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• 1.3 lbs premium hot dogs
• 2 lbs ground beef
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• 1/2 lb chorizo sausage

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This 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.

Eat a Heart-Healthy Diet

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.

Insulin/leptin resistance

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.

Genetics

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.

Live a Heart-Healthy Lifestyle

Physical activity

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.

Sleep

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 management

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)

Boost Your Heart-Healthy Nutrients

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

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 fat

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

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.

Polyphenol-rich foods

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)

Nuts

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.

Soluble fiber

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)

Summary

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.

Here is The Roundup, Edition 5, bringing you the best from around the web from the past two weeks!

Blast from the Past

Last May (2012), I wrote an entire series on salt, including the history of salt in the human diet, the dangers of salt restriction, and my recommendations for a healthy salt intake. There’s no evidence that adding salt to taste to a whole foods, Paleo diet is unhealthy, and salt restriction to the level recommended by the American Heart Association (AHA) is not only completely unnecessary, it’s potentially harmful. There are far more effective ways to reduce blood pressure and the risk for heart disease and stroke than salt restriction, such as increasing dietary intake of potassium, magnesium, and calcium.

Now, a New York Times article explains how a new expert committee, commissioned by the Institute of Medicine (IOM) at the request of the CDC, confirmed that there’s no rationale restricting sodium intake to 2,300 milligrams a day—let alone the AHA target of 1,500 mg per day. The IOM committee also agrees that a sodium intake this low could increase rates of heart attacks and the risk of death in certain populations. It’s incredible to me that this is still considered a controversial topic and that there is so much disagreement between various health organizations on how much salt is “too much” for the general population. It’s perfectly reasonable for most people to consume between 3-4 grams per day, which is right around the world average for salt intake (3,400 mg/day or ~1.5 tsp salt).

Hopefully this (non) issue will be settled soon, and we can focus our attention on the dietary components that really do make a difference in the general population’s health.

Research Report

• New evidence suggests that gluten intolerance may drive at least some cases of IBS.
• Research finds that sunlight prolongs lifespan by lowering blood pressure, demonstrating how the benefits of sun exposure outweigh the risks.
• A new study suggests lowest risk of death occurs at vitamin D levels between 20-36 ng/mL. (Note that 20-30 ng/mL is deficiency according to current standards. I will discuss this on my next podcast.)
• A hospital survey found that kids living in the U.S. who were born elsewhere are 59 percent less likely to have allergic diseases, but their risk increases with time spent in the country.

Worth A Look

• Nourished Kitchen: Jenny explains why she drinks full fat, local, raw milk.
• Mark’s Daily Apple: The top 8 most common reactions to your grain-free diet, and how to respond.
• Forbes.com: A new app allows you to easily boycott Monsanto products—not just food.
• SexyBack Summit: Sean Croxton hosts another great summit, this time focused on all aspects of sexual health.

For the Foodies

• Against All Grain: Watermelon Mint Lemonade
• Food Renegade: Cilantro Lime Chicken Salad on Avocado
• Homemade Mommy: Ghee Mayonnaise
• PaleOMG: Honey Mustard Crunchy Chicken Plantain Salad
• Rubies and Radishes: Chorizo Mashed Yams
• Health-Bent: Italian Sweet & Sour Pork Tenderloin with French Pork & Beans

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 the risk of heart disease. In the second article, I explained it’s not the amount of cholesterol in your blood that drives heart disease risk, but the number of LDL particles. In the third article, I discussed the five primary causes of elevated LDL particle number.

In this article, I will debunk the myth that statin drugs save lives in healthy people without heart disease, and discuss some of the little known side effects and risks associated with these drugs.

Myth #3: Statins save lives in healthy people without heart disease

Statins have been hailed by many in the conventional medical establishment as wonder drugs, with some physicians going as far as suggesting they should be added to the water supply. (The doctor that made that particular suggestion is named John Reckless – I kid you not.) But are statins really the wonder drugs they’ve been made out to be?

Are statins really the wonder drugs they’ve been made out to be?

Before we dive into the statistics on statins, I need to briefly explain the difference between relative and absolute risk reduction. Researchers and pharmaceutical companies often use relative risk statistics to report the results of drug studies. For example, they might say “in this trial, statins reduced the risk of a heart attack by 30%”. But what they may not tell you is that the actual risk of having a heart attack went from 0.5% to 0.35%. In other words, before you took the drug you had a 1 in 200 chance of having a heart attack; after taking the drug you have a 1 in 285 chance of having a heart attack. That’s not nearly as impressive as using the 30% relative risk number, but it provides a more accurate picture of what the actual, or “absolute” risk reduction is.

With that in mind, let’s take a closer look at the efficacy of statins in two broad groups of people: those with pre-existing heart disease, and those without pre-existing heart disease. In the medical literature, these groups are referred to as “secondary prevention” and “primary prevention”, respectively.

Secondary prevention (those with pre-existing heart disease)

There’s little doubt that statins are effective in reducing heart attacks and deaths from heart disease in people who already have heart disease. Several large controlled trials including 4S, CARE, LIPID, HPS, TNT, MIRACL, PROV-IT and A to Z have shown relative risk reductions between 7% on the low end in MIRACL and 32% on the high end in 4S, with an average risk reduction of about 20%.

However, absolute risk reductions are much more modest. They range from 0.8% in MIRACL on the low end to 9% in 4S on the high end, with an average of 3%.

An analysis by Dr. David Newman in 2010 which drew on large meta-analyses of statins found that among those with pre-existing heart disease that took statins for 5 years (1):

• 96% saw no benefit at all
• 1.2% (1 in 83) had their lifespan extended (were saved from a fatal heart attack)
• 2.6% (1 in 39) were helped by preventing a repeat heart attack
• 0.8% (1 in 125) were helped by preventing a stroke
• 0.6% (1 in 167) were harmed by developing diabetes
• 10% (1 in 10) were harmed by muscle damage

A heart attack or stroke can have a significant negative impact on quality of life, so any intervention that can decrease the risk of such an event should be given serious consideration. But even in the population for which statins are most effective—those with pre-existing heart disease—83 people have to be treated to extend one life, and 39 people have to be treated to prevent a repeat heart attack.

Moreover, these results do not apply to all populations across the board. Most studies have shown that while statins do reduce cardiovascular disease (CVD) events and deaths from CVD in women, they do not reduce the risk of death from all causes (“total mortality”). (2)

Nor do these results apply to men or women over the age of 80. Statins do reduce the risk of heart attack and other CVD events in men over the age of 80, and especially at this age, these events can have a significant negative impact on quality of life. However, the bulk of the evidence suggests that statins don’t extend life in people over 80 years of age, regardless of whether they have heart disease, and the highest death rates in people over 80 are associated with the lowest cholesterol levels. (3), (4)

Primary prevention (those without pre-existing heart disease)

Statins do reduce the risk of cardiovascular events in people without pre-existing heart disease. However, this effect is more modest than most people assume. Dr. Newman also analyzed the effect of statins given to people with no known heart disease for 5 years (5):

• 98% saw no benefit at all
• 1.6% (1 in 60) were helped by preventing a heart attack
• 0.4% (1 in 268) were helped by preventing a stroke
• 1.5% (1 in 67) were harmed by developing diabetes
• 10% (1 in 10) were harmed by muscle damage

These statistics present a more sobering view on the efficacy of statins in people without pre-existing heart disease. They suggest that you’d need to treat 60 people for 5 years to prevent a single heart attack, or 268 people for 5 years to prevent a single stroke. These somewhat unimpressive benefits must also be weighed against the downsides of therapy, such as side effects and cost. During that hypothetical 5 year period, 1 in 67 patients would have developed diabetes and 1 in 10 patients would have developed muscle damage (which can be permanent in some cases, as we’ll see later in this section).

In addition, while statins do moderately reduce cardiovascular events such as heart attack in people without heart disease, they’ve never been shown to extend lifespan in this population. This is true even when the risk of heart disease is high. In a large meta-analysis of 11 randomized controlled trials by Kausik Ray, MD and colleagues published in the Archives of Internal Medicine, statins were not associated with a significant reduction in the risk of death from all causes. (6)

This trial included 65,000 people without pre-existing heart disease but with intermediate to high risk of heart disease. It was important because it was the first review that only included participants without known heart disease. Previous studies suggesting that statins are effective in reducing death in people without pre-existing heart disease included some people that did have heart disease, which would have skewed the results.

The lack of significant effect on mortality is even more interesting in light of the fact that LDL cholesterol levels did decrease significantly in the statin group; the average LDL level in those taking placebo was 134 mg/dL and the average in the statin-treated patients was 94 mg/dL—roughly 30% lower. Yet in spite of this marked reduction in LDL cholesterol in the statin group, there was no difference in lifespan between the two groups. This is yet another line of evidence suggesting that the amount of cholesterol in LDL particles is not the driving factor in heart disease.

A meta-analysis of statin trials in people without heart disease by the prestigious Cochrane Collaboration came to a similar conclusion. (7) They also observed that all but one of the clinical trials providing evidence on this issue were sponsored by the pharmaceutical industry. This is significant because research clearly indicates that industry-sponsored trials are more likely than non-industry-sponsored trials to report favorable results for drugs because of biased reporting, biased interpretation, or both. (8)

Adverse effects of statins

If statins were harmless and free, then it wouldn’t matter how many people need to be treated to prevent a heart attack or extend someone’s lifespan. But statins are not free, nor are they harmless. Statin use has been associated with a wide range of side effects, including myopathy (muscle pain), liver damage, cataracts, kidney failure, cognitive impairment, impotence and diabetes.

Unfortunately, studies show that physicians are more likely to deny than affirm the possibility of statin side effects, even for symptoms with strong evidence in the scientific literature. (9) Assuming that physicians would likely not report the adverse reaction in these circumstances, it’s probable that the incidence of statin side effects is much higher than the reported rates.

One of the most troubling side effects of statins that has only recently become apparent is their potential to increase the risk of diabetes, especially in women. A study by Dr. Naveed Sattar and colleagues published in The Lancet in 2010 examined 13 randomized clinical trials involving over 90,000 patients taking statins. They found that statin use was associated with a 9% increased risk in developing diabetes. Note that this is a relative risk, so the absolute risk of developing diabetes while taking a statin is very low. That said, observational data from the Women’s Health Initiative found a 48% increased risk of diabetes in healthy women taking statins after adjusting for other risk factors. (10)

To summarize:

• The only population that statins extend life in are men under 80 years of age with pre-existing heart disease.
• In men under 80 without pre-existing heart disease, men over 80 with or without heart disease, and women of any age with or without heart disease, statins have not been shown to extend lifespan.
• Statins do reduce the risk of cardiovascular events in all populations. A heart attack or stroke can have a significant, negative impact on quality of life—particularly in the elderly—so this benefit should not be discounted.
• However, the reductions in cardiovascular events are often more modest than most assume; 60 people with high cholesterol but no heart disease would need to be treated for 5 years to prevent a single heart attack, and 268 people would need to be treated for 5 years to prevent a single stroke.
• Statins have been shown to cause a number of side effects, such as muscle pain and cognitive problems, and they are probably more common than currently estimated due to under-reporting.

My intention here is not to suggest that statins have no place in the treatment of heart disease, but rather to give you the objective information you need to decide (along with your doctor) whether they are appropriate for you. The decision whether to take them should be based on whether you have pre-existing heart disease, what your overall risk of a heart attack is, how healthy your diet and lifestyle is, what other treatments you’ve already tried, and your own risk tolerance and worldview. It’s clear that statins reduce heart disease as well as the risk of death in those that have already had a heart attack, so if you’re in this group and you’ve already tried diet and lifestyle interventions without much impact on your lipid or inflammatory markers, you are more likely to benefit.

In the next and final article of this series, I’ll discuss three steps to preventing and reversing heart disease naturally, without drugs.

Are you suffering from low libido? Has your sex drive gradually drifted away? Are you looking for ways to connect more deeply with your partner, and cultivate a more rewarding and satisfying sex life?

If you answered yes to any of these questions, you should definitely check out Sean Croxton’s upcoming SexyBack Summit. He’s assembled a group of experts in all aspects of sexual health, including balancing hormones, supercharging sex drive, cultivating intimacy and connection, optimizing nutrition and fitness, and boosting fertility.

