My response to a Wikipedia fund raising letter:

Dear Katherine, 

I will not renew my giving, your practice of inserting yourselves in legitimate scientific debates by selecting one set of disputants to shut out alternative views is unacceptable. Typically, this is done in favor well-known institutions defending theories for which there is little evidence (other than their reputation). Your staff and volunteer editors apparently are unaware just how much dysfunctional science pervades some disciplines.

This degree of dysfunction isn't exactly a secret,  Stanford medical professor and evidence analyst John Ioaniddis is pretty outspoken about the pseudo-scientific practices in nutritional epidemiology (though in fact they are apparent to any stats undergraduate). And yet you allow articles where the mainstream opinion of bodies practicing this bad science to be treated as authoritative when really all they are doing is making appeals to their own authority. That might be appropriate when summarizing political disagreements, but this supposedly is scientific debate.

A good example of this is an article on Nina Teicholz's book The Big Fat Surprise in which the article's editor thought it appropriate to quote Marion Nestle's critique of TBFS as though authoritative. Nestle merely quoted the official statements of organizations like the AHA,and ADA while completely avoiding any of the real and concerning evidence issues that Teicholz competently raised, and that indeed were at the core of her book. 

In essence, Wikipedia has taken to the practice that journalists have been roundly criticized for, choreographing a sham sort of objectivity by having paid corporate shills respond to legitimate critics, often with fabricated evidence. That in this case, the respondent is not a shill but someone whose professional position depends on the adherence to the "party line", or that the data used is inherently speculative rather than fabricated hardly invalidates the comparison. When a respondent in an exchange expressing opinions that merely parrot

powerful institutions and said institutions rely only on weak observational data, it bears

commenting upon, just as surely as pointing out the ties of a commentator to tobacco company.

Your censuring of Malcolm Kendricks work is another example of this. I personally don't know if Kendrick's theory of atherosclerosis is right or not, but I am pretty sure no one really does given the quality of his arguments. Kendrick apparently fell afoul of a wikipedia editor who thought they knew what was and was not settled science. Such a person apparently has little idea that important aspects of arterial physiology and anatomy, with substantial connection to disease processes, such as the glycocalyx and endothelial progenitor cells, were not even discovered until the 90's, decades after the conventional wisdom became enshrined (wisdom which, by the way, has stubbornly failed to produced confirming experimental data). In short, treating Kendrick as a crank or science denialist is another indictment of your faux scientific stance.

In short, within your pool of "experts" evaluating "nutrition war" topics, there apparently is an unwillingness or an inability to appreciate the widely known and understood data issues that drive the contentious of these debates.

Before I can recommend support of Wikipedia, you will need to redress this, perhaps by appointing diverse panels of experts who can negotiate a fair representation of alternative views in contentious sciences (which typically are ones where there actually is not enough hard experimental data to settle disputes). The prime candidates for this sort of review would include nutrition and public health. 

Sorry I've had to come to adopt this position.

Sincerely, ....

WTF?: The New Dietary Guildelines and the Actual Literature on Saturated Fat and Heart Disease

After listening to the Nina Teicholz conversation with a government spokesperson (good job Nina!) about the new dietary guidelines, I am a bit mad. The doubling down on saturated fat is really disturbing given the evidence is so weak (and I know it is nothing new, the current entrenchment of that view is an unfortunate fact of life). 

But how weak is the research? Well, I will tell you that it is so weak that if every Phd or MD (that understands the difference between observational studies and experiments) was required to review the literature on the actual experiments as part of their education, the government recommendations would be defunct or withdrawn in no time because the vast majority of said students would consider that the statement the "evidence is weak" is a charitable interpretation.

Specifically:

1) All but one of the experiments showed replacing sat fat with PUFA (which the various experiments had to do since no one would eat a diet with all the fat removed) showed cardiac deaths unchanged (or increased) as a result of removing sat fat.

2) The one study that did find an effect is the notorious LA Hospital study which inadvertently left more smokers in the sat fat group (1.5 times the number of moderate smokers and 2 times the number of heavy smokers) among other errors and possible confounding factors (e.g, the sat fat group was Vitamin E deficient which is somewhat bizarre given their butter intake, etc).

