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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

1. Alvarez JR, Torres-Pinedo R. Interactions of soybean lectin, soyasaponins, and glycinin with rabbit jejunal mucosa in vitro. Pediatr Res. 1982 Sep;16(9):728-31.

2. Banwell, JG, Howard R, Kabir I, Costerton JW.   Bacterial overgrowth by indigenous microflora in the phytohemagglutinin-fed rat. Canadian Journal of  Microbiology. 1988; 34:1009-13.

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.

4. Boufassa C, Lafont J, Rouanet J M, Besancon P 1986 Thermal inactivation of lectins (PHA)isolated from Phaseolus vulgaris. Food Chem 20 295-304.

5. Buera M P, Pilosof A M R, Bartholomai G B 1984 Kinetics of trypsin inhibitory activity loss in heated flour from bean Phaseolus vulgaris. J Food Sci 49 124-126.

6. Calloway DH, Carol A. Hickey CA,  Murphy EL. Reduction of intestinal gas-forming properties of legumes by traditional and experimental processing methods. J Food Sci. 1971;  36: 251-255.

7. Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet 2008;371(9606): 64–74.

8. Carmalt J, Rosel K, Burns T, Janzen E. Suspected white kidney bean (Phaseolus vulgaris) toxicity in horses and cattle. Aust Vet J. 2003 Nov;81(11):674-6.

9. Caron, M. & Steve, A.P. Lectins and Pathology, Taylor & Francis, 2000, London.

10. Chrispeels, M.J. & Raikel, N.V. (1991) Lectins, lectin genes, and their role in plant defense. Plant Cell 3, 1-9.

11. Collins J L, Beaty B F 1980 Heat inactivation of trypsin inhibitor in fresh green soybeans and physiological responses of rats fed the beans. J Food Sci 45 542-546.

12. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17.

13. Couzy F, Mansourian R, Labate A, Guinchard S, Montagne DH, Dirren H. Effect of dietary phytic acid on zinc absorption in the healthy elderly, as assessed by serum concentration curve tests. Br J Nutr. 1998 Aug;80(2):177-82.

14. FAO/WHO Expert Consultation. Protein Quality Evaluation. Food and Agricultural Organization of the United Nations, FAO Food and Nutrition Paper 51, Rome.

15. Firestein GS, Alvaro-Gracia JM, Maki R.  Quantitative analysis of cytokine gene expression in rheumatoid arthritis. Journal of  Immunology. 1990;144: 33347-53.

16. Francis G, Kerem Z, Makkar HP, Becker K. The biological action of saponins in animal systems: a review. Br J Nutr. 2002 Dec;88(6):587-605.

17. Gee JM, Johnson IT. Interactions between hemolytic saponins, bile salts and small intestinal mucosa in the rat. J Nutr. 1988 Nov;118(11):1391-7.

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.

21. Grant G. Anti-nutritional effects of soyabean: a review. Prog Food Nutr Sci. 1989;13(3-4):317-48.

22. Grant G, More LJ, McKenzie NH, Stewart JC, Pusztai A. A survey of the nutritional and haemagglutination properties of legume seeds generally available in the UK. Br J Nutr. 1983 Sep;50(2):207-14.

23. Grant G, More LJ, McKenzie NH, Pusztai A. The effect of heating on the haemagglutinating activity and nutritional properties of bean (Phaseolus vulgaris) seeds. J Sci Food Agric 1982;33: 1324-1326.

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.

27. Hintz HF, Hogue DE, Krook L. Toxicity of red kidney beans (Phaseolus vulgaris) in the rat. J Nutr. 1967 Sep;93(1):77-86

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. http://www.nutritionistpro.com/

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

68. Piya MK, Harte AL, McTernan PG. Metabolic endotoxaemia: is it more than just a gut feeling? Curr Opin Lipidol. 2013 Feb;24(1):78-85.