The summit will consist of 24 video slideshow presentations, including talks by Dr. Sara Gottfried, Paul Check, Jane Bennett, Elliot Hulse, Dr. Jen Landa and yours truly. The title of my talk is “How Stress Sabotages Your Sex Drive—And What to Do About It.” I’ll discuss the intricate connections between the thyroid, adrenals and ovaries/gonads in both men and women, and how imbalances in one system can lead to dysfunction in the others. Here’s a sampling of other presentations that will be available:

• Get in the Mood, Stay in the Mood by Dan Kalish
• Low T: Causes, Symptoms and Solutions by Reed Davis
• 50 Shades of Better Sex: Secrets of a Harvard Gynecologist by Dr. Sara Gottfried
• Natural Birth Control Alternatives by Jane Bennett
• Chasing the Big O: Overcoming the Inability to Orgasm by Cynthia Pasquella

In case you’re not familiar with the online summit format, here’s how it works. The summit startstakes place over six days, beginning on May 19th and concluding on May 26th. Each day will feature three to four presentations, which can be watched for FREE during a 24-hour period (9am to 9am Pacific). At 9am each morning, the previous day’s presentations are taken down and the next day’s go up. This means you can watch the entire event free of charge. Pretty cool, huh?

Sean is kicking the SexyBack Summit off with some cool free videos covering the top 5 ways to supercharge your sex drive. There’s a video for men (with functional medicine expert Reed Davis), and another for women (with celebrity nutritionist Cynthia Pasquella). To watch the videos and register (for free) for the Summit, just CLICK HERE.

If you’re subscribed to my email list, I’ll send out an email the day before my talk (which is happening on Day 6). I’ll also post reminders on Facebook and Twitter.

I hope you enjoy the Summit!

Note: I may earn a commission if you use the links in this article to purchase any products or programs I mentioned. I only recommend products I would use myself or that I use with patients in my practice. Your purchase helps support this site and my ongoing research.

In this episode I discuss a couple of interesting recent studies, and answer some questions. Enjoy!

In this episode, we cover:

1:35 What Chris ate for breakfast
6:27 Early evidence for meat consumption
18:33 Solving the cholesterol controversy
38:22 More details from Chris’s daily routine (and more treadmill desk)
44:00 Additional sources of magnesium
48:35 When should I stop breastfeeding?
52:49 What to do about anxiety during pregnancy

Links We Discuss:

• Oldowan hunting behaviors at Kanjera South – John Hawks Blog
• Lipids and lipoproteins and risk of different vascular events in the MRC/BHF Heart Protection Study

Full Text Transcript:

Steve Wright:  Hey everyone, welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com, and I’m your host, Steve Wright from SCDLifestyle.com.  With me is integrative medical practitioner and healthy skeptic Chris Kresser.  Chris, how are you doing today?

Chris Kresser:  I’m great, Steve.  It’s absolutely gorgeous today.  It’s been gorgeous the last several days, like in the high 70s, low 80s.  I’ve just been spending a lot of time outside with Sylvie, going on walks in the woods near my house.  Having grown up in Southern California and being used to 300 days of sunshine a year, I have to say this is happy weather for me!

Steve Wright:  Yeah, I actually just got back from a little vacation to Colorado, and even though while I was there it was everything from 25 degrees all the way to 80, it was sun shining every day, and it was the most sun I have seen in the last six months.

Chris Kresser:  Yeah, that’s the thing about Colorado, huh?  It’s very sunny there even when it’s freezing cold a lot of the time in the winter.

Steve Wright:  Yeah, it was beautiful.

Chris Kresser:  Great.  So I think it’s going to be another Q&A show today, but I have a couple studies we’re going to talk about first.

What Chris ate for breakfast

Steve Wright:  OK, well, before we get into the studies, did you have anything special for breakfast today?

Chris Kresser:  Well, I don’t know if it’s special.  I liked it.  I had two duck crépinettes.

Steve Wright:  A what?

Chris Kresser:  A crépinette.

Steve Wright:  Oh.

Chris Kresser:  This is from the charcuterie that I frequent at the farmers’ market.  It’s called The Fifth Quarter.  This guy Scott makes fantastic sausages and salamis and duck and liver pâtes and all kinds of artisanal meats.  And I may get this wrong in terms of the precise description, but a crépinette is like a patty of meat and spices that’s then wrapped in pork fat.  So I just cooked them in a pan.  These ones were duck.  He also makes some lamb crépinettes and, I think, pork crépinettes as well.  They’re really tasty.  They’re amazing.  And then I had some taro sliced really thin with a mandolin and roasted in a little bit of duck fat.  And I had some steamed broccoli with a little bit of olive oil and then a little bit of beet kvass to wash it all down.

Steve Wright:  Sounds pretty gourmet.

Chris Kresser:  It was good.  I’m doing my two-meal-a-day thing today.  It just seems to be the pattern I’m in right now, and it’s working for me.

Steve Wright:  Awesome.  Well, whenever you want to invite me over for breakfast, I’ll try one of these crépinettes.

Chris Kresser:  Anytime.  I think you’d like it.

Steve Wright:  Well, anything wrapped in pork fat, I think, is a hit for myself or anyone listening to this show.

Chris Kresser:  It’s hard to argue with, huh?

Steve Wright:  Yeah.  OK, well, before we get rolling into the studies, I want to tell everybody about Beyond Paleo, Chris.  So I don’t know if you need to… We’re not in the closet today, right?

Chris Kresser:  That’s right.  We’re out of the closet.  I’m committed to making the audio as good as I possibly can, but I discovered there’s a limit to that commitment.  However, I will say that one of our listeners, Mike, stepped up.  He has a lot of audio experience, and he generously donated a lot of his time to explaining several different ideas.  First of all, he said the audio for our show is great, and that’s a testament to you and Jordan and all the help you guys have given me in making this a fantastic show already.  But he said there were a few things we could do just to reduce the echo, which is kind of the main problem that some people have noticed.  So I bit the bullet, bought some extra sound-dampening equipment that I can set up.  I don’t have it yet.  It’s going to be here in time for the next show.  And I think once we get that set up, the audio is just going to be perfect, so I’m excited about that.  And I’m excited to be back in my office overlooking the redwood trees.  It’s much more picturesque than the closet, I’ll tell you.

Steve Wright:  Than a t-shirt?

Chris Kresser:  Yeah.

Steve Wright:  OK, awesome.  Well, huge thanks to Mike, and we’re doing our best to make this the best sounding as well as the best content on the web.  Chris, go ahead and take a break here.  I want to tell everyone about Beyond Paleo.  So if you’re new to this podcast, if you’re new to the paleo diet, or maybe you’re just someone who’s interested in optimizing your health, you’re going to want to check out what over 30,000 other people have already signed up for and started to read.  It’s called Beyond Paleo, and it’s a free 13-part email series on burning fat, boosting energy, and preventing and reversing disease without drugs.  To sign up, head over to ChrisKresser.com, and look for the big red box.  In that box, go ahead and enter your name and your email address, and Chris will go ahead and ship off the first email to your right away.  It’s pretty awesome.  I would highly recommend you start reading this series right away.

Chris, if people want more info from you in between podcasts, they can head over to Facebook and Twitter, right?

Chris Kresser:  That’s right.  Yeah, Facebook, I have a really vibrant community there, lots of great discussion.  I post a lot of studies and just things I’m thinking about throughout the week that don’t make it to my blog, and I do the same thing on Twitter.  So definitely join us there if you’re on Facebook and Twitter.

Steve Wright:  And to get there, if you’re just listening to this on iTunes, go to Facebook.com/ChrisKresserLAc or Twitter.com/ChrisKresser.

Chris Kresser:  All right.

Steve Wright:  Let’s do some studies!

Early evidence for meat consumption

Chris Kresser:  Yeah.  Those of you who follow me on Facebook and Twitter may have already seen my link to these studies, but there was one anthropological study I want to talk about that John Hawks, an anthropologist whose blog I follow and some of you may, reported on earlier in the week.  The earliest evidence of humans butchering animals for meat with stone tools is about 2.6 million years old, and that’s kind of the background for this study.  But the issue with that is that a lot of that could have been scavenging kills from other animals.  So instead of humans purposefully hunting the animals themselves and then eating them, they came across a carcass from an animal that had been hunted by some other prey animal, like a lion, for example.  That in a lot of ways, as John Hawks pointed out, is no less impressive because presumably humans were having to, in many cases, compete with these other animals for the carcass, whether the animals were there at the time or they came back, so it’s still a pretty amazing testament to the collective intelligence and teamwork of our distant ancestors.  But there were a lot of questions still then about whether we were hunting animals ourselves versus just encountering the carcasses that had already been killed.

The first really good evidence for actual hunting is about 1.8 million years old, and that was found at the Olduvai Gorge in Tanzania.  This new study that John Hawks talked about has made a big contribution to our understanding in this area because it analyzed fossil remains from Kenya, from Kandera South, which is an assemblage of artifacts and animal bones from about 2 million years ago.  And this was during what’s referred to as the Oldowan period, which is the earliest stone tool industry, which lasted from about 2.6 million years ago to about 1.7 million years ago.  Now, what was different about this study compared to some of the other ones that have been done before is that the researchers used some pretty smart methods to determine that the animal bones that were found at the site were from animals that were actually hunted and killed by humans rather than scavenged.  And they did this by looking at tooth and cut marks on the bones.  Carnivores who get to chew on bones for a while once they kill an animal, they tend to leave the middle of the bones covered in tooth marks, but if humans get access to the carcass early, they strip off the meat from the midshafts, and then they break those shafts into bits, which leaves different marks on the bones.  So in this study, they compared the tooth and cut marks on the bones that they found, and at this particular site they found marks that were much more consistent with what happens when humans get access to the carcass first, which, of course, suggested that humans had hunted and killed these animals.

Another interesting finding in this study is how our ancestors ate the animals that they killed.  A lot of these animals were really too large to carry in their entirety back to a central place like a cave, campsite, living area where they could all share it.  So what they did is they dismembered the animals on-site where they were hunted, and they only carried back certain parts of the animals, which would, of course, been the parts that were favored and easier to transport.  The parts that they brought back were the legs and the heads, and then they left the rest of the body behind.  So the legs are pretty obvious.  Those of us who eat meat often eat the legs of animals, and they’re some of the best parts there.  But the heads may not be as obvious at least at first glance, but I’ll read from a quote from the paper to explain why they did this, so it says:

But why acquire, transport, and process an abundance of medium-sized heads?  In living animals, these remains contain a wealth of fatty, calorie-packed, nutrient-rich tissues: a rare and valuable food resource in a grassland setting where alternate high-value foodstuffs (fruits, nuts, etc.) are often unavailable.

So essentially the heads contain brains, and brains are very rich in fatty acids, and in particular, the long-chain omega-3 fat DHA, which increasing evidence suggests is essential, meaning not only very important, but the technical definition of essential here from a dietary perspective means a nutrient that we need for proper functioning but cannot synthesize in our body.  Now, historically the shorter chained omega-3, primarily plant-based fat has been considered essential.  That’s alpha-linolenic acid, and it’s found in flaxseeds and walnuts, mostly nuts and seeds.  And it’s true that some alpha-linolenic acid can be converted into DHA, but that conversion is extremely poor in most people.  In fact, in the average person, less than 0.5%, or one-half of 1%, of alpha-linolenic acid gets converted into DHA.  And that’s in relatively healthy people.  That conversion is dependent on enzymes that in turn require adequate amounts of certain nutrients, like B6 and zinc, and a lot of Americans — I think up to about one-third of Americans — are deficient in the nutrients that are involved in that enzymatic conversion.  And especially vegans and vegetarians tend to have higher levels of deficiency of those nutrients.  So that one-half of 1% is kind of a best-case figure.  In reality, it’s probably a lot less than that.  And the problem there is that alpha-linolenic acid has not been shown to have the same benefits as the long-chain omega-3 fats, like EPA and particularly DHA.  So you have a situation where we need DHA, and yet even though in theory we can convert some of the shorter chained fats into DHA, in practice, especially amongst people with chronic illness or any nutrient deficiencies at all, which are really common, very little gets converted into DHA.  So what this suggests is that DHA is really, rather than alpha-linolenic acid, the real essential omega-3 fat.

