The Lipophilia Hypothesis: A Technical Explanation
This essay will introduce you to the Lipophilia Hypothesis, a revelatory theory about why people gain weight and how they can lose it. It is far more complicated and technical than the Caloric Balance Hypothesis -- the idea that calories "count" -- but it appears to do a far better job of explaining the real world evidence.
It's been over 4 years since I wrote this article or edited any of the other content you'll find on this site. :]
During this hiatus, I've had the privilege of talking about these concepts with many renowned authorities in the fields of diet and health, including Gary Taubes... as well as many of his critics.
After researching and thinking for four years, I came to a startling revelation about how to simplify the fat loss question. I call this concept "The Black Box."
I explain it all in a free short report, which you can download via the form below. Check it out! It's a legitimately new idea, and a lot of people (including many respected obesity researchers) have found it compelling. Thank you! - Adam
So let's get to it.
For the basics, let's turn to one of Lipophilia's strongest advocates and contributors to the debate over the low carb diet: science journalist Gary Taubes:
"Obesity... is caused by a hormonal phenomenon, specifically by the consumption of refined carbohydrates, starches and sugars, all of which prompt (sooner or later) excessive insulin secretion. Insulin is the primary regulator of fat storage. When insulin levels are elevated, fat accumulates in our body tissue; when they fall, fat is released and we use it for fuel. By stimulating insulin secretion, carbohydrates make us fat; by driving us to accumulate fat, they increase hunger and decrease the energy we expend in metabolism and physical activity. In short, obesity is caused not by overeating or sedentary behavior, but by hormonal malfunctioning triggered by the consumption of particular types of carbohydrate containing foods."
Like the Caloric Balance Hypothesis, the Lipophilia Hypothesis derives from the first law of thermodynamics. This fundamental rule of physics tells us that, for any system (including the body), the following must be true:
Changes in Energy Stored in the Body = Calories In - Calories Out
Most experts believe that the right side of the equation -- the part dealing with "Calories In" and "Calories Out" -- drives the train. But as Taubes points out, this assumption is based on misconceptions.
"The first law of thermodynamics dictates that weight gain... will be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance... there is no arrow of causality in the equation. It is equally possible, without violating this fundamental truth, for a change in energy stores, the left side of the above equation, to be the driving force in cause and effect; some regulatory phenomenon could drive us to gain weight, which would in turn cause a positive energy balance -- and thus overeating and/or sedentary behavior. Either way, the calories in will equal the calories out, as they must, but what is cause in one case is effect in the other... This simple misconception has led to a century of misguided obesity research."
The Lipophilia Hypothesis flips things around. Something drives us to get fat. This defect causes us to overeat and/or makes us inactive. When you fix that problem (for instance, by eating a low carb diet), you lose excess fat. This fixes your appetite and metabolism.
If you're hearing the idea for the first time, this probably sounds like a 'tail wagging the dog' argument.
But wait. It gets weirder.
In order for the theory to work, we must accept that our fat tissue is essentially in business "for itself." Taubes quotes a Vienna geneticist named Julius Bauer, who wrote about this concept way back in 1929:
"Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant women, the abnormal lipophilic [fat loving] tissue seizes on foodstuffs, and even in the case of under nutrition... It maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists: the adipose [fat] tissue lives for itself and does not fit into the precisely regulated management of the whole organism."
So our fat tissue has its own agenda! (Come on, at some level, we all knew something like this had to be true.)
According to Taubes, the Lipophilia Hypothesis was -- prior to World War II -- the preferred hypothesis of leading European clinicians. But after the war, a new guard of diet researchers abandoned the idea. Not because they refuted it, mind you. But because the original research was conducted in Germany and Austria, two countries few people at the time wanted anything to do with, and for good reason.
So how does the theory all work? Unlike the Caloric Balance Hypothesis, which is simple to the point of absurdity ("calories count!"), the Lipophilia Hypothesis gets quite technical. This essay will attempt to present what appear to be most of its key points. If you crave a deeper understanding of how all the pieces fit together, do a close reading of the second half of Taubes' book, Good Calories, Bad Calories.
