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Sleep | The Paleo Diet
As we move into the colder, darker and shorter days of fall and winter it becomes more difficult to maintain your energy levels, productivity and fight off nasty colds and flu. These common complaints become the norm as the seasons change and people are constantly looking for that “magic bullet” supplement or medication to keep them running on all cylinders. Interestingly, a new study on the daily patterns of modern hunter-gatherer tribes across the globe might hold a few clues in how we can keep ourselves healthy, fit and productive through the winter season.

How Much Sleep Did Our Paleo Ancestors Really Get?

There is a romantic notion that our “hunter-gatherer” ancestors rested their heads with the setting sun in the evening, slept blissfully through the night for 8-10 hours and woke up with the rising sun. They certainly didn’t have cellphones, laptops or external light sources to keep them up. Was it partly down to this that they were so fit, strong, and free of chronic degenerative diseases? Not quite.

An interesting new study on modern day hunter-gatherer tribes – the San of southern Africa, the Tsimane in Bolivia, and the Hadza in Tanzania – found they only sleep an average of 5.7-7.1 hours per night.1 This is very surprising because sleep research today suggests most westerners are sleep deprived, averaging about 6.5 hours of sleep per night, which is approximately 1.0-1.5 hours less sleep than our grandparents got two generations ago. Experts believe we should be aiming for 7.5-8.0 hours per night for better health.

This new research suggests there is much more at play than simply the amount of hours of sleep you get (although, I believe this is also important). Let’s take a closer look at some key factors that could help you improve your sleep and upgrade your energy levels this winter and help fight off colds and flu.

The Tribes Go To Bed Earlier in the Winter

As the year comes to an end, most people are busier than ever at work and home as the holidays approach, rather than winding down to recharge their batteries. If we look to our ancestral roots to find answers to the “best” sleep practices, we find the tribes in the aforementioned study went to bed earlier during the darker days of winter/rainy season and later in the summer/dry season. Their average bedtime was just after 9:00 pm in the winter months, compared to 10:45 pm in the summer (still, not exactly “night owls” by today’s modern standard).
A lot people struggle to get bed before midnight (laptops, cellphones and TVs don’t help) and usually don’t get to bed earlier in the colder, darker, winter months. As we approach the darkest days of the year, we should be getting more sleep (not less), but holiday parties, travel, and work commitments usually ramp up at this time of year. This lack of sleep is shown in the research to suppress your immune system function, putting you at significantly increased risk of catching a cold or flu.2

The Tribes Wake Up Consistently With Morning Light

Hitting snooze is a morning ritual for a lot of people, as they struggle to find the energy to get out of bed and start their day. While I am sure we can all agree that sleeping in feels pretty good, is it what your body really needs? The tribal groups in this study woke up at virtually the same time throughout the entire year with the morning sun (not surprising if you’re an avid camper!).

Many of your key hormones are produced on a natural daily pattern or circadian rhythm that new research shows gets disrupted if you constantly change your sleeping and waking time. Disrupted circadian patterns have been shown to leave you more prone to fatigue (sound familiar?), inflammation, and even change the balance of “good” to “bad” bacteria in your gut.3

If you struggle with fatigue, insomnia or frequent colds and flus, aim to have a consistent bedtime and waking time this winter. Go to bed earlier (don’t sleep in longer in the mornings) to help kick your snooze button habit in the morning. If you really struggle to wake up, try some gentle stretching/mobility/yoga on the floor to ease your way into the day. (Not only that, research shows the later you get to bed the greater your likelihood for weight gain.4 If weight loss is also a goal, get ahead of your new year’s resolution by tucking in earlier at night).

The Tribes Are Exposed To Lots of Morning Light

It’s difficult to wake in the morning and get outside during the cold days of winter. Fatigue, lack of time and general desire to stay warm keep you huddled up in your house, car, and office. However, not exposing yourself to natural light may be having a significant negative impact on your health.

Modern hunter-gatherer communities get up daily with the morning sun and engage in the vast majority of their physical labor in the morning hours exposed to natural light. In contrast, most people are indoors all morning throughout the winter – commuting in cars and working in buildings – not getting nearly enough exposure to natural light. Even on a cloudy day, the natural light outside provides a whopping 100,000-lux (a measure of light intensity), compared to only 5,000-lux in your office or home.

New research shows that this light exposure is crucial for circadian hormone production and thus your energy levels, health and resiliency.5 It’s easy to find yourself stuck in your car, office or house all winter. Instead, get outside to grab your morning coffee, walk a few blocks to your next meeting, or go outdoors in the morning for a light run/jog to start your day. You’ll feel much better for it!

Often we’re drawn to the “shiny new toy” or exotic and complex solutions to our problems, however the real lasting solutions are typically always found in how you eat, move and lifestyle factors. While a Paleo diet will go a long way to keeping you energized and fighting off colds and flu this winter (check out my article on how to Paleo boost your immunity this fall), looking at your daily patterns of sleeping and waking from an ancestral perspective will likely help you dramatically upgrade your energy and vitality this winter.

 

References

  1. Yetish G et al. Natural Sleep and Its Seasonal Variations in Three Pre-industrial Societies. Current Biology. Vol 25, Iss. 21, 2 November 2015, Pages 2862–2868.
  2. Prather A et al. Behaviorally Assessed Sleep and Susceptibility to the Common Cold. Sleep Journal. Vol. 38, Issue 09.
  3. Voigt R et al. Circadian disorganization alters intestinal microbiota. Plos One. 2014 May 21;9(5):e97500.
  4. Asarnow L et al. Possible link between bedtime and change in body mass index. Sleep Journal. Vol. 38, Issue 10.
  5. Czeisler C, Klerman E. Circadian and sleep-dependent regulation of hormone release in humans. Recent Prog Horm Res. 1999;54:97-130; discussion 130-2.

Beans and Legumes | The Paleo Diet

A few days ago I was delighted to learn that Dr. Oz was going to again feature The Paleo Diet on his nationally syndicated television show along with one of my co-authors, Nell Stephenson, of The Paleo Diet Cookbook. I tuned into the Dr. Oz show and was happy about most of what I saw except for Chris Kresser, expounding upon the health virtues of a food group, beans and legumes, that definitely are not Paleo. Please read the following article on beans and legumes, and decide for yourself if beans and legumes are Paleo and feel free to pass this information on to your friends, family and anyone interested in starting a Paleo Diet.

In the decade since I wrote The Paleo Diet, a question that comes up time and again is, “Why can’t I eat beans?”  I briefly touched upon this topic in my first book, but never really was able to get into the necessary detail of why you should avoid not only beans, but all other legumes including peanuts and soy.  Now let me bring you fully up to date on recent developments about our understanding of how beans, soy and other legumes may impact our health.  But most importantly, I’ll show you beyond a shadow of a doubt why legumes are inferior foods that should not be part of any contemporary Paleo Diet.

Toxicity of Uncooked Beans

It may come as a surprise to you, but as recently as 19 years ago imports of red kidney beans into South Africa were legally prohibited because of “their potential toxicity to humans” (63).  Although many people think about kidney beans as nutritious, plant based high-protein foods; few would ever consider them to be toxic poisons.  But indeed toxic they are – unless adequately soaked and boiled kidney beans and almost all legumes produce detrimental effects in our bodies.  Starting in the early 1970’s a number of scientific papers reported that consumption of raw or undercooked red kidney beans caused nausea, vomiting, abdominal pain, severe diarrhea, muscle weakness and even inflammation of the heart (42, 52, 60).  Similar symptoms were documented in horses and cattle (8).  Further, raw kidney beans were lethally toxic to rats when fed at more than 37 % of their daily calories  (24, 27, 51).  Like the proverbial canary in a coal mine, these clues should make us proceed cautiously as we consider the nutritional benefits and/or liabilities of beans and legumes.  Before I get into why raw or partially cooked beans, legumes and soy are toxic, I want to first point out the obvious – these foods (even when fully cooked) are nutritional lightweights when compared to meat, fish and other animal foods.

 The Nutrient Content of Beans and Legumes

If we examine the USDA’s My Plate, governmental nutritionists have arbitrarily created five food groups: 1) grains, 2) vegetables, 3) fruit, 4) dairy and 5) protein foods (61).  On the surface, these categories seem reasonable, and I would basically agree that most common foods could logically be placed into one of these five categories except for one glaring exception – protein foods.

Upon more careful inspection of this category we find the USDA has decided that protein foods should include: 1) meat, 2) poultry, 3) fish, 4) eggs, 5) nuts and seeds and 6) dry beans and peas.  I have little disagreement that meat, poultry, fish and eggs are good sources of protein.  However, digging a little bit deeper, we soon find that the USDA tells us that these six protein food groups are equivalent and can be used interchangeably with one another (61) – meaning that animal protein sources (meats, poultry, fish and eggs) are nutritionally comparable to plant protein sources (nuts, seeds, dry beans and peas).  OK? It gets better still.  I quote the USDA My Plate recommendations:

“Dry beans and peas are the mature forms of legumes such as kidney beans, pinto beans, black-eyed peas, and lentils.  These foods are excellent sources of plant protein, and also provide other nutrients such as iron and zinc.  They are similar to meats, poultry, and fish in their contribution of these nutrients.  Many people consider dry beans and peas as vegetarian alternatives for meat.” (61).

The Paleo Diet

OK let’s let the data speak for itself and really see how “dry beans and peas” stack up to meats, poultry, fish and eggs in terms of protein, iron and zinc as alluded to by the USDA.  In the figure below [data from (66)] you can see that on a calorie by calorie basis, legumes are utter lightweights when compared to the protein content of lean poultry, beef, pork and seafood. Nuts and seeds fare even worse.  Beans, peas and other legumes contain 66 % less protein than either lean chicken or turkey, and 61 % less protein than lean beef, pork and seafood.  What the USDA doesn’t tell us is that our bodies don’t process bean and legume proteins nearly as efficiently as plant proteins – meaning that the proteins found in beans, peas and other legumes have poor digestibility.

The Food and Agricultural Organization (FAO)/World Health Organization (WHO) of the United Nations have devised a protein quality index known as the Protein Digestibility-Corrected Amino Acid Score (PDCAAS).  This index reveals that beans and other legumes maintain second-rate PDCAAS ratings which average about 20 to 25 % lower than animal protein ratings (14).  So to add insult to injury legumes and beans not only contain about three times less protein than animal foods, but what little protein they do have is poorly digested.  Their poor PDCAAS scores stem from a variety of antinutrients which impair protein absorption (20, 29, 44) and from low levels of two essential amino acids (cysteine and methionine) (66).  I don’t know about you, but I have no idea how the USDA concluded that legumes are, “excellent sources of plant protein . . . similar to meats, poultry, and fish in their contribution of these nutrients.

Now let’s take a look at the average zinc and iron content of eight commonly eaten legumes (green peas, lentils, kidney beans, lima beans, garbanzo beans [chick peas], black-eyed peas, mung beans and soybeans).  In the two figures below, I have contrasted the average iron and zinc content [data from (66)] of these eight legumes to lean chicken, turkey, beef, pork and seafood.

