Tuesday, May 21, 2013

Review of Gather: The Art of Paleo Entertaining

Gather-Front-Cover-700x707Gather, the Art of Paleo Entertaining by Bill Staley and Hayley Mason, is a brand new Paleo cookbook designed to inspire year-round celebrations with family and friends. No gathering of loved ones is complete without a table full of delicious food, yet it can be difficult to prepare multi-course meals that can be enjoyed by those who are following a Paleo diet. Bill and Hayley’s book is proof that it’s possible to eat and entertain like a gourmet without gluten, grains, or other “non-Paleo” ingredients.

Gather is not only visually stunning, it also contains impressive multi-course meals perfectly designed for a variety of holidays and celebrations throughout the year. The index is divided by the four seasons, and each season has its own set of menus to guide and inspire you for your own gathering of friends and family.

If you’re on a Paleo diet and you love food, Gather is the cookbook for you.Tweet This

With Gather, you’ll be able to organize a casual Sunday brunch in the spring, a Tuscany-inspired dinner party in the summer, a Paleo Thanksgiving feast in the fall, and lovely winter holiday meal. The menus cover a variety of cuisines, such as Chinese, Cuban, and Caribbean, and there are kid-friendly menus, including a Halloween spooky supper, and even a birthday party, complete with chicken nuggets and birthday cake – all grain-free of course!

The best part of serving food from Gather is that you can feel confident you’re serving your loved ones nourishing food while pleasing their palates. A lot of early Paleo cookbooks were long on health and short of flavor and creativity. Gather is the best of both worlds: the dishes are worthy of a 5-star restaurant, with nutrient-dense ingredients such as pastured meats, wild seafood, green and root vegetables, and healthy fats like coconut oil and grass-fed butter.

Gather would also make a wonderful gift for a friend or family member who is tempted to try Paleo but is concerned that the idea of a “diet” is restrictive, or insist that they can’t live without their favorite foods. This book will be more than enough to convince them that they can eat healthily without sacrificing flavor and enjoyment. (But you might try cooking them a recipe from the book first!)

If you’re a Paleo foodie like I am, Gather is a must on your kitchen shelf. The book releases today (April 30th, 2013), and can be ordered on Amazon.com.

Tagged as: bill staley, book review, gather, hayley mason, paleo, primal palate

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50 Shades of Gluten (Intolerance)

breadsThis article was first featured at The Huffington Post. Click here to see the original article.

Celiac disease (CD) was initially described in the first century A.D. by a Greek physician named Aretaeus of Cappadocia. (1) But neither Aretaeus nor anyone else knew that CD is caused by an autoimmune reaction to gluten, a protein in wheat. That didn’t become clear until 1950 — several centuries later — when Dr. Willem Dicke, a Dutch pediatrician, conclusively proved that gluten was the culprit. (2) Dicke’s discovery saved millions of children and adults from the perils of untreated celiac disease, including malnutrition, stunted growth, cancer, severe neurological and psychiatric illness and even death.

Since then, the mainstream view of gluten intolerance has been relatively black or white: Either you have celiac disease, in which case even a small amount of gluten will send you running to the bathroom in three seconds flat, or you don’t, and you can chug down beer and bagels without fear. This “all-or-nothing” view has led to some doctors telling patients that suspect they’re sensitive to gluten but test negative for CD that they’re simply imagining an affliction that doesn’t exist.

It turns out those doctors are wrong.

In order to explain why, I have to give you a quick lesson in the biochemistry of wheat and wheat digestion.

Wheat contains several different classes of proteins. Gliadins and glutenins are the two main components of the gluten fraction of the wheat seed. (They’re essential for giving bread the ability to rise properly during baking.) Within the gliadin class, there are four different epitopes (i.e. types): alpha-, beta-, gamma- and omega-gliadin. Wheat also contains agglutinins (proteins that bind to sugar) and prodynorphins (proteins involved with cellular communication). Once wheat is consumed, enzymes in the digestive tract called tissue transglutaminases (tTG) help to break down the wheat compound. In this process, additional proteins are formed, including deamidated gliadin and gliadorphins (aka gluteomorphins).

