One of the most hotly debated subjects over the past few years has been the cause of the obesity epidemic, and along with that, the best strategy for weight loss.

Some folks (Atkins, Taubes, Eades, etc.) believe that carbohydrates are to blame. Others (Ornish, Campbell, Esselstyn, Fuhrman, etc.) believe that fat is the problem. More recently, researchers like Seth Roberts and Stephan Guyenet and clinicians like Dr. Sharma have raised awareness of another hypothesis, called the food reward theory, which holds that the consumption of highly palatable foods leads to overeating and weight gain. And Paul Jaminet and others have argued that micronutrient deficiencies, toxins and infections may play a significant role in the obesity epidemic.

Here’s what I think: the most accurate answer to “why do people get fat?” and “what’s the most effective weight loss strategy?” is: “it depends.”

Separating cause from mechanism and effect

One of the biggest mistakes often made in this debate is the confounding of cause, mechanism and effect. A classic example is the assumption that if reducing carbohydrate or fat intake leads to weight loss, then the original weight gain must have been caused by excess carbohydrate or fat consumption.

While it’s tempting to make such an assumption, the logic is faulty. It’s kind of like saying “Advil cures headaches. Therefore, headaches must be caused by Advil deficiency.”

Let’s look at some definitions.

Cause: something that brings about an effect or a result

Mechanism: the fundamental processes involved in or responsible for an action, reaction, or other natural phenomenon

Effect: an outward sign

Obesity is an effect. Insulin resistance, leptin resistance, lipotoxicity, disruption of the mesolimbic dopamine reward pathway and inflammation of the hypothalamus are presumed mechanisms. Excess consumption of carbohydrates, fat, highly palatable food and food toxins (wheat, seed oils, liquid fructose, etc.), exposure to environmental toxins (chemicals), stress, infections, etc. are presumed causes.

Say we do a study on obese people and we observe that they eat a lot of carbohydrates and are insulin and leptin resistance. It’s easy to assume that the chain of causality worked like this: normal weight person eats high-carbohydrate diet, becomes insulin and leptin resistant, and then becomes obese.

But again, this is faulty logic. There’s no proof that A (high carbohydrate intake) was what led to B (insulin and leptin resistance) was what led to C (obesity).

In fact, we could disprove that theory simply by observing another individual or group that eats a very high carbohydrate diet, but does not develop insulin or leptin resistance and obesity. Guess what? Such individuals and groups most certainly exist. There goes that theory.

Likewise, we could also disprove this theory by observing people that are insulin and leptin resistant, but don’t become obese. Such people do exist, and I’ve written about them in my series on diabesity here.

A more rigorous approach

How have we developed our theories on obesity and weight regulation? It seems to me they come from a blend of personal experience, belief and facts. And I think it’s time to become more rigorous about keeping them separate. Here’s an example of what I mean:

Personal experience: I lose weight on an low-carb diet, therefore low-carb diets must be best for weight loss.

Belief: carbohydrates are responsible for the obesity epidemic, via their effects on insulin.

Fact: many cultures around the world eat high-carbohydrate diets and are exceptionally lean.

Those who’ve lost a lot of weight on a low-carb diet have a tendency to become convinced that their wife, friends, family, plumber and everyone else will also lose weight following the same diet.

From this personal experience, a belief is formed. And once we believe in something, we have a remarkable ability to filter out any evidence that might contradict that belief.

This is especially true if our reputation or financial livelihood is tied to said belief. As Upton Sinclair famously said:

It’s difficult to get a man to understand something when his salary is dependent upon him not understanding it.

When a belief like “carbs cause obesity” is shared between enough individuals, it becomes a meme. Once that happens, it is accepted by most as fact – regardless of whether it has any scientific basis. Hence we had the idea for decades that eating fat makes you fat, and now the more recent idea that eating carbs makes you fat.

There’s no single cause (or treatment) of obesity

Perhaps one of the reasons it’s so easy to confuse cause, mechanism and effect and personal experience, belief and fact is that obesity is an incredibly complex disease. Just how complex is it?

Click on the Obesity Systems Influence Diagram below to find out.

Click image for larger version

Wow. That should give you a rough idea of how many variables are potentially involved in weight regulation. Now you know why it has been such a challenge to come up with a single, unified theory of obesity.

That said, of all of the hypotheses advanced to explain the mechanisms behind obesity, I think the food reward theory is the most inclusive.

