“Choose whole, unprocessed foods over refined, processed foods.”
How much have you heard something like this?
It’s pretty much common knowledge at this point. Everyone knows processed foods aren’t as healthy as whole foods, right?
Potato or potato chip? The potato is healthier – it wasn’t fried in industrial seed oils.
Steak or Slim Jim? Obviously the steak – it’s a cut of meat straight from the animal.
Orange or a glass of orange juice? The orange wins. The amount of sugar you’ll get from a glass of orange juice is an order of magnitude higher than what you’ll get from a single orange.
Corn or high-fructose corn syrup? . . . is that even a question?
If you presented each of these to your dietitian or doctor, or consulted the dietary guidelines, they’d get it right. Sometimes the choice is between two inappropriate foods, and choosing the one less likely to do damage. Still – most of the time, they’d manage to choose the less harmful option.
But there’s one that they get wrong, and it’s a whopper to get wrong. I argue that it’s the single biggest blunder we’ve ever made as far as mainstream nutrition advice goes, and the guidelines have gotten a lot wrong. Nothing else has been more disastrous for our health than this.
Butter or margarine?
Tallow or canola oil?
Lard or Crisco?
A fatty ribeye steak cooked in its own fat, or a lean pork chop fried vegetable oil?
Saturated fat or polyunsaturated fat?*
A Big Fat Mistake
If there’s something we’ve been conditioned to fear, it’s saturated fat.
If you ask a dietitian or consult the guidelines, saturated fat should be avoided because it causes atherosclerosis and heart attacks, diabetes, strokes, Alzheimer’s disease, cancer, and leads to a life of chronic disease and a premature death. It might be accompanied by a sound-bite like one of these: “Saturated fat will raise your LDL cholesterol, which is a risk factor for heart disease.” “A new study shows that saturated fat-rich red meat increases your risk of heart disease by 9% for every 3 oz portion consumed daily.”
There is so much wrong with this, it’s hard to decide where I should begin.
Take a look at this poorly-framed picture I took at a barbeque restaurant when I lived in Texas.
The Dietary Guidelines for Americans recommend that you limit your saturated fat to 7% of your daily calorie intake. (I will address calories at length in other posts, I have issues with how we use the term, but let’s stay focused on fats.) The American Heart Association (AHA) recommends an even lower amount, 5-6%. The pediatric Nutrition Care Manual I was given to refer to in graduate school said saturated fat should be minimized “as much as possible while consuming a nutritionally adequate diet”.
They’re wrong. But why do they say this? Why do they think it’s a good idea to strictly limit saturated fat, even to eliminate it to the greatest extent possible?
The whole idea centers around this “logical” progression. High levels of low-density lipoprotein (LDL) cause heart disease. Eating a diet high in saturated fat causes LDL levels to rise. Therefore, saturated fat causes heart disease. A -> B, B -> C, therefore A -> C.
And if LDL causes heart disease and a statin lowers your LDL, then a statin reduces your risk of heart disease. And if high intakes of polyunsaturated fatty acids (PUFAs) lower LDL, then guess what – they’re good for your heart too.
Here’s the thing, though.
LDL doesn’t cause heart disease. A does not cause B. So even if B and C are related (which, in the case of LDL and cardiovascular disease, is a dubious claim at best) , A does not cause C. And the use of the words “risk” and “cause” is completely and utterly inappropriate.
It has never been established in any study ever that LDL causes heart disease or any disease at all. Full stop. The same goes for saturated fat. It has never been established in any study ever that saturated fat causes heart disease or any disease at all.
Some mechanistic studies suggest that LDL particles, especially those containing high amounts of unstable PUFAs like linoleic acid, that have been damaged by oxidation or glycation, may play a role in the development of atherosclerosis, but no causal role has been established experimentally in humans in vivo here either (hello ethics), and it’s only one part of the pathophysiology of cardiovascular disease, which is primarily inflammatory in nature.
Risk, Cause, and Effect
And, another aspect of the argument I have a big issue with is the use of two words: “cause” and “risk”.
There’s a lot that has to happen before you can establish cause and effect. The Bradford Hill criteria are one commonly-accepted set of conditions that should be met to infer causality. And when it comes to all the literature and all the studies and papers written on food, nutrients, dietary patterns, human nutrition, and health outcomes, none of them even come close to providing the evidence to establish a causal relationship between any nutrient, food, food group, or dietary pattern and any chronic disease.
Risk is another word that is inappropriate to use when describing the results of any observational, epidemiological, or associative study. Saying that doing something like eating 3 ounces of red meat daily increases the risk of heart disesase by 9% implies that the study supporting that statement is able to inform on risk, which is a statement of cause and effect.