The Paleo Diet

The Paleo Diet

Notice that the iron content of legumes appears to be similar to seafood and about twice as high as in lean meats and eggs.  Once again, as was the case with legume protein, this data is misleading because it doesn’t tell us how legume iron is handled in our bodies.  Experimental human studies from Dr. Cook’s laboratory in Switzerland and (30) from Dr. Hallberg’s research group in Sweden (26) have shown that only about 20 to 25 % of the iron in legumes is available for absorption because it is bound to phytate.  So in reality, the high iron content of legumes (2.2 mg/100 kcal) plummets by 75 – 80 %, thereby making legumes a very poor source of iron compared to animal foods.  A similar situation occurs with zinc, as phytate and other antinutrients in legumes severely reduce its absorption in our bodies (13, 19, 57).  Given that this information has been known for more than 30 years, it absolutely defies logic how the USDA could misinform the American public by declaring that, “These foods are excellent sources of plant protein, and also provide other nutrients such as iron and zinc.  They are similar to meats, poultry, and fish in their contribution of these nutrients.” 

Antinutrients in Beans and Legumes

From the picture I have painted so far, you can see how misleading it can be to evaluate the nutritional and health effects of beans and other legumes by simply analyzing their nutrient content on paper, as the USDA has done.  Before we can pass nutritional judgment on any food, it is absolutely essential to determine how it actually acts within our bodies.  Beans are not good sources of either zinc or iron, and they have low protein digestibility because these legumes are chock full of antinutrients that impair our body’s ability to absorb and assimilate potential nutrients found in these foods.

As with whole grains, the primary purpose of most antinutrients in legumes is to discourage predation and prevent destruction of the plant’s reproductive materials (e.g. its seeds) by microorganisms, insects, birds, rodents and large mammals (10, 25).  We most frequently refer to legume seeds as beans, but don’t forget that peanuts are not really nuts at all, but rather are legumes.  In the table below I have listed some of the more commonly known legume seeds along with their scientific names.

Table of Commonly Consumed Legumes

The Paleo Diet

Part of the reason for doing this is to point out that many different versions of the beans we frequently eat actually are the exact same species – and as such contain comparable concentrations of toxic antinutrients.  Notice how many times you see the scientific name, Phaseolus vulgaris, repeated in the table above.  If you enjoy Mexican food then you have probably tasted Phaseolus vulgaris as either refried beans or black beans, since these two beans are one in the same species, differing only by color.  Great northern beans, green beans, kidney beans, navy beans, pinto beans and white kidney beans also are members of the same species, Phaseolus vulgaris.  I bring this information up because all beans that are members of Phaseolus vulgaris contain some of the highest concentrations of antinutrients known.

The list of antinutrients found in legumes, beans and soy is seemingly endless and includes: lectins, saponins, phytate, polyphenols (tannins, isoflavones), protease inhibitors, raffinose oligosaccharides, cyanogenetic glycosides, and favism glycosides.  I know that this list appears somewhat formidable at first because of all the scientific terms, but don’t be worried – the concepts underlying how these toxins may impair our health are easily understood.  Let’s briefly go through this list so you can clearly understand why you should avoid legumes.

Lectins

All beans and legumes are concentrated sources of lectins.    Lectins are potent antinutrients that plants have evolved as toxins to ward off predators (10).  You remember from earlier in this chapter that raw or undercooked kidney beans caused severe cases of food poisoning in humans and were lethally toxic in rats.  Although several kidney bean antinutrients probably contributed to these poisonous effects, animal experiments indicate that a specific lectin found in kidney beans was the major culprit (2, 44).  Kidney beans and all other varieties of beans (black beans, kidney beans, pinto beans, string beans, navy beans etc.) within the Phaseolus vulgaris species contain a lectin called phytohemagglutinin (PHA).  The more PHA we ingest, the more ill we become.  This is why raw beans are so toxic – they contain much higher concentrations of PHA than cooked beans (4, 23. 46).  However, cooking doesn’t completely eliminate PHA, and even small amounts of this lectin are known to produce adverse health effects, providing they can penetrate our gut barrier.

The trick with lectins is that they must bypass our intestinal wall and enter into our bloodstream if they are to wreak havoc within our bodies. So far, no human studies of PHA have ever been conducted.  However, in laboratory animals, PHA easily breeches the gut barrier and enters into the bloodstream where it may travel to many organs and tissues and disrupt normal cell function and cause disease (45, 49).  Human and animal tissue experiments reveal that PHA and other food lectins can cause a “leaky gut” and enter circulation (24, 34, 35, 45, 47, 49, 64, 65) .  A leaky gut represents one of the first steps implicated in many autoimmune diseases (67).  Impaired intestinal integrity produced by dietary lectins may also my cause low level inflammation in our bloodstreams (15, 43, 48, 62) – a necessary step for atherosclerosis (the artery clogging process) and cancer.

Besides  kidney beans and other bean varieties within Phaseolus vulgaris species, all other legumes contain lectins with varying degrees of toxicity ranging from mild to lethal.   Soybean lectin (SBA) is also known to impair intestinal permeability and cause a leaky gut (1, 35).  Peanut lectin (PNA) is the only legume lectin to have been tested in living humans by Dr. Rhodes’ research group in London.  Within less than an hour after ingestion in healthy normal subjects, PNA entered their bloodstreams (64) – whether the peanuts were cooked or not.   Later I will show you how peanuts and PNA are potent initiators of atherosclerosis.

The lectins found in peas (PSA) and lentils (LCA) seem to be much less toxic than PHA, SBA or PNA, however they are not completely without adverse effects in tissue and animal experiments (9, 21, 25, 38 ).  Unfortunately, no long term lectin experiments have ever been conducted in humans.  Nevertheless, from animal and tissue studies, we know that these antinutrients damage the intestinal barrier, impair growth, alter normal immune function and cause inflammation.

Saponins

The term, saponin, is derived from the word soap.  Saponins are antinutrients found in almost all legumes and have soap-like properties that punch holes in the membranes lining the exterior of all cells.  As was the case with lectins, this effect is dose dependent – meaning that the more saponins you ingest, the greater will be the damage to your body’s cells.  Our first line of defense against any antinutrient is our gut barrier.  Human tissue and animal studies confirm that legume saponins can easily disrupt the cells lining our intestines and rapidly make their way into our bloodstream (1, 16, 17, 18, 32 ).  Once in the bloodstream in sufficient quantities, saponins can then cause ruptures in our red blood cells in a process known as hemolysis which can then temporarily impair our blood’s oxygen carrying capacity (3).  In the long term, the major threat to our health from legume saponins stems not from hemolysis (red blood cell damage) but rather from their ability to increase intestinal permeability (3, 16, 17, 18, 32)  A leaky gut likely promotes low level inflammation because it allows toxins and bacteria in our guts to interact with our immune system.  This process is known to be is a necessary first step in autoimmune diseases (67) and may promote the inflammation  necessary for heart disease and and the metabolic syndrome to develop and progress (68).

The other major problem with legume saponins is that cooking does not destroy them.  In fact, even after extended boiling for two hours, 85-100 % of the original saponins in most beans and legumes remain intact (55).   On the other hand, by eating fermented soy products such as tofu and tempeh, or sprouted beans you can lower your saponin intake (39).  The table below shows you the saponin content of some common beans, legumes and soy products.

Saponin Content of Selected Beans, Legumes and Soy Products

The Paleo Diet

Consumers beware! Notice that the concentration of saponins in soy protein isolates is dangerously high.  If you are an athlete or anyone else trying to increase your protein intake by supplementing with soy protein isolates, I suggest that you reconsider.  A much healthier strategy would be to eat more meats, fish and seafood.  These protein packed foods taste a whole lot better than artificial soy isolates and are much better for your body.  If we only eat legumes occasionally,  saponin damage to our intestines will quickly repair itself, however when legumes or soy products are consumed in high amounts as staples or daily supplements, the risk for a leaky gut and the diseases associated with it is greatly increased.

Phytate

We’ve already discussed this antinutrient in great detail, so there is really not much else to say.  Because phytate prevents the full absorption of iron, zinc, calcium, magnesium and copper present in legumes and whole grains, then reliance upon these plant foods frequently causes multiple nutritional deficiencies in adults, children and even nursing infants.  Boiling and cooking don’t seem to have much effect upon the phytate content of legumes, whereas sprouting and fermentation can moderately reduce phytate concentrations. Also, vitamin C counteracts phytate’ s inhibitory effects on mineral absorption.  Nevertheless, the best tactic to reduce phytate in your diet is to adopt The Paleo Diet – humanity’s original legume and grain free diet.

Polyphenols: Tannins and Isoflavones

Polyphenols are antioxidant compounds that protect plants from UV sunlight damage as well as from insects, pests and other microorganisms.  Just like sunscreens protect our skin from UV damage, polyphenols are one of the compounds plants have evolved to escape the harmful effects of ultraviolet (UV) radiation from the sun, along with damage caused by animal and microorganism predators.  Polyphenols come in many different varieties and forms and are common throughout the plant kingdom.  When we eat these compounds, they seem to have both healthful and detrimental effects in our bodies.  For instance, resveratrol is a polyphenol found in red wine that may increase lifespan in mice and slow or prevent many diseases.    On the other hand, at least two types of polyphenols (tannins and isoflavones) within beans, soy and other legumes may have adverse effects in our bodies (59).

Tannins are bitter tasting polyphenols and give wine its astringent qualities.  As with all antinutrients, the more tannin you ingest, the greater is the potential to disrupt your health.   Tannins are similar to phytate in that they reduce protein digestibility and bind iron and other minerals, thereby preventing their normal absorption (29, 59).  Some, but not all tannins damage our intestines causing a “leaky gut” (59).   By now you can see that legumes, beans and soy represent a triple threat to our intestinal integrity since three separate antinutrients (lectins, saponins, and tannins) all work together to encourage a leaky gut. Let’s move on to the next category of polyphenols.

Isoflavones are some of nature’s weirder plant compounds in that they act like female hormones in our bodies.  Certain isoflavones which are concentrated in soybeans and soy products are called phytoestrogens – literally meaning, “plant estrogens”.  I’ve previously mentioned that isoflavones from soy products can cause goiters (an enlargement of the thyroid gland), particularly if your blood levels of iodine are low.  Two phytoestrogens in soy called genistein and daidzen produce goiters in experimental animals.  You don’t have to develop full blown goiters by these soy isoflavones to impair your health.  In a study of elderly subjects, Dr. Ishizuki (31) and colleagues demonstrated that when subjects (average age, 61 years) were given 30 grams of soy daily for three months they developed symptoms of low thyroid function (malaise, lethargy, and constipation), and half of these people ended up with goiters.

For women, regular intake of soy or soy isoflavones may disrupt certain hormones that regulate the normal menstrual cycle.  In a meta analysis of 47 studies, Dr. Hooper and co-workers (28) demonstrated that soy or soy isoflavones consumption caused two female hormones, follicle stimulating hormone (FSH) and luteinizing hormone (LH), to fall by 20 %.  The authors concluded, “The clinical implications of these modest hormonal changes remain to be determined.”

I wouldn’t necessary agree with this conclusion, nor would I call a 20 % reduction in both FSH and LH “modest”.  In one study, seven of nine women who consumed vegetarian diets (containing significant quantities of legumes) for only six weeks stopped ovulating (69).  One of the hormonal changes reported in this study, concurrent with the cessation of normal periods, was a significant decline in luteinizing hormone (LH).  Because western vegetarian diets almost always contain lots of soy and hence soy isoflavones, it is entirely possible that soy isoflavones were directly responsible for the declines in LH and the disruption of normal menstrual periods documented in this study.

I have received email from women all over the world who’s menstrual and infertility problems subsided after adopting The Paleo Diet (see Chapter 13). Their stories paint a credible picture that modern day Paleo Diets contain multiple nutritional elements that may improve or eliminate female reproductive and menstrual problems.  Unfortunately scientific validation of these women’s experiences still lies in the future.