However, as even its proponents would agree, it doesn’t tell the whole story because there are people and groups that eat large amounts of highly palatable foods that do not become obese.

My opinion is that the modern lifestyle (i.e. food and environmental toxins, stress, poor gut health, infections, micronutrient deficiencies, sleep deprivation, etc.) interfere with hypothalamic hormonal regulation, dopamine signaling, leptin and insulin sensitivity at the cellular level, glucose metabolism and a range of other mechanisms that lead to obesity.

This is consistent with the observation that obesity is extremely rare or nonexistent in traditional cultures that do not consume modern foods and do not live a “modern” lifestyle.

But even this theory is incomplete, because there are people fully exposed to the modern lifestyle that do not become overweight or obese. This suggests that genetics, and perhaps other undiscovered factors, also play a role.

We’re not robots

Humans are not robots. We’re living, breathing, dynamic organisms influenced by varying genetics and environmental conditions.

Anthropological evidence combined with modern research has helped us to reveal the basic template of a species-appropriate diet. However, it has also shown us that humans can thrive on a wide variety of macronutrient ratios and foods within that basic template.

This is not a belief. It’s a fact, supported by the evidence as a whole. Ignoring the evidence doesn’t make it go away. Believing passionately in something doesn’t make it true. Experiencing something personally doesn’t make it fact for everybody else.

19th century philosopher Charles Peirce said:

The state of belief is a calm and satisfactory state which we do not wish to avoid, or to change to a belief in anything else.

And Tolstoy said:

I know that most men, including those at ease with problems of the greatest complexity, can seldom accept even the simplest and most obvious truth if it be such as would oblige them to admit the falsity of conclusions which they have delighted in explaining to colleagues, which they have proudly taught to others, and which they have woven, thread by thread, into the fabric of their lives.

Recognizing this basic human trait, philosopher of science Karl Popper advised every researcher to earnestly try to discredit their own hypotheses.

That is no easy task, and it asks a lot of us. Yet intellectual rigor, emotional maturity and personal integrity are characterized by the capacity to question our own beliefs, no matter how deeply cherished they are or how much is at stake.

I sometimes wonder why we’re all so sure of ourselves. It helps me to remember that at every point in history scientists (and the general public) were convinced they had the right answers. At one time the world was flat, the earth was the center of the solar system and disease was caused by foul humors and could be cured by bloodletting.

Nowadays we look back on those fallacies with a smirk. But are we so arrogant to assume that our great-grandchildren won’t do the same?

The truth is, there’s far more we don’t know than we do know.

Over the last couple of years, as the popularity of the Paleo diet has expanded, a lot of controversy has emerged over exactly what a Paleo diet is.

Part of the problem is that there are now a number of authors and bloggers – from Mark Sisson to Kurt Harris to Robb Wolf to Paul Jaminet to myself – that advocate what might generally be called a Paleo diet, but with slight variations in each case. This has unfortunately led to some confusion for people new to the “Paleo diet”.

It has also spawned new terminology in an effort by each author/blogger to clarify the differences in their approach, such as Mark Sisson’s “Primal diet”, Paul Jaminet’s “Perfect Health Diet”, and Kurt Harris’ former “PaNu or Paleo 2.0″ and current “Archevore” concepts.

So what’s the controversy or confusion all about? It usually revolves around the following questions:

• Is the Paleo diet low-carb or low-fat? Is saturated fat permitted? If so, how much?
• How much protein should someone eat on a Paleo diet?
• Does the Paleo diet include dairy products – or not? Which kinds of dairy?
• Are any grains at all permitted?

In the early days, following Loren Cordain’s book, The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat, the Paleo diet was considered to be moderate in carbohydrate and low in saturated fat (though monounsaturated fat wasn’t restricted).

Then, as low-carb diets rose in popularity and many low-carbers switched over to Paleo, it seemed that the lines between low-carb and Paleo began to blur. For these folks, the Paleo diet is high in fat – especially saturated fat – and low in carbohydrates, with a moderate amount of protein.

More recently, some authors/bloggers have advocated a diet based roughly on Paleo principles but that also may include dairy products and even certain grains like white rice and buckwheat, depending on individual tolerance. Still others have suggested that a high carb, lower fat diet – provided the carbs come from starchy vegetables and not grains – may be optimal.

So what is a Paleo diet? Is it low-carb? Low-fat? Does it include dairy? Grains?