This is also the study that people quote when they refer to the idea taking sat fat out will make you die of cancer instead of a heart attack because even after screwing up the design of the experiment, the death rate between sat fat and PUFA groups were he same. Chris Masterjohn put it well when he suggested a more accurate description of the results is that sat fat protects you from cancer. The other thing found in some experiments of this type is that the death rate from neurologically related causes (accidents, suicides) also goes up.

Even the observational data taken in its entirety is not even strong enough to probably have justified the experiments in the first place. (Which was the conclusion of a recent WHO expert panel after doing a review of the existing observational data). If I were a betting man, I would lay money on the proposition that all this is going to be considered one of the great scientific scandals some day.

The Chris Masterjohn review of the literature is my favorite because it is so targeted

followed by Peter Attia's talk which is much broader than just looking at the experiments, you can also view the video version here.

Obesity and Sin

A few years ago I had lost a fair amount of weight eating a low carb diet and had kept it off successfully longer than any previous weight loss attempt. I was however realizing, for whatever reason, that I probably was going to have to make the diet a lifestyle, not a one time or "as needed" intervention.

I also still had more weight I wanted to lose so I thought I should be more deliberate about my eating choices (one of the great things about low carb was that it was easy both to endure and to logistically plan). I also realized I had many questions about the long term health consequences of my new lifestyle choice that I was fuzzy on. So I began a period of reading and contemplation about what the science said. That period (for reasons I didn't anticipate at all) has never ended and probably will never.

At first I started out with a basic question, how much protein I needed and (its logical follow on) how much fat. Before too long I realize I had stepped into a hotbed of controversy. And the controversy was not just about distinct questions on the nature of healthy eating but was also enmeshed in larger debates about the practices of entire scientific disciplines. But let me stick with the low carb issues for now.

As most people who have had success with low carb diets will attest, the diet is just easier than other diets because one is not constantly fighting hunger. In fact, the diet is not about portion size or calorie counting, it is simply about choosing what to eat. If you're hungry on a low carb diet, you could well be doing it wrong. So how can this possibly work?

Though Atkins is the controversial figure who is most associated with LC (actually the preferred term these days is the acronym LCHF, low carb/high fat), these diets preceded him and the science supporting them has developed considerably after him. But Atkins, and his supporters such as the Eades (a couple of married physicians) did know fairly early on that the issue in obesity was not calories but insulin.

Most physicians have been trained in medical school since the 1960's that obesity results from digesting more calories than are expended. And they are also taught the actual biochemical mechanism by which energy is stored in (and released for use from) fat cells is controlled by the hormone insulin. Now it is often not realized that the two things that doctors believe to be the mechanism of weight gain are really distinct, and even contradictory, explanations. More about that later. (And when I talk about weight gain with respect to obesity, I am referring specifically to the increase of adipose - fat - tissue, no one worries when you weigh more because of added muscle or, if you're a child, bone.)

Basically, doctors rely on the caloric excess theory of obesity (also known as "calories in/calories out" or CICO). People eat too much and don't burn off what they ate through activity.  Actually someone once nailed a description of most doctors' attitude about obesity as CICO + shame. In other words, people were fat because they lack the knowledge or (more likely) self-discipline to make healthy choices. And in fact, I've had people in my own family talk about their weight problems as "sinfulness".


One obvious problem with this shaming, is that it doesn't really address that some diets are experienced by their practitioners as "easy" and some definitely not. Where does sin or personal knowledge come into that? Some doctors would retort diet pills and heroin are easy paths to weight loss as well, echoing the widespread belief among doctors that Atkins and related diets must somehow be unhealthy "cheating".  Is a LCHF some kind of cheating?

Now it turns out that CICO was not the first theory of obesity around in the 20th century. There was a pre-existing theory which had been developed by the most prominent researchers of the pre-WWII era. That school of thought was that obesity was primarily driven by insulin and caloric excess having at best a minor role. These earlier researchers came to these conclusions not knowing the exact biochemical mechanisms since these were not worked out until the early 60's. Even so, the effects of insulin on patients' fat deposition was observable in many ways.  Why CICO came into the picture and supplanted the earlier theory seems to have been due to a variety of reasons, none of them really connected however to scientific evidence. If you're interesting in this history, science journalist Gary Taubes is the person to read.

