In this “Grab Bag Q&A” episode of the podcast, I discuss the role of nutrition in healing, obstacles to optimal health, macronutrient ratios and more.

Questions include:

• Do you feel with the right nutrition the body is capable of healing itself?
• In your practice, what do you find to be the biggest barrier stopping people from reaching their optimal health?
• Should I eat low-carb, low-fat, or do macronutrient ratios not matter?
• Do you have anything you could teach on the problem of developing gastritis AFTER going paleo?
• Does the food combining theory have any scientific merit?

As part of the recent re-branding of the site from The Healthy Skeptic toward Chris Kresser, I will also be changing the name of the podcast soon. I haven’t settled on a name yet, but keep an eye out for the change.

The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
- Peter @Hyperlipid

I don’t think there are too many people out there familiar with the mechanisms of diabetes and insulin resistance that would disagree with that statement.

But just because a low-carb diet causes fat loss in this population, that doesn’t mean that carbs caused the fat gain or damaged metabolism in the first place.

I wrote about this in a previous article, There is No Single Cause of (or Treatment or) Obesity, but based on some of the comments and discussion I’ve been seeing online recently, I think it bears repeating: in order to properly frame this debate, it’s essential to separate the causes and treatment of obesity. If we don’t do this, we might as well not even have a debate at all because we won’t be talking about the same thing.

We know without a doubt that statins lower cholesterol. But does that mean high cholesterol is caused by a statin deficiency? If you break your arm, your doctor will probably put a cast on to help it heal. Does that mean we should all wear casts on our arms to make sure they don’t break?

Metabolically damaged vs. healthy: apples & oranges

Another important distinction that should be made – but often isn’t – is the difference between how people that are metabolically healthy and metabolically damaged respond to food. Of course excess carbohydrates are more likely to cause problems in someone with leptin and insulin resistance and impaired glucose tolerance. But it doesn’t follow that the same will be true in someone without metabolic problems.

People without gall bladders don’t digest fat very well. Does that mean fat causes indigestion? I have patients with iron overload due to a genetic condition called hemachromatosis. They need to limit their red meat intake because of this. Does this mean we should all avoid red meat to prevent iron overload?

We’re not robot clones. We have different genes, lifestyles, gut flora, immune fitness and exposures to toxins, stress and infections, as well as different emotional and psychological relationships with food. All of these factors play a role in weight regulation.

This explains why two people can react to the same diet in entirely different ways. And it also explains why it’s so ridiculous to extrapolate something that you experience personally to everyone else. (If I read another comment from someone saying that a low-carb diet worked for them, so the insulin-carb theory must be correct, I’m going to lose it. And it takes a lot to make me lose it!)

My unified theory of obesity

For what it’s worth, here’s my “unified theory” on what causes obesity.

Modern lifestyle + genetic predisposition = obesity.

It really is that simple.

Modern lifestyle includes processed, refined and highly rewarding and palatable foods, excess fructose, unprepared grains (especially flour), industrial seed oils, environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.

But the modern lifestyle doesn’t cause obesity in all people. I’m sure we all know someone who eats a horrible diet, doesn’t exercise, is under tons of stress and lives a shockingly unhealthy lifestyle – but doesn’t gain a single pound.

That’s where genetics come in.

Human evolution didn’t stop in the Paleolithic

A commonly held belief in the Paleo-sphere (I held it myself, until fairly recently) is that our genes haven’t changed much since the Paleolithic era. But recent evidence suggests a much more rapid pace of genetic change in humans than was previously estimated.

The birth of agriculture introduced significant selection pressure, and thus mutation, because humans were not well-adapted to this new way of life. And the evolutionary response to agricultural diet differs because different peoples adopted agriculture at different times and in different places.

Agriculture began in the Middle East 10,000 years ago, but it was never adopted by Aboriginal Australians. Might we expect the descendants of people from these two regions to have different responses when exposed to agricultural diets?

Absolutely. Researchers in Iceland have discovered a gene that regulates blood sugar tolerance. (I discussed the role of genetics in obesity and diabetes in a previous article, Are You At Risk For Diabetes and Obesity?) And we know that Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.

Lactase persistence is another example. During Paleolithic times, humans stopped producing lactase (the enzyme required to digest lactose, the sugar in milk) shortly after weaning. There was no need for it, since Paleo people didn’t raise cattle or drink milk. Skeletal remains from northern Europeans 8,000 – 9,000 years ago confirm that there was no lactose tolerance at that time.

However, skeletal remains from northern Europeans living in the Bronze Age 3,000 years ago show roughly 25% of adults produced lactase. And today, in certain Scandanavian countries, more than 95% of adults are now lactose tolerant. ¹

All of these genetic changes happened within the last 8,000 years, after the advent of agriculture.

The hand you were dealt: life isn’t always fair

What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet.

But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.

Does it even matter what causes obesity? I just want to lose weight!

Some might argue that this discussion is irrelevant, since once someone become obese it’s clear their metabolism is damaged. There are two main problems with that argument.