Here’s the crucial thing to understand: Celiac disease is characterized by an immune response to a specific epitope of gliadin (alpha-gliadin) and a specific type of transglutaminase (tTG-2). But we now know that people can (and do) react to several other components of wheat and gluten — including other epitopes of gliadin (beta, gamma, omega), glutenin, WGA and deamidated gliadin – as well as other types of transglutaminase, including type 3 (primarily found in the skin) and type 6 (primarily found in the brain). (3, 4, 5, 6, 7, 8)

This is a huge problem because conventional lab testing for CD and of gluten intolerance only screens for antibodies to alpha-gliadin and transglutaminase-2. If you’re reacting to any other fractions of the wheat protein (e.g., beta-gliadin, gamma-gliadin or omega-gliadin), or any other types of transglutaminase (e.g., type 3 or type 6), you’ll test negative for CD and gluten intolerance no matter how severely you’re reacting to wheat.

Official statistics suggest that Celiac disease affects between 0.7 percent and 1 percent of the U.S. population. (9) But considering the limited scope of the testing, it’s possible that the actual incidence might be much higher.

In addition, CD is only the tip of the iceberg when it comes to gluten intolerance. Celiac disease is caused by a distinct autoimmune response to wheat proteins and transglutaminase enzymes in the gut. But CD is just one possible expression of gluten intolerance; there are many other ways that sensitivity to gluten can manifest in the body. These are collectively referred to as “Non-Celiac Gluten Sensitivity,” or NCGS.

There’s no consensus definition of NCGS yet, but the most common understanding is that it’s a reaction to gluten that is not autoimmune (like CD) or allergic (like wheat allergy). Another definition I’ve seen is, “a reaction to gluten that resolves when gluten is removed from the diet and CD and allergy have been ruled out.” (10)

It’s difficult to estimate the prevalence of NCGS because there is no definitive diagnostic test for it. As I mentioned above, the currently available tests for gluten sensitivity are primitive and only screen for a small fraction of the components of wheat that people react to. Another issue is the variety of symptoms caused by CD and NCGS. While most people assume that gluten intolerance always causes digestive distress, this is not the case. Almost 50 percent of new patients diagnosed with CD do not have gastrointestinal symptoms. (11) Moreover, for every one case of CD that is diagnosed, there are 6.4 cases that remain undiagnosed – the majority of which are atypical or silent forms without gastrointestinal symptoms. (12)

Gluten intolerance can affect nearly every tissue in the body, including the brain, skin, endocrine system, stomach, liver, blood vessels, smooth muscles and even the nucleus of cells. CD and NCGS are associated with an astonishing variety of diseases, from schizophrenia and epilepsy, to Type 1 diabetes and osteoporosis, to dermatitis and psoriasis, to Hashimoto’s hypothyroidism to peripheral neuropathy. (13) Because the range of symptoms associated with gluten intolerance is so broad and nonspecific (e.g., can be attributed to any number of conditions), many patients and doctors don’t suspect gluten may be the cause.

Even with these limitations, some estimates suggest NCGS may occur in as many as 1 in 20 Americans. (14) And while some mainstream medical professionals continue to insist that NCGS doesn’t exist, several studies have validated it as a distinct clinical condition — including gold-standard, double-blind, placebo-controlled trials. (15)

With all of this in mind, the obvious question that arises is, “What’s the best way to test for gluten intolerance?” Because of the limitations of current laboratory testing I described above, most experts on gluten sensitivity agree that the only reliable test is a “gluten challenge.” This involves removing gluten from the diet completely for a period of at least 30 days, and then adding it back in after that. If symptoms improve during the elimination period, and return when gluten is reintroduced, a diagnosis of NCGS can be made.

However, for many people a gluten-free diet isn’t enough. Some grains that don’t contain gluten, such as corn, oats and rice, contain proteins that are similar enough in structure to gluten to elicit an immune response in people with CD or NCGS. In addition, about 50 percent of patients with CD show signs of intolerance to casein, the protein in milk. (16) This may explain why up to 30 percent of CD patients continue to have symptoms or clinical signs after adopting a gluten-free diet. (17) For this reason, I recommend a completely grain- and dairy-free diet during the gluten challenge period.

