Do High-fat Diets inhibit Load-Induced Muscle Hypertrophy in Humans?

By Matt Lalonde

To the uninitiated, making sense of the vast and ever-expanding nutrition literature may appear to be an incredibly daunting, if not impossible, task. Where does one start and what is the best way to identify legitimate research? Having a scientific background certainly helps but I’d argue that, with sufficient determination, any individual could sift through papers in the field of nutrition and make sense of the mayhem. I thought I would offer a few tips by answering George’s question:

Hi Robb –

I’ve subscribed to an email newsletter put out by Dr. Gabe Mirkin for years. Dr. Mirkin is an MD and endurance athlete (a competitive 71 year-old bicyclist). He writes a lot about sports nutrition, and I’ve found that his advice generally runs about 180 degrees from yours. Below is a snippet from today’s email where he cites a new study that shows that a high-carb low-fat diet provides better muscle growth than a low-carb high-fat diet. I’d love to hear your take.




Dr. Gabe Mirkin’s Fitness and Health E-Zine? January 24, 2010

Obesity and High-Fat Diet May Both Prevent Muscle Growth

A study from the University of California, Davis shows? that a high-fat diet prevents exercising mice from enlarging their? muscles (Journal of Physiology, December 2010). The mice ?received either a low fat, high carbohydrate diet or a high fat,? low carbohydrate diet for 14 weeks. Each group was divided into? those who performed progressive resistance exercises with their? plantaris muscles or those that did not do this exercise.? Those who exercised on the low fat, high-carbohydrate diet had? substantially larger muscles than those who exercised on the? high-fat diet. Chemical analysis of their muscles showed that the ?high fat diet group had lower levels of polysomes (Akt and S6K1)? necessary for making protein.? If this study can be applied to humans, it will mean that ?not only does a high-saturated-fat diet make you fatter, it also? keeps you from enlarging your muscles. We know that both full fat? cells and eating large amounts of saturated fats (the dominant fat? in meat) turns on your immunity to cause inflammation that can ?prevent the body from making protein necessary for enlarging? muscles. (Journal of Nutrition, January 2009). A high saturated-fat? diet also blocks insulin receptors and thus prevents your body from? responding to insulin, which is necessary for muscles to heal from ?intense workouts. Insulin drives amino acids, the protein building? blocks, into muscles to help them heal faster. Anything that blocks? muscles’ ability to respond to insulin will decrease amino acid? entry into muscles and thus delay healing so you can’t recover as? fast for your next workout. Further journal references and? recommendations can be found at

The study in question is “Chronic High Fat Feeding Attenuates Load-Induced Hypertrophy in Mice” M. Sitnick, S. C. Bodine, J. C. Rutledge J. Physiol 2009, 587(23), 5753–5765. The first thing to do when evaluating research is to download the full paper and carefully read in its entirety. This may sound obvious but most people make the mistake of focusing exclusively on the abstract, or worse yet, on the conclusion. Details that may make or break a paper can be found anywhere in the body of the text. I particularly like to scrutinize the methods section (a.k.a. procedures, experimental details, or supporting information). I always ask myself the following questions when attempting to assess the legitimacy of nutrition research: a) Was this a controlled trial or an observational study (epidemiological, cohort, and prospective studies are similar in nature to observational studies)? b) Was the research performed on human subjects? c) What are the sources of funding for this research and do the authors have any conflicts of interest or specific agendas that could bias the study’s outcome? Getting answers to these questions will save you a lot of time.

I tend to ignore anything that is an observational, epidemiological, cohort, or prospective study because they can only establish correlation between monitored variables, not causation. I’m not going to elaborate any further on the subject. Instead, I’ll refer readers to an excellent post by Dr. Eades that highlights the shortcomings of observational studies.

Controlled trials are typically more reliable than observational studies. These trials attempt to establish cause and effect by performing experiments where specific variables are isolated and manipulated while others are kept constant. The caveat here is that, in a living system, changing only one variable while keeping the others constant is nearly impossible. As such, there is a very real possibility that the observed experimental outcome is the result of manipulating an unknown variable that is dependent on the variables that were controlled.