First, not all obese people have deranged metabolisms. Research over the past several years has defined a subset of “metabolically healthy obese” (MHO) people with normal fasting glucose, triglycerides, insulin sensitivity and other markers. I wrote about this in my article Not All Fat People Get Diabetes, and Not All Diabetics Are Fat.

Second, separating the cause and treatment of obesity is necessary to prevent confusion. Something I see all the time in my practice and in the blogosphere is normal or even underweight people following zero- or very-low-carb diets. Why? Because they’ve absorbed the notion that “carbs are bad” from the “carbs-insulin-fat gain” theory, and they avoid them in a misguided attempt to promote health. While this may work for some people, it doesn’t for many others. I know because they end up coming to me with complaints like low energy, hair loss, bad breath, constipation and more.

Food reward vs. the carbohydrate hypothesis: setting the ground rules

I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation.

Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.

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?

In a recent article I wrote on my other blog, 9 Steps to Perfect Health – #1: Nourish Your Body, I explained that saturated (SFA) and monounsaturated fats (MFA) are the preferred fuel source of the body. Another important benefit of LCSFA, and to a lesser degree MFA, is that they are stable at high temperatures and thus the safest fats to cook with.

With this in mind, here’s a list of my favorite cooking fats. Not just because they’re safe to cook with, but because they taste so good.

Ghee

Ghee is clarified butter, and it’s popular in Indian cooking. Because the milk solids have been removed, it’s very low in lactose and is almost entirely fat – mostly saturated. I tend to use ghee to brown meat and sautee garlic and onions when I make soups or stews, and I sometimes scramble my eggs in it. A tablespoon of ghee contains 8g SFA, 3.7g MFA fat and 0.5g PUFA.

Coconut oil

Along with ghee, coconut oil is one of the best fats to cook with because it’s almost entirely saturated. In fact, coconut oil is more than 90% saturated fat. While this makes it the devil according to the so-called medical authorities, we know better. In addition to being a great fuel source for the body, coconut oil has some unique properties. It is a special type of saturated fat called medium chain triglyceride (MCT). Unlike other fats, MCTs do not require bile acids for digestion. This means they are easily absorbed in the upper part of the small intestine. Coconut oil is also rich in lauric acid, a fatty acid found in mother’s milk that is anti-fungal, anti-bacterial and anti-viral. Coconut oil has 4g of SFA, 0.3g of MFA and <0.1g of PUFA.

Leaf lard

No self-respecting French chef would ever be without lard. Leaf lard is obtained from the visceral fat deposit surrounding the kidney and loin, and is considered the highest grade of lard because it has little pork flavor. This is why it’s prized in baking, where it’s used to make flaky, moist pie crusts, croissants and other non-Paleo delights. Lard is an incredibly versatile fat. I use mostly to roast vegetables. Unlike olive oil, vegetables roasted in lard do not get soggy or greasy. They stay crisp and almost dry, with a wonderful flavor. This surprises people because they think of lard as “greasy”. Not so. A tablespoon of lard has about 6g MFA, 5g SFA and 1.6g PUFA.

Duck fat

Let me just say this, if you’ve never had potatoes roasted or fried in duck fat, you haven’t had French fries. I mean that literally. Duck fat was what folks in Europe used to make the original French fries before industrial seed oils came along. Once you taste potatoes – or any vegetables – roasted or fried in duck fat, you’ll know why. A tablespoon of duck fat has 6 g MFA, 4 g LCSFA and 1.6 g PUFA.

Butter

Butter has a lower smoke point than the fats listed above, which makes it less suitable for high temperature cooking. However, it’s a great fat to use on top of fish or meat in the oven, or in stews or slow-cooked meals at lower temperatures. “Butter makes everything better” is exactly right. A tablespoon of butter contains 7.2g of SFA, 2.9g of MFA and 0.4g of PUFA.

What are you favorite uses for these fats? Let us know in the comments section.

In a previous article in this series on diabesity I briefly mentioned the role of gut health in obesity and diabetes. I’d like to go into more detail on that subject here, especially since it’s not a very well known relationship.

Our gut is home to approximately 100,000,000,000,000 (100 trillion) microorganisms. That’s such a big number our human brains can’t really comprehend it. One trillion dollar bills laid end-to-end would stretch from the earth to the sun – and back – with a lot of miles to spare. Do that 100 times and you start to get at least a vague idea of how much 100 trillion is.

The human gut contains 10 times more bacteria than all the human cells in the entire body, with over 400 known diverse bacterial species. In fact, you could say that we’re more bacterial than we are human. Think about that one for a minute.

We’ve only recently begun to understand the extent of the gut flora’s role in human health and disease. Among other things, the gut flora promotes normal gastrointestinal function, provides protection from infection, regulates metabolism and comprises more than 75% of our immune system. Dysregulated gut flora has been linked to diseases ranging from autism and depression to autoimmune conditions like Hashimoto’s, inflammatory bowel disease and type 1 diabetes.