Perhaps the most worrisome effects of soy isoflavones may occur in developing fetuses with iodine deficient mothers and in infants receiving soy formula.  A recent (2007) paper by Dr. Gustavo Roman (54) at the University of Texas Health Sciences Center has implicated soy isoflavones as risk factors for autism via their ability to impair normal iodine metabolism and thyroid function.  Specifically, the soy isoflavone known as genistein may inhibit a key iodine based enzyme required for normal brain development.  Pregnant women with borderline iodine status can become iodine deficient by consuming a high soy diet.  Their deficiency may then be conveyed to their developing fetus which in turn impairs growth in fetal brain cells known to be involved in autism.  Infants born with iodine deficiencies are made worse if they are fed a soy formula.  Once again, the evolutionary lesson repeats itself.  If a food or nutrient generally was not a part of our ancestral diet, it has a high probability of disrupting our health and that of our children.

Protease Inhibitors

Unless you are a biologist by trade or are involved in a very narrow area of human nutrition, very few people on the planet know about protease inhibitors.  But I can tell you that when you eat beans, soy or other legumes you should be as aware of protease inhibitors as you are of a radar trap on the freeway – that is – if you don’t want to get a ticket or eat foods that can have unfavorably effects upon your health.

When we eat any protein, we have enzymes in our intestines which break protein into its component amino acids.  These enzymes are called proteases and must be operating normally for our bodies to properly assimilate dietary proteins.  Almost all legumes are concentrated sources of antinutrients called protease inhibitors which prevent our gut enzymes from degrading protein into amino acids.  Protease inhibitors found in beans, soy, peanuts and other legumes are part of the reason why legume proteins have lower bioavailability than meat proteins (20).  In experimental animals ingestion of protease inhibitors in high amounts depresses normal growth and causes pancreatic enlargement (21, 39, 41).  Heating and cooking effectively destroys about 80 % of protease inhibitors found in most legumes (5, 11), so the dietary concentrations of these antinutrients found in beans and soy are thought to have little harmful effects in our bodies.  Nevertheless, at least one important adverse effect of protease inhibitors may have been overlooked.

When the gut’s normal protein degrading enzymes are inhibited by legume protease inhibitors, the pancreas works harder and compensates by secreting more protein degrading enzymes.  Consequently, consumption of protease inhibitors causes levels of protein degrading enzymes to rise within our intestines.  One enzyme in particular, called trypsin, increases significantly.  The rise in trypsin concentrations inside our gut is not without consequence, because elevated trypsin levels increase intestinal permeability in animal experiments (53).  Once again we see yet another antinutrient found in legumes that contribute to a leaky gut, which as I have explained early is not without consequence.

Raffinose Oligosaccharides

Here’s another big scientific term for a little problem almost every one of us has had to deal with at one time or another after we ate beans.  Beans cause gas or flatulence.  Almost all legumes contain complex sugars called oligosaccharides.  In particular, two complex sugars (raffinose and stachyose) are the culprits and are the elements in beans that give us gas (6).  We lack the gut enzymes to breakdown these complex sugars into simpler sugars.  Consequently, bacteria in our intestines metabolize these oligosaccharides into a variety of gases (hydrogen, carbon dioxide and methane).  Beans don’t affect us all equally.  Some people experience extreme digestive discomfort with diarrhea, nausea, intestinal rumbling and flatulence, whereas others are almost symptomless (6).  These differences among people seem to be caused by varying types of gut flora (microorganisms).

Cyanogenetic Glycosides

Upon digestion, antinutrients in lima beans called cyanogenetic glycosides are turned into the lethal poison, hydrogen cyanide, in our intestines.  Fortunately, cooking eliminates most of the hydrogen cyanide in lima beans.  Nevertheless a number of fatal poisonings have been reported in the medical literature from people eating raw or undercooked lima beans (70).

Although most of us would never consider eating raw lima beans, the problem doesn’t end here.  Upon cooking most of the hydrogen cyanide in lima beans is converted into a compound called thiocyanate which you can add to soy isoflavones as dietary antinutrients that impair iodine metabolism and cause goiter (70).  In iodine deficient children, these so-called goitrogens are suspect dietary agents underlying autism (54).

Favism  Glycosides

Unless you are a bean connoisseur, most of us in the United States have never tasted broad beans which are also known as fava or faba beans.  In Mediterranean, Middle Eastern and North African countries broad beans are more popular.  Unfortunately, for many people in these countries, particularly young children, consumption of fava beans can be lethal.  It has been intuitively known for centuries that fava bean consumption was fatal in certain people.  However, the biochemistry of the disease (called favism) has only been worked out in the past 50 years or so (7).

Favism can only occur in people with a genetic defect called G6PD deficiency.  This mutation is the most common human enzyme defect – being present in more than 400 million people worldwide.   It is thought to confer protection against malaria.  People whose genetic background can be traced to Italy, Greece, the Middle East or North Africa are at a much higher risk for carrying this mutation.  If you or your children don’t know if you have the genes causing favism, a simple blood test available at most hospitals and medical clinics can diagnose this problem.  Consumption of fava beans in genetically susceptible people causes a massive rupturing of red blood cells called hemolytic anemia and may frequently be fatal in small children unless blood transfusions are made immediately (7, 71).  Not all people with G6PD deficiency experience favism symptoms after they eat broad beans; however if your family background is from the Mediterranean region you may be particularly susceptible.

Although it is not completely known how broad bean consumption causes favism, three antinutrient glycosides (divicine, isouramil and convicine) found in these legumes likely do the damage (72).  These compounds enter our bloodstreams, and in people with the G6PD mutations interact with red blood cells in a manner that causes them to rupture.   So, you can now add fava beans along with lima beans to the list of legumes which are lethally toxic.

Peanuts and Heart Disease

What’s wrong with Peanut Oil and Peanuts?  Most nutritional experts would tell us that they are heart healthy foods because they contain little saturated fat and most of their fat is made up of cholesterol lowering monounsaturated and polyunsaturated fats.  Hence, on the surface, you might think that peanut oil would probably be helpful in preventing the artery clogging process (atherosclerosis) that underlies heart disease.  Your thoughts were not much different from those of nutritional scientists – that is until they actually tested peanuts and peanut oil in laboratory animals.  Starting in the 1960’s and continuing into the 1980’s scientists unexpectedly found peanut oil to be highly atherogenic, causing arterial plaques to form in rabbits, rats and primates (73-78) – only a single study (79) showed otherwise.  Peanut oil was found to be so atherogenic that it continues to be routinely fed to rabbits to produce atherosclerosis to study the disease itself.

Initially, it was unclear how a seemingly healthful oil could be so toxic in such a wide variety of animals.  Dr. David Kritchevsky and co-workers at the Wistar Institute in Philadelphia were able to show with a series of experiments that peanut oil lectin (PNA) was most likely responsible for it artery clogging properties (36, 37).  Lectins are large protein molecules and most scientists had presumed that digestive enzymes in the gut would degrade it into its component amino acids.  Consequently, it was assumed that the intact lectin molecule would not be able to get into the bloodstream to do its dirty work.  But they were wrong.  It turned out that lectins were highly resistant to the gut’s protein shearing enzymes.  An experiment conducted by Dr. Wang and colleagues and published in the prestigious medical journal Lancet (64) revealed that PNA got into the bloodstream intact in as little 1-4 hours after subjects ate a handful of roasted, salted peanuts.   Even though the concentrations of PNA in the subject’s blood were quite low, they were still at concentrations known to cause atherosclerosis in experimental animals.  Lectins are a lot like super glue – it doesn’t take much.  Because these proteins contain carbohydrates, they can bind to a wide variety of cells in the body, including the cells lining the arteries.  And indeed, it was found that PNA did its damage to the arteries by binding to a specific sugar receptor (58).  So, the practical point here is to stay away from both peanuts and peanut oil and all legumes.

 Summary

I’d like to make a final departing comment before we leave the topic of beans and legumes.  As you adopt The Paleo Diet or any diet, listen to your body.  If a food or food type doesn’t agree with you or makes you feel ill or unwell, don’t eat it.  I should have listened to my own advice 25 years ago when I was experimenting with vegetarian diets.  Whenever I ate beans or legumes, I experienced digestive upset, gas and frequently had diarrhea.   Since embracing The Paleo Diet almost 20 years ago, these symptoms have become a thing of the past.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

REFERENCES

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3. Baumann E, Stoya G, Völkner A, Richter W, Lemke C, Linss W. Hemolysis of human erythrocytes with saponin affects the membrane structure. Acta Histochem. 2000 Feb;102(1):21-35.

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18. Gee JM, Wal JM, Miller K, Atkinson H, Grigoriadou F, Wijnands MV, Penninks AH, Wortley G, Johnson IT. Effect of saponin on the transmucosal passage of beta-lactoglobulin across the proximal small intestine of normal and beta-lactoglobulin-sensitised rats. Toxicology. 1997 Feb 28;117(2-3):219-28.

19. Gibson RS, Bailey KB, Gibbs M, Ferguson EL. A review of phytate, iron, zinc, and calcium concentrations in plant-based complementary foods used in low-income countries and implications for bioavailability. Food Nutr Bull. 2010 Jun;31(2 Suppl):S134-46.

20. Gilani GS, Cockell KA, Sepehr E. Effects of antinutritional factors on protein digestibility and amino acid availability in foods. J AOAC Int. 2005 May-Jun;88(3):967-87.

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24. Greer F,  Pusztai A. (1985).  Toxicity of kidney bean (Phaseolus vulgaris) in rats: changes in intestinal permeability. Digestion. 1985 32: 42-46.

25. Gupta YP. Anti-nutritional and toxic factors in food legumes: a review. Plant Foods Hum Nutr 1987;37:201-228.

26. Hallberg L, Hulthén L. Prediction of dietary iron absorption: an algorithm for calculating absorption and bioavailability of dietary iron. Am J Clin Nutr. 2000 May;71(5):1147-60.

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28. Hooper L, Ryder JJ, Kurzer MS, Lampe JW, Messina MJ, Phipps WR, Cassidy A. Effects of soy protein and isoflavones on circulating hormone concentrations in pre- and post- enopausal women: a systematic review and meta-analysis. Hum Reprod Update. 2009 Jul-Aug;15(4):423-40.

29. Hughes JS, Acevedo E, Bressani R, Swanson BG.  Effects of dietary fiber and tannins on protein utilization in dry beans (Phaseolus vulgaris). Food Res Int 1996;29:331-338.

30. Hurrell RF, Juillerat MA, Reddy MB, Lynch SR, Dassenko SA, Cook JD. Soy protein, phytate, and iron absorption in humans. Am J Clin Nutr. 1992 Sep;56(3):573-8.

31. Ishizuki Y, Hirooka Y, Murata Y, Togashi K.  The effects on the thyroid gland of soybeans administered experimentally in healthy subjects. Nippon Naibunpi Gakkai Zasshi. 1991 May 20;67(5):622-9.

32. Johnson IT, Gee JM, Price K, Curl C, Fenwick GR. Influence of saponins on gut permeability and active nutrient transport in vitro. J Nutr. 1986 Nov;116(11):2270-7.

33. Keukens EA, de Vrije T, van den Boom C, de Waard P, Plasman HH, Thiel F, Chupin V, Jongen WM, de Kruijff B. Molecular basis of glycoalkaloid induced membrane disruption. Biochim Biophys Acta. 1995 Dec 13;1240(2):216-28.