This research in some way contributes to our understanding of why this might be.  I mean, we might wonder, why is that conversion so poor?  Well, if our ancestors were eating a lot more DHA, preformed DHA, like from the brains of animals that they hunted or from fish, for example, then the need to make that conversion from the short-chain omega-3 fat into DHA would have been a lot less.  And in fact, most studies do suggest that this is true.  Historically speaking, our ancestors’ intake of DHA — and for that matter, the long-chain omega-6 fat, which is arachidonic acid — our ancestors’ intake of those longer chained polyunsaturated fats was much higher than our average intake today, so it’s very likely that they didn’t really have a need to make those conversions.

This is an interesting study for me for a number of different reasons, both the evidence that we were hunting and not just scavenging animals as long ago as 2 million years ago and that we were eating the brains, which implies that we had a significant source of long-chain omega-3 fats, which could explain some of the problems we see in the conversion and adds some data to the idea that DHA rather than alpha-linolenic acid is essential.  Now, of all of the reasons that I think vegan and vegetarian diets aren’t optimal for many people for long-term health, this is probably one of the biggest because DHA is so important to the function of the brain and our vision and the growth and development of the fetus, and it just plays so many important roles that a diet that doesn’t have any preformed DHA, which a vegetarian and vegan diet would not, is really kind of difficult to support from a nutritional perspective.  This doesn’t, of course, address the various ethical and perhaps social reasons or religious reasons that people might choose to do a vegetarian or vegan diet, but I’m just speaking right now in terms of a nutritional perspective.  Vegans and vegetarians, I highly recommend taking an algae supplement.  Algae is where fish get DHA from, so it does contain preformed DHA, certain types of microalgae.  It has to specifically be for DHA.  There are a few out there.  Unfortunately, they’re quite expensive, and you have to take a lot of it to get the recommended amount of DHA, but it’s better than not taking any at all.

Let’s see if I have anything else to say about that study… Yeah, I don’t think so.  That’s it for that.

Steve Wright:  It think it’s an awesome new piece of research to definitely add to, I guess, our stack of research that supports all the recommendations we always make on this show.  I really appreciate you just going through that study, so thanks, Chris.

Solving the cholesterol controversy

Chris Kresser:  Yeah.  I’m fascinated by medical anthropology, and if I could go back to college now, I would probably study medical anthropology.  It’s a really interesting subject to me, and I think it has a lot to teach us as well.

The second study I wanted to talk about is actually a paper published in the journal Circulation, and it made kind of a big splash, at least within the research community, so some of you might have seen it already.  But this paper, what they were trying to do is determine which measures of cholesterol and lipoproteins are most predictive for a future risk of heart attack in a very high-risk population.  I’ve actually been writing a series on the blog the last couple of weeks about this, about cholesterol and lipoproteins and the difference between the two and which tests are best in terms of predicting your heart disease risk.  And there’s a fair amount of controversy still in this area, and some studies, for example, in the past have shown that the ratio of total cholesterol/HDL is just as good as a marker as LDL particle number, which is the number of LDL particles that are actually moving around in the bloodstream.  And then there have been a lot of other studies that have shown that LDL particle number or ApoB, which is a kind of proxy marker for LDL particular number, are much better predictors of risk.  So that’s what this study was setting out to look at, that question.

What made this a little bit different than some previous studies that have been done in this area is that the previous studies were observational in nature, so they were looking at observational or epidemiological data, and this study looked at data from a randomized clinical trial that was done.  This particular trial was the Medical Research Council/British Heart Foundation Heart Protection Study, and it was 20,000 high-risk men and women, and they followed them for an average of five years.  And the original trial was actually looking at the effect of a statin drug versus an antioxidant, but they measured a whole bunch of stuff, as they often do in randomized clinical trials, so in this paper the researchers just harvested some of that data.  They looked at levels of total cholesterol, LDL cholesterol, HDL, total cholesterol/HDL ratio, and then all of the different lipid subfractions like LDL particle number.  They looked at LDL particle size, you know, small LDL versus large LDL.  They looked at HDL particle number, HDL size, so they had a lot of information to work with.  And what they found in this study was that all of the LDL measurements were equally predictive for a heart attack in this high-risk population, so LDL cholesterol, LDL particle number, and ApoB, which again is a kind of proxy for measuring LDL particle number, were all relatively similar in terms of their ability to predict a heart attack in the future.

They also found that HDL was a lot less predictive, particularly in those that had pre-existing heart disease, and this is interesting, this has come up before in other studies, and what it suggests — and what some other research also suggests — is that the function of HDL decreases in people with heart disease, so there’s kind of a reverse causality there.  And one of the reasons we might see low HDL or low HDL particle number or even a normal HDL particle number but increased risk of heart disease or higher incidence of heart attack in people that have already had heart disease is that the heart disease itself actually weakens the function of HDL so it can’t carry out its protective function as well as it does in someone that doesn’t have heart disease.  So that was interesting.

And in this study there was a much stronger correlation between LDL cholesterol and LDL particle number.  As I wrote in a recent article on my website, LDL cholesterol and LDL particle number are sometimes related.  They’re often related, but not always.  And in fact, in people with metabolic syndrome, insulin resistance, they can have normal or even low levels of total and LDL cholesterol and high LDL particle number, in which case they’ll be at increased risk.  So this study showed a correlation of about 0.79, which is quite strong.  It’s certainly not perfectly correlated, but it’s stronger than the correlation that has been observed in previous studies, which was closer to 0.6.  It was 0.62 or 0.63, I think.  So the data in this is a little bit different in terms of the relationship between LDL cholesterol and LDL particle number.

There was an accompanying editorial in the journal about this study, and it was written by a doctor, and his main point is that we don’t need these extra fancy tests for estimating heart disease risk because this study shows that the standard markers are just fine in terms of predictive value.  And the other point he makes is that most people who have a heart attack have at least one risk factor.  It doesn’t just happen out of the blue.  He points to a study that looked at 21,000 deaths from fatal heart attacks, and exposure to at least one clinically elevated major risk factor was present in 87% to 100% of the people who died from a heart attack, and ‘risk factor’ in this study was defined as total cholesterol of at least 240 mg/dL, systolic blood pressure of 140, diastolic blood pressure of at least 90, cigarette smoking, and clinical diabetes.  So one of those was present in 87% to 100% of people who had a fatal heart attack, the point being that we kind of know already what the risk factors are for heart disease.  The basic lipid markers that we have are sufficient, so we don’t really need to do any more advanced testing.

I definitely agree with parts of that analysis.  I do think, as I’ve argued many times, that heart disease is a complex, multifactorial process and that it’s heavily influenced by lifestyle factors.  There was the famous INTERHEART study that looked at heart disease in over 50 countries around the world, and they found that 9 out of 10 heart attacks could have been prevented by modifiable diet and lifestyle factors, which, similar to the statistics here, it suggests that maybe 1 in 10 heart attacks are due primarily to genetics or maybe some other lifestyle or diet factor that wasn’t measured, like perhaps chronic stress or maybe gut dysbiosis or some kind of emerging factor that we don’t fully understand yet how it contributes and that isn’t often easy to measure and isn’t often measured in these studies.  So I definitely agree with that.

Also, as I pointed out in the High Cholesterol Action Plan, the ratio of total cholesterol/HDL is often in a general sense, or we should say on average, it’s just as predictive as LDL particle number, but the problem is we don’t treat averages in the clinic.  I mean, any clinician knows this.  We treat individual patients.  So studies are really good at determining trends and average effects.  They take a whole bunch of people, they measure what happened, and they average out the results and come up with a basic finding that then can be applied to clinical settings, and that’s how research is used to make treatment decisions and determine what the standard of care is.  And I’m not suggesting that I have a better way to do it, necessarily, but what I am saying is that there are always outliers on either side of the equation.  And in fact, in the editorial he says:  “It is useful to seek better discrimination of risk in those at the margins, but it is not where our greatest effort should be focused.”  And again, it’s true.  In most cases, most people just need to clean up their diet, clean up their lifestyle, get their blood pressure down, lose weight, improve their insulin sensitivity and glucose tolerance, and stop smoking.  You know, they need to take care of the basics.  That’s absolutely true.  But in the population of people that I work with, I’m hard-pressed to think of any of my patients, maybe two, that smoke cigarettes.  And many of my patients are not overweight significantly, they don’t have high blood pressure, they don’t have diabetes, they don’t fit this normal risk profile.  And yet some of them have very high LDL particle number with normal total cholesterol.  Some have high LDL particle number with high cholesterol.  Some have high cholesterol with normal LDL particle number.  So all of these situations are outside of what most doctors are seeing in their average clinical practice, and they deserve a different approach than those situations because a lot of the data that we have on the relationship between these lipid markers and heart disease doesn’t really necessarily apply to people that are on the margins, so to speak.

So I think this study adds some really important information in terms of determining a kind of general approach in standard practice, but I don’t think it invalidates the use of LDL particle number or some of the more advanced markers in one-on-one patient care, especially when someone has a more specialized practice and is treating people who are already pretty healthy, at least from a cardiovascular perspective, and are mostly interested in optimizing their health.

I will say, though, that one thing that has been really consistent in these studies is that LDL particle size does not add any predictive value once LDL particle number is known.  I think the confusion in the past where we did see these relationships between LDL particle size and heart disease is that at that time, LDL particle number was often not being measured, and so it appeared that the particle size was significant in terms of predictive value, but now when you adjust for LDL particle number, when you know the particle number, adding particle size doesn’t add any additional value.  Part of what helped us figure this out is the observation that people with familial hypercholesterolemia, which is a genetic condition that leads to very high LDL particle number and cholesterol levels, they often have large, buoyant, fluffy LDL, and yet they’re still at three times greater risk of death from heart disease than people without familial hypercholesterolemia.  So I think we can safely not worry too much about particle size as long as we know particle number, and as always, like most other diseases, heart disease is, as I said, complex and multifactorial.  There are a number of different things to consider when we’re determining the overall picture of risk.  I still think LDL particle number is a better lipid marker than LDL or total cholesterol or even the total/HDL cholesterol ratio, but total/HDL ratio for most people is a good surrogate for LDL particle number, and if you can’t afford to get or don’t have access to ApoB or LDL particle number, that can be a good substitute for many people.

Steve Wright:  Hey, Chris, let’s bring it really home for our listeners, if you can.  We just talked about total cholesterol, we talked about the ratio total/HDL, we talked about LDL-P.  Can you just give us your numbers that we should be trying to hit?  People are going to listen to this.  They’re probably going to get these things checked.  Our listeners are like your population, most likely, so can you give us some of your functional numbers for people to go after?

Chris Kresser:  Well, it’s quite complex.  I wish I could answer that question really simply.  Now, that’s part of the reason I ended up doing the High Cholesterol Action Plan, is that I realized that there was no simple way I can answer the question.  The course ended up being nine weeks long because it is really quite an involved process to determine your heart disease risk, and the reason I’ve been hesitant to just throw out a certain number is that it really varies in the sense that you have to consider the rest of the context.  Let’s say, for example, that I said you want your total cholesterol/HDL ratio to be under 4 — and that is a standard target — so if you divide your total cholesterol by HDL, it should be less than 4.  Some say less than 3 is much better and more optimal.  But let’s take two hypothetical people.  Let’s say one person has a total cholesterol/HDL ratio over 4, but they have no other risk factors for heart disease.  They’re in excellent shape, they’re fit, they exercise regularly, they’re physically active, they don’t sit a lot, they eat a really healthy diet, they manage their stress, they sleep well, etc.  They’re like the poster child for health except they have this ratio that’s above 4.  Maybe it’s 4.1 or 4.2.  And then you have another person who has the same exact total/HDL ratio, but they have high blood pressure, they’re obese, they’re not exercising, they’re not managing their stress, and they’re eating a standard American diet, and they’re 20 years older than the other people.  Obviously those two people are going to have really different heart disease risk, and even though their total/HDL ratio is the same, they’re not at all in the same boat.  And one person might need a lot of treatment, a crash course in diet changes, everything else.  The other person may not need any treatment at all, depending on the situation, maybe their family history and things like that.  So that’s kind of my hesitation, but the general target for total/HDL ratio is less than 4.