Finally, though the gluten challenge is still the gold standard test for gluten intolerance, there is a relatively new lab (Cyrex Laboratories) offering a comprehensive blood test which screens for all of the wheat and gluten proteins and transglutaminase enzymes I mentioned above. This can be a helpful diagnostic tool, but it should never replace a gluten/Paleo challenge. (Note: It must be ordered by a physician or health care practitioner.)

Now I’d like to hear from you. Do you suspect you may have gluten intolerance? If so, has removing gluten resolved your symptoms — or have you found it necessary to remove grains and dairy as well? If you haven’t tried a gluten challenge, what’s holding you back?

Tagged as: Celiac Disease, digestion, gluten intolerance, research, statistics

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The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number

cholesterol test

To read more about heart disease and cholesterol, check out the special report page.

Cardiovascular disease is one of the most misdiagnosed and mistreated conditions in medicine. In the first article in this series, I explained the evidence suggesting that eating cholesterol and saturated fat does not increase cholesterol levels in the blood for the majority of the population.

In this article, I will debunk the myth that high cholesterol in the blood is the cause of heart disease.

Part of the confusion about cholesterol and its role in heart disease is caused by imprecise terminology. So, before I explain why high cholesterol is not the underlying cause of heart disease, we have to cover some basics.

Cholesterol is not technically a fat; rather, it’s classified as a sterol, which is a combination of a steroid and alcohol. It’s crucial to understand that you don’t have a cholesterol level in your blood. Cholesterol is fat-soluble, and blood is mostly water. In order for cholesterol to be transported around the body in the blood, it has to be carried by special proteins called lipoproteins. These lipoproteins are classified according to their density; two of the most important in cardiovascular disease are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

I know this can get confusing quickly, so let me use an analogy to make this more clear. Imagine your bloodstream is like a highway. The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.

The crucial test for heart disease risk you’ve probably never heard of.Tweet This

Coronary arteries are essentially hollow tubes, and the endothelium (lining) of the artery is very thin—only one cell deep. The blood, which carries lipoproteins like LDL, is in constant contact with the endothelial lining. So why does the LDL particle leave the blood, penetrate the endothelium and enter the artery wall? The answer is that it’s a gradient-driven process. Going back to our analogy, the more cars there are on the road at one time, the more likely it is that some of them will “crash” into the fragile lining of the artery. It’s not the number of passengers (cholesterol) the cars are carrying that is the determining factor, but the number of cars on the highway.

The significance of this in terms of determining your risk of heart disease is profound. When you go to the doctor to get your cholesterol tested, chances are he or she will measure your total, LDL and HDL cholesterol. This tells you the concentration of cholesterol (passengers) inside of the lipoproteins (cars), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood.

LDL cholesterol levels and LDL particle number are often concordant (i.e. when one is high, the other is high, and vice versa), and this is probably why there is an association between LDL cholesterol and heart disease in observational studies. The elevated LDL cholesterol was more of a proxy marker for elevated LDL particle number in these cases. But here’s the kicker: they can also be discordant. In layperson’s terms, it’s possible to have normal or even low cholesterol, but a high number of LDL particles. (1) If this person only has their cholesterol measured, and not their particle number, they will be falsely led to believe they’re at low risk for heart disease. Even worse, the patients that are the most likely to present with this pattern are among the highest risk patients: those with metabolic syndrome or full-fledged type 2 diabetes. The more components of the metabolic syndrome that are present—such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL—the more likely it is that LDL particle number will be elevated. (2)

On the other hand, patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease. In fact, studies suggest they’re at even lower risk than patients with low LDL-C and low LDL-P. (3) Yet they will often be treated with statin drugs or other cholesterol lowering medications, because the clinician only looked at LDL-C and failed to measure LDL particle number. This is a concern for two reasons. First, statin drugs aren’t harmless. (I’ll go into more detail on this in the third post of the series.) Second, studies suggest that low cholesterol can increase the risk of death, especially in women and the elderly.