The study by Sitnick and coworkers is in fact a controlled trial. The researchers acquired 5-week-old male mice and put them on a low-fat diet for 2 weeks (10% fat). After two weeks, the animals were randomly assigned either to a high-fat diet (HFD, 45% fat) or a low-fat diet (LFD, 10% fat). After a period of 14 weeks on the diets, the mice were randomly assigned either to a sedentary group or a functional overload group until the end of the study. Contrary to Dr. Mirkin’s impression, the mice were not separated into sedentary and exercise groups. Mice can’t perform back squats and deadlifts, so the researchers induced mechanical overloaded in the animals’ plantaris muscles by surgically ablating the soleus and gastrocnemius muscles. I’m not kidding, here is the procedure as described by the authors:

Briefly, mice were anaesthetized with 2–4% isoflurane, and using aseptic surgical procedures, an incision was made to the lower hind limb exposing the ankle extensor muscle complex. The soleus and one-third of the lower medial and lateral gastrocnemius were carefully removed with particular attention to preserving the neural and vascular supply to the plantaris muscle. The incision site was irrigated with sterile saline and closed using subcuticular sutures. This procedure was performed on both hind limbs. At 3, 7, 14 and 30 days post surgery, animals were anaesthetized with 2–4% isoflurane and the plantaris muscles were excised, weighed and flash frozen in liquid nitrogen.”

There is plenty of material to delve into here but let’s start with the diets. Click on these links to see the composition of the high-fat and low-fat diets. The caloric breakdown for the high-fat diet is 20% protein, 35% carbohydrate, and 45% fat. The carbohydrate content of the HFD is too high for it to be considered a ketogenic diet (where 10% of calories from carbohydrate is typically the norm). This is just a detail; let’s continue with our analysis.

The protein source in both the HFD and LFD is casein (200g), which is supplemented by a minute amount of L-cystine (3g). Incidentally, casein is the most problematic protein fraction in milk with regards to the leaky gut syndrome and autoimmune diseases.

Half of the carbohydrate content of both diets is table sugar (a source of glucose and fructose) whereas the rest is derived from cornstarch and maltodextrin 10 (sources of glucose). Vitamins and a few other goodies are thrown in the mix to make sure the mice don’t die prematurely while on this wholly inadequate diet.

Things get interesting when we look at the fat sources. In the HFD, 177.5 grams of fat come from lard and 25 grams from soybean oil. On the other hand, the LFD contains 25 grams of fat from soybean oil and 20 grams from lard.

Now the fun part. Here is what happened to the mice on the HFD:

At the end of the experiment, the control HFD mice were 31% heavier than the LFD mice (Fig. 1 and Table 1). Furthermore, following 14 weeks on the high fat diet, mice were hyperinsulinaemic, having a 7.6-fold increase in fasting insulin levels relative to LFD mice (Table 1).”


“In both LFD and HFD mice, functional overload led to a significant increase in plantaris mass at all time points studied (Fig. 2); however, significant differences were noted in the absolute growth response between mice in the two diet groups at 14 and 30 days. At 7 days the growth response of the LFD mice (mean LFD – mean HFD/mean LFD°—100) was8%greater (P >0.05) relative to the HFD mice and increased to a significant difference of 10 and16% (P <0.05) at 14 and 30 days, respectively. At 30 days of FO, the relative difference between control and overloaded muscles (mean FO/mean control) was 2.1- and 1.7-fold in the LFD and HFD mice, respectively. These data reveal that diet-induced obesity resulted in a significant impairment in the response of skeletal muscle to increased mechanical loading.”

So the mice on the HFD developed symptoms of metabolic syndrome and their plantaris muscles showed less hypertrophy compared to those of the mice on the LFD. And this is in spite of the fact that the HFD mice were heavier. Now that must be telling us that fat is really bad right? Wrong!

Stephan Guyenet recently pointed out that the symptoms of metabolic syndrome observed in rodents fed a high-fat diet are actually due to an omega-6 : omega-3 imbalance caused by the low omega-3 and/or high omega 6 content of the fat sources employed in the studies. This is a perfect example of how controlled trials can reach erroneous conclusions by inadvertently manipulating variables that were not taken into consideration. Unbeknownst to the researchers, modifications in the amount of saturated fat consumed by the rodents changed the omega-6 : omega-3 balance of the diet, which increased inflammation (1).