34. Kilpatrick DC, Pusztai A, Grant G, Graham C, Ewen SW. Tomato lectin resists digestion in the mammalian alimentary canal and binds to intestinal villi without deleterious effects. FEBS Lett. 1985;185:299-305

35. Knudsen D, Jutfelt F, Sundh H, Sundell K, Koppe W, Frøkiaer H. Dietary soya saponins increase gut permeability and play a key role in the onset of soyabean-induced enteritis in Atlantic salmon ( Salmo salar L.). Br J Nutr. 2008 Jul;100(1):120-9.

36. Kritchevsky D et al.  Influence of native and randomized peanut oil on lipid metabolism and aortic sudanophilia in the vervet monkey. Atherosclerosis 1982;42:53-58.

37. Kritchevsky D, Tepper SA, Klurfeld DM. Lectin may contribute to the atherogenicity of peanut oil. Lipids 1998 Aug;33(8):821-3

38. Liener IE.   Nutritional significance of lectins in the diet.  In The Lectins: Properties, Functions, and Applications in Biology and Medicine, pp. 527-52 [I.E. Liener, N. Sharon, I.J. Goldstein, editors]. Orlando; Academic Press, 1986.

39. Liener IE (1994) “Implications of antinutritional components in soybean foods.” Crit Rev Food Sci Nutr., vol. 34, pp. 31-67.

40. Lochner N, Pittner F, Wirth M, Gabor F. Wheat germ agglutinin binds to the epidermal growth factor receptor of artificial Caco-2 membranes as detected by silver nanoparticle enhanced fluorescence. Pharm Res. 2003 May;20(5):833-9

41. Losso JN. The biochemical and functional food properties of the bowman-birk inhibitor. Crit Rev Food Sci Nutr. 2008 Jan;48(1):94-118.

42. Noah ND, Bender AE, Reaidi GB, Gilbert RJ. Food poisoning from raw red kidney beans. BrMed J. 1980 Jul 19;281 (6234):236-7.

43. Muraille E, Pajak B, Urbain J, Leo O. Carbohydrate-bearing cell surface receptors involved in innate immunity: interleukin-12 induction by mitogenic and nonmitogenic lectins. Cell Immunol. 1999 Jan 10;191(1):1-9.

44. Pusztai A, Clarke EM, Grant G, King TP. The toxicity of Phaseolus vulgaris lectins. Nitrogen balance and immunochemical studies. J Sci Food Agric. 1981 Oct;32(10):1037-46.

45. Pusztai A, Greer F & Grant G. Specific uptake of dietary lectins into the systemic circulation of rats. Biochemical Society Transcations. 1989;17, 527-528

46. Pusztai A, Grant G.  Assessment of lectin inactivation by heat and digestion. In: Methods in Molecular Medicine: Vol. 9: Lectin methods and protocols.  J M Rhodes, JM, J D Milton JD (Eds). Humana Press Inc. Totowa, NJ, 1998.

47. Pusztai A, Ewen SW, Grant G, Brown DS, Stewart JC, Peumans WJ, Van Damme EJ, Bardocz S. Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins. Br J Nutr. 1993 Jul;70(1):313-21

48. Pusztai A.. Dietary lectins are metabolic signals for the gut and modulate immune and hormone functions. European Journal of Clinical Nutrition. 1993;47: 691-99.

49. Pusztai A, Ewen  SWB, Grant G, Peumans WJ, Van Damme EJM, Rubio LA, Bardocz S. Plant (food) lectins as signal molecules: Effects on the morphology and bacterial ecology of the small intestine.  In Lectin Reviews, Volume I , pp. 1-15 [D.C. Kilpatrick, E. Van Driessche, T.C. Bog-Hansen, editors].  St. Louis: Sigma, 1991.

50. Pusztai A, Grant G, Spencer RJ, Duguid TJ, Brown DS, Ewen, SWB, Peumans WJ, Van Damme EJM, Bardocz S.  Kidney bean lectin-induced Escherichia coli overgrowth in the small intestine is blocked by GNA, a mannose-specific lectin. Journal of Applied Bacteriology. 1993;75: 360-68.

51. Rattray EAS, Palmer R, Pusztai A. Toxicity of kidney beans (Phaseolus vulgaris L.) to conventional and gnotobiotic rats. Journal of the Science of  Food and Agriculture. 1974; 25:1035-40.

52. Rodhouse JC, Haugh CA, Roberts D, Gilbert RJ. Red kidney bean poisoning in the UK: an analysis of 50 suspected incidents between 1976 and 1989. Epidemiol Infect. 1990 Dec;105(3):485-91.

53. Róka R, Demaude J, Cenac N, Ferrier L, Salvador-Cartier C, Garcia-Villar R, Fioramonti J, Bueno L. Colonic luminal proteases activate colonocyte proteinase-activated receptor-2 and regulate paracellular permeability in mice. Neurogastroenterol Motil. 2007 Jan;19(1):57-65.

54. Román GC. Autism: transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007 Nov 15;262(1-2):15-26

55. Ruiz RG, Price KR, Arthur AE, Rose ME, Rhodes MJ, Fenwick RG.  Effect of soaking and cooking on saponin content and composition of chickpeas (Cicer arietinum) and lentils (Lens culinaris). J Agric Food Chem 1996;44:1526-30.

56. Ryder SD, Smith JA, Rhodes JM.  Peanut lectin: a mitogen for normal human colonic epithelium and human HT29 colorectal cancer cells. Journal of the National Cancer Institute. 1992;84:1410-16.

57. Sandberg AS. Bioavailability of minerals in legumes. Br J Nutr. 2002 Dec;88 Suppl 3:S281-5.

58. Sanford GL, Harris-Hooker S.  Stimulation of vascular proliferation by beta-galactoside specific lectins. FASEB J 1990;4:2912-2918.

59. Singleton VL. Naturally occurring food toxicants: phenolic substances of plant origin. Adv Food Res. 1981;27:149-242.

60. Tuxen MK, Nielsen HV, Birgens H.  [Poisoning by kidney beans (Phaseolus vulgaris)]. Ugeskr Laeger. 1991 Dec 16;153(51):3628-9.

61.  U.S.D.A. Choose My Plate.

62. van den Bourne BE, Kijkmans BA, de Rooij HH, le Cessie S, Verweij CL. Chloroquine and hydroxychloroquine equally affect tumor necrosis factor-alpha, interleukin 6, and interferon-gamma production by peripheral blood mononuclear cells. Journal of Rheumatology. 1997;24: 55-60.

63. Venter FS, Thiel PG. Red kidney beans–to eat or not to eat? S Afr Med J. 1995 Apr;85(4):250-2.

64. Wang Q, Yu LG, Campbell BJ, Milton JD, Rhodes JM. Identification of intact peanut lectin in peripheral venous blood. Lancet. 1998;352:1831-2

65. Wilson AB, King TP, Clarke EMW, Pusztai A.   Kidney bean (Phaseolus vulgaris) lectin-induced lesions in the small intestine. II. Microbiological studies. Journal of  Comparitive Pathology. 1980; 90:597-602.

66. Nutritionist Pro Dietary Software. //www.nutritionistpro.com/

67. Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012 Feb;42(1):71-8

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71. Schuurman M, van Waardenburg D, Da Costa J, Niemarkt H, Leroy P.Severe hemolysis and methemoglobinemia following fava beans ingestion in glucose-6-phosphatase dehydrogenase deficiency: case report and literature review. Eur J Pediatr. 2009 Jul;168(7):779-82

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76. Kritchevsky D et al.  Influence of native and randomized peanut oil on lipid metabolism and aortic sudanophilia in the vervet monkey. Atherosclerosis 1982;42:53-58.

77. Kritchevsky D et al. Lipid metabolism and experimental atherosclerosis in baboons– influence of cholesterol free, semi-synthetic diets. Am J Clin Nutr 1974;27:29-50.

78. Boyle EM et al.  Atherosclerosis. Ann Thorac Surg 1997;64:S47-56.

79. Alderson LM et al.  Peanut oil reduces diet-induced atherosclerosis in cynomolgus monkeys.   Arteriosclerosis 1986;6:465-74.

Betaine | The Paleo Diet
The modern Paleo Diet is focused on lean meats, but we love vegetables too. However, many Westerners need to beef up their vegetable intake because over 87% of adults are not eating enough of them each day.1 Although, the Paleo Diet favors foods with a lower glycemic impact, 2 you can’t beat the nutritional benefits of beets. They are rich in calcium, iron, magnesium, vitamin C, potassium, manganese, phosphorous, as well as carotene and B complex.3 Beets provide anti-inflammatory, antioxidant and detox support in the body. They also support healthy bile flow,4 stimulate liver cell function, and provide a protective effect for the liver and bile ducts.5

Beets are a great source of betaine, also called betaine anhydrous or trimethylglycine (TMG). Betaine is a substance that’s made in the body that’s required for healthy liver function, cellular reproduction, and to make carnitine.6 Further, there is a growing body of evidence that betaine is an important nutrient for the prevention of chronic disease.7 It is also a metabolite of choline8 and an essential biochemical component of the methionine-homocysteine cycle.9

Specifically, betaine also plays a role in reducing levels of the amino acid homocysteine in the blood.10 Homocysteine is a toxic substance in the body that can lead to osteoporosis and is an indicator of an increased risk of heart disease.11

Beets are a great alternative for endurance athletes looking for a nutrient dense option for post workout food to replenish from workouts.12 Studies have shown that eating beets prior to exercise, led to a 16% increase in workout times.13 They are also rich in antioxidants14 to aid in recovery between exercise sessions. Whether you are an avid exerciser or not, adding beets to your Paleo Diet is a win-win as they are a nutritional powerhouse.

Although typically eaten cooked, beets can also be eaten raw. Thinly slice or grate and serve over dressed lettuce greens. To roast whole beets, place them in a covered roasting pan for 45-60 minutes (until you can pierce them with a fork) in a 375 °F oven. Once cooked, the skin will easily peel away with your fingers.

This hearty, Paleo Roasted Beet and Tomato Soup offers a simple way to introduce cooked beets into your Paleo Diet.  It is a festive, bright dish to commence any holiday meal or as an accompaniment to your favorite Paleo sandwich.

Paleo Roasted Red Beet & Tomato Soup

Paleo Soup | The Paleo Diet

Serves 4

Ingredients

  • 1 tablespoon coconut oil
  • 1 red onion, sliced
  • 1 small carrot, diced
  • 2 (14.5 oz.) cans of no salt added organic diced tomatoes or homemade canned tomatoes
  • 1 large roasted, peeled, red beet (about 2 cups cubed)
  • Black pepper to taste

Directions

  1. Sauté the red onion and carrot in the coconut oil until the onions turn translucent and the carrot is soft.
  2. In a blender, combine the diced tomatoes, the cubed roasted beet, and the cooked onion mixture.
  3. Blend until very smooth.
  4. Pour the mixture into a soup pot.
  5. Simmer for 10-20 minutes, season with black pepper to taste and serve!

References

1. Available at: //epi.grants.cancer.gov/diet/usualintakes/pop/2007-10/. Accessed on November 8, 2015.

2. Cordain, Loren. The Paleo Diet Revised: Lose Weight and Get Healthy by Eating the Foods You Were Designed to Eat. Houghton Mifflin Harcourt, 2010.