In one study of over 52,000 Norwegians, researchers found that women with total cholesterol levels below 195 mg/dL had a higher risk of death than women with cholesterol levels above that cut-off. (4) And a study published in the American Journal of Medicine found that people over 70 years of age with total cholesterol levels below 160 mg/dL had twice the risk of death than those with cholesterol levels between 160-199 mg/dL. (5) Low cholesterol is also associated with increased risk of disease—especially mental health and brain disorders. For example:

A study in the Journal of Psychiatric Research found that men with low total cholesterol levels were 7 times more likely to die prematurely from unnatural causes such as suicide and accidents than other men in the study. (6)A 1993 study published in The Lancet found that depression was 3 times more likely in men over 70 with low cholesterol than in those with normal or high cholesterol. (7)A Swedish study found that women with the lowest cholesterol suffered significantly more depressive symptoms than other women in the study. (8)A study in the journal Neurology showed that low cholesterol is associated with increased risk of dementia. (9)A paper published in the European Journal of Internal Medicine linked low cholesterol levels with Alzheimer’s disease. (10)

It’s important to note that all of these studies were observational, which means that they don’t prove that low cholesterol was the cause of the increased risk of death or disease that was observed. It’s possible, for example, that these patients had another disease that caused both the lower cholesterol and increase in disease or mortality. However, given what we know about the important roles of cholesterol in the body, it’s certainly plausible that low cholesterol is capable of contributing to these problems directly.

Before concluding, I’d like to point out that although LDL particle number is superior to LDL cholesterol as a marker for heart disease, it’s still just that—a marker. A marker is not a disease. It’s a risk factor for a disease. Having a risk factor for a disease does not guarantee that you will get that disease—it just increases the chance that you will. There are still several gaps in our knowledge about LDL-P and its usefulness in a clinical setting. For example:

Imagine two people with an LDL-P above 2,000, which puts them in the highest risk group. Person A follows a Paleo diet and lifestyle, gets plenty of sleep, manages stress and has no other significant risk factors for heart disease. Person B eats a Standard American Diet, doesn’t exercise, doesn’t get enough sleep, is stressed out and has several other risk factors for heart disease. Logic would dictate that Person A would be at much lower risk for heart disease than Person B, but there isn’t any comparative data to quantify the difference in risk and it’s unlikely such a study will ever be done. (Who would pay for it?)Imagine two people following a healthy Paleo-type diet and lifestyle. Person C has no conventional risk factors for heart disease. Person D has no conventional risk factors either, but does have an LDL-P of 2,000. Logic here would dictate that Person D is at higher risk than Person C, but again, we don’t have actual data to quantify the difference in risk.

Heart disease is a complex, multifactorial process. The likelihood that we’ll have a heart attack depends on numerous factors, including genetics, diet, lifestyle and living environment. The purpose of this article is not to suggest that LDL-P is the only risk factor that matters, or that other risk factors shouldn’t be taken into consideration. It is simply to point out that existing evidence suggests that LDL-P is a much better predictor of heart disease risk than LDL or total cholesterol, and that it appears to be one of the better markers available to us now.

I was going to follow this article with one on statin drugs. But I’m almost certain that all of you are going to ask what increases LDL particle levels after reading this, so I think I’ll cover that next and then move on to statins after that.

Note: if you’re interested in a much more thorough discussion of how to determine your risk of heart disease and how to use diet, supplements and lifestyle changes to protect yourself and those you love, check out the High Cholesterol Action Plan.

Tagged as: cardiovascular, cholesterol, Heart Disease, LDL-C, LDL-P, particle number, risk

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What Causes Elevated LDL Particle Number?

geneticsTo read more about heart disease and cholesterol, check out the special report page.

In the last article in this series, I explained that LDL particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol. In this article, I’m going to briefly outline the five primary causes of elevated LDL-P.