Recent research has shown that the gut flora, and the health of the gut in general, also play a significant role in both obesity and diabetes. I’ve seen this anecdotally in my practice as well. Nearly every patient I treat with a blood sugar issue also has a leaky gut, a gut infection, or some other chronic inflammatory gut condition.

We now know that the composition of the organisms living in your gut determines – to some extent, at least – how your body stores the food you eat, how easy (or hard) it is for you to lose weight, and how well your metabolism functions. Let’s take a closer look at the mechanisms involved.

Intestinal bacteria drive obesity and metabolic disease

A study published this year in Science magazine found that mice without a protein known as toll-like receptor 5 (TLR5) in their gut gain excessive weight and develop full-blown diabetes and fatty liver disease when fed a high-fat diet. If we think of the gut flora as a community, TLR5 is like a neighborhood police force that can keep the houligans in check. Without TLR5, bad bacteria can get out of control.

The study authors found that these bad bacteria caused a low-grade inflammation in the mice, which caused them to eat more and develop insulin resistance. They also found that treating these mice with strong antibiotics (enough to kill most of the bacteria in the gut) reduced their metabolic abnormalities.

But the most interesting part of this study is what happened when the researchers transferred the gut flora from the TLR5-deficient overweight mice into the guts of skinny mice: the skinny mice immediately started eating more and eventually developed the same metabolic abnormalities the overweight mice had. In other words, obesity and diabetes were “transferred” from one group of mice to the other simply by changing their gut flora (as shown in the image below).

Other studies have shown that the composition of the gut flora differs in people who are obese and diabetic, and people who are normal weight with no metabolic irregularities.

One possible mechanism for how changes in the gut flora cause diabesity is that different species of bacteria seem to have different effects on appetite and metabolism. In the study on TLR5 deficient mice I mentioned above, the mice with too much bad bacteria in their guts experienced an increase in appetite and ate about 10 percent more food than their regular relatives. But it wasn’t just that these mice were hungrier and eating more; their metabolisms were damaged. When their food was restricted, they lost weight – but still had insulin resistance.

Other studies have shown that changes in the gut flora can increase the rate at which we absorb fatty acids and carbohydrates, and increase the storage of calories as fat. This means that someone with bad gut flora could eat the same amount of food as someone with a healthy gut, but extract more calories from it and gain more weight.

Bad bugs in the gut can even directly contribute to the metabolic syndrome by increasing the production of insulin (leading to insulin resistance), and by causing inflammation of the hypothalamus (leading to leptin resistance).

How modern life screws up our gut and makes us fat and diabetic

What all of this research suggests is that healthy gut bacteria is crucial to maintaining normal weight and metabolism. Unfortunately, several features of the modern lifestyle directly contribute to unhealthy gut flora:

• Antibiotics and other medications like birth control and NSAIDs
• Diets high in refined carbohydrates, sugar and processed foods
• Diets low in fermentable fibers
• Dietary toxins like wheat and industrial seed oils that cause leaky gut
• Chronic stress
• Chronic infections

We also know that infants that aren’t breast-fed and are born to mothers with bad gut flora are more likely to develop unhealthy gut bacteria, and that these early differences in gut flora may predict overweight and obesity in the future.

It’s interesting to note that the diabesity epidemic has neatly coincided with the increasing prevalence of factors that disrupt the gut flora. I’m not suggesting that poor gut health is the single cause of obesity and diabetes, but I am suggesting that it likely plays a much larger role than most people think.

How to maintain and restore healthy gut flora

The most obvious first step in maintaining a healthy gut is to avoid all of the things I listed above. But of course that’s not always possible, especially in the case of chronic stress and infections, and whether we were breast-fed or our mothers had healthy guts.

If you’ve been exposed to some of these factors, there are still steps you can take to restore your gut flora:

• Remove all food toxins from your diet
• Eat plenty of fermentable fibers (starches like sweet potato, yam, yucca, etc.)
• Take a high-quality probiotic, or consider more radical methods of restoring healthy gut flora
• Treat any intestinal pathogens (such as parasites) that may be present
• Take steps to manage your stress

In the first part of this series on diabesity, we “got under the hood” to look at the underlying mechanisms of both obesity and diabetes. We’ve now moved on to discussing the environmental and lifestyle risk factors that drive these conditions. In the last article we learned about the top 3 dietary causes of diabesity. In this article, we’re going to see how stress can independently cause both obesity and diabetes.

A huge – and I mean huge – amount of research over the past two decades shows that stress causes both obesity and diabetes in a variety of ways. Studies also show that stress makes it hard to lose weight. This is one reason why some people just can’t seem to lose weight no matter how well they eat or how much they exercise. I believe stress is one of the most important – yet most often ignored – factors driving the diabesity epidemic.

Stress is a bigger problem than you think

Hans Selye, the famous physiologist who coined the term “stress”, defined it this way:

…the nonspecific response of the body to any demand made upon it.

The prominent psychologist Richard Lazarus offers a similar definition:

…any event in which environmental demands, internal demands, or both tax or exceed the adaptive resources of an individual…

Most people only think of psychological stress when they hear the term “stress”. When asked what causes stress, they might say things like losing a job, having a fight with your spouse, driving in traffic or getting audited by the IRS.