69. Pirke KM, Schweiger U, Laessle R, Dickhaut B, Schweiger M, Waechtler M. Dieting influences the menstrual cycle: vegetarian versus nonvegetarian diet. Fertil Steril. 1986 Dec;46(6):1083-8

70. Conn EE. Cyanogenic glycosides.  In:  Encyclopedia of Plant Physiology. New Series. Volume 8. Secondary plant products [Bell, A.E.; Charlwood, B.V. (Editors)]. 1980 pp. 461-492

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

72. Arese P, Bosia A, Naitana A, Gaetani S, D’Aquino M, Gaetani GF. Effect of divicine and isouramil on red cell metabolism in normal and G6PD-deficient (Mediterranean variant) subjects. Possible role in the genesis of favism. Prog Clin Biol Res. 1981;55:725-46

73. Gresham GA et al.  The independent production of atherosclerosis and thrombosis in the rat. Br J Exp Pathol 1960;41:395-402.

74. Scott RF et al.  Short term feeding of unsaturated vs. satruated fat in the production of atherosclerosis and thrombosis in the rat. Exp Mol Pathol 1964;3:421-443.

75. Wissler RW et al. Aortic lesions and blood lipids in monkeys fed three food fats. Fed Proc 1967;26:371.

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.

Inuit | The Paleo Diet

The Inuit have long been used as a shining example that low carbohydrate approaches to diet can work.1 2 3 4 In fact, traditionally they consumed very little vegetables or any other typically Western foods, and subsisted mainly on fish, sea mammals, and land animals.5 And despite this diet (which would horrify most mainstream dieticians) the Inuit traditionally had very low rates of disease.6

By contrast, the traditional Western diet has been correlated with a plague of health issues.7 8 9 As a further example of just how nutritionally poor the Western diet can be, one third of all cancer deaths have been linked to continued intake of low quality foods – which are everyday staples of the Western diet.10

Interestingly, when consumed in a very low carbohydrate version, a Paleo Diet looks very similar – if not identical – to the traditional Inuit diet. Since this way of eating is higher in fat than most North American diets, it is commonly presumed (erroneously) that high fat diets must somehow be “bad.”11 12 What gets (purposely) left out of these arguments is the fact that the type of fat consumed is very important.13 14 15 16 17 Consuming omega-3 fatty acids is highly beneficial for health – while consuming industrial trans fat is pretty much the worst thing you can do for your health.18

To bring all this background knowledge to a head, new research published last week, showed that the Inuit have special mutations in genes involved in fat metabolism.19 These genetic mutations may allow them to thrive on their very low carbohydrate diet. This is thought provoking because these genetic mutations are found in nearly 100% of the Inuit. By contrast, only a mere 2% of Europeans exhibit the same mutations. This means that those of us from European ancestry may synthesize omega-3 polyunsaturated fatty acids differently than the Inuit.

While the initial buzz of this paper was high, in practice it really doesn’t change anything we know about consuming a healthy Paleo Diet. Omega-3 fatty acids, like those found in wild-caught fish, are still extremely beneficial for our health. In fact, researchers have found that omega-3 fatty acids have widely beneficial anti-inflammatory properties.20 This proves beneficial for inflammatory and autoimmune diseases, in addition to maintaining good health for those without specific health conditions. The advice to consume omega-3 fatty acids is great for mitigating coronary heart disease, depression, aging, and cancer.21

Beyond this, arthritis, Crohn’s disease, ulcerative colitis and lupus erythematosis are autoimmune diseases which may be helped by adequate omega-3 consumption.22 Of the omega-3 fatty acids available, DHA (docosahexaenoic acid) is the best, for a variety of reasons.23 24 Look for foods naturally high in DHA (such as wild-caught fish) and avoid inflammatory seed oils – like those commonly used by most major restaurants. This crucial step will help you stay healthy in the long term – no matter what genes and ancestry you may have.

REFERENCES

[1] Dewailly E, Mulvad G, Sloth pedersen H, Hansen JC, Behrendt N, Hart hansen JP. Inuit are protected against prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(9):926-7.

[2] Bjerregaard P, Dewailly E, Young TK, et al. Blood pressure among the Inuit (Eskimo) populations in the Arctic. Scand J Public Health. 2003;31(2):92-9.

[3] Mulvad G, Pedersen HS, Hansen JC, et al. The Inuit diet. Fatty acids and antioxidants, their role in ischemic heart disease, and exposure to organochlorines and heavy metals. An international study. Arctic Med Res. 1996;55 Suppl 1:20-4.

[4] O’keefe JH, Harris WS. From Inuit to implementation: omega-3 fatty acids come of age. Mayo Clin Proc. 2000;75(6):607-14.

