I would remind you to notice where the claim of consensus is invoked. Consensus is invoked only in situations where the science is not solid enough. Nobody says the consensus of scientists agrees that E=mc2. Nobody says the consensus is that the sun is 93 million miles away. It would never occur to anyone to speak that way.
― Michael Crichton
In the previous post I got all worked up over a news article claiming that eating red meat raises the risk of developing diabetes. I may still be slightly worked up, so you might want to go have some chocolate and get back to me tomorrow.
The article was biased from the outset, was not a real “study” at all, relied on notoriously inaccurate data, and ignored important variables altogether. Not to mention that no hypothesis was formed for the purpose of testing and truth-finding. No, we skipped that inconvenient step completely and just jumped to calling it a full-fledged theory and telling everyone how to eat based upon it.
But really, what’s wrong with doing that? I mean, stuff like heart health or diabetes is so important that we really don’t have the luxury of waiting till we get the final word, right? Heading in the general direction the evidence seems to point is really good enough, right?
Plus, wouldn’t it be unethical to put a person with heart disease or diabetes risk on a high-fat diet, or deny them a low-fat, high-carb diet? Even in the interests of science? Isn’t that pretty much the same thing as Nazis deliberately injecting prisoners with deadly diseases in order to test their serum antidotes?
No, it isn’t.
It would only be unethical if there was actual proof that a high fat diet hurt people, and that’s the whole point: we’ve never proved that. We just took a hypothesis, declared it truth and then instead of conducting proper, controlled studies with…VOLUNTEERS…we decided instead to issue nutrition guidelines that radically changed people’s macronutrient intake proportions and involuntarily enrolled the entire population of the United States in a giant, uncontrolled experiment.
That’s right. You were a “volunteer” in this giant experiment. Your grandparents or great-grandparents were much more likely to have grown up thin and healthy than you have. They also ate more animal fat, more red meat, and fewer carbs than you do. When they did eat carbs they ate them with plenty of fat–full fat ice cream, cake and pie with whipped cream and ice cream, mousses and creams, and biscuits with gravy and butter and bacon. Fat slows down glucose absorption rates so the sugar doesn’t hit your bloodstream in an instant, viciously spiking your blood sugar like your low-fat ice cream and granola bar do. When they ate soup, they made it from scratch from animal bones and gelatin. You buy it, or make it from bouillon containing sugar and grain thickeners. When they ate a snack they ate leftovers from a real meal containing meat and fat. You eat a low-fat glucose bomb like pretzels, or low-fat chocolate pudding, or mini-fudge pops, or fat-free popcorn, or sorbet. As children, they ate things like bacon and eggs for breakfast: you ate things like Frankenberry cereal , toaster pastries, whole grain bagels, and fruit smoothies.
We’ve been obeying the dietary guidelines suggested in the late 60s and enshrined on tablets of stone in 1980. We really have. We eat less fat. We eat less red meat. We eat more whole grains. We exercise more and more and more.
And it’s clearly helping, right?
No, obviously that is sarcasm. Something unusual for me, so try not to let it throw you. But if you read some of those links up there you get the insane picture, don’t you? “Americans are ______ than ever before,” but “still not enough.” When it’s not working just keep doubling down on the advice.
The proper, scientific way to do things is illustrated in this article:
Even the title is instructive. It makes no suggestions; no assumptions. It’s not “Diet could affect Alzheimer’s.” There is no judgment about whether this effect is good or bad. It simply states the truth–we’ve found that a certain diet has an effect on certain brain proteins that have been linked to Alzheimer’s.
A low-fat, low-carb diet altered levels of lipid-depleted beta-amyloid peptides in a small clinical trial, suggesting a biochemical explanation for past observations connecting lifestyle factors to risk of Alzheimer’s disease, researchers said…A similar but smaller difference in lipid-depleted, 40-mer beta-amyloid (AB40) that failed to reach statistical significance (P=0.15) was seen as well, the researchers reported online in JAMA Neurology.
Note the directness, the honesty. It “altered” levels. Right now we think altering them is a good thing: but we need more testing before we say it “improved” levels. Some of the findings weren’t statistically significant.
In an accompanying editorial, Deborah Blacker, MD, ScD, of Massachusetts General Hospital in Boston, noted that the study did not address whether the biochemical changes would have a clinical effect.
This is so refreshing to read: a researcher who realizes that just because you saw something happen in a lab doesn’t mean it will have a clinical effect.
This is a nice change from those “scientists” in the 1980s who observed that cholesterol-lowering statin drugs improved overall heart health and then extrapolated that, since the main effect of statins is to lower cholesterol, a diet which lowers cholesterol will have exactly the same effect. Without testing this hypothesis, they then went about promoting a cholesterol-lowering diet to the world. Which has worked beautifully so far, hasn’t it? We’ve nearly wiped out heart disease, right?
“But what could it possibly hurt to recommend a diet that lowers cholesterol if a drug that does it lowers your heart disease risk?” Well, because drugs have multiple actions within the human body, and diets are not the same as drugs. As bio-statistician Richard Kronmal says: “Claiming that statins reduce the risk of heart disease by lowering cholesterol is like saying that aspirin reduces the risk of heart attack by reducing headaches.” Maybe they do work because they lower cholesterol. Again the point is no one knows, because no one tested anything properly.
Some more from the excellent Alzheimer article:
She added that the study had no immediate clinical implications…Nevertheless, Blacker said, the study is important in showing that dietary changes can affect amyloid chemistry in the brain, potentially a step toward solving the puzzle of Alzheimer’s disease etiology.
See that? A “first step.” The article ends with this excellent note:
Limitations to the study cited by the authors included its small size and short duration. Also, because both fat and carbohydrate content were manipulated in the diets, it was unclear whether one or the other was primarily responsible for the effects seen.
It’s rare these days to see scientists or reporters admitting to serious limitations in their work. And I was thrilled to see the last sentence, since that was a concern of mine from the first paragraph of the article: how could you tell if it was the lack of fat, the lack of carbohydrates, or some combination of the two that caused the effect?
You only get jumping ahead of the scientific method when there isn’t enough evidence to support your hypothesis. Then suddenly it’s all about consensus. “Oh, you can’t eat that much fat. Doctors agree that fat is bad for you.” No one says that “Doctors agree that arsenic is bad for you” or “Doctors agree that heart attacks are bad for you” or “Doctors agree that stabbing yourself in the eye with a pencil is bad for you.”
We’ve got to have some evidence.
Plato says he’s hungry
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