Here are what appear to be the critical propositions of the Lipophilia Hypothesis, the theory that argues for the low carb diet:
- When we eat carbohydrates (particularly 'simple carbs,' like sugar and flour) our blood sugar levels rise.
- To deal with this sugar, our pancreas secretes the hormone insulin to draw glucose into cells where it can be oxidized for fuel. The more carbohydrates we eat, the more insulin we secrete.
- An array of other factors -- some related to our diet, some entirely unrelated (e.g. medications, genes, natural hormonal shifts, how much sleep we get, etc) can also influence how much insulin we secrete and how our body responds to insulin and blood sugar.
- When insulin drives glucose into the fat cells of our adipose tissue, the sugar gets burned ('oxidized'). This results in the creation of a molecule called alpha glycerol phosphate, also known as 'activated glycerol,' glycerol 3 phosphate dehydrogenase or glycerol phosphate dehydrogenase (GPDH).
- Alpha glycerol phosphate in turn interferes with a key cycle in our fat tissue called the fatty acid / triglyceride cycle. What happens is as follows. Fat comes in essentially two forms: triglycerides (TGs) and fatty acids. Inside our fat cells, triglycerides and fatty acids are in a state of constant flux. It's a biochemical dance. Fatty acids are constantly getting "bound up" into TGs -- which are by definition just 3 fatty acids chemically connected by a glycerol molecule -- and these TGs are simultaneously "falling apart" into their constituent fatty acids. There's a natural equilibrium between TGs and fatty acids. But when you add alpha glycerol phosphate into the mix, it tilts the balance so that more fatty acids get made into TGs and fewer TGs break down into their constituent fatty acids.
- Since triglycerides are bigger than fatty acids, they can't escape our fat cells. So the more the fatty acid / triglyceride cycle gets tweaked by alpha glycerol phosphate, the more triglycerides we'll make inside our fat cells, and the more fat will get stuck in our fat tissue.
- Over time, this process causes our fat tissue to increase in size and thus we get "fatter."
- Once it has been "disregulated," our fat tissue (per Bauer) "maintains its stock... independent of the requirements of the organism." So if we try to starve our fat away, it won't just let us. Instead, it will seek to survive by driving us to be hungry; and if we don't give our fat the calories it craves, it can literally strip energy away from our muscles and organs to maintain itself - it's that powerful. Similarly, if we try to "exercise off" our fat, it will cause us both to get hungry and to slow down our metabolism in order to "maintain its stock." Thus, attempts to lose weight by doing things like starving yourself, working out like a madman, taking drugs to diminish your appetite, and so forth are all doomed to fail.
- The reason we don't accumulate excess fat when we eat protein on a low carb diet is that the byproducts from protein digestion don't have much of an effect on insulin or the fatty acid / triglyceride cycle.
- The reason we don't fatten when we eat fats on a low carb diet -- even saturated fats -- seems to be as follows: When we digest fats, we break them down into both triglycerides and fatty acids. But only the fatty acids can enter the fat tissue. The triglycerides are too big to fit through from the outside. They have to be assembled inside the fat cells in order to get stuck inside. And in order to get triglycerides into the fat tissue (and thus to "get fatter"), you need alpha glycerol phosphate. But in order to have a sufficient amount of alpha glycerol phosphate to mess up the fatty acid / triglyceride cycle enough so that you "get fat," you need a sizable concentration of insulin and blood sugar. That's why, theoretically, one might be able to gorge on saturated fat all day long and not gain weight -- because in order for the fat you eat to be stored in the fat tissue, it needs to be converted into triglycerides inside the fat tissue itself.
- The reason we maintain any fat in our fat tissue at all on a low carb diet is as follows. When carbs are restricted, the body's metabolism changes to be able to convert amino acids (from protein) into sugar. This sugar can in turn enter fat cells to be burnt for fuel, thus creating a modicum of alpha glycerol phosphate, thus allowing us to store some fat.