Conventional medicine is primarily focused on suppressing symptoms. If your blood pressure is high, you take a medication to lower it. If your blood sugar is high, you take a medication to lower it. If your cholesterol is high, you take a medication to lower it. In most cases there is rarely any investigation into why these markers are high in the first place, with the possible exception of some basic (but often incorrect) counseling on diet and exercise.

On the other hand, functional medicine—which is what I practice—focuses on treating the underlying cause of health problems instead of just suppressing symptoms. If your blood sugar, blood pressure or cholesterol are high, the first question a functional medicine practitioner will ask is “why?” If we can identify the root cause of the problem, and address it at that level, medication is often unnecessary.

To use a simple analogy, if you have weeds in your garden, what happens if you just cut the weeds from the top? They grow right back—and sometimes faster than before! If you really want to get rid of them once and for all, you have to pull them up by their roots.

With this in mind, let’s look at some of the potential causes of elevated LDL particle number. If your LDL-P is high, it makes sense to test for and treat any of the conditions below (with the exception of the last, which is genetic and thus can’t be treated) before—or at least along with—taking pharmaceutical drugs.

5 common causes of elevated LDL particle number that can increase your risk of heart disease.Tweet This

LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.

As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.

Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (1) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.). (2)

Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.) Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3, 4)

Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone. (5)

Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori, which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (6) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL. (7)

Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens. This has been confirmed by studies showing that mice with defective LDL receptors—and thus very high levels of LDL—are protected against infection by gram-negative bacteria like H. pylori. (8)

One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation. (9) Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins. (10)

Though more research is needed in this area, the studies above suggest that a leaky gut could increase the level of LPS and other endotoxins in the blood, and thus increase LDL particle number as a result. I have seen this in my practice. I recently had a patient with high LDL-P and no other risk factors. I tested his gut and discovered H. pylori and small intestine bacterial overgrowth (SIBO). After treating his gut, his LDL-P came down to normal levels.

The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a mutation of a gene that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB). The LDL receptor sits on the outside of cells; the LDL particle has to attach to the LDL receptor in order to deliver the nutrients it’s carrying and be removed from the circulation. ApoB is the part of the LDL particle that binds to the receptor. If we use a door lock as an analogy, apolipoprotein B would be the key, and the LDL receptor is the lock. They both need to be working properly for LDL to deliver its cargo and to be removed from the bloodstream.

Homozygous carriers of FH have two copies of the mutated gene. This condition is very rare. It affects approximately 1 in a million people. And people that are homozygous for this mutation have extremely high total cholesterol levels, often as high as 1000 mg/dL. And unfortunately they usually die from severe atherosclerosis and heart disease before the age of 25.

Heterozygous carriers, however, only have a single copy of the mutated gene, and the other copy is functioning normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL, along with very high LDL particle number. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.

It’s important to note that people with FH have primarily large, buoyant LDL particles, and yet are still at much higher risk for cardiovascular disease. While it’s true that small, dense, oxidized LDL particles are more likely to cause atherosclerosis, large, buoyant particles can also be harmful when their concentration is high enough. This is one reason why LDL particle number is a superior marker to LDL particle size.

In the next article in this series, I will debunk the myth that statins extend lifespan in healthy people with no pre-existing heart disease.

Tagged as: cholesterol, conditions, genetics, infection, insulin resistance, LDL-P, metabolic syndrome, thyroid

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The Diet-Heart Myth: How to Prevent and Reverse Heart Disease Naturally

Senior couple on cycle rideThis is the final article in the Diet-Heart Myth series I’ve been writing over the past several weeks. If you missed the previous articles, you can find them on the special report page for heart disease.

Ben Franklin said, “An ounce of prevention is worth a pound of cure.” Heart disease is no exception. According to the INTERHEART study, which examined cardiovascular risk factors in 51 countries, 9 out of the 10 strongest risk factors for heart disease are modifiable by changes in diet and lifestyle. (1)

While taking action now does not guarantee that you’ll never get heart disease (as age is perhaps the strongest risk factor), it does vastly improve your chances of avoiding it or at least delaying it significantly. In this article, I’ll teach you how to do that in three simple steps: Eat a Heart-Healthy Diet, Live a Heart-Healthy Lifestyle, and Boost Your Heart-Healthy Nutrients.