In other words, doing something or being exposed to something increases the risk (has a direct effect on the likelihood) of some outcome. Moving around on the x-axis has an effect on something on the y-axis, like the chance of a certain outcome. That cannot be determined by any observational study. Observational studies can only establish relative rates of incidence or prevalence. A non-experimental study cannot tell us anything about risk, by its very design.
It’s often said that correlation does not imply causation, and it’s true. Just because one thing is associated with another, that doesn’t mean the one causes the other. But when we use words like “risk”, “relative risk”, “impact”, “lead to”, “cause”, “give rise to”, “effect” or “bring about” when describing the results of any non-experimental study, we are misrepresenting what the data is able to tell us. And even then, the experiments we do don’t have nearly the level of control, statistical power, and elimination of all possible confounders and variables required to provide good and valid data.
Even if you do all the statistics right on the data, if the data themselves are no good, then the conclusions reached from those data will also be no good.
When it comes to epidemiology and associative studies, remember this: garbage in, garbage out. No matter how good the process in between is.
Disproving Causation
We’ve established that just because an association exists, that doesn’t imply or indicate there’s a causal relationship at play between the two variables being considered.
Here’s the thing though:
Lack of association can disprove causation.
If A is not correlated or associated with B, then A does not cause B. Correlation is necessary (but not sufficient) to infer causality.
And this is what we see in the studies and meta-analyses on saturated fat and heart disease. Meta-analyses (which mostly combine low-level, non-experimental data from observational studies like cross-sectional and cohort studies) on saturated fat and heart disease show no association.
A note about epidemiological studies – the “relative risk ratios” that these authors are so proud of and the media loves to run with – 1.09, 1.16, or 1.2 – are statistical noise, especially since the lower end of their 95% confidence intervals are often very close to 1. When it comes to observational studies, anything below a 2 in terms of so-called “relative risk” (more rightly called “relative incidence” or “relative prevalence”, depending on whether the study was prospective or not) can essentially be dismissed as a non-significant finding. Even if it is statistically significant, it isn’t clinically significant. Terms like “statistically significant”, “positive, linear association/correlation” and “link between/relationship between” are abused by many to bolster arguments that would fall apart immediately when looking at the strength of the relationship (r squared-value, correlation coefficient ρ [rho]) and the fact that there can be no causality inferred.
(As a point of comparison, the “relative risk” (read: relative incidence) of lung cancer between smokers and non-smokers is about 25. Even though we would certainly suspect a causal relationship with a ratio that high, it would have to be proved experimentally while controlling for all other possible factors to use the word “cause”, which isn’t ethical.)
The signal to noise ratio in these observational studies makes the results even more meaningless, and there are always confounders and various biases that further muddy the waters.
The use of 24-hour recalls or food frequency questionnaires that rely on self-reporting by itself confounds the results of the study. When describing the results of such a study, the authors aren’t comparing what the participants ate to the variables being examined, they’re comparing what the participants said they ate and those variables. That is an enormous source of error. Healthy user bias is also a major confounder, one that often goes unackowledged.
Not to mention all the “adjusting” that goes on in the statistical manipultion of the results. Scientists report on what they observe through rigorous, tightly controlled experimental endeavor. Altering the results with statisical methods is a fabrication, which can be influenced or conducted in such a manner to show results favorable to the views or biases of the authors conducting the study, or the source funding it. Case in point: Adventist Health Study 2. Not that it necessarily happens every time; it’s certainly a possiblity though. Scientists report what they observed, without adjusting the outcomes to suit some motive – financial, professional, or otherwise.
There are three kinds of lies: lies, damned lies, and statistics.
Mark Twain
“lDl iS bAd ChOlEsTeRoL” – ignorant people
The whole idea that saturated fat is bad for you and you should replace saturates with polyunsaturates centers around the idea that LDL causes or increases the risk of heart disease.
This is wrong. LDL does not cause heart disease, and the data available on the topic show no association between saturated fat intake and heart disease. LDL is not “bad cholesterol” (it isn’t cholesterol at all, in fact), and HDL is not “good cholesterol”. Both classes of lipoproteins are good and necessary and have important functions, and neither one causes disease. Our lipoprotein system which moves fat-soluble substances throughout the body has survived millions of years of both positive and negative natural selection pressures. LDL and HDL and the genes that encode for them are there for a reason. Neither one is inherently bad, or has any individually predictive value for any chronic disease, at any physiological concentration.
Certain relative concentrations of the lipoproteins and lipids in the blood may show association with various health outcomes and display certain patterns that correlate with disease incidence, but again, no causation can be inferred. The disease and the “deranged” blood lipids may indeed have a common cause, and the lipids may merely serve as an indicator which associates with the incidence or prevalence of the disease because they reflect a deeper problem that drives the disease.
