to the low carb time of 81min the subjects cycled for 206min on the high carb diet.

Since then, the consensus has been to feed athletes large amounts of carbohydrates to fill glycogen stores to the max, and this is still the norm. Close to everything about exercise performance and diet has been about trying to increase glycogen stores, because glycogen depletions and fatigue coincide. Athletes are commonly recommended a diet of 60 – 70% carbohydrate for optimal performance. In addition, during prolonged activity it is common to consume large amounts of sugary beverages to stock up on carbs.

Last, but not least there is an important physiological mechanism behind the whole “carbs for competition.” Unlike carbohydrates, fat cannot be oxidized under anaerobic conditions. This means that as soon as we reach high intensities, as we commonly do during competition speeds, carbohydrates has to be our primary energy source.

As seen in the above figure, carbohydrates are the main fuel source during high intensities while fat dominates at lower intensities. When exercise intensity increases the body cannot take up and supply sufficient oxygen to support the oxidation of fat. During prolonged low intensity activity the blood flow in the adipose tissue increase. This increases the rate of fat delivery from fat tissue. During high intensity exercise sympathetic vasoconstriction decrease adipose tissue blood flow, fatty acids accumulate in the fat tissue and the amount of fat transported to muscles decrease. This also contributes to the low fat oxidation rates at high intensities.

I know this last bit seems a crucial point. No competition exercise is performed at low “fat burning” intensities. Even in marathons or triathlons intensities goes up and down and an athlete need the ability to sprint or to rely on glycogen for shorter periods of time. But maximal fat oxidation rates differ immensely and in some fat oxidation is not suppressed until intensities reach well above 80% VO2max.

Muscle glycogen and plasma glucose can contribute 130kJ of energy per min (32kcal/min) during high intensities. Fat is more slowly used and can supply in the area of 6-7kcal/min. The carbohydrate stores are quickly depleted during prolonged high intensity exercise, but the stores are also quickly refilled when carbohydrates are eaten.

In the end carbohydrates can supply more energy per time unit. It can supply energy even at high intensities, but the depletion of glycogen is when exhaustion sets. Fat on the other hand is burned slowly. It cannot supply energy during high intensities, and eating a high fat diet may lead to smaller glycogen stores. However, the amount of fat stored is never a limiting factor for performance.

I’ll admit that, based on the above, the case for going high fat is not strong. But there is still hope. The rules governing the human metabolism are not set in stone. They can be bent and stretched to better suit our needs. The body is adaptable, very adaptable.

Adaptation to high fat eating and maximal fat oxidation
A chronic high fat diet cause a marked shift in substrate use compared to high carbohydrate diets. Interestingly, the adaption in substrate use caused by high carbohydrate intake is close to instantaneous, whereas the adaptation to a high fat diet can take weeks.

In addition, the adaptation persists for some time after carbohydrate intake is increased and glycogen stores refilled. It is possible to maintain an increased fat oxidation while having full glycogen stores. This strategy, though similar to carbohydrate loading is actually more of a fat loading and very much like the “train low-race high” principle.

When we start eating high fat we gradually get better and better at burning fat. If we are well trained, we also burn more fat at higher intensities. Fat is released faster and in greater amounts from the fat tissue, it is also transported faster into the muscles and the mitochondria. The muscles also store more energy as fat and get better at using this fuel as well. Full adaptation takes time tough, and it is likely that optimal adaptation need >4 weeks. High fat diets cause a shift in the expression of our genes into coding for several of proteins involved in fat metabolism.

After adapted to high fat diets we can oxidize more fat during exercise and we get a higher maximal fat oxidation. Endurance trained athletes are particularly adept at burning fat. An endurance athlete adapted to a high fat diet is a fat burning machine. Still, endurance trained athletes are not a homogenous group and may differ greatly in their fat burning capacity.

Achten and Jeukendrup tested 55 endurance trained athletes to find maximal fat oxidation and at what level of intensity it occurred. Maximal fat oxidation averaged 0,52g/min at an intensity level of 63% VO2max. But there were large variations in both maximal fat oxidation and the rate of fat oxidation. Although the average intensity for maximal fat oxidation was at 63% VO2max some athletes cycled at more than 85% VO2max before fat oxidation declined, while in others it went downhill when reaching 50% VO2max. This study used a high carb diet and the exercise was performed after an overnight fast.

Knechtle and coworkers found a higher fat oxidation at 75% VO2max than at 65% and 55% VO2max for both men and women and in both running and cycling. This intensity was related to the lactate threshold for both sexes in cycling.