3 simple steps to living a heart healthy lifestyle that your doctor has never told you about.Tweet This

When most people hear the phrase “heart-healthy diet”, they think of egg-white omelettes, a salad with no dressing or similar low-fat, low-cholesterol fare. But if you’ve been reading this series, or my blog in general, you know better. The “Paleo Template” approach I’ve written about here is an excellent starting place. It includes all of the necessary micronutrients in their most bioavailable form, emphasizes an optimal balance of fats, eliminates highly processed and refined foods, and reduces other food toxins that interfere with nutrient absorption. On the other hand, the American Heart Association’s “heart healthy” diet emphasizes nutrient-poor foods such as whole grains and vegetable oil, and unnecessarily restricts nutrient-dense foods like red meat, animal fat and cholesterol.

But which version of the “Paleo Template” is best for preventing heart disease? In this series we’ve been focusing on LDL particle number as one of the primary drivers of atherosclerosis. We also discussed the five main causes of elevated LDL-P, including insulin/leptin resistance, genetics, poor thyroid function, infections and leaky gut. If you have elevated LDL-P while on a Paleo diet, the key is to first discover what’s causing it and then tailor your diet accordingly. In this article, I’m going to focus on insulin/leptin resistance and genetics, since those are the two most common causes of elevated LDL-P that I see in my practice.

In this case, the best approach is often a low-carb Paleo diet. When I say low carb, I generally mean between 50–100 grams of carbohydrate per day in the form of fruit and starchy vegetables like sweet potatoes, potatoes, plantain, yuca and taro. I do not count non-starchy vegetables toward the carbohydrate intake, because I don’t believe they make a significant enough contribution to matter. The purpose of this approach is to improve insulin and leptin sensitivity and promote weight loss, which will in turn decrease LDL-P.

If you have high LDL-P, but normal triglycerides, HDL, small LDL-P and your lipoprotein insulin resistance (LP-IR) score on the NMR LipoProfile is normal, and you’ve ruled out thyroid problems, infections and leaky gut, than it’s very likely that you have one of the many genetic variants that can lead to increased LDL particle number. In this case, a low-carb Paleo diet will often increase—rather than decrease—LDL-P. In my practice I will often recommend what I call a “Mediterranean Paleo diet” in these cases. This means following the basic Paleo approach, but reducing intake of fat and increasing intake of fruit and starchy vegetables. You can still eat fat as it naturally occurs in food, but try not adding as much additional fat to meals, and using more monounsaturated fat than saturated fat. In many cases this will decrease LDL-P quite significantly.

The trickiest situation is when someone has both insulin and leptin resistance and a genetic issue. A low-carb diet will usually drive up LDL-P in that situation, but it will improve many other markers that are also risk factors for heart disease, including triglycerides, HDL, fasting insulin, fasting glucose, etc. So I will usually recommend a low-carb diet for these patients, and if their LDL-P goes up, try to use natural therapies to bring it down.

Exercise has been shown to reduce LDL particle concentration even independently of diet. (1) Regular exercise prevents the development and progression of atherosclerosis, improves lipids, and reduces vascular symptoms in patients that already have heart disease. The benefits of exercise are related to maintenance of body weight or weight loss, blood pressure control, return of insulin sensitivity, and beneficial changes in lipids, all of which in turn promote endothelial stabilization and vascular health.

In addition to distinct periods of exercise, it’s also important to sit less and stand and walk more. In fact, some research suggests that this “non-exercise” physical activity may have a greater impact on our cardiovascular health than exercise. Dan’s Plan has some fantastic recommendations for physical activity, as well as a great software and hardware-based tracking system.