3. Available at: //nutritiondata.self.com/facts/vegetables-and-vegetable-products/2348/2. Accessed on November 8, 2015.

4. Gu, X., and D. Li. “Fat nutrition and metabolism in piglets: a review.” Animal Feed Science and Technology 109.1 (2003): 151-170.

5. Kanbak, Güngör, Mine İnal, and Cengiz Bayçu. “Ethanol‐induced hepatotoxicity and protective effect of betaine.” Cell biochemistry and function 19.4 (2001): 281-285.

6. Craig, Stuart AS. “Betaine in human nutrition.” The American journal of clinical nutrition 80.3 (2004): 539-549.

7. Craig, Stuart AS. “Betaine in human nutrition.” The American journal of clinical nutrition 80.3 (2004): 539-549.

8. Abdelmalek, Manal F., et al. “Betaine, a promising new agent for patients with nonalcoholic steatohepatitis: results of a pilot study.” The American journal of gastroenterology 96.9 (2001): 2711-2717.

9. Craig SA. Betaine in human nutrition. Am J Clin Nutr 80: 539–549, 2004.

10. Olthof, Margreet R., et al. “Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women.” The Journal of nutrition 133.12 (2003): 4135-4138.

11. Homocysteine Studies Collaboration. “Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis.” Jama 288.16 (2002): 2015-2022.

12. Lomangino, Kevin. “Moving With the Beet: Can It Enhance Athletic Performance?.” Clinical Nutrition Insight 38.9 (2012): 6-7.

13. Bailey, Stephen J., et al. “Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans.” Journal of Applied Physiology 107.4 (2009): 1144-1155.

14. Trejo-Tapia, G., et al. “Effect of screening and subculture on the production of betaxanthins in Beta vulgaris L. var.‘Dark Detroit’callus culture.” Innovative Food Science & Emerging Technologies 9.1 (2008): 32-36.

Gluten Free | The Paleo Diet

Last week, The New York Times published an op-ed by Roger Cohen, its International Affairs and Diplomacy correspondent, regarding…wait for it – gluten!1 Has gluten become the nefarious “sticking point” that underlies our most critical diplomatic issues? Or was this just another of Cohen’s haughty rants against people who purchase organic food, implement health-optimizing diets, and keep abreast of nutrition science research? Spoiler alert – it’s the latter.

The gist of Cohen’s latest article, “This Column is Gluten-Free,” is that wheat has gotten a bad rap, despite graciously feeding the world for the past 12,000 years. Cohen acknowledges that gluten is harmful for the roughly 1% of the population that has celiac disease, but what about the remainder of the estimated 30% of Americans who are cutting back on gluten or going gluten-free?2

Does non-celiac gluten sensitivity (NCGS) exist? Is there evidence that gluten can be harmful for the general population? According to Cohen, people who eschew gluten (celiac patients excluded) are “self-indulgent” narcissists with imaginary food intolerances. “Having a special dietary requirement,” Cohen asserts, “is one way to feel special in the prevailing ‘me’ culture.”

Narcissism seems to be Cohen’s favorite buzzword when describing nutrition-motivated people, particularly those who buy organic food and avoid gluten. In this capacity, he uses the n-word no less than three times in his latest article, and in a previously article, he scolds the “affluent narcissism” of the upper middle class, people who purchase organic food while the poor “get a lot more nutrients from the two regular carrots they can buy for the price of one organic carrot.”3

This gets to the crux of Cohen’s ethos. He takes issue with individualism and self-determination, preferring a social structure whereby the balance of power is significantly tilted toward the state. In yet another recent article, he comments on a Pew Global Attitudes survey for which Americans and Europeans were asked which is more important,

  1. “freedom to pursue life’s goals without state interference,” or
  2. “state guarantees that nobody is in need.”

Much to Cohen’s dismay, 58% of Americans say the former is more important (compared to 62% of Europeans who prefer the latter).4 He then suggests the government should be more empowered to dictate how people eat, starting with a “coordinated policy action” designed to reduce sugar consumption, but where would it end?

What if the government decided that gluten is only dangerous for those with celiac disease? Could it outlaw a generalized form of “gluten-free” labeling? After all, because the US government supports GMO foods and deems them absolutely safe, it has repeatedly thwarted legislative attempts to implement mandatory GMO labeling. Not surprisingly, Cohen also strongly supports GMO foods:

“To feed a planet of 9 billion people,” he insists, “we are going to need high yields not low yields; we are going to need genetically modified crops; we are going to need pesticides and fertilizers and other elements of the industrialized food processes that have led mankind to be better fed and live longer than at any time in history.”5

Feeding the poor is a noble goal, even with subsistence-level nutrition, but so is health optimization for individuals, which is a primary goal of nutrition science research. These goals, however, are not incompatible; they are complementary. Nevertheless, Cohen’s steadfast resolve to restore wheat’s “amber waves” reputation prevents him from critically assessing and/or acknowledging the scientific research on gluten, the dangers of which extend far beyond just celiac patients.

Just last month, for example, researchers at the National Institutes of Health published a randomized, double-blind, placebo-controlled, cross-over trial on people who don’t have celiac disease but believe themselves to be gluten sensitive. The results? “The severity of overall symptoms increased significantly during 1 week of intake of small amounts of gluten, compared with placebo.”6

For further reading on the science behind how gluten can damage the gut and compromise health, check out Trevor Connor’s excellent 5-article review, “The Wheat Series.” Nutrition is always vulnerable to politicization, but rather than choosing sides, why not seek mutually beneficial solutions to complex, interdependent challenges? Being kind and respectful also helps immensely (leave the diet-shaming for the narcissists).

References

1. Cohen, R. (October 19, 2015). This Column is Gluten-Free. The New York Times. Retrieved from //www.nytimes.com/2015/10/20/opinion/this-column-is-gluten-free.html?_r=0

2. Strom, S. (February 17, 2014). A Big Bet on Gluten-Free. The New York Times. Retrieved from //www.nytimes.com/2014/02/18/business/food-industry-wagers-big-on-gluten-free.html

3. Cohen, R. (September 6, 2012). The Organic Fable. The New York Times. Retrieved from //www.nytimes.com/2012/09/07/opinion/roger-cohen-the-organic-fable.html

4. Cohen, R. (August 5, 2015). Incurable American Excess. The New York Times. Retrieved from //www.nytimes.com/2015/08/07/opinion/roger-cohen-incurable-american-excess.html

5. Cohen, R. (August 5, 2015). Incurable American Excess. The New York Times. Retrieved from //www.nytimes.com/2015/08/07/opinion/roger-cohen-incurable-american-excess.html

6. Di Sabatino, A., et al. (September 2015). Small Amounts of Gluten in Subjects With Suspected Nonceliac Gluten Sensitivity: A Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial. Clin Gastroenterol Hepatol, 13(9). Retrieved from //www.ncbi.nlm.nih.gov/pubmed/25701700

Leptin Resistance | The Paleo Diet

What’s all the buzz about leptin? With over half the American population trying desperately to lose weight,1 it’s no wonder we’ve become fascinated with a hormone that prompts us to think obesity or starvation.

Robert H. Lustig, MD, professor of pediatrics at UCSF and a member of the Endocrine Society’s Obesity Task Force explains “Leptin is a protein that’s made in the fat cells, circulates in the bloodstream, and goes to the brain; it’s the way your fat cells tell your brain that your energy thermostat is set right…and you have enough energy stored in your fat cells to engage in normal, relatively expensive metabolic processes.” Dr. Lustig goes on to discuss that levels are likely genetically set for each person. When an unbalance occurs exceeding your leptin threshold, the brain responds to the energy sufficiency, allowing you to “burn energy at a normal rate, eat food at a normal amount, engage in exercise at a normal rate, and you can engage in expensive processes, like puberty and pregnancy.”2

When the body doesn’t respond to the signal, it cannot stimulate your metabolism or suppress your appetite, inducing leptin resistance. This can make losing weight difficult if not impossible. With insulin resistance, pre-diabetes, and ultimately a diagnosis of Type II Diabetes on the rise, so too are the number of individuals diagnosed with leptin resistance.

The Standard American Diet (SAD), leading a predominantly sedentary lifestyle, too much stress, and not enough sleep all contribute to leptin resistance.3 Assessing whether leptin resistance is contributing to shedding stubborn pounds once and for all, shouldn’t start with the notion of a magic bullet, but an overhaul of lifestyle.

Sure, it’s easy to find leptin supplements online that promise the oomph you need to kickstart your new weight loss regime. But are they effective? Not according to research.

Because leptin is a digestible protein that doesn’t enter the bloodstream, the body just breaks it up. Further, leptin supplements sold online don’t actually contain leptin, but rather ingredients that are purported to help improve leptin functioning or feelings of fullness.4

So what’s the answer? As always, we need to go back to basics and look at the problem, rather than the symptom.

Leptin and insulin communicate and work in conjunction with other hormones to control our energy balance and as insulin levels rise, so do leptin levels. If we start by following a balanced, Paleo eating plan, which prevents blood sugar spike to begin with, we regulate our blood sugar and leptin release, reducing our chances of developing leptin and insulin resistance.

The takeaway: stop doing your body a disservice. Ask yourself:

  1. Am I eating right?
  2. Are my macronutrients balanced?
  3. Is my food timing in check?
  4. Am I exercising regularly?

If you answered ‘No’ to any of these questions, you may be hindering your weight loss and setting yourself up for additional adverse effects, like increasing your risk for cardiovascular disease (CVD) and other metabolic diseases.

“With obesity, leptin cannot tell our brain to stop eating, but it can still tell our brain to increase the activity of the cardiovascular system,” said Dr. Eric Belin de Chantemele, physiologist in the Department of Physiology at the Medical College of Georgia at Georgia Regents University. 5

Researchers have also shown that fat-derived leptin directly activates aldosterone synthase expression in the adrenal glands, resulting in production of more of the steroid hormone aldosterone. Increased aldosterone directly effects blood pressure by regulating salt-water balance in the body, contributes to widespread inflammation, blood vessel stiffness and scarring, enlargement and stiffness of the heart, and impaired insulin sensitivity. High levels of aldosterone are an obesity hallmark and a leading cause of metabolic and cardiovascular problems6

Avoid widespread inflammation. Stop insulin resistance in its tracks. Keep blood sugar low. These three key health tenants fit the bill and are easily achieved by following a Paleo diet. Add a little patience into the mix and avoid the urge for ‘get results fast!’ and Viola! We give our bodies the time to calm inflammation, shed the extra weight, and reset its hormonal cascade.

Take action now, before you need medical intervention!