[5] Kuhnlein HV. Nutrition of the Inuit: a brief overview. Arctic Med Res. 1991;Suppl:728-30.

[6] Stefansson V. The friendly arctic. The MacMillan Co, NY. 1921.

[7] Manzel A, Muller DN, Hafler DA, Erdman SE, Linker RA, Kleinewietfeld M. Role of “Western diet” in inflammatory autoimmune diseases. Curr Allergy Asthma Rep. 2014;14(1):404.

[8] Myles IA. Fast food fever: reviewing the impacts of the Western diet on immunity. Nutr J. 2014;13:61.

[9] Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;56(8):365-79.

[10] American Cancer Society. Cancer facts & figures 2004. Atlanta: American Cancer Society, 2004.

[11] Guldstrand MC, Simberg CL. High-fat diets: healthy or unhealthy?. Clin Sci. 2007;113(10):397-9.

[12] Schwingshackl L, Hoffmann G. Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis. J Acad Nutr Diet. 2013;113(12):1640-61.

[13] Abumrad NA, Piomelli D, Yurko-mauro K, Merrill A, Clandinin MT, Serhan CN. Moving beyond “good fat, bad fat”: the complex roles of dietary lipids in cellular function and health: session abstracts. Adv Nutr. 2012;3(1):60-8.

[14] Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr. 1991;54(3):438-63.

[15] Daley CA, Abbott A, Doyle PS, Nader GA, Larson S. A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutr J. 2010;9:10.

[16] Loef M, Walach H. The omega-6/omega-3 ratio and dementia or cognitive decline: a systematic review on human studies and biological evidence. J Nutr Gerontol Geriatr. 2013;32(1):1-23.

[17] Swanson D, Block R, Mousa SA. Omega-3 fatty acids EPA and DHA: health benefits throughout life. Adv Nutr. 2012;3(1):1-7.

[18] Ip C. Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals. Am J Clin Nutr. 1997;66(6 Suppl):1523S-1529S.

[19] Fumagalli M, Moltke I, Grarup N, et al. Greenlandic Inuit show genetic signatures of diet and climate adaptation. Science. 2015;349(6254):1343-7.

[20] Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280-9.

[21] Harris WS, Dayspring TD, Moran TJ. Omega-3 fatty acids and cardiovascular disease: new developments and applications. Postgrad Med. 2013;125(6):100-13.

[22] Robinson DR, Knoell CT, Urakaze M, et al. Suppression of autoimmune disease by omega-3 fatty acids. Biochem Soc Trans. 1995;23(2):287-91.

[23] Horrocks LA, Yeo YK. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999;40(3):211-25.

[24] Conquer JA, Holub BJ. Dietary docosahexaenoic acid as a source of eicosapentaenoic acid in vegetarians and omnivores. Lipids. 1997;32(3):341-5.

4 Paleo Cornerstones to Increase Your Metabolism | The Paleo Diet

Many individuals who are desperate to lose weight do not realize that they can – and should – eat lots of calories.1, 2, 3 Crash diets do not work, when it comes to long term fat loss.4, 5 In fact, they usually have the opposite effect – weight and fat gain.6, 7, 8 There are, however, some very easy tricks to incorporate into your routine to help ramp up your metabolism.

However, as a disclaimer, if you’re after a quick fix to mimic the effects of steroids or other illegal drugs, you’ll be looking at a harsh reality dead in the eyes. These drugs are dangerous, and are illegal for a reason.

Follow these simple, easy steps to hone in on the last 10% to push you over the edge and help you lose those few extra stubborn pounds!

4 Paleo Cornerstones to Increase Your Metabolism | The Paleo Diet

Mullur, Rashmi, Yan-Yun Liu, and Gregory A. Brent. “Thyroid Hormone Regulation of Metabolism.” Physiological Reviews. American Physiological Society, 1 Apr. 2014. Web. 2 June 2015.

1. KEEP CALORIES IN CHECK

Make sure you are eating plenty of calories. Skip the starvation diets and/or “cleanses” please. Secondly, make sure that you are including “good” calories, and leaving out “bad” ones. This means making your diet as nutrient dense as possible, which the Paleo diet will accomplish for you automatically (I told you this was easy!). Leaving out the “bad” calories can be trickier, but you simply choose between avoiding ice cream and achieving their weight loss goal, or downing a pint and keeping those extra pounds. Ultimately, the choice is yours.