So why is the original theory better than CICO? First of all, insulin is a hormone (it's made in a gland, the pancreas, and travels through the blood to signal cells throughout the body) and the fact that a hormone is central to the story of weight gain is actually quite profound. It suggests that body weight is controlled by a "regulated" system.

The body has to maintain many conditions in a balance within very narrow bounds to sustain life. Examples of this include, temperature, blood acidity, blood sugar, urea levels. The list goes on. Hormones are key to many of the systems that maintain these balanced conditions, acting as means to signal various body organs or systems to do their job, e.g., to either produce or breakdown some chemical.

Now the fact insulin is a hormone strongly suggests that body weight is a regulated system. It is a serious evolutionary disadvantage if the body had inadequate energy stores (i.e., fat).  Without enough fat, individuals may not survive dips in the food supply such as seasonal scarcity. Too much energy diverted to fatty tissue means not enough energy available for other important activities (like obtaining food or reproduction). So it makes sense the most important chemical controlling weight gain is the hormone insulin because evolution should have programmed us to maintain a stable (not too fat, not too thin) body weight. Fat storage is a regulated system.

Well, if the body is trying to maintain a some target percentage of body fat, then it follows that other factors of caloric intake and expenditure, must be regulated too. What does that mean? It means that our appetite and energy level (i.e., how much we want to be active) are being controlled by the same mechanisms that want to maintain body fat.  Indeed, anyone who has ever dieted by conventional means understands that they at times face powerful feelings of hunger and urges to eat and severe disinclination to do anything but sit on a couch. This is not lack of self-discipline (aka sloth) it is our body doing what it is designed to do.

But then what explains why people get fat (since they obviously do)? How can that happen if body weight is self-regulating? Why would the body want you to have one weight when young and another heavier weight as you get older (say freshman year of college or your 40's)?  The answer is that the body is not changing its weight target, what is happening is that we are throwing a wrench into the system by changing the levels of the key hormone, insulin.

How do we do that? Easy, we eat carbohydrates. Of the three macro-nutrients (these are the broad categories of nutrients: protein, fat, carbohydrates)  the most profound effect is by carbs. Protein does cause insulin levels to rise but it also causes another hormone to be released that lowers insulin in time.  Carbs just cause the levels to go up. What about fat? Hmmm.

This is important. Remember how I mentioned that the calorie story and the insulin story were different and even contradictory? Fat has no effect on insulin levels. Zip. If you eat a thousand calories of fat, if your insulin levels are low, it is difficult - perhaps impossible - for your body to store any of the calories.

By the same token, when insulin levels are high your fat stores are locked up. Obese people often feel intense hunger and that is probably because the body believes it is starving since it can't gain access to its fat stores. In short, none of this is about will power, it is about the body telling you when to eat and expend energy and how we ignore and mess up the very important tool of appetite by eating the wrong things.

Why are carbs so disruptive to our systems? Didn't we evolve to eat them? Short answer: no.

You can never eat another carb (sugar or starch) for the rest of your life and you will be fine. You cannot cut out either fat or protein without it killing you.  The reason carbs are different and unnecessary is because prior to the rise of agriculture ten thousand years ago there were not very many available. For the two million years before that (i.e., 200 times as much time as we've been eating carbs, primarily as grain) most of our nutrients came from animal meat and fat. When we say humans are omnivores, I would suggest it is not quite right. When we diverged from chimpanzees, we were already omnivores (it wasn't known until the 1950's that chimpanzees actually kill and eat monkeys). It is more accurate to say we've been evolving towards being carnivores for the last 2 million years and changes in our body structure (such as the length of our intestinal tract) reflect that.

In evolutionary terms, we are not used to carbs and other sugars. We should suspect that in some circumstances, they are toxic to us. When we overeat and resist exercise that is not personal failure, it is the effect of eating food that confuses the body's strategy to achieve a healthy balance. Appetite is our friend, and a useful one at that. If that goes against traditional or religious views of morality, I think I have to go with the science.