References

1. “Americans’ Desire to Shed Pounds Outweighs Effort.” Gallup.com. N.p., n.d. Web. 19 Oct. 2015

2. “Leptin Hormone & Supplements: Do They Work for Obesity & Weight Loss?” WebMD. WebMD, n.d. Web. 19 Oct. 2015

3. Galland, M.D. Leo. “Leptin: How to Make This Fat-Burning Hormone Work for You.” The Huffington Post. TheHuffingtonPost.com, n.d. Web. 19 Oct. 2015

4. “The Facts on Leptin: FAQ.” WebMD. WebMD, n.d. Web. 19 Oct. 2015

5. “Satiety Hormone Leptin Plays a Direct Role in Cardiovascular Disease in Obesity.” ScienceDaily. ScienceDaily, n.d. Web. 19 Oct. 2015

6. Anne-Cécile Huby, Galina Antonova, Jake Groenendyk, Celso E. Gomez-Sanchez, Wendy B. Bollag, Jessica A. Filosa, Eric J. Belin de Chantemèle. The Adipocyte-Derived Hormone Leptin is a Direct Regulator of Aldosterone Secretion, Which Promotes Endothelial Dysfunction and Cardiac Fibrosis. Circulation, 2015; CIRCULATIONAHA.115.018226 DOI: 10.1161/CIRCULATIONAHA.115.018226

Eating Disorder | The Paleo Diet

There are currently 30 million people in the United States alone who suffer from eating disorders,1 where the related science and mental health are overlooked in their diagnoses.2 3 A new study, published by the journal of Psychosomatic Medicine, found new evidence of an association between the gut microbiota and the eating disorder anorexia.4

Researchers (and more mainstream sources) are beginning to understand just how much impact our gut has on nearly everything in our body – including our brain.5 6 7 Since nearly 90% of the body’s serotonin is made in the digestive tract – what’s going on in your gut – may be causing what’s going on inside your brain.8

Montiel-castro AJ, González-cervantes RM, Bravo-ruiseco G, Pacheco-lópez G. The microbiota-gut-brain axis: neurobehavioral correlates, health and sociality. Front Integr Neurosci. 2013;7:70.

Holzer P, Farzi A. Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 2014;817:195-219.

The researchers’ findings were remarkable. Individuals suffering from anorexia nervosa have not only one of the highest mortality rates,9 but also have very different microbial populations residing inside their guts, compared with healthy populations.10 How does this relate to a Paleo diet? Quite simply – what you eat plays a huge role in influencing your microbial population.11

There are of course a host of other factors, excluding diet that can influence your microbiome, but for our purposes, think of it as a basic equation: Bad food = bad microbial population in your gut = depression and anxiety, among other conditions. Good food = the opposite.

This is certainly an over-simplification, but for practical purposes, it works well. I’ll preface this with the importance of keeping your health and wellness in perspective and go from one extreme to another. A Paleo approach is meant to guide your lifestyle, not consume it. Since a Paleo diet focuses upon food qualitynot calories – it is oftentimes a good antidote to those who have food restriction behaviors.

If you were to go back to the 1950s, and tell a scientist or member of the general populace that what we have in our guts, in terms of microbes, would affect our weight or behavior – they would have escorted you away to a psychiatric ward. But, in the fascinating world of present day modern science, studies have shown the gut microbiome is indeed linked to weight gain, behavior, and even attention deficit disorders like ADHD.12 13 14 15 It’s not all so farfetched after all.

In the context of eating disorders, the microbiome is basically that of a spiral. The worse you eat, the worse your microbe population becomes, and the worse your mood and behavior fairs. Again, this is an oversimplification, but the analogy works. In a life filled with constant stressors, unpredictability, and other problems, if you follow the simple paradigm to make positive changes to our health and lifestyle, we can take back control.

A Paleo diet will provide your body with a wide array of beneficial nutrients that allow your gut bacteria to thrive, not hurt you. The human microbiome is basically an interface between our genes and our history of environmental exposures. Eating a healthy diet can only positively influence your gut microbiome.16

The science is far from definitive yet, but explorations of our microbiome continue to provide the chance of providing new answers into our own neurodevelopment – and behavior. If you or a loved one are suffering from an eating disorder, know that you are not alone and that healing your relationship with food and your body is possible, and professional counseling to help you overcome it is available.

For general information on mental health and to locate treatment services in your area, call the Substance Abuse and Mental Health Services Administration (SAMHSA) Treatment Referral Helpline at 1‑877‑SAMHSA7 (1‑877‑726‑4727). SAMSHA also has a Behavioral Health Treatment Locator on its website that can be searched by location.

References

1. Wade, T. D., Keski-Rahkonen A., & Hudson J. Epidemiology of eating disorders. In M. Tsuang and M. Tohen (Eds.), Textbook in Psychiatric Epidemiology (3rd ed.). New York: Wiley, 2011. p. 343-360.

2. Bulik CM, Tozzi F. Genetics in eating disorders: state of the science. CNS Spectr. 2004;9(7):511-5.

3. Wilson GT. Eating disorders, obesity and addiction. Eur Eat Disord Rev. 2010;18(5):341-51.

4. Kleiman SC, Watson HJ, Bulik-sullivan EC, et al. The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology. Psychosom Med. 2015.

5. Gareau MG. Microbiota-gut-brain axis and cognitive function. Adv Exp Med Biol. 2014;817:357-71.

6. Holzer P, Farzi A. Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 2014;817:195-219.

7. Montiel-castro AJ, González-cervantes RM, Bravo-ruiseco G, Pacheco-lópez G. The microbiota-gut-brain axis: neurobehavioral correlates, health and sociality. Front Integr Neurosci. 2013;7:70.

8. Kato S. Role of serotonin 5-HT₃ receptors in intestinal inflammation. Biol Pharm Bull. 2013;36(9):1406-9.

9. American Journal of Psychiatry, Vol. 152 (7), July 1995, p. 1073-1074, Sullivan, Patrick F.

10. Available at: //www.sciencedaily.com/releases/2015/10/151005121310.htm. Accessed October 8, 2015.

11. Conlon MA, Bird AR. The impact of diet and lifestyle on gut microbiota and human health. Nutrients. 2015;7(1):17-44.

12. Petra AI, Panagiotidou S, Hatziagelaki E, Stewart JM, Conti P, Theoharides TC. Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation. Clin Ther. 2015;37(5):984-95.

13. Turnbaugh PJ, Ridaura VK, Faith JJ, Rey FE, Knight R, Gordon JI. The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. Sci Transl Med. 2009;1(6):6ra14.

14. Sweeney TE, Morton JM. The human gut microbiome: a review of the effect of obesity and surgically induced weight loss. JAMA Surg. 2013;148(6):563-9.

15. Sampson TR, Mazmanian SK. Control of brain development, function, and behavior by the microbiome. Cell Host Microbe. 2015;17(5):565-76.

16. Gonzalez A, Stombaugh J, Lozupone C, Turnbaugh PJ, Gordon JI, Knight R. The mind-body-microbial continuum. Dialogues Clin Neurosci. 2011;13(1):55-62.

Vitamin E | The Paleo Diet

Symptoms of vitamin E deficiency are rare, but according to at least four national surveys, most Americans consume less than the government’s Recommended Daily Allowance (RDA) of this essential nutrient.1 The authors of an August 2015 study published in PLOS-One call vitamin E a “shortfall nutrient” because over 90% of Americans consume insufficient quantities and because low vitamin E status has been linked to multiple health consequences, including increased total mortality.2

Vitamin E is clearly important, but can the Paleo diet provide adequate levels? After all, some of the most frequently cited “best dietary sources” aren’t Paleo compliant. Are supplements necessary? The RDA for males and females above 14 years of age is 15 mg daily. The following table shows vitamin E values for 100 grams of various foods and their corresponding RDAs.

Vitamin E

The foods highest in vitamin E are predominantly seeds/nuts and their oils. Seed oils are excluded from the Paleo diet, however, primarily because they contain excessive amounts of polyunsaturated fatty acids (PUFAs). Almonds, hazelnuts, and sunflower seeds are good Paleo vitamin E sources. Fruits and vegetables are also good, but they contain very low amounts. Those small amounts accumulate, however, so collectively they are indeed significant.

Probably the best Paleo vitamin E source is olive oil. One tablespoon packs 1.9 mg, which is 10% of the RDA. You can add a few tablespoons of olive oil on salads or cooked vegetables, or use it for cooking. Olive oil becomes even more attractive when you consider its relatively low levels of PUFAs.

We should note that vitamin E functions primarily as an antioxidant, which means it protects against cellular damage by scavenging for free radicals. PUFAs have a high propensity to oxidize and oxidation creates free radicals. Therefore, high levels of PUFAs can negate vitamin E’s benefits. If we refer back to our chart, we see that many foods rich in vitamin E are also PUFA-rich.

Back in 1988, Brazilian scientists theorized that total vitamin E content is not the best indicator of vitamin E activity for vegetable oils. Using high-pressure liquid chromatography, they analyzed various oils for vitamin E activity and determined that high PUFA content offsets vitamin E activity and that oil refinement causes vitamin E losses upwards of 22%, especially during steam deodorization.3 They proposed that for vitamin E, unrefined oils beat their refined counterparts and that the ratio of vitamin E to PUFA better indicates vitamin E potential compared to absolute vitamin E levels.

A British Journal of Nutrition study published this month (October 2015) reiterates the same point: “The vitamin E requirement will increase with an increase in PUFA consumption and with the degree of unsaturation of the PUFA in the diet.”4 Another just-published study is also raising interest about vitamin E, particularly for its conclusion that those who have metabolic syndrome (about one-third of the US population) don’t absorb vitamin E as effectively as those who are healthy.5 Lead author of this latter study, Richard Bruno, commented, “Dietary requirements of nutrients are generally defined only in the context of what a healthy person needs, but considering that two-thirds of Americans are overweight or obese, a healthy person might not be representative of our society. This work tells us that at least one-third of Americans have higher vitamin E requirements than healthy people.”6

With all this in mind, one might conclude that supplementation is the best way to maintain adequate vitamin E levels. In the 1980s, scientists began to understand how free radicals contribute to atherosclerosis, cancer, vision loss, and various other chronic conditions. This sparked interest in the preventative potential of antioxidant supplements, particularly vitamin E. Several observational studies, including the Nurses’ Health Study, suggested 20 – 40% reductions in heart disease risk among people taking vitamin E supplements.7

Follow-up randomized controlled trials, however, dampened enthusiasm for vitamin E supplements, both for heart disease and cancer prevention. One meta-analysis even concluded that high-dose vitamin E supplementation may increase all-cause mortality and should be avoided.8 For those who are interested, the Harvard School of Public Health has an excellent summary on the history of research on vitamin E supplementation.

In conclusion, supplementation may provide benefits for certain conditions, but food sources of vitamin E are widely considered to be superior. Many of the richest food sources, however, are high-PUFA seed oils. High levels of PUFAs counteract vitamin E’s antioxidant capacity. It’s best to eliminate vegetable seed oils from your diet. The Paleo Diet provides plenty of vitamin E via olive oil, small quantities of seeds and nuts, and large amounts of vegetables.

References

1. National Institutes of Health, Office of Dietary Supplements. (June 2013). Vitamin E Fact Sheet for Health Professionals.

2. McBurney, M., et al. (August 19, 2015). Suboptimal Serum α-Tocopherol Concentrations Observed among Younger Adults and Those Depending Exclusively upon Food Sources, NHANES 2003-2006. PLOS-One.

3. Desai, D., et al. (June 1988). Vitamin E content of crude and refined vegetable oils in Southern Brazil. The Journal of Food Composition and Analysis, 1(3).

4. Raederstorff, D., et al. (October 2015). Vitamin E function and requirements in relation to PUFA. British Journal of Nutrition, 114(8).

5. Mah, E., et al. (October 7, 2015). α-Tocopherol bioavailability is lower in adults with metabolic syndrome regardless of dairy fat co-ingestion: a randomized, double-blind, crossover trial. American Journal of Clinical Nutrition [epub ahead of print].

6. Caldwell, E. (October 7, 2015). Metabolic syndrome leads 1 in 3 Americans to need more vitamin E. Ohio State University (Press Release).

7. Institute of Medicine. (2000). Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academies Press.

8. Miller, ER., et al. (January 4, 2005). Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Annals of Internal Medicine, 142(1).

Wheat | The Paleo Diet

Click Here to Start The Wheat Series from the Beginning!