There are a few other things to consider here. First, mice consume mostly plants (leaves, roots, seeds, stems) and insects in the wild and most likely did not evolve while consuming large quantities of fat, let alone lard. As such, it seems appropriate to assume that mice are not adapted to a high-fat diet. Second, regardless of the diet, how can we possibly assume that an experiment involving mice who’s muscles were artificially loaded can tell us anything about the ideal dietary requirements for lean muscle mass gains in human beings? Seriously!? This may seem obvious to most folks but it is important to underscore the fact that the conclusions of scientific research are only relevant within the specific context under which the experiments were conducted. In this case, the findings of the study only apply to mice. For this reason, I tend to ignore studies that were not conducted on human subjects. I acknowledge the fact that there are many gene sequences that are conserved between humans and mice (as well as other mammals and other species). I don’t consider studies that are performed on mice (or other species) to be completely useless. Like observational studies, they are useful for testing and generating new hypotheses. Nevertheless, I don’t consider the results of these studies to be applicable to human beings until the hypotheses have been specifically tested in human beings (2). When scientists extrapolate the findings of a study to another species, as in “this may apply to humans”, they are either speculating or generating a new hypothesis that will need to be validated with further research (on human subjects). Dr. Mirkin did highlight this fact in his newsletter when he wrote, “If this study can be applied to humans”. Unfortunately, the remainder of Dr. Mirkin’s newsletter is written in a fashion that gives the reader the impression that the outcome of the study does apply to humans. Dr. Mirkin proceeds to reference more flawed research to support his belief that consumption of saturated fat is detrimental to human health. The tone of Dr. Mirkin’s newsletter, as well as the fact that his advice runs counter to Robb’s (according to George), indicate that he is biased toward low-fat diets. He even comments that “high-saturated-fat diet make you fatter”. I would recommend that Dr. Mirkin read Gary Taubes’ Good Calories Bad Calories for an alternative interpretation of the research on the subject. It appears as though the diet-heart hypothesis is on its death bed and that the weight of the evidence is making prominent researchers reconsider their lipophobic stances (see Whole Health Source Blog here and here).

In the end, my take on this study is very different than Dr. Mirkin’s. I don’t think the outcome of the Sitnick study is at all relevant to human beings. Aside from the fact that mice were used as subjects, there exists the possibility that the high-fat diet induced obesity and metabolic syndrome through an omega-6 : omega-3 imbalance. As such, saturated fat itself may not be detrimental to the health of rodents. Even if we were to assume that the saturated fat itself was responsible for the obesity and symptoms of metabolic syndrome observed in the mice, would that give us any insight into the effect of saturated fat on the metabolism of human beings (a species that evolved while consuming some saturated fat)? Absolutely not!

It is interesting to look at the conclusion of the study:

“The present study represents the first investigation to show that diet-induced obesity has a negative impact on the ability of skeletal muscle to adapt to growth signals such as mechanical loading. A decrease in the ability of muscle to respond to growth signals could adversely affect glucose homeostasis, as well as prevent recovery from injuries and accelerate the effects of ageing. Additional studies are required to investigate the mechanisms by which obesity interferes with the response of skeletal muscle to growth stimuli.”

Note the use of the words “diet-induced obesity” instead of “high-fat diet-induced obesity” or “saturated fat-induced obesity”. This correctly states that the obesity was induced by the diet but leaves open the question as to what exactly caused it and the metabolic disorder.

Ultimately I do understand why the researchers performed the study with mice as opposed to humans. An equivalent study with human subjects would have required real food, dieticians, coaches, accurate methods for determining increases in lean muscle mass in living subjects, and would be prohibitively expensive.

My personal experiment of one tells me that a ketogenic diet is excellent for gaining lean muscle mass while avoiding gains in fat mass (I have now gained a total of 15 pounds of lean muscle mass). I readily acknowledge that a ketogenic diet might not be ideal for everyone seeking to gain muscle mass and that my experiment of n=1 has little to no scientific value. Then again, ketogenic diets have been shown to improve insulin sensitivity in human beings and Dr. Mirkin acknowledges the importance of insulin sensitivity in muscle repair and recovery. It’s almost as if personal experience that is guided by legitimate scientific research trumps the nutritional advice offered by mice. Go figure.

(1) The high- and low-fat diets in the Sitnick study provided equal amounts of soybean oil. As such, we would have to assume that the lard originated from grain-fed pigs and contained a significant amount of omega-6 fatty acids as a result.