I have come to believe that chronic sleep deprivation is one of the most pernicious—yet under-recognized—contributors to the modern disease epidemic. Sleep deprivation has been associated with weight gain, insulin resistance, increased appetite and caloric intake, overconsumption of highly palatable and rewarding food, decreased energy expenditure and a reduced likelihood of sticking with healthy lifestyle behaviors. Sleep duration and quality are inversely associated with blood pressure in epidemiological studies, and high blood pressure is one of the strongest independent risk factors for cardiovascular disease (CVD). (2) Finally, the Nurses Health Study found that those who reported fewer than 5 hours of sleep at night had a 38% greater risk of coronary heart disease (CHD) than those reporting 8 hours of sleep. (3)

For tips on how to improve your sleep, see my article “Sleep More Deeply“.

Stress increases the risk of cardiovascular disease in numerous ways. It increases intestinal permeability, impairs blood sugar control, depresses immunity (which increases the risk of infection), contributes to fat storage in the liver, and promotes consumption of comfort and junk foods. But perhaps the most significant contribution stress makes to CVD is that it promotes inflammation. Stress has been shown to increase circulating inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6), both of which are associated with heart disease (4). On the other hand, stress management can have a profound impact on heart disease risk. One recent randomized trial showed that regular meditation decreased the risk of death from heart attack, stroke and all causes by 48%—a much greater reduction than what is observed with statins even in the highest risk population. (5)

In addition to the basic heart-healthy versions of the Paleo template I mentioned above, there are several specific foods/nutrients that have been shown to improve cardiovascular health.

Cold-water, fatty fish are an excellent source of EPA and DHA, long-chain omega-3 fats with several cardiovascular benefits. An analysis of randomized trials since 2003 suggests that regular fish consumption or consumption of fish oil would reduce total mortality or deaths from all cause by 17%. (6) This is remarkable when you consider the fact that statin drugs only reduce total mortality by 15%, and even then, only in certain populations.

Monounsaturated fats have been shown to reduce LDL and triglycerides and increase HDL. They also decrease oxidized LDL, reduce oxidation and inflammation in general, lower blood pressure, decrease thrombosis, and they may reduce the incidence of heart disease. (7) The best sources of monounsaturated fat are olives, olive oil, macadamia nuts, and avocados.

Antioxidant-rich foods protect against heart disease in a number of important ways. Our antioxidant defense system is what protects us from oxidative damage, which as you now know is a major risk factor for heart disease. Strengthening this system has two sides: reducing our exposure to oxidative stress and increasing our intake of antioxidant-rich foods. When most people think of antioxidants, they think of fruits and vegetables like dark, leafy greens and fruits like berries. But while it’s true that these foods are rich in antioxidants, what a lot of people don’t know is that red meat and organ meats are also very rich in important antioxidants that aren’t found in significant amounts in plant foods, like CoQ10 and retinol, which is preformed vitamin A. A good rule of thumb is to eat the rainbow, choosing a variety of colors of fruits and vegetables, as well as organ meats, meats, eggs, and grass-fed dairy.

Polyphenols are a diverse class of molecules made by plants, certain fungi, and a few animals. They serve a lot of purposes including defense against predators and infections, defense against sunlight damage, chemical oxidation, and coloration. The color, in fact, of many fruits and vegetables like blueberries, eggplants, red potatoes, and apples comes from polyphenols. Some of the best studied polyphenol-rich foods are tea, especially green tea; blueberries; extra-virgin olive oil; red wine; citrus fruits; hibiscus tea; dark chocolate; coffee; turmeric; and other herbs and spices. Polyphenol-rich foods have been shown to have a number of beneficial health effects. For example, dark chocolate has been shown to lower blood pressure and LDL cholesterol and improve insulin sensitivity, red wine has been shown to prevent the increase in oxidized fats that occur after consuming a meal high in oxidized and potentially oxidizable fats, several studies have shown that hibiscus tea lowers blood pressure in people with hypertension, and blueberries have been shown to lower blood pressure and oxidized LDL in men and women with metabolic syndrome. (8)

Some studies have shown that nut consumption may reduce the risk of cardiovascular disease. In a recent analysis of NHANES data from 1999 to 2004, investigators found that nut consumption was associated with a decrease in a wide range of cardiovascular disease risk markers, including body mass index, waist circumference, and systolic blood pressure, compared to non-consumers of nuts. (9) This is observational data so we can’t be sure that it was the nuts, rather than some other factor that wasn’t adequately controlled for, that led to the improvements. That said, a review of five large prospective studies (including NHANES) as well as clinical trials examining the effects of nut consumption on lipid parameters found similar results. (10) I favor macadamia nuts, almonds and hazelnuts because they are lower in omega-6 linoleic acid, which research suggests may contribute to CVD when consumed in excess.

