In a contest among phrases that are both commonly spoken but overtly flawed, “you are what you eat” is a sure winner.  In our combined 6 decades of experience in academic nutrition, incessantly we’ve heard this sound-bite used to deter people from eating foods containing fats and cholesterol.  And perhaps most interestingly, it seems no amount of logic can lead its users into the light.

With just a little bit of thought, perhaps you can perceive our problem with this.  Let’s take the example of a highly trained male distance runner who eats a 60% carbohydrate, 20% fat diet.   If he is what he ate, his body should contain more carbohydrate than fat.  If our runner weighs 145 pounds and has about 10% body fat, however, his body energy stores translate into 50,000 kilocalories (kcal) of fat and perhaps 2000 kcal of carbohydrate (glucose and glycogen).  Putting it another way, if you are what you eat, how does eating three times more carb than fat translate into having1/25th as much carbohydrate as fat in the body’s fuel reserves?  The answer, of course, is that on a high carbohydrate diet, the high blood insulin levels it induces promote carbohydrate oxidation – carbohydrates are rapidly oxidized to carbon dioxide and water (at least in an insulin-sensitive athlete).

Now let’s go to the other end of the dietary spectrum – to the aboriginal diet of the Arctic Inuit or the nomadic Native Americans of the Great Plains.  If we give our hypothetical runner a diet that is 5% carbohydrate and 75% fat (neither of these cultures over-indulged in protein) and allow him/her to eat to satiety for a month, what becomes of body fuel stores?  Surprisingly, total body glycogen reserves are only reduced by half to about 1000 kcal, whereas body fat content will typically either stay the same or decline somewhat (i.e., 40,000 – 50,000 kcal).

How can this possibly be true?  Of course if you eat mostly rice, your body doesn’t become a big blob of starch.  But what most people don’t realize is that if you eat mostly fat, neither do you automatically turn into a dollop of butter.  What’s happening here is that the remarkable adaptability of human metabolism adjusts the body’s fuel flow to burn the available fuel.  When dietary carbohydrate intake is low, insulin levels fall even lower than the initially low values typically found in highly trained athletes.  The rise in fat oxidation in response to decreased insulin is a steep curve (see Figure), so even a modest drop in insulin in this range can dramatically enhance the body’s capacity for fat oxidation.

While we have presented this here as a thought experiment, in truth this is a study we first did 3 decades ago (1,2)   In that study, bicycle racers were tested before and after a month of adaptation to an Inuit-type diet.  Neither body composition nor aerobic performance changed significantly after a month of eating upwards of 80% of their energy as fat.  Muscle glycogen was reduced by half, but its rate of use during exercise fell by 75%.  What changed dramatically was their bodies’ ability to burn fat.  During exercise at over 900 kcal per hour, their fat oxidation doubled from about 45 grams per hour on a high carb diet to 90 grams per hour after a month adapting to the Inuit diet.  Thus this adaptation allowed these highly trained athletes to power about 85% of their work output from fat.

We have named this process keto-adaptation, because to get insulin low enough to unleash fat as a performance fuel, the body shifts into nutritional ketosis.  In this clinically benign state, blood glucose is mostly replaced by circulating fatty acids and ketones to fuel the muscles and brain, respectively.  And please don’t make the unfortunately common mistake of confusing nutritional ketosis (in which blood ketones are regulated by low levels of insulin) with ketoacidosis, in which ketones are unregulated in the complete absence of insulin.  In ketoacidosis, ketones are typically 10-times higher than in nutritional ketosis.

Our primary point here is that the body’s metabolism in a healthy human is remarkably adaptable, allowing humans to eat a high fat diet without accumulating excess body fat.  In a way, this is similar to a healthy body’s tolerance of a very high carbohydrate diet without accumulating excessive amounts of glycogen in muscles and liver.

We know that in just these few paragraphs we’ve assaulted some of nutrition’s most treasured icons, as well as the results of many well done research studies.  There are, for example, all of those classic studies (3,4) demonstrating that a high carb diet supported better sports performance than one low in carbohydrate.  But upon careful  review, you will find that these studies were all of less than 2 weeks duration, whereas keto-adaptation requires at least 4-6 weeks of sustained nutritional ketosis while following a well-formulated low carb diet.  The simple analogy is that you can’t enjoy a Hawaiian vacation if you are afraid to fly your plane more than half way there.  Furthermore, many published ‘low carbohydrate diet studies’ were not “well-formulated” – a term that encompasses a range of issues discussed in our recent book ‘The Art and Science of Low Carbohydrate Living’.

But then there’s the common concern that high fat, low carb diets lead to the accumulation of saturated fats and cholesterol in the body, and logically from there to heart disease or stroke.  Please trust us that this is not an issue that we take lightly.  Because both of us have been consuming ketogenic diets for a decade or longer, there’s more than a bit of personal well-being at stake here.  Thus you won’t be surprised that we have been studying the effects of low carbohydrate diets on blood lipids and fatty acids for about twice that long.  Rather than bore you with all of this research, suffice it to say that you are not what you eat.  You are what you save from what you eat.  In the context of a well-formulated low carbohydrate diet, saturated fats become the body’s preferred fuel and thus get burned rather than stored.  Similarly, cholesterol has many fates in the body, and in the keto-adapted state, cholesterol is shunted into the beneficial blood lipids (the so called ‘good cholesterol’) independent of its content in the diet.

So what’s our key point here?  The metabolic fates of fat and cholesterol are very complex, and they are remarkably altered for the better when sugars and refined carbohydrates are restricted and the body given an adequate time to adapt.  Once we embrace this complexity, the science of nutrition will take a giant step forward.

Work cited

1. Phinney SD, Bistrian BR, Evans WJ, Gervino E, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation. Metabolism. 1983 Aug;32(8):769-76.
2. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism. 1983 Aug;32(8):757-68.
3. Christensen EH, Hansen O. Arbeitsf’~ihigkeit und Ern~ihrung. Skand. Arch. Physiol. 1939 81, 160-172.
4. Bergström J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol Scand. 1967 Oct-Nov;71(2):140-50.
5. Volek JS, Phinney SD. The Art and Science of Low Carbohydrate Living.  www.amazon.com/Art-Science-Low-Carbohydrate-Living/dp/0983490708/