LDL particle number is really contextual, in my opinion.  I mean, the National Lipid Association and folks like Dr. Dayspring, who has written a lot about LDL particle number, and the NLA has been really responsible, to a large degree, for getting the word out there about LDL-P.  They want to see it below 1000, which is below the 20% percentile.  It’s separated into quintiles.  So if you’re below 1000, you’re in the zero to 20th percentile.  If you’re 1000 to 1299, I think, you’re in the 20th to 40th percentile.  If you’re 1300 to 1599, I think, you’re in the 40th to 60th.  1600 to — I may be getting this slightly wrong because I think I just missed — 1600 or 1700 to 1999, you’re in the 60th to 80th.  And then above 2000, you’re in the 80th to 100th percentile.  The NLA wants to see people below 1000, and they will medicate anybody with statins regardless of their other risk factors or their ‘picture.’  They’ll medicate anyone with a statin to get their LDL-P below 1000.  I’m not so sure that that’s necessary.  I think context does matter.  So if somebody comes to see me and they have an LDL-P of 1300, which puts them still in the sort of low moderate risk, maybe moderate risk group, if they have no other risk factors, I think it’s hard to justify medication in that situation, given the current evidence and what we know about the multifactorial nature of heart disease.  And as I just said, in people who had fatal heart attacks in the study that we talked about in the editorial, 87% to 100% of them had a major risk factor.  So I’m a little less aggressive as far as that goes and a lot more likely to look at the other factors.

Steve Wright:  OK, well, thanks for taking a shot at that.

Chris Kresser:  Sure.  So I think that’s it for that study.  We have time for a few questions now before we finish.

More details of Chris’s daily routine (and more treadmill desk)

Steve Wright:  OK, let’s transition.  The first question that we have here comes from Laura, and she wants to know more about your standing desk, Chris.  She says that she has transitioned to a standing desk while at the corporate office and has the opportunity to use a treadmill desk as well.  “What are your thoughts on decompressing the spine after long periods of standing?  I’ve learned that in order to help improve recovery after endurance events that you should spend time upside down or with your feet up against a wall.  What are your thoughts on this related to long periods of standing?  If I work standing for 8 hours, should I end my day with 8 minutes of time lying on the ground with my legs vertically against the wall?  Is there anything that you would recommend doing to balance out the body after standing all day?”

Chris Kresser:  Yeah, that’s a good question.  Truthfully, this isn’t an area of expertise for me.  This might be something I would defer to my wife on.  She has a lot more advanced understanding of biomechanics and has spent a lifetime studying that.  She had a treadmill desk, right?  Not just the standing desk?

Steve Wright:  I think she says she has both.

Chris Kresser:  Um-hum.  So one thing I mentioned, I think, when we first started talking about treadmill desks is there’s actually some research that suggests that standing for long periods is not that beneficial and possibly harmful.  I’m not sure that standing for 8 hours is an improvement from a health… I think it probably is an improvement over sitting for 8 hours, but I think if your choice is standing desk or sitting desk, maybe a mixture of both, actually, throughout the day is a better idea than just standing for the entire day at the desk, based on what some of the research about standing for too long suggests.  I myself actually switch back and forth between several different postures and positions.  I have a standing desk, of course, and then I have the treadmill desk, and then I have a sitting desk with a really nice chair, a Herman Miller chair that I will often sit on the edge of so that my back is still straight.  And then I have a balance disc, or a sitting disc they’re called, and I can put that on my chair, and when I’m sitting on it, I have to continually kind of adjust my posture.  It scoots me forward on my sits bones, so it’s really hard to slouch while I’m sitting on it.  And then I have a yoga ball as well.  So I alternate back and forth between all of those different positions throughout the day, and I find that I feel best when I do that.  If I walk for too long, that actually can start tightening the hamstrings, and I feel a little bit too sore at the end of the day or just stiff, and it doesn’t feel good.  If I stand for too long, certainly I have that issue, and of course, if I sit for too long, I don’t feel good.  So for me, a mixture back and forth is ideal.  But if you do stand or even walk or some combination of both for the entire day, then something like what you described is probably helpful, and I can’t see how it would be harmful, so by all means, give that a shot.

Steve Wright:  So also has a follow-up question that I think is appropriate to address.  She also wanted to know if you had any thoughts or preferences about the shoes that you wear during the day and using an anti-fatigue mat for the standing desk.

Chris Kresser:  I do have an anti-fatigue mat, but unfortunately it’s now under the treadmill!  The treadmill is resting on it.  The reality is, along with what I just said, I stand comparatively little to walking.  I probably walk most, then I sit on the yoga ball and the chair and the sitting disc a distant second, and then third would probably be standing.  And that’s in part because the way my desk is set up now, the treadmill is under the desk.  So if I’m standing, I’m standing on the treadmill, which isn’t actually ideal from a biomechanical perspective, the way that it’s set up, and then the anti-fatigue mat is under the treadmill, so I’m not standing on that.  In terms of footwear, I’m barefoot.  If I’m in my home office, I’m barefoot whether on the treadmill or sitting or whatever.  Occasionally I’ll be wearing very thin-soled… I have some Patagonia shoes that are really kind of more barefoot than any other barefoot shoes I’ve tried except for Vibrams and maybe a few others.  And so sometimes I’ll wear those if I’ve been outside and I’ve just come back or something like that.  But I think minimalist footwear is always a good idea for this kind of thing.

Additional sources of magnesium

Steve Wright:  All right, awesome.  I think this next question is very appropriate for this podcast.  Eden wants to know, “Where did humans traditionally get magnesium in their diet?”

Chris Kresser:  Yeah, this is a question that often comes up, and I’m not entirely sure.  One thing that I’ve heard and read about quite a few times and I’ve been searching around in the scientific literature for something to corroborate this, but I’ve found general references to nutrient depletion in the soil that would include magnesium, but I haven’t found any specific comparisons between soil from preindustrial times or maybe a place that hasn’t been developed with monocropping and industrialized agriculture in a more rural place, but there’s this idea that the diversity and the quality of nutrients in soil has changed quite a bit since the industrialization of agriculture.  And it’s not just an idea.  I mean, there is data to support this.  So there was probably more magnesium in nuts and seeds and even some vegetables and fruits and starches like plantains than there is now, so there was just more magnesium in the diet due to better soil quality.

But in terms of the diet now and historically, nuts and seeds have been one of the highest sources of magnesium.  One of the issues there, though, is traditional cultures almost always prepared nuts and seeds by soaking them and then drying them.  And we know that nuts and seeds have phytate, phytic acid, which inhibits the absorption of magnesium and that these traditional preparation methods, like soaking and drying, break down the phytate so that more of the nutrients and minerals in the food can be absorbed.  So it’s possible that they got most of their magnesium from nuts and seeds.  Today in the sort of modern diet, pumpkin seeds and Brazil nuts are relatively high in magnesium.  Like 6-8 Brazil nuts have about 107 mg of magnesium.  A half ounce of pumpkin seeds has about 75 mg.  Buckwheat is actually a seed.  It’s not related to wheat at all, in spite of its name, and a cup of buckwheat flour has about 300 mg of magnesium.  And actually plantains are a good source of magnesium.  One medium plantain has about 65 mg of magnesium.

But I generally would recommend that people get 400 to 500 mg of magnesium, if not more if they’re dealing with constipation or muscle pain or some other symptoms, and that, in my experience, it’s just really difficult to get from the diet, so that’s one of the reasons I recommend it as one of the few nutrients that most people benefit from supplementing with.

Steve Wright:  Do you do anything special in your daily life to ensure that you get magnesium, like supplement?  Or do you do it all through food?

Chris Kresser:  I take a magnesium supplement.  Magnesium and fermented cod liver oil are the only two supplements that I take.  I have tried to get magnesium from food, and I notice a difference when I’m not supplementing with magnesium, so as I said, along with fermented cod liver oil, it’s the only one I take on a regular basis.

When should I stop breastfeeding?

Steve Wright:  Awesome.  All right, let’s move on to the next question.  This question comes from Christina, and Christina has a little bit of a paragraph here, so bear with me.  She has a soon-to-be 1-year-old son, and she has yet to have her first period.  She’s still nursing him two to three times a day plus pumping once at night.  She works part time, so the pumping at night is for during the next day.  Her pediatrician said that she should ditch the pump when he turns 1, despite knowing all the benefits of breastfeeding.  “I have to say that I’m ‘pumped’ to get rid of it.  Bad pun, but anyway, I’m wondering how normal this is.  He’s my first son, and I have a history of irregular periods.  Do some people have amenorrhea until they completely wean their child?  Is there any risk involved with not having a period?  My biggest concern is that my husband and I would like to start trying again, and knowing that I am getting my period would help me a lot.  Would you recommend acupuncture treatments to help me get things started again?  Thanks for all your help.”

Chris Kresser:  OK, so I just want to take a step back and throw in my plug for complementary nursing until at least 22 months.  I know she’s pumped to stop pumping, and I completely understand that.  I’ve worked with a lot of women who have had to pump a lot, and I know it can be difficult, but there’s a considerable amount of research that suggests that along with exclusive breastfeeding to 6 months that there’s a real and measurable benefit to continuing to do supplemental breastfeeding up to 22 months.  And the recommendation is to just do it on demand, meaning you offer it when baby wants it.  Of course, that’s not necessarily practical in this situation, given the work schedule and the pumping and things like that.  But I would encourage you to at least consider biting the bullet and continuing for up to 22 months or as close to that as you can get because I think the research suggests that there’s some significant benefit there.  The benefit seems to stop from a health perspective at around 22 months.  I mean, of course, that’s an estimate.  It’s going to vary from baby to baby, but that’s a general guideline.  The decision to nurse beyond 22 months really depends more on parenting philosophy and questions of attachment and development and things like that.  It’s not really related to nutrition in most cases.

In terms of the amenorrhea, it’s not unusual to be amenorrheic at one year if you’re nursing.  And different women have a different ‘normal’ here.  Some women start menstruating really relatively quickly even if they’re still nursing.  Other women take quite a while to get back to menstruation when they’re nursing.  And it doesn’t necessarily indicate any kind of pathology or problem; different women just have a different rhythm and pattern there.  In some cases, it can indicate a problem, a hormone imbalance, something that’s not clicking back into place after the birth, but I wouldn’t suspect that at 1 year, especially given the history of irregular menstrual cycles before.  And someone who has a history of irregular menstrual cycles is more likely, in my experience, to be a little bit slower getting back into their normal rhythm since their rhythm wasn’t really normal in the first place.  It sounds to me like there isn’t anything to be concerned about, but of course, that’s something you should also double-check with your OB/GYN or midwife or whoever’s care you’re under.

What to do about anxiety during pregnancy

Steve Wright:  All right, so let’s move on to the next question.  “What are your thoughts on supplemental support with PharmaGABA and/or L-theanine during pregnancy?  What about certain adaptogens, like ashwagandha, during pregnancy?  This would be in regards to anxiety during pregnancy.  Thanks for your consideration.  Ben”

Chris Kresser:  GABA is the major inhibitory neurotransmitter, for anyone who doesn’t know what GABA is.  It’s kind of like the off-switch in the brain and elsewhere.  It leads to feelings of calmness and relaxation, and so the idea, of course, is supplementing with GABA would reduce anxiety.  But GABA is a very large molecule, and it shouldn’t actually cross the blood-brain barrier, is my understanding.  And so if you take GABA and you have a response, some practitioners kind of actually use that as a way of diagnosing leaky brain.  We’ve talked a lot about leaky gut, I’ve even written a bit about leaky skin, but the blood-brain barrier is another barrier system in the body that’s designed to keep certain things out and let certain things in, and large molecules are not supposed to pass through the blood-brain barrier.  There’s one school of thought that says that supplementing with GABA shouldn’t work, and if it does work, it’s actually indicative of a leaky blood-brain barrier and that’s what should be investigated and treated.