- If and when we gain too much fat, in order to change our fat tissue back to normal (i.e. to "lose weight"), we should not try consuming fewer calories and/or burning off "excess" calories via exercise, since doing so does nothing to fix the underlying metabolic defect or defects. This is why almost all diets that advise you to "eat less and exercise more" ultimately fail and, conversely, why the low carb diet seems to be uniquely effective.
- If people DO lose weight on calorie restricted diets, chances are the weight loss could easily be attributable to the fact that the low calorie diet is often a low carb diet in disguise. After all, most of the calories we eat -- and thus most of the calories we end up restricting on a low calorie diet -- come from carbohydrates (Note: this link tells us that we're eating less fat than we were before the obesity epidemic and more calories - all the "excess" calories are from carbohydrates. This makes sense. After all, the "empty calories" in most junk foods are just simple carbs by another name.)
- A better way to address the problem of excess fat accumulation is to identify and repair the metabolic defect or defects causing the disregulation of the fat tissue.
- For most people the best diets to do this involve carbohydrate restriction. A low carb diet works because, when we cut carbs, we reduce insulin secretion; thus reducing the amount of glucose that enters our fat tissue; thus reducing the concentration of alpha glycerol phosphate in our fat cells; thus allowing the cycling of fatty acids and triglycerides to normalize; thus allowing excess triglycerides to break up and escape our fat tissue as free fatty acids; thus allowing our muscles to burn fatty acids instead of glucose; thus allowing us to lose excess fat and get thinner.
- But even a low carb diet can fail because theoretically anything that messes up your fat tissue metabolism can cause you to gain or lose weight. Sure enough, as we'll explore, a plethora of non-dietary factors seem to be able to do this, including: medications, hormones, diseases, brain injuries, insomnia and so on.
So the Lipophilia Hypothesis is not as simple and clean as 'eat less and exercise more.' But the explanatory power of this theory about the low carb diet is revelatory. As we will show in the upcoming pages, the Lipophilia Hypothesis blows away the Caloric Balance Hypothesis whenever you look at evidence in real life -- whether you're looking at diet studies, epidemiological data, or even personal experience. As the adage goes, an explanation should be as simple as possible, but no simpler.
Now obviously, this site's authors are not doctors, researchers, or nutritionists, and it's fairly likely that this simplification of low carb diet science has left out/mangled key points. To really get a handle on this theory, read the relevant pages of Good Calories, Bad Calories. As far as the site's authors know, Taubes' explanation is the most comprehensive.
That being said, it's not like Taubes invented these ideas; he merely aggregated a lot of the research and helped put some of the pieces together. But you can find a lot of the "pieces" elsewhere. For instance, want to know more about how/why insulin makes us fat and other key points of low carb diet theory?
Here are just a few of the contributors to the science of the low carb diet and Lipophilia -- whom Taubes cites in GCBC:
- Hugo Rony
- Carl von Voit and Max Rubner
- Hilde Bruch
- Carl von Noorden
- Eugene Du Bois
- John Yudkin
- William Harvey
- Vilhjalmur Stefansson
- Alfred Pennington
- Blake Donaldson
- George Thorpe
- Margaret Ohlson
- Charlotte Young
- Robert Kemp
- Stephen Ranson and Albert Hetherington
- Graham Lusk
- Julius Bauer
- Rosalyn Yalow and Solomon Berson
- James Neel
- Robert Atkins
- Peter Cleave
- Jacques Le Magnen
- M.R.C. Greenwood
For a five minute summary about the theory behind the low carb diet: check out this article by Taubes in the January 2008 issue of The New Scientist.
Or if you have an hour or so to spare: check out Taubes' online lecture about the Lipophilia Hypothesis.
Okay, whew. At long last, we've gotten through this alternative idea about what makes us fat and why the low carb diet seems to work. But what specifically does it predict? In order to compare it effectively to the Caloric Balance Hypothesis, we need to know its testable predictions. If the evidence somehow contradicts these, then maybe the hypothesis is wrong or needs to be changed.
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1.Taubes, Gary. "Good Calories, Bad Calories." New York: Knopf (2007).