It’s one of the most commonly used analogies in existence and it’s about a game that few want to play. A revolver is loaded with a single bullet. The hapless players take turns putting the gun to their heads and pulling the trigger. The analogy is often used to make a point about the high stakes of luck. Eventually someone gets a loaded chamber and pays the ultimate price.

There is a second side to the analogy, however that is frequently overlooked. Regardless of whether you have extremely good or bad luck, you first have to willingly pull the trigger.

We’ve known for a while that most chronic diseases such as cancer, autoimmune disease, and heart disease have a genetic component.1 – 10 Genetics are the loaded bullet that we sadly have no control over.

For celiac disease, the “bullet” is a genetic variant in HLA-DQ.11, 12 However, a large number of people with the variant never express the disease. Further, those who do develop the condition usually resolve it by removing gluten from their diet.13, 14 In other words, the bullet might be in the chamber, but often the gun is never fired.

Environmental factors ultimately pull the trigger.

In the first four parts of this series we talked about how wheat (and to a degree other gluten-containing grains such as rye and barley) is highly effective at dysregulating the immune system of our guts. In fact, it’s the only food we know of that affects all three pathways of dysregulation:

  1. Opening up the tight junctions of our gut (Part 2)
  2. Excess and chronic bacterial stress (Part 3)
  3. Harmful dietary antigens (Part 4)

In this final part, we’ll talk about how the resulting chronic inflammation leads to a pathological state that essentially “pulls the trigger” on disease. But just as importantly, we’ll discuss how there has to be a bullet in the chamber first. The genetic susceptibility has to be there.

It’s Not So Easy to Pull the Trigger

Our genetics have not changed in the last 100 years. Yet, chronic disease such as autoimmune conditions and cancer have risen dramatically. Faster than rate of population growth.

In other words, going with our analogy, the number of bullets hasn’t changed, but for some reason the trigger is getting pulled a lot more often. Which is surprising considering no one wants to pull it.

Imagine for a minute what it takes for a person to get to the point where they will voluntarily put a gun to their heads. None of us handed a revolver and told we have a five in six chance would exclaim “sure, those sound like good odds.”

From what little we understand, Russian Roulette players essentially have to build up to it, engaging in other risky behavior, and slowly desensitizing themselves. As it turns out, a lot of behavior altering substances help too.15

Likewise, our bodies have a lot of defenses to avoid ever pulling the trigger on disease, even when the bullet is there.

So, while we hopefully made the case in the previous four parts that wheat is not good for us, one piece of bread isn’t going to give you cancer. Despite all the dysregulation of our immune system caused by wheat, it still takes a lot to build up to the point of disease.16, 17

Building Up to It…

In fact, as we discussed in Part 1, all the inflammatory processes activated by wheat are both normal and necessary processes designed to deal with regular bacterial stress. Mice breed without these inflammatory responses suffer severe tissue damage and wasting disease.18, 19

Even the temporary shift in the balance between two critical immune cells – Tregs and TH17 cells – is a natural response to this inflammation. Let’s explore these two cells a little more.

In a healthy state, Tregs dominate. Their role is to suppress the immune system20 – 24 preventing it from damaging our own bodies. People unfortunate enough to have dysfunctioning Tregs suffer severe autoimmune diseas.25

TH17, on the other hand, have a murkier and less benign role. Only discovered in 2006, they solved an important puzzle for researchers. Scientists knew that T cells were involved in many conditions but none of the known T cells at the time fully explained disease development.26

With the discovery of TH17, they had their answer.26, 27

Proving to be highly inflammatory cells, TH17 effectively explained the damage in a multitude of chronic diseases16, 28 – 31 such as asthma,32 heart disease,33, 34 and most autoimmune conditions30, 35 including celiac disease,36, 37 type I diabetes,38, 39 Crohn’s disease,40, 41 rheumatoid arthritis,31, 42 and multiple sclerosis.43

A question remained, however: Why would our bodies produce such a self-destructive cell?

The reason lies in their role. It was believed that TH17 cells evolved to deal with harmful bacterial infections and effectively handling the invasion means doing some damage to our own bodies.19, 44, 45

This damage seems to be acceptable to our bodies and even part of a healthy immune response as long as one essential condition is met – the shift towards TH17 dominance is short-lived and ends. Once an infection is dealt with and the resulting inflammation quiets down, TH17 cells die off and Tregs return to dominating our immune system.24, 46

So what happens if the inflammation doesn’t end?

According to one emerging theory, the result is an out-of-control pathogenic form of the TH17 cell.10, 23, 24 In other words, if normal bacterial stress causes a little risky behavior by inciting beneficial TH17, chronic inflammation causes the buildup that leads to the pathogenic TH17 putting the gun to our heads and pulling the trigger.

Chronic Inflammation – Putting the Gun to our Heads

The diagram below shows the different responses between normal and chronic inflammation.30

Chronic Inflammation | The Paleo Diet

Kamada, N., et al., Role of the gut microbiota in immunity and inflammatory disease. Nat Rev Immunol, 2013. 13(5): p. 321-35.

Let’s explore this destructive shift a little more closely. Bear with me – this gets technical.

Under normal inflammation, the number of Treg cells increase alongside the TH17 cells allowing Tregs to continue controlling TH17’s destructive potential and maintain some balance.30, 47

But in chronic inflammation, a dramatic shift occurs. More and more innate immune cells such as dendritic cells and CD14+ macrophages (explained in Part 3) are activated or recruited to the digestive immune system.17, 28, 48, 49

Over time, these cells change the chemical milieu of the gut to one that is high inflammatory. Il-23 is released which both promotes the destructive form of TH17 and inhibits Tregs.27, 47, 50, 51 Newly recruited CD14+ macrophages also suppress Tregs.52

In fact, it gets worse. The chronic inflammation causes Tregs to “flip” and start behaving like TH17 contributing to the inflammation instead of preventing it.47, 52, 53

The result is that chronic inflammation breaks the Treg/ TH17 balance. Treg lose their ability to control the immune system and TH17, now uninhibited, take on a more destructive form traveling from the gut45 throughout the body pulling the trigger:30

Gut Microbiota | The Paleo Diet

Kamada, N., et al., Role of the gut microbiota in immunity and inflammatory disease. Nat Rev Immunol, 2013. 13(5): p. 321-35.

This is the point where you may want to remind me that this is the fifth part in a series about wheat. Where does wheat come into all of this?

Wheat, as we’ve shown in the previous parts, creates the chronic inflammation that sets off this cascade. In fact, in one study of mice, that tested many dietary antigens, wheat was the only one that could activate inflammatory TH17 cells.54

Put simply, wheat sets in motion the build-up that causes our bodies to ultimately put the gun to our heads and pull the trigger.

Why Aren’t More Guns Going Off?

The very sobering thought is that the chronic inflammation, which wheat is so effective at creating (in fact it took three parts to explain all the ways wheat can cause it,) appears to be common to everyone.17, 20, 55

So why aren’t we all sick?

This is where we need to flip things around and remember there are two parts to the Russian Roulette analogy. Wheat causes our immune system to put the gun to our heads and pull the trigger, but there still needs to be a bullet in the chamber. The genetic susceptibility has to be there.

Sure enough, a genetic susceptibility to chronic inflammation has been identified in many conditions. Often taking the form of a hyper-sensitivity to inflammation or a failure of the Treg system to suppress it.

CD14+ macrophages appear to be particularly potent in rheumatoid arthritis.56 Celiacs are hyper-sensitive to Il-15 – one of the key proteins used by wheat to produce inflammation.3 Much higher levels of inflammatory CD14+ macrophages exist in the guts of people with Irritable Bowel Disease (IBD).57 IBD sufferers also appear to be more responsive to IL-23.29 In type II diabetes, the immune cells that destroy the pancreas exist in healthy and afflicted subjects, but Treg cells appear to be less functional in diabetics.1, 2

Making a further case for the importance of genetics, people with one of these conditions are often more susceptible to the others.58-63

Still, There Are a Lot of Bullets…

The need for a “genetic bullet” in order for a disease to materialize has led many to breathe a sigh of relief. An example is the recent Washington Post article “For many, gluten isn’t the villain it gets cracked up to be.”

But the fact is that there are many chronic disease and they are all on the rise. A lot more guns are actually going off now.

Recent research is showing more and more that inappropriate chronic inflammation is at the heart of almost every “disease of civilization” including cancer,64, 65 metabolic disorders,66, 67 Alzheimer’s disease,68 most autoimmune conditions,30, 35 and heart disease where aberrant macrophages (immune cells) form the atherosclerotic plaques.69, 70

That amounts to a whole lot of genetic bullets.

While the research is still small, several of these conditions including celiac’s disease, diabetes, and     IBD are improved when wheat is removed from the diet.13, 14, 71 – 73

So feel free to do as the Washington Post article says, eat your bread, and trust your luck that the chamber is empty. But with that many potential bullets in the revolver and chronic inflammation – so effectively produced by wheat – ready to pull the trigger, I’m personally going to avoid putting the gun to my head.