Achten and Jeukendrup also showed that the first increase in lactate coincided with maximal fat oxidation.

Studies of HFD and performance
Venkatraman et al (2001) examined the effects of increasing dietary fat on endurance exercise as measured at 80% VO2max. 14 trained runners serially consumed a 15% fat diet, a 30% fat diet and 40% fat diets for four weeks each. In the last week of each diet period the subjects ran to exhaustion at 80% of their VO2max. On the 15% diet, the women ran 39.2 min. and the men ran 44.3 min. Increasing dietary fat to 30% significantly increased the running time to exhaustion by 19% for women (46.6 min) and 24% for men (54.9 min). Increasing the dietary fat to 40% did not significantly increase endurance time, compared to the 30% diet.

30% fat is not a high fat diet, but the results mirror many similar studies that indicate a negative effect of reducing fat to below “normal” levels. For example, in 2000 Horvath et al examined 12 male and 13 female runners who ate diets providing 16% and 31% fat for four weeks. In addition, six men and six women increased their fat intakes to 44%. Endurance and VO2max were tested at the end of each diet period. Although the diets were designed to be isocaloric the runners on the low fat diet ate 19% fewer calories than on the medium or high fat diets. The endurance test was a run to exhaustion at 80% VO2max.

The table below shows the timed run to exhaustion after the different diets.

From Horvath et al 2000

The endurance time to exhaustion in the subjects on the medium fat diet increased 20% in females and 8% in males compared to the low fat diet.

Muio et al (1994) examined the effects of dietary manipulations on six trained runners. The runners were given diets of 38%, 24% and 15% fat each for 7 days. Running time to exhaustion at 75- 85 % VO2max was greatest after the 38% diet with 91.2min as compared with the 15% diet with 75.8min and the 24% diet with 69.3min. VO2max was also higher on the 38% diet. The results imply that restriction of dietary fat may be detrimental to endurance performance.

A much quoted study is one from Stephen D. Phinney from 1983. He put 5 endurance trained athletes on a ketogenic (85% fat) diet for 4 weeks. After the diet period the athletes did not have a significant reduced performance on a 150min test at 62-64% VO2max, and the results almost seemed to point to an advantage. However, four of the cyclists showed little change while one participant had an almost abnormally large improvement. It is difficult to say if this improvement was caused by diet or whether this athlete just had a very good day.

In 1999 Silvia Pogliaghi and Arsenio Veicsteinas had fourteen untrained men sequentially submitted to 4 weeks eucaloric diets (30%, 15%, 55% fat). After each diet period, VO2max and endurance (time to exhaustion at 75% VO2max) were measured. Neither VO2max nor endurance time were significantly modified by the different diets. Although time to exhaustion was greater during high fat than low fat the difference was not statistically significant.

Vogt et al (2003) also saw no decrements in performance after a HFD. 11 athletes did 5weeks of HFD (53%) or low fat diet (17%) and were tested at both moderate and high intensities. Half marathon running time differed only 12sek between diets. Vogt also showed that glycogen stores were maintained on the HFD.

In contrast to Vogt, Lambert and colleagues (1994) who used a 2 week 67% fat or 12% fat diet, showed reduced glycogen stores in 5 trained cyclists. But unlike Vogt they observed an improved performance measured as time to exhaustion at 60% VO2max. The study shows that a diet with more than 60% fat may make it hard to maintain full glycogen stores, but also that these stores do not necessarily play an important role at these intensities. The same study observed no differences between the diets when tested at 85% VO2max. The actual time to exhaustion on the 60% VO2max test was 79.7min in the HFD and 42.5min in the low fat group.

In 2003, Fleming and coworkers, assigned twenty non-highly trained men to either a HFD (61% fat) or control (25% fat). The men were tested before and after 6 weeks. The HFD group lost on average 2.2kg, but also showed small decrements in peak power output and endurance performance. The HFD group also reported increased ratings of perceived exertion. Interestingly, the average reported energy consumption in the two groups was 2335kcal and 1815kcal in the HFD and low fat groups respectively.

Rowlands and Hopkins (2002) compared the effects of 2 weeks HFD (66% fat), high-carbohydrate (16% fat) and a 11.5-day high-fat diet followed by 2.5-day carbohydrate-loading, on metabolism and short- and ultra-endurance. Participants were tested for 5 hours and all groups ingested carbohydrates during testing. The diets had no statistically significant effect on 15-minute performance, although the high-fat condition tended to reduce distance covered by -2.4% (not significant) relative to the fat with carbo-loading condition. In a 100-km time trial, the HFD and the HFD with carbohydrate loading attenuated the decline in power output observed in the high-carbohydrate condition. The corresponding improvement in performance time of 3% to 4% was not statistically significant. The authors concluded that “…there was some evidence for enhanced ultra-endurance cycling performance relative to high-carbohydrate.