(2) Interesting side note; beta-lactam antibiotics are toxic to guinea pigs. We would have seriously missed out if we had initially tested these antibiotics on guinea pigs instead of humans.

Categories: Paleo/Low Carb


Robb Wolf’s 30 Day Paleo Transformation

Have you heard about the Paleo diet and were curious about how to get started? Or maybe you’ve been trying Paleo for a while but have questions or aren’t sure what the right exercise program is for you? Or maybe you just want a 30-day meal plan and shopping list to make things easier? Then Robb Wolf’s 30 Day Paleo Transformation is for you.


  1. Jason says

    This is a hellva post. I gonna need to take small bites of it just to digest it all.

    @Robb your gonna generate a ton of new podcast questions with this one. :)

  2. Harold says


    This is a very nice post, thank you. As a statistician, I am very pleased to see your primer on how to interpret scientific results. Too often observational studies sway opinions. Though observations can be very good, perceived success can also come from what we call a confounding variable–some other uncontrolled variable in the experiment that contributed to the outcome.

    OK, I have a question that this post alludes to, and I have been thinking about and personally experimenting with for a long time. You may well have answered this previously, but I haven’t seen it. Apologies in advance if that is the case. I have just enough info about this stuff to constantly confuse myself. Any clarification is appreciated.

    My understanding is that fat converts to energy when we are working in the oxidative pathway. This is good to know if you’re an endurance athlete or even if you’re doing longish WODs, like Murph, Hansen, etc.

    However, much of the work a typical crossfit athlete does is within the glycolytic path, in which case we rely on higher glycogen stores and less on fat since glucose doesn’t need the same amount of oxygen to convert into energy.

    So, things like Fran, Helen, or sub 15 minute WODs (approximately) require us to put different things in our bodies to power through those quickly.

    Now, crossfit totally randomizes the WODs, and this isn’t something I agree with, for lots of reasons. I like some randomness, but within a clear structure. One of the reasons more structure makes sense, IMHO, is because you can tailor your nutrition to match the kind of work you are doing. So, when a cyclist is doing his speed work for the month, he can modify his nutritional plan to match his energy needs. OTOH, when he is doing his long rides for endurance, he can change food intake to match this phase. Most sports periodize in some fashion, and within a periodization phase, you can align nutrition to match the work output of the athlete.

    I have done a few things in the past two years. I have gone almost ketogenic with prescribed zone levels of fat. This was the worst I ever felt. I dropped a significant amount of weight and I lost energy. People were often asking me if I was OK. I was unfocused at work too.

    I have done high fat with very low carbs (but more than needed to be ketogenic). In this phase, I did well with strength WODs and even set a few PRs. But, when it came to met-con work, I plummeted, badly.

    Now, I am doing a high fat and “sufficient” carb diet. I am making up my own definition of sufficient. I am basically just trying to find the right amount of carbs to bring in to support the glycolytic path work I do. So, I’m just tweaking and trying to bring in enough to power through a WOD, recover, and do it again.

    So, to preface my question, my personal experience has been that high fat, very low carbs don’t seem to match the work capacity needs of a crossfit athlete when much of that work is in the glycolytic phase. OK, here is my question?

    1) If fat converts to energy when performing in the oxidative phase, and most crossfit-related activities are in the glycolytic phase, does a ketogenic diet make sense for a crossfit athlete?

    2) If my “sufficient” carb hypothesis is about right, do you have any sense of what sufficient might mean? I see so many numbers for athletes my head turns. I see anywhere from 5 grams to 15 grams per pound of bodyweight depending on the length of physical activity.

    This is really hard stuff to understand, Robb. So, any reactions are appreciated.

  3. says

    Oh, Dr.Mirkin…Mark Rippetoe mentions Dr.Mirkin’s website in his article “Silly Bullshit.” Mirkin also believes that exercise can’t strengthen a muscle, because if it could, long distance runners would be the strongest athletes.

    Oh Dr.Mirkin…

  4. Ryan says


    Great post. I read that ketogenic diets might increase the risk of developing kidney stones? If this is the case, do you recommend any (i.e. potassium citrate) supplements to reduce the risk?