We’re not robots: variation amongst groups and individuals

The answer to that question depends on several factors. First, are we asking what our Paleolithic ancestors ate, or are we asking what an optimal diet for modern humans is? While hard-core Paleo adherents will argue that there’s no difference, others (including me) would suggest that the absence of a food during the Paleolithic era does not necessarily mean that it’s not nutritious or beneficial. Dairy products are a good example.

Second, as recent studies have revealed, we can’t really know what our ancestors ate with 100% certainty, and there is undoubtedly a huge variation amongst different populations. For example, we have the traditional Inuit and the Masai who ate a diet high in fat (60-70% of calories for the Masai and up to 90% of calories for the Inuit), but we also have traditional peoples like the Okinawans and Kitavans that obtained a majority (60-70% or more) of their calories from carbohydrate. So it’s impossible to say that the diet of our ancestors was either “low-carb” or “low-fat”, without specifying which ancestors we’re talking about.

Third, if we are indeed asking what the optimal diet is for modern humans (rather than simply speculating about what our Paleolithic ancestors ate), there’s no way to answer that question definitively. Why? Because just as there is tremendous variation amongst populations with diet, there is also tremendous individual variation. Some people clearly do better with no dairy products. Yet others seem to thrive on them. Some feel better with a low-carb approach, while others feel better eating more carbohydrate. Some seem to require a higher protein intake (up to 20-25% of calories), but others do well when they eat a smaller amount (10-15%).

The Paleo diet vs. the Paleo template

I suggest we stop trying to define the “Paleo diet” and start thinking about it instead as a “Paleo template”.

What’s the difference? A Paleo diet implies a particular approach with clearly defined parameters that all people should follow. There’s little room for individual variation or experimentation.

A Paleo template implies a more flexible and individualized approach. A template contains a basic format or set of general guidelines that can then be customized based on the unique needs and experience of each person.

But here’s the key difference between a Paleo diet and a Paleo template: following a diet doesn’t encourage the participant to think, experiment or consider his or her specific circumstances, while following a template does.

In my 9 Steps to Perfect Health series, I attempted to define the general dietary guidelines that constitute the Paleo template:

• Don’t eat toxins: avoid industrial seed oils, improperly prepared cereal grains and legumes and excess sugar (especially fructose)
• Nourish your body: emphasize saturated and monounsaturated fat while reducing intake of polyunsaturated fat, favor glucose/starch over fructose, and favor ruminant animal protein and seafood over poultry
• Eat real food: eat grass-fed, organic meat and wild fish, and local, organic produce when possible. Avoid processed, refined and packaged food.

Within these guidelines, however, there’s a lot of room for individual differences. When people ask me whether dairy products are healthy, I always say “it depends”. I give the same answer when I’m asked about nightshades, caffeine, alcohol and carbohydrate intake.

The only way to figure out what an optimal diet is for you is to experiment and observe. The best way to do that is to remove the “grey area” foods you suspect you might have trouble with, like dairy, nightshades, eggs, etc. for a period of time (usually 30 days is sufficient), and add them back in one at a time and observe your reactions. This “30-day challenge” or elimination diet is what folks like Robb Wolf have recommended for a long time.

As human beings we’re both similar and different. We share the same basic physiology, which is why a Paleo template makes sense. There are certain foods that, because of their chemical structure, adversely affect all of us regardless of our individual differences. These are the foods I mentioned in my “Don’t Eat Toxins” article.

On the other hand, each of us is unique. We grew up in different families, with different dietary habits, life experiences, exposures to environmental toxins and lifestyles. Many of our genes are the same, but some are different and the way those genes have been triggered or expressed can also differ.

For someone with an autoimmune disease, dairy products, nightshades and eggs may be problematic. Yet for others, these foods are often well-tolerated. This variation merely underscores the importance of discovering your own optimal diet rather than blindly following someone else’s prescription.

I think it’s a complete waste of time and energy to argue about what a Paleo diet is, because the question is essentially unanswerable. The more important question is, what is your optimal diet?

I imagine some of you have heard about the new study published in the Annals of Internal Medicine claiming that low-carb, meat-based diets raise the risk of heart attacks, other cardiovascular events and death. With headlines in the media like “Low carb, high meat diet has high risks” and “Low-carb diets might be deadly“, you might be (understandably) concerned.

Well, as they say in NYC, “fuggedah-bout-it.”

As many preposterous and poorly designed studies as I read (and let me tell you, I read a lot of them), I haven’t lost the ability to be shocked by a particularly bad one. I know the researchers who publish them aren’t stupid. And in general, I think their motivations are good. But it is truly astonishing to see how easily highly trained scientists can completely abandon reason and critical thinking.