It is important to remember that although some averages are not statistically significant, an improvement of for example 4% during the last 42km of a triathlon would equate to a 6min 36sek improvement in a goal time of 2h 40 min.

Although many studies show only small or no performance improvements, not many studies show an obvious decrease in performance.

In 1989 Kathleen O’Keefe and colleagues had seven highly trained female cyclists follow a low carbohydrate diet (13% carbs), a medium carbohydrate diet (54% carbs) or a high carbohydrate diet (72% carbs). The diets were isocaloric and followed for one week. After each week the subjects exercised at 80% VO2max to fatigue. Average time to fatigue was 60min for low carb, 98min for medium carb and 113min for high carb. Thus a low carb diet in this case caused a marked decrease in exercise performance. However, mark the 1 week intervention.

In 1999 Julia H. Goedecke and colleagues tested a 15 day HFD period in 16 endurance trained cyclists. They were randomly assigned to control diet (30% fat) or HFD (69% fat). The cyclists were tested on a 2.5hour constant load ride at 63% VO2max followed by a 40km time-trial. 90min before each trial subjects consumed 400ml 4.3% MCT solution. At the start of the trial the same solution was ingested containing 10% glucose. Thereafter 200ml of the glucose+MCT was consumed every 20 min until 40 min into the time-trial. 40km time trial went from 69.9 min to 65.6min in the control diet (-3.3min) and from 69.3 to 63.4min in the HFD group (-5.9min) indicating an advantage of HFD.

Several studies have examined the effects of HFD periods followed by carbohydrate loading on performance. One of these studies was performed by Burke and coworkers. The strategy was 5days HFD followed by 1 day high carb. Average time trial time was 8% faster with this strategy compared to constant high carb. More interesting is the observation that the increased performance was mostly due to two participants who improved greatly following the HFD. The same subjects showed symptoms of severe fatigue and hypoglycemia toward the end of testing on high carb diet.

This observation might indicate that HFD can be especially effective in individuals who may experience hypoglycemia during prolonged activity where carbohydrates are not ingested during exercise.

Neither high fat diets, nor high carbohydrate diets, have shown consistent improvements in scientific studies. All in all the results indicate that HFD have a greater positive effect in trained athletes than in untrained.

This was also the finding in a meta-analysis by Erlenbusch and colleagues who concluded that; “…endurance performance is enhanced following a high-carbohydrate diet, compared to a high-fat diet, in untrained individuals, while the performance response in trained individuals appears to be blunted.

But there are major weaknesses with many of the studies if we want to know whether HFD actually work. First of all is the time to adaptation. Often studies are done with less than 4 weeks intervention which is not much time for the body to fully adapt. There are also many other nutritional factors which are little controlled for, e.g. protein intake, vitamin and mineral status and fatty acid composition, carbohydrate type, etc.

Summary
There is little clear evidence of a performance enhancing effect of high fat diets. However, there are too few longitudinal studies to conclude sufficiently and the studies we do have differ in their results. Although the big picture looks inconclusive there exist definite findings of performance enhancement. In addition there is some circumstantial evidence from studies – individual performances, and there are the stories from athletes using the approach.

The studies we have to base our conclusions on are generally not designed to optimize all conditions and are often of too short duration.

There are many nutritional factors beyond macronutrient composition that affects fat oxidation during exercise. The existence of these influencing nutritional factors make it difficult to interpret results, but make it likely that conditions can be optimized and, if so, yield better results than the observed averages in many of the studies. It is natural that any performance enhancing effects of high fat diets are most likely to be seen in long duration sports such as marathon or triathlon. The “train low-race high” strategy, where carbohydrates are used at specific times to enhance performance, is likely a good strategy and also make physiological sense.

The death of a theory


«
If I haven’t seen further than others it’s because giants were standing on my shoulders« – Richard Feinman quoting Hal Abelson quoting his roommate. 

