Saturated Fat Still Not Bad For You

This article has been a long time coming. The nonsense surrounding saturated fat is one of the main reasons I got sucked into independent health research in the first place. And I’ve had an article ready to go on this topic in one revision or another for several months. But I decided that that article was a diatribe and it’d be better to try and keep this to the point. So I rewrote it.

There are two main theories to understand when discussing saturated fat and heart disease. The first is the lipid-hypothesis, and the second is the diet-heart-hypothesis. The lipid-hypothesis is based on the observation that heart disease usually correlates with elevated cholesterol levels and that arterial plaques contain a fair amount of cholesterol. The lipid-hypothesis puts forth the theory that the elevated cholesterol is a causal agent in the formation of arterial plaques.

The diet-heart-hypothesis is the theory that dietary saturated fat, via its ability to raise serum cholesterol, is causal to heart disease. It is important to note that the diet-heart-hypothesis must be tested separately and independently of the lipid hypothesis.

Now before we move on here, I just want to say a few things. First, all the evidence points to heart disease (and the other degenerative diseases) being problems of oxidation and inflammation. Note that this has nothing directly to do with cholesterol. Second, cholesterol is an extremely important lipid. It is a critical component of cell membranes, the precursor to all steroid hormones, a precursor to vitamin D, and the limiting factor that brain cells need to make connections with one another called synapses, making it essential to learning and memory. Third, there is no evidence that elevated cholesterol is causal to heart-disease. That is, the lipid-hypothesis has not been proven.

Now a little bit on atherosclerosis. How does all that cholesterol get in there? Generally via foam cells. A foam cell is a dead macrophage that was supposed to have helped clear up an infection. It could have been damaged by an oxidized LDL particle or infected by a germ it was unable to kill due to excess cortisol. Once a macrophage becomes a foam cell, it is itself highly inflammatory and furthers the process of inflammation. An atheroma is like a puss filled blister on the surface of your skin, except it’s inside your artery. The cholesterol is just a lot of left over junk from the inflammatory response.

The standard method of treating this problem is to try and reduce the amount of cholesterol in the blood to such a low level that only a few macrophages can turn into foam cells, rather than identifying and treating the source of the chronic inflammation. We’re getting away from the original topic of saturated fat, so I’d like to bring this around and tie it together.

We talked about cholesterol levels and correlation, and it is true, cholesterol levels are a marker for heart disease. What we should be concerned about here though is dyslipidemia and not elevated cholesterol per se. (Dyslipidemia simply means having an abnormal blood lipid profile.) This is because dyslipidemia is probably an indication that the inflammatory process that causes atherosclerosis is ongoing in your body. But there are better measures than total LDL, total HDL, and total cholesterol. You have to understand that these are somewhat arbitrary measures that happen to be easy to measure at most clinics, but which have a weak correlation with heart disease. There are better measures, such as the size of your LDL (pattern A or pattern B) and the total LDL particle count. I do not want to get into the physiology here but there are much better explanations as to why LDL particle size and count would affect heart disease as opposed to just total LDL cholesterol.

Getting back to saturated fat, it is well accepted that dietary saturated fat does increase total cholesterol levels, including LDL. In fact it increases both LDL and HDL. And this is where it becomes important to test the diet-heart-hypothesis directly. I would like to point out here that although saturated fat increases total LDL cholesterol, it does so by producing fewer and larger LDL molecules, an improvement in the overall lipid profile.

And what of the diet-heart-hypothesis itself? Here are a couple quotes:

“The diet-heart hypothesis has repeatedly been showing to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even government agencies. The public is being deceived by the greatest health scam of the century.”

--George V. Mann, Coronary Heart Disease: The Dietary Sense and Nonsense

“The commonly held belief that the best diet for the prevention of coronary heart disease is a low saturated fat, low cholesterol diet is not supported by the available evidence from clinical trials. In the primary prevention, such diets do not reduce the risk of myocardial infarction or coronary or all cause mortaility…
“Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested…”

--Corr LA and Oliver MF. The low fat/low cholesterol diet is ineffective. European Heat Journal 1997; 18: 18-22

Primary prevention means preventing a first occurrence. Secondary prevention means preventing a second occurrence. Also, another term brought up here is “all cause mortality”, and it is a major point. Reducing our risk of heart disease only matters if it’s not increasing our risk of dying from other factors (i.e. by reducing endogenous production of cholesterol). That is to say, our life expectancy should be increasing. I’m not entirely sure the numbers on this, but anybody on a cholesterol-lowering diet or taking statins should be aware that although it prevents a few deaths from heart disease, it increases the number of deaths from other causes.