  5. says

    Hi Mat and Robb,

    First of all, I’d like to say that I’m really enjoying what you guys are puttin’ down! Mat, I attended the 1st Crossfit Nutritional Cert you gave with Bobbi in Albany last year….learned a lot, and you confirmed much of my own findings, as well.
    This post is another gem…Speaking for both my clients, and myself- thank you. Keep on spreading the Low Carb Paleo Diet gospel!

    Be Well,


  6. Steve says


    One thing I was kind of disappointed in with Cordain’s books (PD and PDfA) is that a significant portion of them are dedicated to n=1 observational studies/claims instead of delving into the nitty gritty real research.

    This seems to be true of a lot of fad diet books, and it is frustrating that Cordain’s books seem to follow the same pattern. I realize these books have to appeal to a large audience, but what of the skeptics, who have seen these arguments over and over again from various books, all claiming a bunch of stuff that may or may not be true…

    All that said, so far my experience on Paleo has been a positive one. The science of it one way or another notwithstanding, at the end of the day, if it works for me, I’ll be happy.

    • says

      that’s a tough gig. If you hammer folks with studies it;s easy to lose them. These anecdotal stories are very easy for folks to relate to. And the reality is we only have a few legit, metabolic ward type studies looking at a “paleo” diet. They are very favorable but not a lot to go on from that angle. I’ll warn you now, my book will not be dissimilar in this regard but I am well aware of what you are describing. And like you said, so long as it helps people…

  7. A says

    Mat, nice breakdown. While I don’t agree with your pov wrt epidemiology (I think a lot of hypotheses into potential biochemical mechanisms germinate in the findings of nutritional epi studies), I am amused by the conclusions the good doctor reaches as well. You’re right: the title and the abstract completely throw the casual observer off course. It’s curious that the researchers can only speculate about the role of dietary fat in the response – and I wonder if they would have observed the same results in obese rats whose obesity was induced via a hypercaloric (but not necessarily “high fat”) diet. Attributing the results they saw to the macro composition of the diet as opposed to, perhaps, obesity itself may be misleading.

  8. says

    I don’t know I recon you could extrapolate this study to humans. The “high fat diet” fed to the mice was 20% protein, 35% carbohydrate, and 45% fat. That looks to me like a high fat AND high carbohydrate diet mislabeled as simply “high fat”.

    If for example my daily intake was around 2,800 calories, 35% of that as carbs would equate to 980 calories from carbs or 245g. That’s about 5 times more than someone on a low carb, solid amount of fat, paleo type diet would get.

    The conclusion? If humans eat a lot of high-carb high-fat foods (think fast food, and so forth) they tend to get fat. Wow, thanks science! Ground breaking stuff!


  9. Mike says

    I know when I first switched over to paleo, it was pretty low carb, probably ketogenic or close to it most of the time. Within about a month or so, people started asking me what I was doing and saying I looked like I lost about 15 lbs… yet I weighed the same the whole time, so I must have added lean mass in the process.

    Also when I think back to my early days getting into fitness stuff & weight training, I put on muscle much faster when I wasn’t worrying about what I then thought was a “healthy low fat diet.”

    Another n=1 experiment, but it seems there are a lot of them pointing to the same conclusion.
    Nice writeup Mat!

  10. Jamie@CFA says

    make that n=2 Mat… up 11 pounds, no increase in body fat… deadlift up 20lbs, backsquat up 15lbs, over 11 weeks.. previously I carried the same 1rm on deadlift for over a year

  11. Jay says

    Hey Robb,
    In one of your podcats could you please look at the notion of exercising for health versus exercising for performance? I’ve been reading a lot of stuff on paleolithic or evolutionary fitness and it would seem to me that sometimes performance and health cannot occupy the same space. Specifically I would really like to know if CrossFit is too intense over the long term for health and longevity and if it is, what better programming for health/longevity might look like? I enjoy that CrossFit increases my work capacity and is functional (I am not sure how bicep curls continually make it into the Evolutionary Fitness theory when they too decry functionality), but is there a point where your work capacity (and the training to keep it there) becomes so high it affects your health/longevity? Sorry for the convoluted question but this is one that has been bugging me for awhile.

  12. says

    Given the amount of metabolic derangement present in the “average” American is it possible to get any conclusive evidence from a study which uses “average” Americans as test subjects? It seems like the inconsistencies in biological behavior brought on by the myriad of conditions created by the western diet would create uncertainty in the results of any experiment. Maybe researchers could attempt to remove these abnormalities by using a normalized (read fit) group like say paleo-eating crossfitters?