2. EAT QUALITY OVER QUANTITY

Of these quality calories, protein is probably the most important.9, 10 Most of us do not eat enough protein, and the more protein we eat, the more satiated we will be and the more muscle we can build – both important cornerstones of true weight loss.11, 12 Thermogenesis requires adequate protein – as does muscle growth.13 Without protein, you will never become leaner and meaner.

3. FATTEN UP

The next step (which is so commonly overlooked) is indulging in lots of healthy fats.14 This means extra virgin olive oil, coconut oil, avocados and other Paleo Diet staples.

4. SLEEP IT OFF

One of the biggest secrets to fat loss, is so simple, and yet so overlooked. As I’ve previously written, getting enough sleep is absolutely vital to fat loss.15 In fact, sleep deprivation will cause fat gain!16 Getting an appropriate amount of sleep may be the most unrecognized and underreported secret to fat loss – and yet so many of us struggle to achieve it.17 Why is this? Examine your lifestyle and see what you can strip away (another secret to fat loss – eliminate activities and stressors – don’t add them!)

So to review, boost your metabolism and get rid of stubborn body fat by getting enough calories (quality here is vital), eat plenty of quality proteins and fats, and get lots of high quality sleep (8-9 hours per night). These four Paleo cornerstones will ramp up your metabolism and help you lose body fat.

4 Paleo Cornerstones to Increase Your Metabolism

Mullur, Rashmi, Yan-Yun Liu, and Gregory A. Brent. “Thyroid Hormone Regulation of Metabolism.” Physiological Reviews. American Physiological Society, 1 Apr. 2014. Web. 2 June 2015.

Perhaps two more key notes should be mentioned here. The first is to avoid sugar at all costs. Sugar is your enemy when it comes to fat loss.18 1-2 servings of fruit are all you usually need, and it’s vital (if you want to lose fat) to keep your carbohydrate intake to starchier sources, like sweet potatoes.

The second key is to give it time! Weight loss does not happen overnight – it really does take patience. I have had so many clients who have given up after a week of not achieving their goal, which is truly heartbreaking. I know that if they were to simply hold on for another few weeks, they would see very good results, and stick with it.

A Paleo diet and lifestyle will provide you with all the tools you need to maximize your metabolism and lose weight.19, 20 If you have very complex metabolic or health issues to deal with, you may need to see a doctor or practitioner, but this isn’t always necessary.

Go home, get rid of all the processed and man-made foods from your house, keep exercising and sleeping, and reap the rewards of a Paleo-driven, fuel-efficient metabolism!

 

REFERENCES

[1] Purnell JQ. Obesity: Calories or content: what is the best weight-loss diet?. Nat Rev Endocrinol. 2009;5(8):419-20.

[2] Finer N. Low-calorie diets and sustained weight loss. Obes Res. 2001;9 Suppl 4:290S-294S.

[3] Kowalski LM, Bujko J. [Evaluation of biological and clinical potential of paleolithic diet]. Rocz Panstw Zakl Hig. 2012;63(1):9-15.

[4] Kline GA, Pedersen SD. Errors in patient perception of caloric deficit required for weight loss–observations from the Diet Plate Trial. Diabetes Obes Metab. 2010;12(5):455-7.

[5] Kelley DE, Wing R, Buonocore C, Sturis J, Polonsky K, Fitzsimmons M. Relative effects of calorie restriction and weight loss in noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab. 1993;77(5):1287-93.

[6] Shah M, Miller DS, Geissler CA. Lower metabolic rates of post-obese versus lean women: Thermogenesis, basal metabolic rate and genetics. Eur J Clin Nutr. 1988 Sep;42(9):741-52.

[7] Bray GA: Effect of caloric restriction on energy expenditure in obese patients. Lancet 1969; 2:397-398

[8] Keys, Ancel. The Biology of Human Starvation: Volume I. Minneapolis: University of Minnesota Press, 1950. Print.

[9] Westerterp-plantenga MS, Lemmens SG, Westerterp KR. Dietary protein – its role in satiety, energetics, weight loss and health. Br J Nutr. 2012;108 Suppl 2:S105-12.