While it’s true that psychological challenges like this are major stressors, what many people don’t realize is that stress is also caused by physiological challenges, such as:

• insomnia
• chronic infections
• inflammation
• autoimmune disease
• environmental toxins
• dieting
• too much exercise

Even if your levels of psychological stress are pretty low, any of the conditions listed above can provoke a chronic stress reaction in your body. And as we’ll see in the next section, chronic stress can make you both fat and diabetic.

10 ways stress makes you fat and diabetic

When stress becomes chronic and prolonged, the hypothalamus is activated and triggers the adrenal glands to release a hormone called cortisol. Cortisol is normally released in a specific rhythm throughout the day. It should be high in the mornings when you wake up (this is what helps you get out of bed and start your day), and gradually taper off throughout the day (so you feel tired at bedtime and can fall asleep).

Recent research shows that chronic stress can not only increase absolute cortisol levels, but more importantly it disrupts the natural cortisol rhythm. And it’s this broken cortisol rhythm that wreaks so much havoc on your body. Among other effects, it:

• raises your blood sugar
• makes it harder for glucose to get into your cells ¹
• makes you hungry and crave sugar
• reduces your ability to burn fat
• suppresses your HPA-axis, which causes hormonal imbalances
• reduces your DHEA, testosterone, growth hormone and TSH levels ²
• makes your cells less sensitive to insulin
• increases your belly fat and makes your liver fatty
• increases the rate at which you store fat
• raises the level of fatty acids and triglycerides in your blood

Each one of these consequences alone could make you fat and diabetic, but when added together they’re almost a perfect recipe for diabesity.

Our bodies aren’t made for chronic stress

One of the reasons chronic stress is so destructive is that our bodies didn’t evolve to deal with it. We’re set up to handle short-term, acute stress fairly well. In paleolithic times, this might have been caused by getting chased by a lion or hunting for our next meal. In fact, this type of stress may even be beneficial for our bodies because it improves our ability to react to the challenges of life.

What we’re not adapted for, however, is the chronic, unrelenting stress that has become so common in modern life. This type of stress provokes feelings of hopelessness and helplessness – what psychologists call a “defeat response”. And it’s the defeat response that leads to increased fat storage, abdominal obesity, tissue breakdown, suppression of the immune system, and all of the other effects I listed above that directly cause obesity and diabetes.

A closer look at insomnia, dieting and exercise

I’d like to take a closer look at three often stressors that can make us fat and diabetic: insomnia, dieting and exercise.

More than a third of American suffer from insomnia, with 42 million prescriptions for sleeping medications filled in 2007. Several studies show that sleep deprivation elevates cortisol and makes it more likely that you’ll get fat and develop diabetes.

A very recent paper showed that restricting sleep to 5 hours a night for just one week significantly reduces insulin sensitivity. Another study earlier this year showed that even one night of sleep loss increased appetite in young, healthy adults. Sleep restriction is associated with impairment of carbohydrate tolerance, and research has shown that a loss of 3 hours of sleep each night causes a weight gain of 4-5%.

It’s estimated that between 50-60% of Americans are dieting at any given time. That’s a huge number. And while it may seem counter-intuitive that dieting contributes to obesity and diabetes, it makes perfect sense when you understand that dieting is a stressor that disrupts our cortisol rhythm.

A 2001 study showed that “cognitive dietary restraint” (translation: stressing about food or doing overly restrictive diets) raises your cortisol levels. Studies have also shown that caloric restriction – as is common in low-fat diets – increases cortisol levels. And a recent study reported on by Stephan Guyenet at Whole Health Source found that caloric restriction is especially harmful when combined with sleep deprivation.

Finally, although not common in the general population, too much exercise can also predispose you to weight gain and diabetes by raising cortisol levels, breaking down muscle tissue and increasing fat storage. This is especially true if cortisol levels are already elevated or disrupted by other stressors like gut infections, insomnia, food toxins or psychological factors.

It’s not uncommon (in the paleo/fitness subculture, at least) to encounter someone who eats well and exercises their brains out, but cannot lose weight. In fact, several of my patients fall into this category. They are often surprised when I tell them they need to exercise less if they want to lose weight and recover their health. What they may not realize is that cortisol is a catabolic hormone. It breaks the body down.

While this might sound like a good thing for those trying to lose weight, it’s not. Muscle tissue is metabolically active and actually helps us lose weight. A reduction of lean muscle tissue may drop a few pounds in the short-term, but it will predispose you to weight gain in the future by impairing your metabolism. (This is another reason why caloric restricted diets, which break down muscle tissue, don’t work in the long-term and even make things worse.)

So if you’re struggling with weight or blood sugar control, don’t diet, get plenty of sleep and take it easy with exercise. You’ll be a lot better off.