And don’t get me started on the mainstream media. They’re hopeless. Do they even read the junk that comes across their desk before regurgitating it as a sensationalized and vapid news story? I know that news outlets have science reporters on staff. Where do they find these people? I could explain this study to a ten-year old in simple language, and they’d understand right away how ridiculous and worthless it is.

Maybe these researchers and reporters need to eat more meat and fat so their brains work better. Because stuff like this is pretty embarrassing for them.

When I saw this study, I knew I’d have to write about it. After all, a low-ish carb, meat-based diet is exactly what I advocate for optimal health. Fortunately, several of my esteemed blogger colleagues have already dissected, dismantled and otherwise disposed of this piece of scientific garbage. Rather than re-create the wheel, I’m simply going to link to their articles and provide a brief summary of the key points here.

The study claimed that a plant-based, low-carb diet (which we’ll call the Vegetable group) is associated with a lower risk of mortality and disease, while an animal-product based low-carb diet (which we’ll call the Animal group) is associated with an increased risk of mortality and disease.

Does the study support those claims? Hardly. Here’s why:

• The so-called low-carb diet in the study wasn’t remotely low-carb. The participants got between 37% – 60% of calories from carbohydrates, which is what most low-carb experts would call, um, “high-carb.”
• People in the Animal group were more likely to smoke and be overweight than the Vegetable group. Smoking and overweight are risk factors for heart disease. This alone could explain the results, but it also suggests that the Vegetable group may have been more health conscious in other ways (like exercise, stress management, etc.) that were not accounted for in the study. This, of course, is the problem with attempting to draw conclusions from epidemiological research – as we’ve discussed several times here before.
• The Vegetable group didn’t exactly eat a vegetable-based diet. They got almost 30% of calories from animal products (vs. 45% from the Animal group).
• When you examine the data in the study closely, differences in death rates were unrelated to animal product consumption. That means something else (not eating meat) described the differences seen in the study.
• Epidemiological (observational) studies about meat intake are notoriously inaccurate, because people tend to lie (or forget) how much meat they actually eat. Since this study was based on nurses and doctors, who firmly believe the “meat is bad for you” hype, and are invested in the medical establishment, the participants may have been more likely to under-report their meat intake.

Of course Dean Ornish has jumped on the bandwagon claiming this study vindicates his completely unscientific claims that a plant-based diet is healthier than a meat-based diet. It does nothing of the sort, as you’ll see when you read the following articles. (I’ve lost all respect for the Dean Ornish’s integrity. I think his heart is in the right place, but he so clearly believes eating meat is bad and wrong that he entirely ignores any evidence that conflicts with his belief, and eagerly distorts any evidence that vaguely appears to support his belief.)

For a full analysis of the absurdity of this study, check out the following articles:

• Why the latest low carb scare study is flawed, by Jenny Ruhl at Diabetes Update
• Brand-spankin new study: are low-carb meat eaters in trouble?, by Denise Minger at Raw Food SOS: Troubleshooting on the Raw Food Diet
• The Atkins study (ahem, ahem) according to Ornish, by Tom Naughton at Fat Head
• New study shows that lying about your hamburger intake prevents disease and death when you eat a low-carb diet high in carbohydrates, by Chris Masterjohn at The Daily Lipid. (That headline says it all, doesn’t it?)

Summary:

• The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
• Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
• Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
• Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
• The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.

Not all cholesterol is created equal

By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.

But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”

Words to live by.

The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.

But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.

In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.

You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).

Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.

It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.

The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.

In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.

On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.

Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.

Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.

Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.

Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.

I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.

Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol

Here’s where the story gets even more interesting. And tragic.

Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.

It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.

Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.

In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.

Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.

Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.

Here’s what the authors said about their results:

Translation: following the advice of the American Heart Association is hazardous to your health.

Eating cholesterol reduces small LDL

The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.

Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.

Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.

If you’re confused right now I certainly don’t blame you.

Let’s review what we’ve been told for more than 50 years:

1. Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
2. Reducing intake or saturated fat and cholesterol protects us against heart disease.

Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:

1. Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
2. Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.

Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”

In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.

I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.

We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.

Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?

Really?

Sometimes it seems like everything is backwards.

How to reduce small LDL

Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.

Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.

As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.

In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.

Testing your small LDL level

I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.

If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.

However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.

First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.

The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.

Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.

If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:

1. LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
2. The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.