References and Further Reading:
The Cholesterol Wars: Steinberg Strikes Back
Chris Masterjohn reviews Daniel Steinberg’s book “The Cholesterol Wars: The Preponderance of Evidence”. I include this book because in it, Steinberg attempts to prove the diet-heart-hypothesis and I believe Masterjohn’s rebuttal is fairly solid.

Cholesterol and Health – Functions and Foods
Again from Masterjohn. This time an overview of the functional roles and importance of cholesterol.

The Potbelly Syndrome
An in depth look into the causes of modern degenerative diseases. I don’t agree entirely with what this book has to say, but I like its emphasis on cortisol as an important aspect. It contains a lot of information on the process of atherosclerosis. It is also where I got the two quotes I used in this post.

http://www.youtube.com/watch?v=dBnniua6-oM
Robert Lustig’s rant against sugar. This isn’t directly about saturated fat or lipid profiles, but there is a good rebuttal of Ancel Keys’ Seven Countries Study from 32:30 to 36:00.

http://freetheanimal.com/2009/09/saturated-fat-intake-vs-heart-disease-stroke.html
The interesting thing about the internet is the availability of information. Does lower cholesterol really correlate with lower mortality? A follower of the blog Free the Animal compiles some publicly available data from the British Heart Foundation into some easy to read graphs.

Dirty Little Secret of Heart Disease
Diet-Heart Controlled Trials: a New Literature Review
Saturated Fat Consumption Still Isn’t Associated with Cardiovascular Disease
Stephan Guyenet is a person I respect for well thought out, clear-minded opinions and he has written a lot on the issues of saturated fat and heart disease. So I’m throwing out a few links to his website.

What is Causality

“You need to be healthy to lose weight, not lose weight to be healthy.” So begins Diana Schwarzbein in her book “The Schwarzbein Principle: The Program”. Although this blog is not an endorsement of Schwarzbein or her program, it is a look into what we can learn when we let go of our concepts, open ourselves up to new sources of information, and keep a critical perspective.

And today’s topic: causality... or more specifically: the direction of causality. We’ll be focusing on causilty as it relates to obesity. The beauty of Schwarzbein’s statement is that it reverses the direction of causality. The direction of causality as it relates to disease and obesity is something we’ve always implicitly taken for granted. Yet, here’s an M.D. achieving clinical results telling us that in her experience, it works the other way around. Unfortunately, “what causes what?” is a question we need to ask a lot when it comes to health and nutrition.

This is just a short post, intended to spur your mind in a different direction. I will summarize it now, with a couple images to visualize Schwarzbein’s statement.



This is the current model. I’ve never been able to find an adequate explanation of how the extra fat tissue, just sitting around there, is causing these diseases, but hey, look at the bright side: With this model you get to take all the blame when the model your diet is based on is proven wrong (oops, I mean when you fail the diet)!



A different model. Note that in this model “undesired fat storage”, “increased appetite”, and “low energy” are results, not causes. Furthermore, they don’t maintain any direct links with each other, which means that you don’t affect one result (undesired fat storage) by ignoring another (increased appetite). I don’t have anything to indicate that this model is incorrect as opposed to the overeating model. In fact, my research has lead me to believe this model is more correct. More to come on that. And intuitively, to me at least, it makes more sense.

Finally, I want to make one more addition to the diagram that the research so far seems to support.



Again, more on these themes in future posts.

What Makes us Fat

There’s an idea that’s been accepted by the mainstream. This idea is a theory although most people don’t know that. This theroy has no inherent strength over any opposing theories. It is not supported by any controlled studies. It fails to fit much of the observable evidence. And although it at first sounds intuitive, on deeper thought it lacks common sense. What is it? It’s the idea that eating too much makes you fat.

“Say what!?” I can hear some of you saying, but bear with me. I’m going to break this argument apart so you never think about it the same way again.

Let’s start out by stating exactly what we mean by “fat”. We mean a high body-fat percentage. And we mean primarily abdominal obesity, the type that’s associated with all the degenerative diseases.

Let’s start off with the energy balance equation:
change in energy stores = calories consumed – calories expended
On the face of it this seems straightforward enough. You can’t really get around it, so any argument based on the energy balance equation has an air of certainty. But going from there to “eating too much makes you fat” is a big leap. Let’s look at some of the assumptions we’re ignoring in making this leap.