I’ve been reading a fantastic book lately. Lee Smolins “The trouble with physics – The Rise of String Theory, the Fall of a Science, and What Comes Next.” The book is exactly as great as the title sounds, although admittedly, I only understand a fraction of it. Lee Smolin discusses string theory, how is came to be the leading theory in theoretical physics and how it might prove to be one of the greatest dead ends in the history of science. I’m by no means qualified to discuss theoretical physics, but as always when reading science my head draws parallels to my own area of research. String theory, as the leading theory in theoretical physics, does have a lot in common with the leading theory in obesity treatment, the low fat theory.
There is little doubt that the “low fat diet for weight loss” theory is a theory that should have been rejected a long time ago. There are good reasons it should be rejected. It only indirectly addresses the physiological causes of excess fat storage. And because it only indirectly addresses the real problem, it only works temporarily.

«They will devise numerous articulations and ad hoc modifications of their theory in order to eliminate any apparent conflict.» – T. Kuhn

In the near future the low fat theory might be considered one of the greatest blunders in health science. At least, it has the potential to be considered as such. Some theories have been shown to be near immortal and this is definitely one of them.

It is easy to draw parallels between the low fat theory and string theory. String theory is an attempt to unite different aspects of physics, general relativity and quantum mechanics, into one great unifying theory, a complete theory of nature. It is based on simplicity and beauty, but what seems intuitively logic is not necessarily logic at all.

Before Keppler, the planetary orbits were thought to be circular. A circle is beautiful and symmetric and it seemed logic that this was how the planets moved. And yet, observations showed the planetary orbits to be elliptical. The low fat theory is also intuitively logic. Fat contains much more energy than other nutrients of the same weight and excess energy is stored as fat. Thus eating fat in excess makes the body store fat in excess. Fat from foods makes fat in the body. It is simple, beautiful, logic and wrong.

String theory, like the low fat theory, does not have a good track record as far as theories go. It started as a simple theory, and many people think that a theory that incorporates all of physics should be simple. But there were fundamental problems with string theory right from the start. In order to get it to work on paper a lot of dimensions had to be added (the 3 dimensions we are used to, were by far enough), new and unobserved particles were invented and the theory had to be background dependent to work when the whole point was that it should be background independent. It also made few predictions and proved close to impossible to falsify by experiment. A theory has to be falsifiable, because only by opposing repeated attempts of falsification does a theory evolve into truth.

«A nice adaptation of conditions will make almost any hypothesis agree with the phenomena. This will please the imagination, but does not advance our knowledge.» – J. Black

Still, string theory survived. It survived because it was constantly added ad hoc additions and because conditions were constantly changed. Now, this is a normal scientific process. Few theories are perfect when they emerge. The question is, how many conditions can be changed and alterations be made before the theory should be replaced by a new one?

Like the string theory, the low fat theory needs to rest on several assumptions in order to survive. The low fat theory is based on the belief that energy intake and energy expenditure are independent factors. Little scientific data support this, and it is not possible to consider the body to be a closed system. It is also based on the assumption that we can all control our energy intake and expenditure by will. Low fat diets don’t work in the long run. Upon discovering this we can change the theory or consider it faulty. Because it didn’t work, modifications were made; People are lazy, have poor self control, exercise too little and so on. None of these assumptions are justified. They are often not given directly, but disguised by the fact that they are logical consequences of the theory.

Both the low fat and string theory were the leading theories in their field for a long time and in many ways still are. Other theories, even better theories, has constantly been placed in the shadow and were given little financial support. People who worked on alternative theories to string theory were automatically outsiders, low in the field’s hierarchy, just like the researchers working on low carb diets was given less attention than they deserved.

This is painful for many who have invested years and even decades of their working lives in string theory. If it is painful for me, imagine how some of my friends who have staked their whole careers on string theory must feel. Still, even if it hurts like hell, acknowledging the reduction ad absurdum seems a rational and honest response to the situation. It is a response that few people I know have chosen. But it is not one that most string theorists choose.”  – Lee Smolin

Although there’s still some hope for string theory, there is none for the low fat theory. We’ve tried it. It didn’t work. We are getting fatter than ever. Often the scientific standards themselves are reduced in order to keep these gargantuan theories alive. Intentionally or not, the result of this is sometimes the death of science itself and the people considered scientists are no longer scientists in the true definition of the word. The death of a theory is replaced by the death of science.

It doesn’t take an expert
There are usually no sides in science. Sometimes people ask me; what do you believe in/ who do you believe to be right or what dietary method do you teach? The way I see it the only correct answer is that I don’t believe anything. I know what some of the facts are. I can make some calculated guesses on what is less certain, and there is a lot I don’t know. Of course, I cannot actually give this answer. People need substance, and as soon as I mention carbohydrates, I’m on the low carb side. But there are no sides. Science is not a battle between teams, it is a unified search for truth.