But as far as this question goes, supplements during pregnancy are always a tricky thing because we don’t have a lot of data on the safety of supplements during pregnancy, and we never will because those studies are unethical to do.  Imagine a trial where you take two groups of pregnant women and you give one group a supplement and give the other a placebo and then you watch what happens to them and their babies.  I mean, obviously no one is going to sign up for that study and they shouldn’t.  It’s completely unethical.  So we’re left kind of wondering a lot about the effect of various supplements, and the only way to really know is to, in some cases, look at the history of safe use of those supplements by herbalists and other types of health care practitioners throughout history.  You can consider the mechanism of how the substance works and whether it’s likely to shift anything around in pregnancy, although it’s pretty sketchy to do it that way because we just don’t know.  I mean, there are so many profound changes in pregnancy that it’s really difficult to predict how something might impact the developing baby or the mother.

So my general philosophy on supplementation during pregnancy is to be extra cautious, to do as much as possible with lifestyle-based interventions and diet, and when using supplements, to use only the ones that have the longest record of safe use and that are the least likely to cause any harm or difficulty.  For anxiety during pregnancy, I will tend to recommend acupuncture.  It seems to really take the edge off for a lot of women.  The only side effects are typically feeling better, for the most part, and it’s pretty affordable these days if you find a community acupuncture clinic.  Mindfulness-based stress reduction, which we’ve talked about numerous times on the show, and the Rest Assured program are two ways of inducing the parasympathetic nervous system, and mindfulness-based stress reduction, particularly, is clinically proven to reduce anxiety in several different studies, and that you can search online for a class nearby or you can even download some free audio programs.  The body scan is one way of doing MBSR, mindfulness-based stress reduction.  You can download some of those for free from the Internet to learn how to do it.

Then there are some botanicals, like skullcap — Chinese skullcap, not American skullcap.  There are two different varieties.  It’s really important.  Chinese skullcap is generally considered by most herbalists to be safe during pregnancy, particularly when taken as a tea.  Lemon balm and chamomile are two other botanicals that are generally considered to be safe.  And if you use one of the over-the-counter teas that have them in it or you combine those together, they’re generally, again, considered to be safe.  Now, if you search for some of these on the Internet, you might see some mixed views, and that’s in part because of what I just said before.  We don’t have randomized clinical trials that give us this type of information, and different people have a different take, but the vast majority of even mainstream sources consider chamomile and Chinese skullcap and lemon balm to be safe.  American skullcap is not considered to be safe.

5-HTP, which is an intermediate between tryptophan and serotonin and is often used for depression and anxiety in non-pregnant people, is questionable.  There are mixed opinions, again, about that.  And I would be hesitant myself to prescribe it during pregnancy because we just don’t know.  On the other hand, a lot of doctors do prescribe SSRIs, prescription antidepressants that, I think, have probably an even greater impact on serotonin metabolism than taking 5-HTP, and a lot of women take SSRIs during pregnancy.  I’m not arguing for that, and two wrongs don’t make a right, of course, but I guess it depends on the extent of the anxiety and depression because that can be harmful for the baby as well, especially if it leads to harmful behavior in the mother.

So if you’re going to explore any of those more, 5-HTP or anything like that, absolutely do it in conversation with your healthcare provider or under the supervision of whomever you’re working with.  Otherwise, the lifestyle interventions, like acupuncture and mindfulness-based stress reduction, spending time outdoors, making sure to get plenty of sleep if possible — I know that’s sometimes challenging when you’re pregnant, especially in the later stages — and then considering using some of those teas, when you add all of those kind of smaller interventions up, they can actually equal a larger intervention.

Steve Wright:  Awesome.  Well we’ve covered a lot of different topics today from science on why we should be eating what we’re eating and pregnancy to standing desks to all kinds of things.

Chris Kresser:  Yeah, and it was a lot more enjoyable than being in the closet.

Steve Wright:  You just like the window!

Chris Kresser:  Hopefully the sound is good, and next time it’ll be even better because I’ll have my fancy new sound-dampening equipment, which I’m excited about.

Steve Wright:  Awesome.  Well, as always, Chris, thanks for all the wealth of information.

Chris Kresser:  Thank you, Steve.  Pleasure, and see you all next time.

Steve Wright:  Yeah.  Thanks, everyone, for listening today.  If you would, please keep sending us your questions to ChrisKresser.com.  I swear I still have them, and we’re plowing through the list as we go.  When you get to ChrisKresser.com, use the podcast submission link to send them over to me.  And if you enjoyed listening to the show, please head over to iTunes and leave us a review.  Thanks.  We’ll talk to you next time.

A recent study by published in the New England Journal of Medicine (NEJM) has proposed a new link between eggs and coronary heart disease (CHD) that doesn’t involve cholesterol. A team of researchers, led by Dr. Stanley Hazen, showed that dietary choline—a nutrient found largely in eggs, beef liver and other animal foods—is metabolized by bacteria in our gut and then converted by the liver into TMAO.

They demonstrated this with a “choline challenge”: feeding volunteers two large hard-boiled eggs (with approximately 250 mg of choline each) along with 250 mg of supplemental choline that was tagged with a heavy isotope. The isotope acts like a chemical “label” that allowed the researchers to track what happened to the choline after it was ingested. Their data did indeed show an increase in both labeled TMAO and total TMAO (in urine and blood) in the volunteers after they consumed the eggs and supplemental choline.

In a second study, Dr. Hazen’s group showed that increased levels of TMAO in the blood are associated with cardiovascular disease (CVD). The researchers followed roughly 4,000 adults for three years. At the end of the study period, those with the highest levels of TMAO had a 2.5-fold increased risk of heart attack, stroke and death.

On the surface this sounds like very bad news for omnivores. But let’s take a closer look at the studies to see if it’s really time to swap your morning eggs for a tofu scramble.

Do choline-rich foods increase TMAO levels?

Dr. Hazen’s team did show a temporary increase in total TMAO after eating eggs. However, as Dr. Chris Masterjohn pointed out to me in an email dialog, the researchers’ own data show that there’s no way that the “choline challenge” could have contributed to this increase in total TMAO. If it had, we would expect to see an initial increase in labeled TMAO followed by an increase in labeled TMAO. This would indicate that the labeled choline supplement (that participants ate with the eggs) had been metabolized by the gut bacteria and then converted into TMAO in the liver.

But that’s not what happened. I re-created Figure 1C and 1D from the study. Figure 1C (below) shows an increase in total serum TMAO at one hour after the choline challenge. But by hour four, total TMAO is back to baseline and by hour 8 it’s even below baseline (i.e. the participants had lower TMAO at 8 hours than they did before they ate the eggs/choline).

However, Figure 1D (below) shows that labeled TMAO did not increase at all until hour four, and it didn’t increase significantly until hour six! This shows that the eggs and supplemental choline the participants ate had nothing to do with the increase in total TMAO that occurred one hour after the challenge.

What’s more, the researchers didn’t mention that other commonly eaten foods have a much more significant impact on TMAO than eggs. A 1999 study tested the effects of 46 different foods on the urinary excretion of TMAO in 6 human volunteers. (1) Eggs had no effect on TMAO excretion compared to a light control breakfast, yet 19 out of 21 types of seafood tested did. In fact, halibut generated over 53 times as much TMAO as eggs! This is not surprising, because although all species of seafood contain lower amounts of choline than eggs, they do contain trimethylamine and TMAO. Dr. Hazen’s team was aware of this study, because they referenced it briefly in the discussion section of the NEJM paper. They acknowledged that “TMAO has been identified in fish” and “the ingestion of fish raises urinary TMAO levels.” But remarkably, they did not explain how much greater fish’s impact on TMAO was when compared to eggs.

Finally, this paper did not prove that eating choline-rich foods (or any other foods) increases TMAO levels over time. In fact, the researchers themselves seem to suggest this is unlikely in the discussion section of the paper. They said: “the high correlation between urine and plasma levels of TMAO argues for effective urinary clearance of TMAO.” In other words, even if eating food does increase total TMAO levels, most people are able to quickly and efficiently clear that TMAO from their blood by excreting it in the urine. This makes it doubtful that dietary factors alone explain chronic elevations in TMAO.

Instead, there are several other factors that are more likely to explain such an increase, including:

• Impaired urinary clearance of TMAO due to impaired kidney function. This is at least partially supported by data in the NEJM paper. Those with the highest levels of TMAO had an average glomerular filtration rate (GFR) of 69 mL/min. According to National Kidney Foundation guidelines, a GFR between 60–89 ml/min is indicative of a reduced capacity to filter blood through the kidneys. (2)
• Differences in the gut microbiota that predispose toward increase TMAO production. Previous work by Dr. Hazen’s group has shown that people with higher levels of Prevotella bacteria in their gut produce higher levels of TMAO. (3) (Interestingly enough, other research has shown that consumption of whole grains—not animal products—is associated with higher levels of Prevotella bacteria.) (4)
• Enhanced conversion of trimethylamine to TMAO in the liver. An enzyme called Fmo3 carries out this conversion, and its activity is affected by genetic factors, iron or salt overload, and a number of common pharmaceutical drugs used to treat arthritis, GERD and infections. (5)
• Diabetes and metabolic syndrome. Fmo3 activity is upregulated in cases of insulin resistance and insulin deficiency. (6)

If food really did make a significant contribution to TMAO levels, and high TMAO levels cause heart disease, then we’d expect to see much higher rates of CHD among people who eat more fish—since fish has a much greater effect on TMAO than eggs. Yet this is the opposite of what studies indicate: Eating more fish (especially cold-water, fatty fish) has consistently been shown in both observational and randomized controlled trials to reduce the risk of death from heart disease. (7, 8)

Do choline-rich food cause heart disease?

At the end of their paper, Dr. Hazen’s group cautions against “excessive consumption of dietary phosphatidylcholine and choline” and recommends a high-fiber, vegetarian diet as a means of protecting against heart disease.

Yet as I’ve argued above, they failed to present convincing evidence that eating eggs significantly increases TMAO over time—especially when compared to other foods like fish. Moreover, if eating choline-rich foods did increase the risk of heart disease (via TMAO or any other mechanism), we’d expect to see higher rates of CHD in those that eat more eggs. Yet numerous studies have failed to find any such association. For example, a meta-analysis of prospective studies involving a total of 474,000 participants followed from 8 to 22 years published in the British Medical Journal found no association between higher egg consumption (up to one per day) and CHD or stroke. (9) An analysis of data from the National Health and Nutrition Examination Study found an inverse association between egg consumption and stroke, and a cohort study from Japan found that consumption of animal products including eggs was associated with reduced risk of death from stroke. (10, 11) The lack of association—or inverse association—between egg consumption and CVD is even more impressive when you consider that those who eat more eggs are also more likely to smoke and be physically inactive. (12)

Some studies suggest that eggs may even prevent heart disease. Egg consumption leads to the formation of larger, less dense LDL and HDL particles, which may be protective against atherosclerosis. (13) Eating eggs frequently may even lead to lower cholesterol; one study found that those eating four or more eggs per week had lower total serum cholesterol than those eating one or fewer per week.  (14) This same study found that egg consumers had diets higher in nutrients that have been shown to reduce the risk of cardiovascular disease compared to non consumers, including vitamins E, B12 and folate.

Finally, as I pointed out above, some research suggests that consuming large amounts of whole grain increase Prevotella bacteria in the gut, which were associated with the highest levels of TMAO in Dr. Hazen’s previous study on TMAO. If this is the case, consuming large amounts of fiber from whole grains may actually increase the risk of heart disease.

The hypothesis that increased serum TMAO is associated with heart disease is interesting and should be investigated further. But the data presented by Dr. Hazen’s group doesn’t support the conclusion that dietary choline is a major cause of increased TMAO, nor does it support their advice to avoid choline-rich foods like eggs, liver, beef and pork.

To 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.

Insulin resistance and metabolic syndrome

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

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)

Infections

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)

Leaky gut

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.

Genetics

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.

Here 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.

Blast from the Past

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!

Research Report

• 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 disorder
• A 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.

Worth A Look

• 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.

For the Foodies

• Mark’s Daily Apple: Crock Pot Pork-Stuffed Peppers
• PaleOMG: Easy Delicious Breakfast Hash
• NomNomPaleo: Spicy Salmon Cucumber Bites
• Against All Grain: Baked Omelette with Ham and Gruyere
• Civilized Caveman: Dill Roasted Carrots
• The Food Lovers: Korean Inspired Beef and Vegetable Noodle Bowl

Gather, 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.