  13. Steve says


    I think its great your explaining how people can attempt to sift through literature and come up with their own logical conclusions for particular studies.

    One point I wanted to make is with the assertion observational studies are similar to epidemiological, cohort and prospective studies. As an epidemiologist I was trained to understand and construct a variety of studies including the ones just mentioned. I wanted to add that there are stark differences in the information that can be collected with this studies and to think of them as similar is not entirely correct.

    An excellent reference detailing all aspects of epidemiology is A Dictionary of Epidemiology. 4th ed by John M. Last. It gives a good, though not an in depth, discussion of all things related to epidemiology. In there, as well as my training in school, it is discussed that RCTs are also epidemiological studies. I do not want to go into the history of epidemiology here it just seems a broad brush was used to dismiss epidemiology studies when its application provides very useful information…

  14. Brad says

    At first, I though that study was some kind of joke. Then I read the entire paper.. now I know it was a joke. What a f-ing joke. Kick his ass Robb.

  15. Preston says

    Now THAT is how to take apart a paper. Thanks for modeling how to do this. I find that most people either aren’t willing to put in a little time/effort to go through the details of the experimental setup or they just glaze over because they’ve never learned how to read/analyze scientific papers. Someone should start a blog or seminar teaching lay people how to really scrutinize experiments and evaluate their conclusions.

    I find that everytime one of these studies that ‘proves’ the superiority of high-carb/low-fat is cited, I only need to go to the methods/techniques section and look at the feeding protocol to realize the whole thing is bogus. For simplicity and cost sake, they usually use MICE and feed them CRAP.

    I’m still going through Krauss’ recent paper on sat. fat and CVD:
    Any thoughts on this one?

  16. Mathieu Lalonde says


    I am only pointing out that the studies are similar with respect to the fact that they can’t establish cause and effect. Some regression (both ways) and Monte Carlo analyses will give you a better chance at correctly identifying the cause but it doesn’t change the fact that the studies cannot establish causation with certainte. With regards to randomized controlled trials and nutrition, I do elude to the fact that they are not as solid as controlled trials performed in the field of say chemistry. Too many interdependent variables.

  17. Mathieu Lalonde says


    That is exactly what I was eluding to. Most high-fat diet trials are performed with diets that are 35% carbohydrate. Even if the carbohydrate percentage is lower, the caloric intake is high enough to take the daily dose of carbohydrate upwards of 150g.

  18. Mathieu Lalonde says


    You mentioned that “I think a lot of hypotheses into potential biochemical mechanisms germinate in the findings of nutritional epi studies”.

    I absolutely agree. When I write that “I tend to ignore these studies” what I really mean is that I ignore the press coverage of these studies. The press constantly picks up these types of studies to publish attention grabbing headlines like “Meat causes Cancer”. I do read the studies, however, and keep the correlations in mind while examining the scientific literature.

  19. William Davidson says

    That’s it, it’s official and I’m announcing it to the world.
    I have a massive man-crush on Mr. Lalonde.
    Additionally, count me in the “League of Bullshit Research Evaluation” as one of his proud comrades.

    • says

      Get in line…everyone want’s to hump Mat’s knee. I’m not sure which person my wife would leave me for first, Mat or Ido. I can’t figure out WHY though…I mean Mat’s younger, stronger, smarter and better looking. DAMN YOU MAT LALONDE!!!!

      Ok, I’m fine now…

  20. Mark says

    Hey Mat and Robb,
    Just wondering your thoughts on this. While I know you both prefer pretty low carb approaches to Paleo, do you think it is necessary to go down to ketogenic levels or do you think it would be just as fine to take in about 25% of calories through carbs (or standard zone levels) if they were a mix of veggies and higher glycemic stuff like white rice, sweet potatoes, and corn tortillas. What I’m shooting at is avoiding all wheat and most fruit in favor of some higher GL foods. Knowing what we know about fructose, I would think that it would be better to eat relatively non-nutritious stuff like white rice than to eat fruit. Since the carbs will still be relatively low (compared to other approaches) and they will be measured, do you see harm in this? I just think that there are people out there that like to eat some more carbs instead of subbing fat for them. So pretty much, higher protein (>1g/lb/bdwt), moderate carbs (1g/lb/bdwt)? Matt Stone at 180 Health has seen some pretty impressive postprandial (sp?) blood glucose levels even after eating lots of higher GI foods. His main evils are veggie oils, wheat, and fructose/sugar, not higher carbs. Sorry for the long comment, I appreciate it. Thanks guys.