The reason that mathematics invented the idea of proof and made it the criterion for belief is that human intuition has so often proved faulty– Lee Smolin 
Basic scientific principles are not difficult to understand and they are independent of scientific subject. When scientific standards are reduced, any lay person can see the faulty logic. Tom Naughton is being accused of writing about things he does not have the authority to write about. But, he does know what he is talking about, much more so than many of the experts in the field. You do not have to be a nutritionist or even a scientist to address the core problems related to basic scientific principles. A beginners mind easily spots the obvious flaws. Diabetes means you can’t handle dietary carbohydrates, yet a doctor may easily tell you to cut fat from your diet after diagnosing you. The doctor’s mind is that of an expert, clouded by experience.

«…insist that we should change the rules of science just to save a theory that has failed to fulfill the expectations we originally had for it. – Lee Smolin


Why aren’t we all fat?

I have noticed that there is one argument used in the nutrition debate that is used by both the low carb and the low fat community (in this context, dividing it into two sides make perfect sense). The same argument keep flying back and forth but I feel it is rarely given the response it deserves.

It goes something like this; “If carbohydrates make us fat, why aren’t all the people of the world, like many Asian people, who live on high rice diets, fat?”

For the record, I am fully aware that the composition of a traditional Asian diets is debated and that a general shortage of food may protect against any harmful effects of a high carb diet. The above argument is a poor argument for another more important reason.

In the low carb world the same argument is used, often in a form resembling the following; “Eating fat cannot make us fat. Because, if fat made us fat, why aren’t all people who live on regular high fat diets, like the Inuit or the Masai fat?”

This argument (and all similar) is easily refuted. Part of the reason these arguments are fallacious is that they rely on an unstated assumption, an assumption we cannot make. A causal factor may affect us differently and may only end up in full blown disease in predisposed individuals. We are not genetic copies. If we were all clones, finding causal factors would be so much easier (there is a reason twins make for popular study subjects). But we’re not. We respond differently to the same stimuli and only by being clones would we all be able to react similarly.

Smokers have a greatly increased risk of lung cancer, yet many smokers smoke their way through long lives with no cancer.

Still, the causal factor is still the causal factor. Insulin and glucose drive fat storage in all of us. Some of us however have counter regulatory mechanisms that may overpower the fat storing effects causing us to remain lean. The above arguments rest on the assumption that we are genetic copies. We’re not.

Ok, I realize the clone analogy is stretching it a bit. After all, as members of the same species we are very similar and we may easily all respond similarly to the same stimuli. But the truth is that the arguments do rest on the assumption that we will respond in the same way and the danger is that the assumption will be used to discard a theory when responses differ.

In some studies of low carb diets the results have been less than expected. My experience is that many of these studies are also easily criticized, but that doesn’t really matter. It also doesn’t matter that studies using body weight may not detect large alterations in body composition. What matters is that the cause for a disease does not necessarily make everybody exposed to the causative agent, sick. Carbohydrates may easily be the main cause of excess fat accumulation in fat cells even if not everybody who eats great amounts of carbs gets fat. We cannot simply reject a theory that points to carbohydrates as the main cause of overweight just because there are people who don’t get fat in the face of plentiful carbohydrates.

«If any and every failure to fit were ground for theory rejection, all theories ought to be rejected at all times.» – T. Kuhn 

Imagine a disease spreading through society and everything points to a virus as a cause. Then some people argument that the virus cannot be the cause of the disease, simply because there are people being exposed that does not get sick. It makes no sense.

On a similar note, the fact that you can lose weight by starving yourself (eating less energy) does not in any way contradict a theory pointing to carbohydrate as the causative agent.

The simple and undeniable fact is that many high quality studies of low carb diets have illustrated the diets efficiency in reducing weight. It makes perfect physiological sense and even evolutionary perspectives support it. These results cannot be rejected simply because someone loses weight by eating less energy. The results still stand. Getting them to fit with results from energy restriction studies is a matter of physiology, not theoretical science.

So, although carbohydrate restriction does not always give the expected positive results, this is not ground for theory rejection. On the other hand, when low fat diets have never given the long term results the theory predicts, this is ground for rejection. Treating overweigh people with low fat diets is a prime example of treating a symptom, the fat stores, rather than treating the cause of the fat storage. Because this is a strategy focusing on a symptom is will not work long term. Science supports this. Low fat diets simply do not work long term. We must reject the theory and try something else.

Is there a chance that such observations have already been made but ignored because, if confirmed, they would be inconvenient for our theorizing?” – Lee Smolin