I got an email from Pamela Schoenfeld, R.D. the other day. She wanted to make me aware of a paper she and her colleagues (Hite, et al)published on Friday in the journal Nutrition. It’s a critique of the Report of the 2010 Dietary Guidelines Committee (DGAC) that recommended that we all go on eating the same low-fat, high-carb diet that has contributed to the epidemics of obesity, diabetes and heart disease (among others).

The paper is open-access, which means you can read the full text for free (PDF). Here’s the gist: the new dietary guidelines proposed by the DGAC aren’t based on scientific evidence. The authors criticize the DGAC for excluding recent research that contradicts their low-fat propaganda, and for conveniently ignoring the fact that disease rates have skyrocketed over the past 30 years in spite of Americans eating less fat and more carbs.

The DGAC report essentially said, “Hey Americans! You’re fat and sick because you haven’t done a good enough job following our advice. What you need to do is eat even less fat (and by extension more carbs), and then you’ll finally lose weight and maybe not die of a heart attack.

Obviously the DGAC has never heard Einstein’s definition of insanity, which is to do the same thing over and over again and expect a different result.

Hite et al start the paper off with this gem of a quote:

What is required is less advice and more information. – Gerald M. Reaven

Amen to that! There’s no doubt we’re in the midst of a serious nutritional crisis, but the DGAC is dead wrong about what’s causing it. Hite et al continue:

Nutritional health covers a wide range of concerns but first and foremost in the mind of the public are whether the standing recommendations for lowering fat intake and increasing carbohydrate intake were ever appropriate for the prevention of obesity, diabetes, and cardiovascular disease;

You took the words right out of my mouth!

The authors go on to dismantle the DGAC dietary recommendations by reviewing all of the available evidence (imagine that!), rather than just focusing on the studies that support their viewpoint. Real science! What a breath of fresh air.

If you’re interested in learning more about how we’ve been collectively duped into the idea that fat is bad and carbs are good, read the paper. It’s not highly technical and is intended, to some degree I think, for a lay audience. But for those of you who don’t have time to read it, I’m going to list a few of the section headings to give you the idea:

“Strong recommendations, weak evidence”

“Animal versus plant protein: Recommendations do not reflect limitations and uncertainties of the science”

This is an important paper. It’s one of the most comprehensive critiques of the mainstream dietary recommendations I’ve seen, and it’s all in one place. So please, share this with as many people as you can. Post it to Facebook. Tweet it. Print it and take it to your doctor. Send it to your Mom & Dad, who might still think butter is bad for them. Tape it on your refrigerator. Get the word out!

In the last article we learned that type 2 diabetes (T2DM) is characterized by chronic inflammation. We also learned that while inflammation often precedes the development of obesity and T2DM, obesity and T2DM contribute to inflammation – creating a vicious cycle of metabolic damage.

In this article we’re going to review the complex and sometimes murky relationship between body weight and type 2 diabetes. There’s a strong association between obesity and T2DM in the scientific literature, and it doesn’t take a rocket scientist to determine that there might be a connection between the two.

But some obese people never develop T2DM, and and some type 2 diabetics are extremely lean. Even more strangely, recent research suggests that obesity may actually protect certain people from developing T2DM.

How do we make sense of this? Let’s find out.

How obesity causes type 2 diabetes

As I explained in the previous article, body fat isn’t just a lump of inert tissue. It’s a metabolically active endocrine organ that secretes inflammatory cytokines and hormones, both of which have profound effects on our physiology.

It has long been known that T2DM is a disease of impaired glucose metabolism. But what is less commonly known is that T2DM is also characterized by impaired fat metabolism. And recent research suggests that this is one way that obesity contributes to type 2 diabetes.

The first step in this process is an abnormal gain of fat mass, usually caused by overconsumption of wheat, fructose, industrial seed oils or other dietary toxins. As fat mass increases, more leptin is secreted. (Remember, leptin is the hormone that tells the brain to decrease appetite, increase metabolic rate and increase physical activity.) Chronically high levels of circulating leptin cause leptin resistance. It’s like leptin is banging on the brain’s door, but the brain has its headphones on and can’t hear leptin knocking.

Leptin resistance causes free fatty acids (FFA) to spill over into tissues other than fat cells, such as the liver, pancreas and heart. This starts a chain reaction of inflammation and toxicity, because fat does not belong in these tissues and damages them when present.

Also, obesity causes excessive growth of fat tissue in two ways: it makes the fat cells larger (hypertrophy) and increases their number (hyperplasia). These overgrown fat cells become unstable and eventually rupture, releasing their fat content and causing further inflammation as the body attempts to clean up the dead or dying fat cells.

The end result of this “lipotoxicity” and inflammation is insulin resistance, which as you know is the defining feature of type 2 diabetes and the metabolic syndrome.

Not all obese people get diabetes

At one point it was assumed that all obese people were at higher risk for developing T2DM. But in recent years, research has proven that assumption to be untrue. We now know that a subset of obese people are “metabolically healthy”, which means that their fasting glucose, triglycerides, and other metabolic markers are normal. This population, referred to as the metabolically healthy obese (MHO) are at no higher risk for type 2 diabetes or cardiovascular disease (CVD) than their metabolically healthy lean counterparts.