[10] Brehm BJ, D’alessio DA. Benefits of high-protein weight loss diets: enough evidence for practice?. Curr Opin Endocrinol Diabetes Obes. 2008;15(5):416-21.

[11] Westerterp-plantenga MS, Nieuwenhuizen A, Tomé D, Soenen S, Westerterp KR. Dietary protein, weight loss, and weight maintenance. Annu Rev Nutr. 2009;29:21-41.

[12] Clifton PM, Keogh JB, Noakes M. Long-term effects of a high-protein weight-loss diet. Am J Clin Nutr. 2008;87(1):23-9.

[13] Acheson KJ, Blondel-lubrano A, Oguey-araymon S, et al. Protein choices targeting thermogenesis and metabolism. Am J Clin Nutr. 2011;93(3):525-34.

[14] Brehm BJ, Seeley RJ, Daniels SR, D’alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88(4):1617-23.

[15] Available at: http://thepaleodiet.com/sleep-loss-making-fat/. Accessed May 30, 2015.

[16] Spivey A. Lose sleep, gain weight: another piece of the obesity puzzle. Environ Health Perspect. 2010;118(1):A28-33.

[17] Durmer JS, Dinges DF. Neurocognitive consequences of sleep deprivation. Semin Neurol. 2005;25(1):117-29.

[18] Kuo LE, Czarnecka M, Kitlinska JB, Tilan JU, Kvetnanský R, Zukowska Z. Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signaling toward neuropeptide Y and leads to obesity and the metabolic syndrome. Ann N Y Acad Sci. 2008;1148:232-7.

[19] Boers I, Muskiet FA, Berkelaar E, et al. Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. Lipids Health Dis. 2014;13:160.

[20] Masharani U, Sherchan P, Schloetter M, et al. Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. Eur J Clin Nutr. 2015;

Speeding Up Your Metabolism | The Paleo Diet

A fast metabolism has wide appeal to modern humans, yet, it is exactly what our hunter-gatherer ancestors avoided to survive during periods of food scarcity. We are genetically designed to store extra calories, so what you feel is a sluggish metabolism, is actually a life saving measure to buy time to find your next meal.

In times of food scarcity (or self-inflicted calorie restriction), insulin-stimulated glucose uptake by tissues is reduced, which prevents the body from relying on protein from muscle tissue as a product for endogenous glucose production.1 This process provided hunter-gatherers the ability to endure famine by retaining more muscle mass to support the physical demands of fleeing from predators and fruitful hunting. Individuals with metabolisms effective at utilizing proteins, carbohydrates and fats have a genetic advantage. When you avoid calorie restriction, you stop encouraging your body to store reserves easily.2

Metabolism isn’t all about burning all of the calories you eat in order to stay thin. It accounts for numerous biochemical reactions that occur in each cell of the body required for basic survival, called basal metabolism. The basal metabolic rate (BMR) accounts for 70% of the calories you need at rest to:

  • circulate blood
  • contract muscles
  • digest food and nutrients
  • maintain body temperature
  • support the functions of the brain and nervous system 3

In addition to BMR, thermogenesis (food processing) and physical activity, determine overall caloric needs. Food processing accounts for 100 calories on average, while physical activity provides the most variability, ranging from 15-35% of your total energy expenditure. BMR slows 3-5% per decade after age 30, which can be attributed to the loss of lean body mass that naturally occurs with age.4

The key to boosting the resting metabolic rate appears linked to the one element we can control: building and maintaining strong skeletal muscles, thus preserving lean body mass.5 In nonobese individuals, skeletal muscle comprises 40% of body weight,6 and can account for 20-30% of the total resting oxygen uptake.7

RESISTANCE TRAINING

Researchers found an extra 100 calories per day were burned after 6 months of resistance training.8 Body weight exercises like pushup and pull-ups can be just as effective as lifting weights to stress muscles enough to build strength.9 As a long term strategy, heavy-resistance strength training programs increase resting metabolic rates (RMR) by increasing lean body mass, sympathetic nervous system activity,10 and insulin action.11

CARDIOVASCULAR TRAINING

Aerobically trained individuals tend to have a higher RMR than those who are untrained.12 An average increase in RMR of 129 calories per day has been shown with cardio exercise 3-5 days per week, for 20-45 minutes, for 16 months.13 Metabolic adaptations associated with traditional aerobic exercise training correlate with improved insulin action14 and glycemic control.15 Insulin resistance is linked to metabolic disorders,16 and performing moderate to vigorous intensity aerobic and resistance exercise for several hours per week can enhance insulin sensitivity.17,18