Ergo, saturated fat does not cause heart disease. And there isn’t a study or combination of studies in the world that can show otherwise, and there will never be, because that would require a decades-long experiment on a large enough population to provide adequate statistical power comprised of similar individuals, ideally identical twins separated at birth, under metabolic ward lock-in conditions, proper control and observation, and changing only one variable while keeping everything else exactly identical.
That is much closer to the level of rigor required to establish a cause-and-effect relationship between saturated fat and heart disease. The funding required would be immense and it would never get past an ethics committee/IRB.
Meaning, we will never to be able experimentally prove that saturated fat does or does not cause heart disease, or any other disease for that matter. The same goes for any other nutrient, food, food group, or dietary pattern.
The fat we are meant to eat
And the entire study on saturated fat and heart disesase risk, if it could be constructed properly to actually be able to inform on risk, would be a crapshoot because humans have subsisted almost entirely on the meat and fat of animals, which is mostly made up of saturated fat, for hundreds of thousands of years in our current speciation, and for millions of years prior to that as pre-human Homo and Australopithecus species. The few plants early humans foraged looked nothing like they do now, they were usually only available seasonally, and contributed very little to the overall diet. They were primarily subsistence foods – eaten when a hunt was unsuccessful, fallback foods if you will – or eaten seasonally to fatten up for a harsh winter. That our ancestors ate this almost entirely carnivorous diet is confirmed by the stable isotope testing of the collagen contained within skeletal remains of early pre-agricultural humans.
It makes no sense at all to blame a nutrient that we’ve been eating in abundance for hundreds of thousands of years – saturated fat from animals – for causing a disease that has been around as a cause of death for less than 150 years – atherosclerotic cardiovascular disease. It’s much more reasonable to believe that the refined plant fats/industrial seed oils are a problem, because they became a part of the global diet during the same period that atherosclerotic cardiovascular disease and all manner of inflammatory chronic disease began to afflict us.
So, your doctor is wrong. Your dietitian is wrong. The associations for heart disease and diabetes and cancer and the guidelines and the textbooks are wrong. Industrial seed oil is not a healthy alternative to the fat on your steak. Margarine is not a healthy alternative to butter. The “science” that supports those wrong ideas isn’t science at all, it isn’t experimental in nature, and it cannot inform on risk or causality. It’s nothing more than an association found by survey-based observational studies and poorly controlled, short-term interventional trials usually conducted on free-living people which don’t have the proper control and rigor to generate any meaningful data.
The healthiest fats are those that come from well-raised animals eating a species-appropriate diet, especially ruminants like cattle, bison, sheep, and deer. Other rendered fats appropriate for our consumption are butter, ghee, tallow, lard, and most of all, the fat that comes with the meat of animals. Egg yolks and the fat in whole, raw dairy are excellent as well, if you tolerate those foods. Meat and fat is what we ate during our pre-agricultural past, and this is what our physiology, anatomy, and genetics are designed for. This is what we evolved eating. This is what is appropriate for our species.
The antithesis of these healthy animal fats are the industrial seed oils, which are a blight on our health. Ideally, no liquid oil of any sort should pass your lips. Anyone who says seed oil is “heart-healthy” because its polyunsaturated fatty acids reduce LDL concentrations and LDL is “bad cholesterol” has no clue what they’re talking about, and they’re spreading dangerous misinformation with no basis in science or physiology. They’ve been deceived by shoddy non-science, inappropriate conclusions drawn from weak observational studies, ideology, and propaganda with heavy influences from industry, and mostly parrot what they’ve been told. And they were told wrong.
Whole, natural foods appropriate for your species are better for you than processed, refined foods. Fats aren’t an exception this. And the fats found in the natural foods we are meant to eat are mostly saturated fats, because the foods we are meant to eat are almost entirely comprised of the meat and largely saturated fat of animals.
If it is a departure from nature, the safer assumption is that it will be to our detriment.
Naturalist Nutrition
Don’t be deceived. Eating the right fats is of monumental importance; eating the wrong fats has led to all manner of chronic disease and ruin. And pretty much everyone has gotten it wrong. It’s time we stop listening to them and return to nature.
Naturalist Nutrition
*I don’t mean to present a false dichotomy here – polyunsaturated fats are not bad. They are essential in the diet – the body is unable to make omega-6 and omega-3 polyunsaturated fats itself, so we must consume them, but not very large amounts are necessary. The amount we get from the meat and fat of animals is perfectly sufficient. The fact that they are oxidized (damaged) when in the form of industrial seed oils is the main problem. They also have toxic metabolites and auto-oxidation problems that will be discussed at length in future posts.