Early studies suggested that up to 1 in 3 obese people were metabolically healthy. But these studies used either insulin resistance or the presence of metabolic syndrome (which includes 3+ risk factors) alone to determine metabolic health. But a newer study that used a stricter definition of metabolic health (the absence of any risk factor known to contribute to T2DM) found that the percentage of metabolically healthy obese is much lower: only 6%.

Though the number of MHO is much lower than was once assumed, it’s still true that a small subset of obese people 1) does not develop type 2 diabetes or metabolic syndrome, and 2) is not at higher risk for cardiovascular disease.

How might that be possible?

Not all obesity is created equal

The most honest answer to that question is, “we still don’t really know”. But there are a few possibilities.

The first is that not all obesity is the same. There are two main areas where we store fat: under the skin (subcutaneous) and in the abdominal cavity (abdominal or visceral). Visceral fat (a.k.a. “beer gut”, “spare tire”, and “wheat belly“) is distinguished from subcutaneous fat by a large waist circumference and waist-to-hip ratio. As it turns out, the amount of visceral fat you have is far more important than body-mass index (BMI) in predicting whether you’ll develop type 2 diabetes or metabolic syndrome.

Let’s take a step back and look at why obesity develops in the first place. You might be surprised to learn that obesity is actually a healthy response to high blood sugar. High blood sugar is extremely toxic. The conversion of glucose to fat is the body’s attempt to protect the liver, brain and other vital organs from glucose poisoning. But this mechanism only works for so long. Eventually the fat cells can’t accommodate any more glucose, and metabolic dysfunction sets in.

Subcutaneous fat has a much larger capacity to store the converted glucose as fat, given its much larger size and distribution throughout the body. This may explain why it appears to be protective against metabolic syndrome, and why men, who possess a smaller amount of subcutaneous fat than women, tend to more easily develop “beer gut” or “wheat belly”.

Visceral fat, on the other hand, is not only a smaller storage depot than subcutaneous fat, it is highly active from a metabolic point of view. It is associated with a higher production of inflammatory cytokines, and it is more susceptible to lipolysis. Visceral fat cells are also subject to sudden pressure variations (cough, physical exercise, etc.) that cause them to rupture more easily than subcutaneous fat cells. And as we saw earlier in this article, ruptured fat cells cause inflammation.

All of this explains why visceral fat is an independent predictor of insulin sensitivity, impaired glucose tolerance, high blood pressure and high cholesterol and triglycerides. That means even if you have a relatively low BMI, you’re at much higher risk for T2DM and cardiovascular disease if you’ve got a lot of visceral fat. It also means that even if you have a high BMI, if you don’t have a lot of visceral fat you may not be at higher risk.

A second factor in determining whether obesity protects against or causes type 2 diabetes is levels of a hormone called adiponectin. Early studies suggested that high adiponectin levels protect against obesity, and it was observed that adiponectin levels were inversely correlated with BMI. But later studies found that increased levels of adiponectin in mice led to remarkable weight gain – that wasn’t accompanied by high blood sugar or other metabolic abnormalities. In fact, the mice with high adiponectin levels are up to 5 times fatter than the control mice, but they still don’t develop type 2 diabetes.

This suggests there may be something about adiponectin that protects against the metabolic abnormalities that cause T2DM, and that adiponectin levels may be another explanation for why some obese people don’t develop diabetes.

A third explanation for the MHO phenotype may be genetics. I’m going to leave it at that for now, because this article is already getting very long, and I will be devoting an entire future article to the contribution of genetics to diabesity.

Metabolically “healthy” obese still isn’t healthy

As we saw above, the MHO are not at higher risk of developing type 2 diabetes or heart disease. However, there’s more to health than normal triglycerides and blood sugar. A group of researchers recently found that the MHO who don’t have T2DM and CVD die at the same rate as those that do. The MHO are at higher risk for cancer and death from any cause than the non-obese, and they are also at higher risk for dying from traumatic injuries.

This highlights the negative impact of excess weight alone. What’s more, weight loss still improves insulin sensitivity and fasting insulin levels in obese people that are metabolically healthy.

Although nearly 1 in 3 Americans are obese today, it hasn’t always been this way. Overweight and obesity have only become common in the last 40 years in the U.S., and is virtually unheard of in traditional hunter-gatherer societies. Leanness is the natural human state, and obesity is a sign that something has gone wrong.

That’s why I think it’s still a good idea for the overweight and obese to lose weight, provided they do it in a responsible way that doesn’t include severe caloric restriction (which won’t work in the long-term anyways, and can actually predispose towards increased weight gain in the future). Given the non-metabolic problems that characterize obesity – such as impaired mobility, joint problems, reduces sexual function, psychological and social status, etc. – all obese individuals will benefit from losing weight.

In part 2 we’re going to discuss the mirror reflection of the metabolically healthy obese phenotype: the “metabolically unhealthy non-obese”, a.k.a. the “skinny diabetic”.