First is the direction of causality. There is a theory known as partitioning. The idea behind it is that your hormones determine which nutrients go where. If, for example, your hormonal state is such that it’s pushing energy into fat cells rather than using it for things like immune function and tissue repair, then the driver here is “change in energy stores”, not “calories consumed”. That hormones would be driving a homeostatic process seems normal, as that is how every other function in the body is regulated. No one would say a child is growing because he eats too much or a bodybuilder has too many muscles because he eats too much. But, for some reason, when it comes to weight and diet, such thinking goes out the window.

The second oversight is independence of the variables. There’s nothing that states they are independent, and the observable evidence would indicate they are not. Dieting and overeating have been shown to regularly produce lowering and raising of the metabolic rate, respectively. In fact, depending on the extremity of the diet, dieters can begin to suffer severe consequences long before desired weight comes off.

A third oversight is what’s hidden in the terms themselves. “Energy stores” could refer to adipose tissue, or it could refer to glycogen stores. And it doesn’t specify where the storage is either. Why would one person store fat primarily in the belly, and another throughout their body, unless it was hormonal? And why wouldn’t the body take the opportunity of the available extra energy to increase all its processes and max out lean tissues?

These are questions any dieter should ask, but I want to move on. Let’s look at some of the readily observable evidence. I have three points here.

First is that animals in their natural environment are usually quite lean, unless they are gaining fat for a specific purpose: i.e. hibernation or living in a cold climate. This leanness is regardless of the abundance or scarcity of food.

Second is what we know of humans in their natural environment. According to what we know of primitive cultures prior to contact with Western civilization, they did not suffer from overweight and obesity. This is documented by researchers such as T.L. Cleave, Western Price, Staffan Lindeberg, and others. This would be the case often in spite of an abundance of food. The Pima indians of the southwestern US are often upheld as examples of the “thrifty gene hypothesis”. What most people don’t realize is that the Pima, like most indiginous cultures, had an abundance of food before white men arrived. Oh, and they were not fat and diabetic.

The third point is what actually happens to people who diet. Long term dieting success rates are abysmal: 5% at the most optimistic. One has to ask the question, “why, if it’s such a simple matter of calories in vs. calories out, should it be so hard?”. Maybe it’s because the body doesn’t want to lose weight. Maybe when you eat too little, the body goes through hormonal changes to make you miserable, lethargic, and obsessed with food. And maybe when you eat too much, the opposite changes happen. In fact, this is what the evidence shows. Most dieters, in order to maintain their weight-loss, need to eat less than appetite and remain hungry. That does not sound right to me. If you’re eating too much, wouldn’t your hunger and satiety signals be telling you that? Or are the hormones out of whack? Hmm…

So the question remains… if overeating isn’t making us fat, what is? The most direct answer that any honest obesity researcher will tell you is we don’t really know yet. Body-weight regulation is turning out to be incredibly complex. But here are some of the theories I think hold promise:
Chronic stress: Most of the degenerative diseases appear to associated with inflammation, including obesity. The stress could come from lifestyle factors, chronic infections, or poor diet.
Poor nutrition: Without adequate nutrients and calories, the body does not have what it needs to regulate its internal environment.
Dieting: I actually think this is the biggest contributer. I don’t really understand how this works, but there appears to be a clear long-term increase in weight for serious dieters. It makes sense from an evolutionary perspective as part of a “famine response”. The other possibility is that extreme dieting causes metabolic damage.

I really don’t think diets are healthy and I think losing weight is a cosmetic goal, not a health goal. Abdominal fat is associated with degenerative diseases, but there is no evidence that it is causal, and there is no evidence that dieting improves long term outcomes. Attempting to lose weight by restricting calories causes a lot of unfavorable hormonal changes in the body. If we take the view that excess abdominal fat is a sign of disregulation, restricting nutrients is probably the last thing we want to do.

References:
The Kitava Study
It’s Not Your Fault You’re Fat
Good Calories, Bad Calories
Medicare’s Search for Effective Obeisty Treatments
Overfeeding Experiment
Semi-Starvation Experiment
Vermont State Prison Overfeeding Experiment
Scott Abel on Metabolic Damage (email from former figure competitor)
Scott Abel on Metabolic Damage (effects of long-term dieting)