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.

A beautiful side dish with a small ingredient list that packs great flavor.

Type of dish: Side Dish
Equipment: Pot with steamer basket and lid, sauté pan
Servings: Makes 4 servings.

Ingredients:

• 2 to 2 1/2 pounds asparagus, washed, tough bottom parts broken off, and sliced into one-inch pieces
• 1 TB traditional fat of choice
• 5 cloves garlic, minced or pressed
• 1/2 cup almonds, sliced or roughly chopped
• juice of one lemon
• salt to taste

Directions:

1. Steam asparagus in covered pot with steamer basket, with one to two” of boiling water, until bright green, about 5 minutes.
2. Remove asparagus from heat and drain any excess water.
3. In a sauté pan, heat the oil over medium heat. Add the garlic and cook for one minute, stirring.
4. Add the almonds and toast lightly, stirring for about another minute.
5. Remove pot from heat and add in the steamed asparagus. Stir well.
6. Finally squeeze in the juice of the lemon and salt to taste. Serve.

Enjoy!

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.

Myth #2: High cholesterol 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.

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.

Wrapping up: The map is not the territory!

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.

Another Q&A episode, which we tried recording in a closet!  The clothes apparently absorb the sound, so I want to hear from you if you notice a difference in the audio quality.  Please leave a comment and let me know how it sounds to you.

Sorry it’s a little late. We got off of our normal schedule because of some commitments I had; we’ll be back to normal starting with the next show.

In this episode, we cover:

1:44 What Chris ate for breakfast
4:03 What supplements should kids take?
7:48 What to eat for lifelong constipation
18:05 How to support adrenals after having a baby
27:08 What to do about low ferritin levels
31:50 Tips for teething babies
34:50 Dealing with disrupted sleep patterns
42:14 How do you explain someone that feels better on a juice fast?

Links We Discuss:

• Green Pastures Fermented Cod Liver Oil (Non-flavored)
• Sounder Sleep Rest Assured Program

Full Text Transcript:

Steve Wright:  Hey everyone, welcome to another episode of the Revolution Health Radio Show.  This show is brought to you by ChrisKresser.com.  I’m your host for the show, Steve Wright from SCDLifestyle.com, and with me is integrative medical practitioner and healthy skeptic Chris Kresser.  So Chris, how’s the closet?

Chris Kresser:  Haha, so we’ve had a suggestion from one of our more audiophilic listeners who has mentioned that there’s sometimes an echo in the background, and that’s probably because I record in my home office, which has high ceilings and it’s acoustically not the best space.  So somebody recommended that we try recording in a closet!

Steve Wright:  Haha, the lengths to which we go for our listeners, Chris!

Chris Kresser:  That’s right.  I’m in a closet.  The clothes apparently absorb the sound, and I will say it’s not the most aesthetically pleasing recording space, so I want to hear from you if you notice a difference in the audio quality, and I’m not yet committing to doing this every time even if you do notice a difference, because so far I’m not a huge fan of the closet recording.  But we’ll give it a shot.  We’ll see how it goes.

Steve Wright:  OK.  All right, well, you’ve been posting pictures all week of traveling and eating, so we have to talk about what you had for breakfast this morning.

What Chris ate for breakfast

Chris Kresser:  Well, let’s see.  Breakfast I skipped.  I had some coffee and cream, and then I had a leftover stew for lunch, which was made with chuck roast from the beef we get from our local farmer, Freestone Ranch, and potatoes, carrots, peas, homemade chicken broth, I think some onions, and some seasonings.  And then I had some homemade raw sauerkraut with ginger, beets, carrots, and cabbage to go along with that.

Steve Wright:  Sounds pretty delish.

Chris Kresser:  Yeah, it was good.

Steve Wright:  Let me know when I can come over and clean up your leftovers.

Chris Kresser:  Haha, all right.  How are you doing, Steve?

Steve Wright:  Well, as of the time of this recording, it’s late in the week, and I’m ready to respect my body and get a long night’s rest.

Chris Kresser:  TGIF, huh?

Steve Wright:  Yeah.  Thank goodness it’s Friday, and I’m looking forward to maybe, like, 10 or 12 hours’ worth of sleep here.

Chris Kresser:  Nice.

Steve Wright:  I’m going to do my best.

Chris Kresser:  Sounds good.

Steve Wright:  OK, well, I think we have a Q&A episode that’s going to be pretty fun today, Chris, and I know that you’re going to be doing most of the talking, so why don’t you get a glass of water or search through the clothes and see what needs to be folded in there, and I’m going to go ahead and tell everybody about Beyond Paleo.  So if you’re new to this podcast, it’s going to be really fun, you should keep listening, but you should also check out Beyond Paleo.  If you’re new to the paleo diet or you’re just interested in optimizing your health, you’re going to want to check out what over 30,000 other people have signed up for.  It’s this mysterious Beyond Paleo that I keep talking about here, and it’s a free 13-part email series on burning fat, boosting energy, and preventing and reversing disease without drugs.  Head over to ChrisKresser.com, and look for the big red box where you can sign up, and Chris will start sending you the first email very shortly.

Chris, how are the clothes?

Chris Kresser:  Everything’s pretty much the same way I left it before.

Steve Wright:  Haha, perfect.

Chris Kresser:  All is well.

What supplements should kids take?

Steve Wright:  Well, everyone loves to hear about Sylvie, so let’s start off with the first question from Brenda, which is, “Does your daughter receive any supplements, and if so, what?”

Chris Kresser:  She only receives one, and it’s debatable that it’s a supplement at all because it’s a whole food, but it’s fermented cod liver oil.  I do kind of think of it as a supplement because most people just don’t eat it as part of their normal diet.  She’s been getting that since she was about 6 months old, 7 months, when we first started her on food.  And the amount has been gradually increasing.  And I think I’ve mentioned this on the show before, but amazingly she just takes it straight in the mouth, no flavor.  Flavors actually aren’t a good idea for really young kids.  She’s getting close to 2 now, so it wouldn’t be that big of a deal for her, but you wouldn’t want to use strong flavors for infants.  But from the beginning she’s liked it, and it got to the point where she’d ask for it after meals, and we’d just shoot it right into her mouth with the little plastic syringe that they give you.  Lately something interesting has happened:  She has been refusing it.  But I don’t think it has anything to do with the taste.  She’s just in this phase where she’s refusing things!  And the more that she senses that we want her to do something, even though we’re really kind of, at least on the surface, laid back about it, we don’t push it at all, but she senses that we want her to have it, and so lately she’s been saying, “No.  No!”

Steve Wright:  Haha, you’re going to have to just leave it on the counter and go into the other room?

Chris Kresser:  Yeah.  Totally pretend that we don’t want her to have it.  But I also heard some of my patients have tried — you might have seen this, Steve — Green Pasture just came out with this new product.  It’s a coconut oil base, but they infuse it with butter oil, fermented cod liver oil, and fermented skate liver oil, which is a different type of fermented fish liver oil, and it has complementary nutritional properties to fermented cod liver oil.  Apparently some of my patients who just couldn’t stomach any of the cod liver oils, even the cinnamon flavor, which I think barely even tastes like cod liver oil, but some of my patients who couldn’t take any of them are able to take the coconut oil based, and I think that would probably be a good one for kids, too.  So if anyone’s having trouble giving their young child cod liver oil, you might want to give that one a shot.

Steve Wright:  Interesting.  I haven’t seen that one yet, but I typically stick to the cinnamon.

Chris Kresser:  Yeah.  To me, the cinnamon is… literally I can barely taste the cod liver oil.  Maybe it’s just that I’m accustomed to it, but the cinnamon is so strong that it’s pretty overwhelming.

Steve Wright:  I would agree.

Chris Kresser:  So that’s it.  We occasionally, every now and then have given her, like if we’ve traveled, a little bit of infant probiotic from Klaire Labs, but that’s pretty sporadic, and she doesn’t really get anything regularly other than that.

Steve Wright:  But she is fond of eating a whole plate of sauerkraut, so you don’t have to worry too much about the probiotics, right?

Chris Kresser:  Haha, absolutely.  We have to keep her away from it.

What to eat for lifelong constipation

Steve Wright:  Haha.  Well, let’s talk about where some more sauerkraut might be needed.  This question comes from Lucy, and she wants to know, Chris:  “What is the best diet for lifelong constipation?”

Chris Kresser:  Hmmm.  That’s actually a hard question to answer because I think it depends on a lot of factors.  I’ll give a general response, and then I’ll mention some extenuating circumstances.  I think, in general, the best diet for lifelong constipation is one that nourishes the gut and doesn’t irritate the gut.  And that’s really general, so let’s go into a little more detail there.

Steve Wright:  Break it down.

Chris Kresser:  Yeah, so foods that nourish the gut would include fermentable fibers, I think.  So we’re talking about water-soluble fiber in fruits and vegetables, starchy tubers.  Resistant starch is in some tubers, and that’s actually insoluble fiber, but it is fermentable.  And a lot of studies have shown that the fermentation of soluble fiber produces short-chain fatty acids like butyrate, in particular.  And these short-chain fatty acids have a number of beneficial effects on digestive health, but not only digestive health, also heart health and even brain health.  They play an important role in the differentiation of colonic enterocytes, which are the cells that make up the lining of the gut.  And so the production of these short-chain fatty acids is probably responsible for a significant portion of the benefits that are seen in observational studies that look at fiber intake and health outcomes.  And you know, we can never draw causal relationships, of course, from these studies, but the observational studies consistently do show that soluble fiber intake, at least, is associated with better health outcomes.  So there are a lot of reasons to use fruits and vegetables and starchy tubers.  One of them is gut health, and constipation is usually caused by a lack of beneficial gut flora, particularly bifidobacteria in the colon.  And one of the best ways to stimulate the growth of that flora in the colon is eating these fermentable fibers in the context of a whole foods diet, like fruits and vegetables and tubers.

Now, the other part of that was avoiding foods that irritate the gut, so these are the food toxins that we often talk about:  refined flour, refined sugar.  Both refined flour and refined sugar can cause unhealthy changes in the gut flora that could predispose toward constipation.  Grains and grain fiber tend to be high in insoluble fiber, which has a mechanically rough action on the gut.  It’s kind of like rubbing a wire brush against an open wound, so that can be really irritating to the gut, especially if the gut is already inflamed.  Industrial seed oils, you know, corn oil, soybean oil, all of these “Franken-oils” have been shown to cause undesirable changes in the gut.  And then gluten and various different compounds in wheat can be aggravating.  I mean, they can be extremely aggravating to the gut if you have celiac disease, of course, but even non-celiac gluten sensitivity.  And some studies suggest… There have been extremely limited, I think just one or two, studies that have shown that gluten might even be inflammatory in people who don’t have any obvious gluten sensitivity or celiac disease, but that’s definitely not a solid finding.  But non-celiac gluten sensitivity is a lot more common than most people believe.  Some statistics range between… I’ve seen some numbers as high as 1 in 12, and then 1 in 20 is another estimate that often gets thrown around.  And celiac disease is actually more common than was previously believed, as we discussed with Dr. Fasano.  A lot of people have some level of gut inflammation, and I think it’s probably best for most people to avoid gluten for that reason, regardless of where they fall on the spectrum of gluten intolerance.

Let’s see.  Regarding fiber supplements, it’s another one of these things that’s kind of accepted without question:  the idea that fiber and fiber supplements benefit constipation.  And it’s true that fiber in the context of the diet appears to be beneficial for regularity, but fiber supplements, when they’ve been tested, have often not been shown to be beneficial for constipation and can actually have the opposite effect.  So you want to be careful with fiber supplements, just as a side note there.