    • says

      Yea, I think his could work fine, especially for someone who is quite insulin sensitive. I will say this, if I have rice or corn too frequently I start getting some acid reflux. All grains have GI irritating lectins. Folks vary in their responsiveness. I’d still stick with yams, squash and similar carb sources for the most part. Experiment, and try both ways and let me know.

  21. Anthony White says

    Proposal for study:
    The study group will consist of twelve tigers and twelve cows. Tigers and cows will be divided into two groups of six. Six tigers and six cows will then be fed a high carbohydrate, low fat, low protein diet (CHOD) of grasses and other flora. The remaining six tigers and six cows will be fed a fat and protein diet (PFD) consisting of whole, freshly slaughtered animals. In order to maintain the specificity of the test diet, the PFD cows will be kept in a flora-free enclosure. Similarly the grass-fed tigers will be kept separate from the cows.

    The tigers and cows will be observed eating the specified diet for six months, then subject to a battery of tests to determine their health.

    This study will test conclusively whether a high carbohydrate, low protein, low fat diet, or a protein, fat, low carbohydrate diet is optimal for humans.

    Now I just need to rustle up some funding.

  22. Bill says

    Great article. I had read the one by M. Eades, but I think this addresses the B.S. things a little bit better. Mat, have you had muscle hypertrophy in your ongoing experiment? Rippetoe stresses the importance of developing larger levers (mass) to move more weight. Although it seems that a pre-agriculutral lifeway would have favored the lean/mean body type as shown in the whale hunting photo in this post: ( I have definitely experienced strength gains since going high-fat low-cho paleo, but weigh the same as ever, or sometimes less. I also suffer from the SBWTBH Robb Wolf body type. (don’t eat enough?)

    Thanks for all the good stuff!

  23. Mathieu Lalonde says


    I gained 15 pounds and lowered my body fat percentage since starting my low-carb paleo experiment. The hypertrophy was most noticeable in my pecs and triceps (not sure why given that I was doing plenty of squats and deadlifts). There is a funny story to tell here. I walked through my old lab after about 3 months into the low-carb paleo experiment and a former female colleague looked at me and said “whoa! you are bigger than I remember”. At which point I looked down my pants and replied “I not sure how you could you tell but that is what your mom keeps telling me”

  24. Bill says

    Wait…did I even ask a question in there? I guess it would be: Is hypertrophy really desirable as long as your strength is adequate, or in some cases are you only able to achieve your strength goals with some additional hypertrophy?

  25. Rafael says

    ello Robb

    You have some article about the percentage of fat / carb / protein “ideals about gaining muscle mass.

    For I am in doubt, refer to Matt which seems to use a larger amount of carbs, than you

    • says

      If you tolerate the carbs, go for it. I do not have specific numbers other than tinkering to find what you do well on. It could be a selection bias but most of the folks who frequent this site seem to do particularly well on lower carb, but they are NOT shooting for maximum muscle gain either.

  26. says

    Thanks for modeling how to do this. I find that most people either aren’t willing to put in a little time/effort to go through the details of the experimental setup or they just glaze over because they’ve never learned how to read/analyze scientific papers.

  27. Andrew Zacharuk says

    I have had a fair amount of objective experience with muscle gaining on both the typical super high carb bulking diet, and a high-fat low-carb diet. I started trying to gain mass when I was 23 years old and weighed in at 115lbs @ 5’8.

    At the peak of my high-carb bulking I was weighing in at 145-150lbs, but I was packing a pretty decent amount of body fat and glycogen/water weight.

    On a high-fat diet I weigh about 130lbs right now, but without a doubt I have seen my best functional mass and real strength gains while being in ketosis.

    Initially when I dropped the 20ish lbs (I went from almost 150 to 125 after going paleo), I was lifting noticeably less than before, but with a few months of hard work I’m lifting close to what I was before but am still weighing 15lbs less.

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