In the previous article in this series, I argued that diabesity is an autoimmune, inflammatory disorder. In this article, we’re going to review the evidence linking inflammation to obesity and type 2 diabetes (T2DM) and learn why inflammation may be the single-most important mechanism driving the diabesity epidemic.

The inflammation-diabesity connection is a hot topic in the scientific literature. A Pubmed search for “inflammation diabetes obesity” turns up more than 1,800 articles. The association between these conditions has been known for decades. In fact, more than 100 years ago high doses of salycilates – a class of anti-inflammatory compounds which includes aspirin – were used to treat T2DM. In 1876, a physician named Ebstein found that sodium salycilate could make the symptoms of diabetes completely disappear. (In case you’re wondering why doctors don’t use this therapy today, it fell out of favor due to the serious side effects caused by high doses of salicylates.)

Though the association between inflammation and diabesity is well-known, questions remain. Does diabesity cause inflammation, or does inflammation cause diabesity? How and why does the body initiate an inflammatory response to diabesity? Does obesity itself cause inflammation, or is inflammation caused by something secondary to obesity (like high blood sugar or triglycerides)?

I’m going to try to answer those questions in this article. Let’s dive in.

How inflammation causes diabesity

There are several lines of evidence that inflammation directly causes obesity and diabetes.

First, inflammation has been shown to precede the development of diabesity. Elevated levels of inflammatory cytokines predict future weight gain, and infusion of inflammatory cytokines into healthy, normal weight mice causes insulin resistance.

The idea that inflammation precedes diabesity is supported by the observation that humans with other chronic inflammatory conditions are at higher risk of developing T2DM. For example, about one-third of chronic Hepatitis C patients develop T2DM, and those with rheumatoid arthritis are also at higher risk.

Second, inflammation begins in the fat cells themselves. Fat cells are the first to be affected by the development of obesity. As fat mass expands, inflammation increases. One mechanism for this may be dysfunction of the mitochondria (the “power plant” of our cells) caused by the additional stress obesity places on cellular function. Another mechanism may be oxidative stress. As more glucose is delivered to the fat cells, they produce an excess of reactive oxygen species (ROS) which in turn starts an inflammatory cascade within the cell.

Third, inflammation of the fat tissue causes insulin resistance, which is the primary feature of T2DM. TNF-α, a cytokine (small protein) released during the inflammatory response, has been repeatedly shown to cause insulin resistance. Several other proteins involved with inflammation, such as MCP-1 and C-Reactive protein, have also been shown to cause insulin resistance.

Fourth, inflammation of the brain (specifically the hypothalamus) causes leptin resistance, which often precedes and accompanies insulin resistance and T2DM. Leptin is a hormone that regulates appetite and metabolism. It does this through its effect on the hypothalamus. When the hypothalamus becomes resistant to leptin, glucose and fat metabolism are impaired and weight gain and insulin resistance result.

Finally, inflammation of the gut causes leptin and insulin resistance. This may occur via an increase in lipopolysaccharide (LPS), an endotoxin produced by Gram-negative bacteria in the gut. LPS has been shown to cause inflammation, insulin resistance in the liver and weight gain.

How diabesity causes inflammation

Up until relatively recently, fat was considered an inert tissue with no biological activity. The idea was that it was just, well, there. It didn’t do much other than store excess energy.

We now know, however, that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. The metabolic activity of fat is the key to understanding its role in diabesity.

Why would obesity cause inflammation? There are two basic theories. The first is that obesity-induced inflammation is actually a protective mechanism that prevents the body from losing mobility or fitness. Fat storage is an anabolic process, which means it builds up the organs and tissues. Inflammation, on the other hand, is a catabolic process. Catabolism breaks down organs and tissues. It’s possible that the activation of catabolism via inflammation is the body’s attempt to keep weight within acceptable bounds. Evidence that experimentally induced local inflammation in fat tissue improves insulin resistance and causes weight loss supports this theory.

The second theory is that obesity-induced inflammation is simply a malfunction that was never selected against in human evolution. Obesity and its related disorders have been extremely rare throughout human history, and have only become common in the past 40 years. The surplus of modern, processed foods that accompanies diabesity is also a relatively new phenomenon. It’s possible that the stresses of obesity are similar enough to the stresses of an infection that the body reacts to obesity in the same way it would to an infection: via inflammation. Supporting this theory is evidence that the same intracellular, inflammatory stress pathways are activated in both obesity and infection.

Whichever theory is correct (and they probably both are, to some extent), it’s clear that diabesity causes inflammation. Insulin and leptin resistance impair glucose metabolism. When fat cells become insensitive to insulin, they can’t store any more glucose and hyperglycemia results. Excess sugar in the blood causes glycation, a process where a sugar molecule binds to a protein or a fat, and leads to the formation of advanced glycation endproducts (AGEs). AGEs are inflammatory and are associated with T2DM.

Obesity also contributes to inflammation by up-regulating certain genes involved with the inflammatory response. These genes control the expression of white blood cells called macrophages that play a key role in inflammation. As the concentration of macrophages in the fat tissue increases, the release of inflammatory byproducts such as TNF-α, IL-6 and MCP-1 also increases. This means that the more fat tissue you have, the more inflammation it will produce.