Now, the extenuating circumstances here are that it often depends what the cause of the lifelong constipation is.  As I said, it’s often insufficient amounts of beneficial bacteria in the gut, particularly bifidobacteria in the colon, and the reason for that is 70% to 80% of the dry weight of stool is bacteria.  So if you don’t have enough good bacteria, the stool won’t have enough bulk, and that will reduce motility.  However, if someone has small intestine bacterial overgrowth, that means they have too much bacteria growing in the upper part of their small intestine.  Those bacteria can feed on fermentable fibers and carbohydrates too, so in those situations, things like starch and foods that are rich in fermentable fibers might actually exacerbate the problem.  So in that scenario, you would probably need to treat the small bowel bacterial overgrowth first — and that can be a common cause of long-term constipation — with a low-carb diet and some antimicrobial nutrients.  And then after that’s treated, it’s probably beneficial to gradually reincorporate some fermentable fibers over time.  And the GAPS diet is a good example of this.  I often see patients in my practice who have been on GAPS or SCD — and Steve, you probably have some thoughts about this — but it worked really well for them for a time, and when they were on the intro GAPS or intro SCD, they were kind of starving out the overgrowth in bacteria.  But then after a long period of being on an almost zero-fiber diet, it also starved the good bacteria in their gut, and then they either went from having diarrhea to having constipation, or maybe they just got more constipated over a period of time.  So at that point, if that starts to happen on one of those diets, it’s probably the right time to start adding back in some starchy tubers or other fermentable fibers.

Steve Wright:  Yeah, I think from what we’ve seen… The message Jordan and I are always trying to get out is that everyone has a custom diet that also is changing with your health.  So as Chris is talking about, as you change your foods, the easiest output to measure is going to be your stool, and as that changes over time and you get healthier, it’s likely a good idea to continue to broaden your horizons.  So like, on our site we like to start with the SCD, get your symptoms under control, and then begin to branch back out to, like Chris was talking about, the starchy tubers, things like that, but with the caveat that Chris already mentioned, which is that constipation is almost like acne.  There’s not a really easy way to explain why it’s happening to you.  There could be a lot of different causes that are at the root of the issue.  Diet is a huge part of it, but if you have SIBO, not everyone can just change their diet to GAPS or SCD and get rid of SIBO.

Chris Kresser:  Right, and there could be other pathogens, like H. pylori, or parasites.  A lot of people think of diarrhea when they think of parasites, but chronic parasite infections can and do lead to constipation.  If a patient were to come see me in the clinic with this complaint of lifelong constipation, the very first thing I would do would be to run some tests for gut pathogens and SIBO because you have to at least rule that stuff out before even proceeding, and the chances are really high that someone has those things, because constipation is not only a result of those problems, it actually increases the risk of those problems, because proper elimination, as you can imagine, is helpful to keep a healthy intestinal environment.  And if you’re not eliminating properly, then you’re going to be at a lot higher risk for getting infections even if you didn’t already have one and that wasn’t the original cause of the constipation.

Steve Wright:  Yeah, I think that’s the huge takeaway right there.  Get some really good, advanced testing because I think that’s going to be the root at which you’ll be able to figure this out.

Chris Kresser:  Yeah.

How to support adrenals after having a baby

Steve Wright:  Cool.  Well, let’s roll on.  This next question comes from Jenny, Chris, and she wants to know about supporting adrenals after eight months of poor sleep due to nursing an infant.  She wants to know about safe supplements.

Chris Kresser:  Yeah, that’s a great question, and it’s frankly not an easy one to answer, again.  I think the hardest part for me as a clinician in treating pregnant women or women who are nursing is that there aren’t really any studies on safety of nutritional supplements during pregnancy and nursing, for obvious reasons, right?  I mean, it’s unethical to do that kind of study where you give pregnant women something of unknown safety and then just watch what happens.  No one is going to sign up for that study, and they shouldn’t because it’s completely unethical and dangerous.  So we’re left kind of wondering about a lot of natural supplements and even drugs, for that matter.  There are some wisdom traditions, like ayurvedic medicine and Chinese medicine, where there’s a history of apparently safe use with certain botanicals over a long period of time.  And if you talk to herbalists, they might tell you that something is safe, but then you go and search on the Internet and it says don’t take this during nursing and pregnancy, and it’s confusing because maybe someone just told you it was safe, but then you research it yourself and it says it’s not safe.  Well, generally if you ever look anything up on the Internet, it’s going to say it’s not safe because there are no studies proving that it’s safe, and due to obvious liability concerns, websites and healthcare practitioners and people in general don’t want to say that something is safe on the Internet when it’s not absolutely known to be safe because if something does happen, then that would be a terrible thing.

So the first thing, the primary thing with adrenal support during pregnancy and nursing would be actually non-nutritional interventions.  So things like Mindfulness-Based Stress Reduction, which is a clinically proven program, and the Rest Assured program, which I’ve talked about before at SounderSleep.com, these two things regulate the nervous system and induce a parasympathetic response, which can definitely help with adrenal fatigue syndrome type of problems.

Acupuncture, I think, can be helpful in this type of situation.  It’s safe to do during both pregnancy and nursing.  There aren’t really any side effects other than feeling better for most people.  The research on whether it works for adrenal fatigue syndrome is a little unclear because in the conventional world, adrenal fatigue syndrome doesn’t really exist, so there haven’t been studies done on that, per se, but there have been studies on acupuncture and anxiety, and acupuncture and depression, and acupuncture and insomnia, and the research is somewhat mixed, but part of the reason for that is that it’s really difficult to study acupuncture in a randomized controlled trial because there’s no obvious way to do a placebo control arm.  I mean, they do this shallow needling or dummy needling at non-acupuncture points.  There are a lot of different ways they’ve tried to do a placebo arm, but what they’ve found is that even some of the placebo needling can actually have physiological effects, so it’s not a true control.  So the acupuncture research is really confounded and not easy to draw conclusions from, but I can just tell you from my own experience doing acupuncture and receiving acupuncture and seeing a lot of people receive acupuncture that it can be very effective for adrenal-fatigue-related problems, and it’s certainly worth a try because it’s safe and it’s one of few things that is safe during pregnancy and nursing.

Another thing would be all of the stuff we’ve talked about in terms of limiting artificial light exposure at night, so turning down the room lights, getting the orange goggles that block out the blue light that suppresses melatonin, reducing your use of electronic media at night, making sure on the flipside that you get out during the day and get some sun or bright light exposure on your eyeballs.  It doesn’t even have to be sun, just bright light, just getting outside in the morning and during the day.  That actually helps regulate the cortisol/melatonin circadian rhythm.  If it’s dark where you live a lot during the day or you’re not able to go outside because of your job or something, a light machine used in the morning can be helpful to reset the circadian rhythm, the type that they use for seasonal affective disorder and depression.

And then there are some medicinals that are generally recognized to be safe.  Now, again, the caveat here is you should talk to your doctor about this, and you should do your own research too and make sure that you feel comfortable, but most herbalists and even most conventional sources and physicians would say that herbs like chamomile and lemon balm are very safe during pregnancy and nursing.  And the Chinese skullcap — not American skullcap.  There are two different versions of skullcap, but Chinese skullcap is an anxiolytic — which means it’s antianxiety — can have a pretty calming effect.  So those are some botanicals that can be used.

From a dietary perspective, you want to make sure that you’re getting plenty of protein, not too low carb, not skipping meals.  For some people, eating every 2 to 3 hours would be really helpful with adrenal fatigue type of symptoms.  And hopefully something in all of that that we just talked about can make an impact, or some combination of all of those things.  I think if you did all of that stuff, it’s pretty likely that you’d start to see some improvement.

Steve Wright:  Yeah, I would think so.  That one about not skipping meals, I think, is a big one for a lot of people I see suffering from adrenal issues.

Chris Kresser:  Yeah.  There was one more thing, which has always been kind of interesting to me.  If you look up 5-HTP, which is an intermediary between tryptophan and serotonin — so tryptophan gets converted into 5-HTP, and 5-HTP into serotonin, and serotonin has a really strong regulatory effect on the nervous system.  It’s kind of responsible for well-being.  It helps with sleep, and it can be really helpful in adrenal fatigue scenarios where the sleep pattern is really disrupted.  And if you look up 5-HTP, it says contraindicated during pregnancy, but what’s interesting to me is that a lot of doctors don’t hesitate to prescribe SSRIs, which have a much more potent effect on serotonin metabolism than 5-HTP does.  That’s maybe something to discuss with your doctor.  If you’re really kind of on the edge and none of the other stuff that I’ve talked about is helping, that might be worth exploring with your doctor as well.

What to do about low ferritin levels

Steve Wright:  All right, let’s roll on.  This next question comes from Krista, and she wants to know the best way to increase ferritin levels, because she’s been taking an iron supplement for about a year and she hasn’t had any change.

Chris Kresser:  Well, I noticed in the question that her ferritin levels were 80, and in my opinion, there’s no need to increase ferritin above 80.  In fact, in women, the upper end of ferritin, the safe range, is about 140 or 150.  If you see ferritin above that in a woman, it means iron overload.  So I’m just not totally clear on why Krista wants to get her ferritin levels above 80.  I don’t think that that’s necessary or even desirable, and maybe her body is self-regulating in some way, although I’m not sure how the body would do that because the only ways to get rid of excess iron are bleeding and chelation, and that’s one of the problems with iron and it’s one of the problems with iron supplements.  So I would say just be happy with your ferritin level of 80.  That’s a good level.

Steve Wright:  What’s the lower end, Chris, for women?

Chris Kresser:  It depends whether they’re premenopausal or postmenopausal.  And it depends sometimes on what point they’re at in their cycle and how heavy the menstruation is and what’s normal for them.  But the lab range for premenopausal women goes down to 13 or 15, but I think that’s too low.  I don’t like to see premenopausal women — or postmenopausal women, for that matter — below about 30.  And when they are below 30, it can be really hard to get them above 30.  There’s kind of this threshold that if you’re below the threshold, it often can take fairly large amounts of supplementation and sometimes even shots to get you above the threshold, but then once you’re above the threshold, it’s easier to stay above it just with eating iron-rich foods like organ meats and things like that, or even just red meat.

I think in premenopausal women, iron deficiency is a bigger problem.  In postmenopausal women, iron overload is actually often a bigger problem because menstruation is one of the primary ways that women lose iron, and when that stops they start accumulating iron just like men do.  So the risk generally kind of shifts as women go into menopause to iron overload, and in fact, some of you might remember the whole HRT debacle, which was the idea that there was an observation that premenopausal women had much lower rates of heart disease than postmenopausal women, and the first theory about why that was was related to estrogen levels.  Postmenopausal women have lower estrogen levels than premenopausal women, so they did a trial and they gave postmenopausal women estrogen, thinking that that would reduce their risk of heart disease, and in fact, they had to stop the trial early because it was dramatically increasing the risk of heart disease in postmenopausal women.  The latest theory now about why that difference exists is iron.  Premenopausal women have lower iron saturation and ferritin levels than both postmenopausal women and men, and when women go into menopause they start to match men in terms of their iron saturation and ferritin levels.  I mean, they’re still on average lower, but they start to accumulate more iron.  So that’s just something to be aware of.  Like most nutrients, there’s a sweet spot for iron.  You don’t want too little, and you don’t want too much.  And what that is depends on your gender and also on the stage of life you’re in if you’re a woman.

Tips for teething babies

Steve Wright:  OK, awesome.  Well, let’s move on to the next question, and this question comes from Tom.  He has a 14-month-old son whose molars are coming in, and Chris, he wants to know, do you have any recommendations for treating teething?

Chris Kresser:  I was going to ask Tom for some recommendations, actually!  Haha.  Sylvie’s getting her two-year molars right now, and actually it’s a little better lately.  It was pretty rough there for a while.  She was in obvious discomfort and rubbing her cheeks, and it was kind of sad.  You know, we’ve done a few things, and I have to be honest, I don’t really understand homeopathy from an allopathic, scientific perspective.  It doesn’t really make sense to me.  But I certainly don’t think it can cause any harm.  There are a couple of homeopathic ointments that a lot of parents swear by, and we’ve tried them.  Like I said, why not?  It couldn’t hurt.  And it’s hard to say.  It’s really hard to say when you’re in just kind of real life whether something clearly is working or not working.  It seems to help her, but I could be just imagining that.

Steve Wright:  You didn’t do any scientific trials?