In the NHANES study, subjects followed for more than 19 years with the highest quartile of dietary soluble fiber intake had a 15% lower risk of heart disease and had a 10% lower risk of cardiovascular events. (11) Soluble fiber binds bile acids or cholesterol; upregulates LDL receptors in the liver; increases clearance of LDL; inhibits fatty acid synthesis by producing short-chain fatty acids like acetate, butyrate, and propionate; improves insulin sensitivity; and increases satiety with lower overall energy intake. (12)

I hope you’ve enjoyed the Diet-Heart Myth series, and that the information I’ve presented will help protect you and those you love against heart disease. I’ve done my best to cover the most important steps you can take, both in terms of diagnosis and treatment. That said, cardiovascular disease is a complex, multifactorial process and it’s difficult to give it the attention it deserves in a blog series. That’s why I created the High Cholesterol Action Plan. It’s a 9-week, digital course that goes into much more depth on these topics than I was able to go into here, including additional tests that help determine your risk, natural alternatives to statins, and a step-by-step framework that helps you determine your own, customized “action plan”. Click here to learn more about it and sign up.

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The Roundup

RoundupHere is The Roundup, Edition 4, bringing you the best from around the web from the past two weeks! This week, I’m focusing on articles that address diabetes, obesity, and related metabolic disorders.

In 2011, I wrote an article explaining the many factors affecting the development of diabetes and obesity, and how many of the proposed mechanisms could conceivably contribute to the development of the disease. As obesity and diabetes research advances, however, the interconnection between these proposed mechanisms is becoming more clear, yet no primary treatment protocol has been established. And as I’ve mentioned before, I doubt one single treatment will ever be devised; after all, we’re not robots!

Recently, two studies were published suggesting alternative treatments that could help obese and diabetic patients lose weight and improve metabolic function. One study found that intermittent fasting (IF) may be a possible treatment protocol to help with weight loss and recover metabolic function, as IF has been found to limit inflammation, boost pancreatic function, and decrease levels of sugars and lipids in circulation. Another study demonstrated that intestinal parasites may be a potential diabetes and obesity treatment, as certain parasites may be able to mitigate inflammation, improve glucose tolerance, and prevent excess weight gain. Perhaps in the future, the recommendation to “eat less and exercise more” will be a distant memory, and these novel treatments will be considered the norm!

Fossil record shows early hominids hunted animals and ate their brains as early as 2 million years ago.A psychiatrist says that ADHD might actually be a misdiagnosed sleep disorderA study shows that increased efforts are needed to regulate the supplement industry.A small clinical trial suggests that fecal transplantation may help reduce or eliminate symptoms of ulcerative colitis in most children and young adults.Collaboration between veterinary and human medicine offers a cross-species perspective on a range of human health problems.Research by the NIH finds that women with sufficient amounts of vitamin D have a 32% lower risk of developing uterine fibroids.Mercola.com: My interview with Dr. Mercola on one of the most important tests for heart disease you can get.Stumptuous.com: Krista Scott-Dixon explains hormones, homeostasis, and why you (probably) need carbs.Ancestralize Me: A young woman shares her experience with using ancestral nutrition to manage her autoimmune condition.Rodale: Carageenan hides out in a lot of your favorite foods, causing inflammation, gut irritation, and potentially even cancer.Chris Kresser I hate spam too. Your email is safe with me.

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Boost fertility naturally & promote lifelong health for you & your baby.

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Break through the energy swings, digestive upset, and obstacles of adopting a Paleo diet.

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