References

  1. Danke, N.A., et al., Comparative study of GAD65-specific CD4+ T cells in healthy and type 1 diabetic subjects. J Autoimmun, 2005. 25(4): p. 303-11.
  2. Richer, M.J., et al., Immunomodulation of antigen presenting cells promotes natural regulatory T cells that prevent autoimmune diabetes in NOD mice. PLoS One, 2012. 7(2): p. e31153.
  3. Harris, K.M., A. Fasano, and D.L. Mann, Monocytes differentiated with IL-15 support Th17 and Th1 responses to wheat gliadin: implications for celiac disease. Clin Immunol, 2010. 135(3): p. 430-9.
  4. Cereijido, M., et al., New diseases derived or associated with the tight junction. Arch Med Res, 2007. 38(5): p. 465-78.
  5. Fasano, A., Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation Living Life on the Edge of the Wall. American Journal of Pathology, 2008. 173(5): p. 1243-1252.
  6. Fasano, A., Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev, 2011. 91(1): p. 151-75.
  7. Ahlbom, A., et al., Cancer in twins: Genetic and nongenetic familial risk factors. Journal of the National Cancer Institute, 1997. 89(4): p. 287-293.
  8. Marenberg, M.E., et al., GENETIC SUSCEPTIBILITY TO DEATH FROM CORONARY HEART-DISEASE IN A STUDY OF TWINS. New England Journal of Medicine, 1994. 330(15): p. 1041-1046.
  9. Heward, J. and S.C.L. Gough, Genetic susceptibility to the development of autoimmune disease. Clinical Science, 1997. 93(6): p. 479-491.
  10. Levin, L. and Y. Tomer, The etiology of autoimmune diabetes and thyroiditis: evidence for common genetic susceptibility. Autoimmunity Reviews, 2003. 2(6): p. 377-386.
  11. Sollid, L.M., et al., EVIDENCE FOR A PRIMARY ASSOCIATION OF CELIAC-DISEASE TO A PARTICULAR HLA-DQ ALPHA-BETA HETERODIMER. Journal of Experimental Medicine, 1989. 169(1): p. 345-350.
  12. Sollid, L.M. and E. Thorsby, HLA SUSCEPTIBILITY GENES IN CELIAC-DISEASE – GENETIC-MAPPING AND ROLE IN PATHOGENESIS. Gastroenterology, 1993. 105(3): p. 910-922.
  13. Johnston, S.D., C. Rodgers, and R.G.P. Watson, Quality of life in screen-detected and typical coeliac disease and the effect of excluding dietary gluten. European Journal of Gastroenterology & Hepatology, 2004. 16(12): p. 1281-1286.
  14. Fasano, A. and C. Catassi, Current approaches to diagnosis and treatment of celiac disease: An evolving spectrum. Gastroenterology, 2001. 120(3): p. 636-651.
  15. Collins, K.A., Adolescent Russian roulette deaths. Am J Forensic Med Pathol, 2010. 31(1): p. 4-6.
  16. Gonzalez-Quintial, R., et al., Systemic autoimmunity and lymphoproliferation are associated with excess IL-7 and inhibited by IL-7Ralpha blockade. PLoS One, 2011. 6(11): p. e27528.
  17. Palova-Jelinkova, L., et al., Gliadin fragments induce phenotypic and functional maturation of human dendritic cells. J Immunol, 2005. 175(10): p. 7038-45.
  18. Muramatsu, M., et al., Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell, 2000. 102(5): p. 553-63.
  19. Reynolds, J.M., et al., Cutting edge: regulation of intestinal inflammation and barrier function by IL-17C. J Immunol, 2012. 189(9): p. 4226-30.
  20. du Pre, M.F. and J.N. Samsom, Adaptive T-cell responses regulating oral tolerance to protein antigen. Allergy, 2011. 66(4): p. 478-90.
  21. Battaglia, M., et al., IL-10-producing T regulatory type 1 cells and oral tolerance. Ann N Y Acad Sci, 2004. 1029: p. 142-53.
  22. Wing, K. and S. Sakaguchi, Regulatory T cells exert checks and balances on self tolerance and autoimmunity. Nat Immunol, 2010. 11(1): p. 7-13.
  23. Williamson, E., G.M. Westrich, and J.L. Viney, Modulating dendritic cells to optimize mucosal immunization protocols. J Immunol, 1999. 163(7): p. 3668-75.
  24. Veldman, C., A. Nagel, and M. Hertl, Type I regulatory T cells in autoimmunity and inflammatory diseases. International Archives of Allergy and Immunology, 2006. 140(2): p. 174-183.
  25. Scalapino, K.J. and D.I. Daikh, CTLA-4: a key regulatory point in the control of autoimmune disease. Immunol Rev, 2008. 223: p. 143-55.
  26. Mesquita Jr, D., et al., Autoimmune diseases in the TH17 era. Braz J Med Biol Res, 2009. 42(6): p. 476-86.
  27. Langrish, C.L., et al., IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med, 2005. 201(2): p. 233-40.
  28. Smith, P.D., et al., Intestinal macrophages and response to microbial encroachment. Mucosal Immunol, 2011. 4(1): p. 31-42.
  29. Ohnmacht, C., et al., Intestinal microbiota, evolution of the immune system and the bad reputation of pro-inflammatory immunity. Cell Microbiol, 2011. 13(5): p. 653-9.
  30. Kamada, N., et al., Role of the gut microbiota in immunity and inflammatory disease. Nat Rev Immunol, 2013. 13(5): p. 321-35.
  31. Tesmer, L.A., et al., Th17 cells in human disease. Immunological Reviews, 2008. 223: p. 87-113.
  32. Cosmi, L., et al., Th17 cells: new players in asthma pathogenesis. Allergy, 2011. 66(8): p. 989-98.
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  43. Du, C., et al., MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis. Nat Immunol, 2009. 10(12): p. 1252-9.
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Sodium Levels | The Paleo Diet

For the majority of people, the problem with sodium is too much of it, not too little. National health organizations and the Paleo diet agree that high levels of dietary sodium should be avoided for healthy blood pressure levels and to reduce the risks of cardiovascular disease.1 However, diets too low in sodium are also dangerous, especially for athletes engaged in endurance sports.  Fortunately, it is possible for athletes to keep their sodium levels in check, without added processed foods, while still following the Paleo diet.

Understanding the Importance of Sodium in the Body

Although the Paleo diet is in inherently a low sodium lifestyle, dietary sodium, from naturally rich sodium foods and no common table salt, is necessary for everyday bodily functions.2 Muscles, including both the skeletal and cardiac types, need sodium to function properly. Twitches, cramps, spasms, and muscle weakness can occur when sodium levels are too low. The nervous system also uses electrolytes, such as ions of sodium, potassium and chloride, to transmit nerve impulses across cell membranes and to trigger muscle contractions.3 Sodium, in conjunction with potassium, is also necessary to maintain normal blood pressure, blood volume, and to balance bodily fluids.4 If that balance is disturbed, problems like heat-related illnesses and hyponatremia, low blood sodium (<130 mmol/L), may occur.5

Do Athletes Require More Dietary Sodium?

One major concern for athletes, especially those engaged in endurance activities, is that high sweat rates in athletes result in loss of both fluids and sodium.6 Low blood sodium can also occur in people who drink too much water, eat too little food, or take medications that deplete the body’s supply of water.7 Research indicates that the amount of sodium consumed in the days prior to exercise, might be more important in maintaining the proper levels during exercise, then in specific supplementation during the activity.8

Additionally, avoiding sodium rich beverages and foods during physical activity has been shown to not impact performance,9 ingesting sodium prior or during intense or prolonged physical activities is linked to an improved rate of absorption of water and carbohydrate in the small intestines.10 An athlete can encourage proper blood serum sodium levels by drinking for thirst and eating whole fruit, such as oranges, for a gradual fructose release.

Pre-and-Post Workout Meals

Pre-and-post workout meals can provide the necessary recovery nutrients rather than turning to processed supplements that are often sickeningly sweet, and contain many unnecessary additives and refined sugars. Surprisingly, they don’t contain exorbitant amounts of sodium. For example, a scoop of powdered electrolyte supplement contains 14 mg of sodium,11 compared to the 97mg available in a dash of table salt.12 An athlete concerned about maintaining adequate sodium levels during their exercise program can focus including naturally sodium-rich foods to their pre-workout meal, and focusing on the main principles of the Paleo diet. Our favorite sodium-rich and Paleo foods include:13

  • 1 large celery stalk (50 mg)
  • 1 beet (65 mg)
  • 4 oz. lamb chop (65 mg)
  • 4 oz. chicken breast (70 mg)
  • 4 oz. grass-fed ground beef (75 mg)
  • 1 cup of spinach (125 mg)
  • 1 cup of Swiss chard (300 mg)

By simply following a Paleo diet, focused on eating a wide variety of mineral rich vegetables, animal organs, and bone broth will supply the necessary nutrients to maintain adequate sodium levels, for both the weekend warrior and the elite endurance athlete under most training conditions. Traditional hunter-gathers participate in rigorous and demanding physical activities required by their hunting, gathering, and foraging lifestyles without needing to supplement their diets with table salt, or electrolyte supplements, to meet their sodium requirements. Dietary sodium is not quite the villain he has been made out to be. However, we don’t need to overcompensate with sodium-rich supplements when a regular Paleo diet offers enough of this essential nutrient to support most individuals, even those who are avid exercisers.

References

1. Mattes, R. D., and D. Donnelly. “Relative contributions of dietary sodium sources.” Journal of the American College of Nutrition 10.4 (1991): 383-393.

2. Centers for Disease Control and Prevention (CDC. “Usual sodium intakes compared with current dietary guidelines—United States, 2005-2008.” MMWR. Morbidity and mortality weekly report 60.41 (2011): 1413.

3. Brodal, Per. The central nervous system: structure and function. Oxford University Press, 2004.

4. Blaustein, M. P. “Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis.” American Journal of Physiology-Cell Physiology 232.5 (1977): C165-C173.

5. Noakes, T. D., et al. “The incidence of hyponatremia during prolonged ultraendurance exercise.” Medicine and Science in Sports and Exercise 22.2 (1990): 165-170.

6. Godek, S. Fowkes, A. R. Bartolozzi, and J. J. Godek. “Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment.” British journal of sports medicine 39.4 (2005): 205-211.

7. Noakes, Timothy D. “The hyponatremia of exercise.” International journal of sport nutrition 2.3 (1992): 205-228.

8. Stofan, John R., et al. “Sweat and sodium losses in NCAA football players: a precursor to heat cramps?.” International journal of sport nutrition and exercise metabolism 15.6 (2005): 641.

9. Merson, Stuart J., Ronald J. Maughan, and Susan M. Shirreffs. “Rehydration with drinks differing in sodium concentration and recovery from moderate exercise-induced hypohydration in man.” European journal of applied physiology 103.5 (2008): 585-594.

10. Murray, Robert. “The effects of consuming carbohydrate-electrolyte beverages on gastric emptying and fluid absorption during and following exercise.” Sports Medicine 4.5 (1987): 322-351.

11. Available at: //nutritiondata.self.com/facts/beverages/9232/2. Accessed on October 7, 2015.

12. Avaialble at: //nutritiondata.self.com/facts/spices-and-herbs/216/2. Accessed on October 7, 2015.

13. //nutritiondata.self.com/

Paleo Recipe | The Paleo Diet

Hawaiian cuisine incorporates five distinct styles of food reflecting the diverse food history of settlement and immigration in the islands.1 Polynesian voyagers brought plants and animals to the islands, contributing to the local fish, taro (which were raised for poi), coconuts, sugarcane, sweet potatoes and yams, and meat, cooked in earth ovens.

Later, large plantations developed with the arrival of Europeans, Americans, missionaries, and whalers who introduced cuisine native to their homelands to Hawaii. In the late 1800s, migrant workers from China, Korea, Japan, the Philippines, and Portugal immigrated to meet the growing labor needs of the pineapple industry in Hawaii, bringing with them rich new foods and flavors that further influenced the region.

Can we say fusion cuisine? Try saying that five times!

When we think of a Paleo autumn recipe, most of us, myself included, don’t think tropical flavors from lands from afar. But since it is fall, and I happen to be writing to you from Kona, why not come up with a Hawaiian twist on a fall favorite?

The hardest part: deciding what type of preparation seems most fitting, captures Hawaiian tradition, but also stays true to the seasonal goodness packed with the wholloping punch of health-packing nutrients of any real Paleo recipe!

A trip to the farmer’s market on Ali’i Drive in downtown Kona2 was just the ticket. Freshly picked pineapple, Japanese sweet potato, sweet onion from Waimea, and locally grown basil were amongst the goodies I encountered. And, while a bit on the starchier and sweeter side than I’d recommend for day-to-day dining, in context of preparing for a long endurance event, absolutely perfect.

Hearty, tasty and ideal for preparing the body’s fuel stores for a day of intense physical activity to come, my Blue Sweet Potato and Pineapple ‘Poke’ is both easy to prepare and easy to enjoy.

Paleoista’s Blue Sweet Potato and Pineapple ‘Poke’

A play on the local island favorite, ‘Poke,’ is a raw salad served as an appetizer in Hawaiian cuisine. This recipe will fill your boots and ensure you’re ready to race or train hard!

Ingredients

  • 2 lbs boiled blue sweet potatoes, cubed into 1” pieces and cooled
  • 1 sweet onion, chopped
  • 1 small pineapple, cored, peeled and cut into 1” cubes
  • 1 small lime, juiced
  • ¼ cup coconut oil, melted
  • ½ cup freshly chopped basil, plus a few leaves for garnish

Instructions

  1. Combine all ingredients in large bowl
  2. Stir to combine
  3. Chill for one hour before serving
  4. Garnish with basil leaves

References

1. Wikipedia. Wikimedia Foundation, n.d. Web. 07 Oct. 2015

2. //www.konafarmersmarket.com

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