Chris Kresser:  Haha, no.  And then there are also analgesics with not-so-nice ingredients in them, but I think if teething gets so bad to the point where sleep is seriously disrupted that using those over-the-counter analgesics can be helpful, because as we’ve discussed many times, there’s really nothing worse than chronic sleep deprivation for your health and for a baby’s health.  So unfortunately, I don’t really have a lot of insight to offer on teething.  The homeopathic stuff sometimes can help.  Giving the baby something to chew on, like frozen fruit.  Sometimes we give Sylvie a frozen strawberry, and she kind of gnaws on that a little bit.  They make, of course, various frozen teething toys.  But maybe some other parents who have had more success than we have could chime in in the comments section and help Tom out.

Steve Wright:  So no whiskey, then?

Chris Kresser:  Haha.  Well, there’s something maybe…

Steve Wright:  Grandma knows best, right?

Chris Kresser:  Believe me, there were a few nights we definitely were thinking along those lines, haha, let me tell you!  We didn’t resort to it because we didn’t actually happen to have any whiskey in the house, which was probably a good thing.

Steve Wright:   Haha, OK.  Well, thanks for the question, Tom, and hopefully our listeners will give everyone some ideas.

Dealing with disrupted sleep patterns

Let’s move on to the next question.  This comes from Joss and it’s a little bit long, so bear with me here.  He has a question regarding his sleep pattern, and it starts off with him falling asleep most days between 9:30 and 10:30 p.m.  Then he sleeps for about 4 to 5 hours pretty deep, undisturbed.  He wakes up around 3 a.m. to go to the bathroom and urinate.  After that, he says:  “I turn and I go in and out of sleep, kind of doze, and I either generally get frustrated or I get rested, but not any real deep sleep.”  Sometimes during this frustrated time of sleep he will read, and it doesn’t matter what happens, it all seems to happen before 6 a.m. when he gets up.  So after that, during the day he feels the urge to nap between 30 minutes to an hour around 3 p.m., and when he does nap, it feels very restorative for his focus and concentration.  In general, he goes on to say that he is following a good diet, he has very good overall health, has a pretty good workout regimen, and has a little bit of coffee but not too much and never past 9 a.m.  So, Chris, his question is, “Should I worry about my sleep pattern?  Is there anything I should do to change and get more complete nights?  Alternatively, should I just embrace it and get up at 3 a.m. and read for an hour?”

Chris Kresser:  Yeah, it’s a good question.  I wouldn’t worry about it, per se, but I think it’s something to address because it’s not normal to wake up at 3 a.m. and be restless and toss and turn for the rest of the time.  And it sounds like he’s holding up pretty well so far, but maybe after a longer period of time with that kind of sleep pattern it’s going to catch up.  That’s the thing about sleep deprivation:  it’s cumulative.  A lot of people are able to deal with some sleep loss for a significant period of time without really obvious effects or symptoms, but over time, it just deepens and becomes harder and harder to get out of, so I think it is important to address.

Some of you might have read about biphasic sleep recently, this idea that for humans the natural sleep pattern was to fall asleep, sleep for maybe 4 hours, then wake up and either just lie awake for an hour or two or actually even get up and do something and then go back to sleep for another 4 hours.  And that may be true, and there are actually references in medieval texts about that kind of sleep pattern.  They called it first sleep and second sleep, and some traditional cultures that have been studied do have that kind of sleep pattern, but here’s the thing:  That works fine if you’re in bed for 12 hours or you’re allocating 12 to 14 hours for rest.  If you go to bed at 8 p.m., and then you sleep until midnight, and then you’re kind of awake until 2 a.m., and then you sleep again from 2 a.m. to 6 a.m., that’s still 8 hours of good-quality sleep, and that’s what’s recommended, 7 to 8 hours.  A biphasic sleep pattern when you’re getting in bed at 10 o’clock and getting up at 6 a.m. isn’t going to work because if you sleep for 3 hours or 4 hours, and then you’re awake for an hour or two, and then you sleep again for a little while, that’s not enough sleep put together.

The first thing I would do in this situation is get an adrenal test, look at cortisol and DHEA levels.  That waking at 3 a.m., even if it’s just to urinate… I mean, if you wake at 3 a.m. and go right back to sleep, that’s not that big of a problem for most people.  Ideally you wouldn’t be waking to urinate.  Maybe drink a little less water, start drinking less water earlier in the day.  If someone just wakes up and goes pee and then goes right back to sleep and sleeps deeply, I’m not really concerned about that.  But if you’re waking up at 3 a.m. and then just not getting any restful sleep after that, to me, chances are really high that there’s an adrenal issue, a cortisol issue there.  Cortisol levels are too high too early, and that’s what’s waking you up or preventing you from getting back to sleep.

Some of the same things that I recommended earlier for Jenny, who was asking about adrenal support during nursing, would apply here.  But since Joss is not nursing, I’m assuming, we have, of course, many other things to consider there.  So depending on what the specific pattern of cortisol dysregulation is, adaptogenic herbs, licorice root extract if cortisol is low, Seriphos or phosphatidylserine if the cortisol is high, pantethine or pantothenic acid, adrenal glandulars, and in some more extreme cases maybe sublingual DHEA and pregnenolone, although those need to be used with caution.  And then, of course, all the same other artificial light and light modification stuff that we talked about would apply here, too.

Steve Wright:  Now, Chris, isn’t it the Chinese realm that says if you wake up at 3 a.m. it’s a liver issue?  Do you put any stock in that?

Chris Kresser:  Not really.  Maybe my former Chinese medicine colleagues will be upset to hear that, but it’s not my orientation right now.  I’m not saying there’s nothing to it.  It’s just not the lens that I look through at this point.

Steve Wright:  OK.

Chris Kresser:  Yeah.  I will say, though, that the liver system in Chinese medicine would be closely related to the kinds of personality types and symptoms and signs that you would expect to see in someone that’s waking up at 3 in the morning.  And it can often be stress related, although it doesn’t seem to be really the case with Joss.  The lifestyle he describes seems pretty grounded and pretty low stress.  But there may be something to that connection.  That’s all I’m saying.

Steve Wright:  OK.  All right.  Well, let’s do one more question, Chris.  You up for it?

Chris Kresser:  Yeah.

How do you explain someone that feels better on a juice fast?

Steve Wright:  OK.  So this question comes from Jeremy.  He says:  “I searched the blog the best I could, and I couldn’t find anything specifically related to this.  Recently I watched Fat, Sick, and Nearly Dead.  I understand that with super-greens your feeling is that unless a person is also eating fats, those micronutrients are not going to absorb well.  My question is, how does one explain the amazing recovery and improvement to health those individuals have after doing a juice fast for 10, 15, or even 60 days?  And second, could someone combine these two diet approaches, where they juice for one meal or more daily and then consume a paleo-based diet for the other meal or two?  And if so, would you add something like olive oil or macadamia nut oil or something of that sort to help the absorbability of some of the micronutrients?”

Chris Kresser:  To answer the first question, how do you explain how someone feels better on a juice fast — or we could ask the same question about a raw food diet, vegan diet, whatever — you always have to consider where people are coming from.  If someone is coming from a Standard American Diet or a diet low in nutrient density and high in a lot of food toxins and they switch to a vegan diet, a raw food diet, juice fast, whatever it is, of course they’re going to feel better.  I mean, they went from eating crap to eating real foods.  And yes, I think the science is pretty clear that if they persist and follow a juice fast type of thing or a raw vegan diet for an extended period of time, a high percentage of people are going to develop nutrient deficiencies, but in the short term it can make you feel really good.  Generally, people are eating fewer calories so that they’re getting the benefits of caloric restriction and fasting.  Autophagy kicks in, like all of the stuff we’ve talked about with intermittent fasting and just eating fewer calories.  So it’s not a surprise at all to me that someone would feel better in the short term doing that.  The question is, is that a sustainable approach over the long term, number one?  Number two, is that appropriate for everybody?  Like, I don’t recommend that for people who have severe adrenal fatigue, for example.  It can actually often take them in the worse direction.  And is it appropriate in the context of a more nutrient-dense, whole foods approach?  If you tolerate carbohydrates well, I don’t see a problem with doing fresh vegetable juices and fruit juices even, too, although you probably want to be moderate with the fruit juice because of the amount of sugar and the lack of fiber.  I know some people are really crazy about this thing called the NutriBullet.  Have you heard about that, Steve?

Steve Wright:  I have.  I have had some people I know go and take the dive.Chris Kresser:  NutriBullet fanatics?

Steve Wright:  Yes.

Chris Kresser:  Yeah, so the NutriBullet is basically like… I don’t have one myself, but what I gather, it’s like an ultra, super-duper-powered blender that you put vegetables and fruits in there, and it turns it into liquid.  And it’s different than juicing because when you juice, it’s removing all of the fiber and pulp, and the NutriBullet, it’s all still in there.  So to me, that’s actually probably better than juicing because the fiber slows down the absorption of the sugars and it also provides some beneficial stuff for the gut bacteria.  But I don’t see a problem with doing, haha, some NutriBulleting.

Steve Wright:  Some extracting?!  That’s what they call it, the Extractor.

Chris Kresser:  Some extracting or some juicing within the context of a paleo type of diet, especially during the summer months when seasonally that feels better and seems more appropriate for the body.  I think that’s fine.

Steve Wright:  Yeah, anecdotally I’ve never done whole lot of experimenting with juicing, but it does seem to be that a lot of people when they do start they do report some sort of increased well-being or energy of some type.

Chris Kresser:  Um-hum.

Steve Wright:  But I’ve never done a whole lot of experimenting myself.

Chris Kresser:  You know, the GAPS diet is pretty big on juicing.  And when I was doing the GAPS intro and then going through the phases way back in the day, I did a fair amount of juicing, and I liked it.  I did almost exclusively vegetable juices because I just felt better with that, but there was a time in my life where that felt good.  I really don’t do it at all anymore.  I don’t feel the need to do it at this point.  And to be honest, cleaning out the juicer is just such a pain in the butt!

Steve Wright:  Haha!

Chris Kresser:  I can’t be bothered to do it!  I guess that’s why people like that NutriBullet, too, because you don’t have to deal with that.  It’s a lot easier to clean out.

Steve Wright:  Yeah, if they made a self-cleaner, man, you could make a million bucks easy.

Chris Kresser:  Yeah, exactly.  So yeah, in summary, I don’t think a 60-day juice fast… I think that absolutely requires supervision.  I think it’s way too extreme for most people.  I wouldn’t recommend it.  But short periods of juice fasting and juicing or NutriBulleting, extracting, whatever you want to call it, within the context of a nutrient-dense diet?  Sure.  Why not?

Steve Wright:  And would there be any reason to throw an ounce or two of some oil into that?

Chris Kresser:  Right, that was the original question!

Steve Wright:  Like a Slurpee?

Chris Kresser:  Yeah, I think adding some coconut oil or some olive oil does absolutely help with nutrient absorption.  I wrote an article called “Eat some vegetables with your butter,” haha, or “Have some butter with your veggies!”  I can’t remember.  Something like that.  And I presented some data in that article showing that the absorption of carotenoids and various other vitamins in green vegetables increases dramatically when you add fat.  So yeah, to really improve the results that you’re going to get from something like that, absolutely.  Add some fat.

Steve Wright:  All right, Chris.  Well, that was a great answer, and I guess if people are extracting nutrients out there, please leave a comment and tell us about your experience with the NutriBullet.  Are you ready to get out of the closet yet, Chris?

Chris Kresser:  I’m really ready to get out of the closet.  It’s a beautiful day here in Berkeley, and I want to go take a walk in the woods near my house.

Steve Wright:  All right, well, with that, thank you for listening.  If you want to get more of Chris in between the shows, please head over to Facebook.com/ChrisKresserLAc, or head over to Twitter.com/ChrisKresser.  Thanks for listening to the show today.  Please keep sending us your questions at ChrisKresser.com using the podcast submission link.  If you enjoyed listening to the show, head over to iTunes and leave us a review.  It helps to get the message out and spread this information to more people.

Chris Kresser:  Thanks, everyone, for listening, and we’ll see you next time!

Note: I earn a small commission if you use the links in this article to purchase the products I mentioned. I only recommend products I would use myself or that I use with patients in my practice. Your purchase helps support this site and my ongoing research.

This 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.

The Many Shades of Gluten Intolerance

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.

Beyond Celiac: Why CD Is Just the Tip of the Iceberg

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)

The Gluten-Free Challenge: Still the Best Test for Gluten Intolerance

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?