Putting it all together

Collectively, these findings are consistent with the theory I presented in the last article that obesity is an autoimmune, inflammatory disorder.

As we’ve seen, inflammation is both the cause and the result of diabesity. Once obesity and/or insulin resistance have been established, each can further stimulate the production of inflammatory cytokines, forming a vicious cycle of inflammation and diabesity.

It follows, then, that the key to preventing and treating diabesity is reducing inflammation. Unfortunately, few clinicians treating diabesity today understand this. Focusing exclusively on regulating blood sugar and fat hormones without addressing other potential causes of inflammation is bound to produce inferior results.

What are these “other causes” of inflammation? In a phrase: the modern lifestyle. Specifically, dietary triggers (fructose, wheat and industrial seed oils), stress, poor sleep, gut dysbiosis and environmental toxins all cause inflammation on their own. When combined together, they are an explosive mix.

We’ll talk about each of those factors in future articles. For now, the takeaway is that inflammation is probably the single most important mechanism driving the diabesity epidemic. Keep this in mind as we discuss the lifestyle factors that contribute to diabesity, because almost all of them relate back to inflammation in some way.

Welcome to the first episode of The Healthy Skeptic Podcast! To listen to this podcast and subscribe to future episodes in iTunes, click here or click the new iTunes podcast button in the sidebar to the right.

If you don’t use iTunes, you can listen to the file by clicking this link. If you’d like to download it, just right-click the link and download it to your computer. If you’re an Android user or prefer subscribing to an RSS feed of the podcast and blog together, click here.

We’re kicking things off with an interview with Dr. Stephan Guyenet, Ph.D. on obesity, body fat regulation, and weight loss. Stephan is a researcher at the University of Washington studying the neurobiology of fat regulation. He also writes one of my favorite blogs on nutrition and health, Whole Health Source.

Topics covered include:

• The little known causes of the obesity epidemic
• Why the common weight loss advice to “eat less and exercise more” isn’t effective
• The long-term results of various weight loss diets (low-carb, low-fat, etc.)
• The body-fat setpoint and its relevance to weight regulation
• The importance of gut flora in weight regulation
• The role of industrial seed oils in the obesity epidemic
• Obesity as immunological and inflammatory disease
• Strategies for preventing weight gain and promoting weight loss

It’s a bit long at 1:20, but I think you’ll enjoy it if you’re interested in this topic.

Please let me know what you think!

From the documentary Fat Head

I came across some interesting research the other day concerning the potential role of Bisphenol-A (BPA) in regulating weight.

BPA is a chemical that is found in several plastics and plastic additives. It’s in the water bottles folks carry to gyms and in the baby bottles moms use to feed their infants. And it’s in almost all of our bodies. A CDC study in 2007 found that 92% of 2,500 subjects studies had detectable amounts of BPA in their urine.

A study published in 2002 by Masuno and colleagues demonstrated that relatively small amounts of BPA significantly reduced insulin sensitivity and accelerated the formation of adipocytes (fat cells). In other words, BPA made the mice fat.

Not only did BPA trigger the conversion of pre-adipocytes to adipocytes, it also stimulated the conversion process once triggering had occurred. This “double-whammy” effect caused a 1,300% increase in fat levels, compared with a 150% increase with insulin alone.

The worldwide obesity epidemic has been primarily explained in terms of poor diet, decreases in exercise, and other lifestyle factors. (I am planning a future series on weight loss, so stay tuned!) However, this research raises the possibility that hormone-disrupting contaminants such as BPA may play a role in regulating weight. BPA triggers and then stimulates two of the key biological mechanisms underlying obesity. It increases the number of fat cells, and it enhances their fat storage.

Health authorities in the US make the claim that the levels of BPA found in most humans are not a risk to human health. However, researchers working in the field have a different view. Ample evidence suggests that BPA can harm lab animals at concentrations below those already occurring in most people.

A report (PDF) published in Reproductive Toxicology by 38 scientists evaluated the strength of data from more than 700 BPA studies.

The panel concluded that BPA exposure in the womb permanently alters the genes of animals, impairs the function of organs in ways that persist into adulthood, and triggers brain, behavioral, and reproductive effects, including diminished sperm production. Effects deemed likely included a heightened sensitivity to carcinogens, impaired immunity, and diminished insulin sensitivity.

Although the jury is still out on BPA’s ability to cause weight gain in humans, I think the consequences of obesity and the diseases it’s linked to far outweigh the “convenience” of drinking out of plastic water bottles. Of course there are several other reasons not to use plastic water bottles, including the waste they generate and their harmful effect on oceans and sea life.

So do yourself and the planet a favor: get a stainless steel water bottle, and abstain from drinking bottled water! I like the Klean Kanteen brand, but there are many others.

It has also been shown that polycarbonate baby bottles heated by microwave leach BPA into milk fed to infants. So Moms, please don’t heat those bottles in the microwave!

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.