“AFTER BURN” BOOST

Excess post-exercise oxygen consumption (EPOC), also called the “after burn effect,” restores the body to its resting state. RMR has been shown to increase for up to 38 hours post-exercise19 contributing to a greater overall calorie expenditure than would be measured without exercise. The EPOC effect is dependent on the intensity and duration of exercise,20 with the greatest effect occurring following high intensity exercise.21 To further boost the overall effect of energy expended post workout, intermittent intervals can be performed throughout the day, as opposed to performing only one continuous period of exercise.22

Physical activity that mimics the movements of hunter-gatherers offers many metabolic advantages, in addition to purely burning calories. Whether your metabolism is fast or slow, you can make vital improvements through a targeted fitness program for optimal performance.

 

REFERENCES

[1] Carey, Andrew L., et al. “Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase.” Diabetes 55.10 (2006): 2688-2697.

[2] Summermatter, Serge, et al. “Thrifty metabolism that favors fat storage after caloric restriction: a role for skeletal muscle phosphatidylinositol-3-kinase activity and AMP-activated protein kinase.” The FASEB Journal 22.3 (2008): 774-785.

[3] Tortora, Gerard J., and Bryan H. Derrickson. Principles of anatomy and physiology. John Wiley & Sons, 2008.

[4] Hunter, Gary R., John P. McCarthy, and Marcas M. Bamman. “Effects of resistance training on older adults.” Sports medicine 34.5 (2004): 329-348.

[5] Wade, 0. L., and J. M. Bishop. 1962. Cardiac Output and Regional Blood Flow. Blackwell Scientific Publications, Oxford, UK.

[6] Owen, 0. E., G. A. Reichard, Jr., G. Boden, M. S. Patel, and V. E. Trapp. 1978. Interrelationships among key tissues in the utilization of metabolic substrate. Adv. Mod. Nutr. 2:517-550.

[7] Wade, 0. L., and J. M. Bishop. 1962. Cardiac Output and Regional Blood Flow. Blackwell Scientific Publications, Oxford, UK.

[8] resistance training. After 6 months, subjects had increased their RMR and were burning an extra 100 calories per day.

[9] Kraemer, William J., et al. “American College of Sports Medicine position stand. Progression models in resistance training for healthy adults.” Medicine and science in sports and exercise 34.2 (2002): 364-380.

[10] Pratley, R., et al. “Strength training increases resting metabolic rate and norepinephrine levels in healthy 50-to 65-yr-old men.” Journal of Applied Physiology 76.1 (1994): 133-137.

[11] Miller, John P., et al. “Strength training increases insulin action in healthy 50-to 65-yr-old men.” Journal of Applied Physiology 77.3 (1994): 1122-1127.

[12] Poehlman, Eric T., et al. “Resting energy metabolism and cardiovascular disease risk in resistance-trained and aerobically trained males.” Metabolism41.12 (1992): 1351-1360.

[13] Potteiger, Jeffrey A., et al. “Changes in resting metabolic rate and substrate oxidation after 16 months of exercise training in overweight adults.”International journal of sport nutrition and exercise metabolism 18.1 (2008): 79.

[14] Hickey MS, Weidner MD, Gavigan KE, Zheng D, Tyndall GL, Houmard JA: The insulin action-fiber type relationship in humans is muscle group specific.Am J Physiol 1995, 269(1 Pt 1):E150-154

[15] Houmard JA, Egan PC, Neufer PD, Friedman JE, Wheeler WS, Israel RG, Dohm GL: Elevated skeletal muscle glucose transporter levels in exercise-trained middle-aged men.

Am J Physiol 1991, 261(4 Pt 1):E437-443.

[16] Bonora, Enzo, et al. “Prevalence of insulin resistance in metabolic disorders: the Bruneck Study.” Diabetes 47.10 (1998): 1643-1649.

[17] Stiegler, Petra, and Adam Cunliffe. “The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss.”Sports Medicine 36.3 (2006): 239-262.

[18] Babraj, John A., et al. “Extremely short duration high intensity interval training substantially improves insulin action in young healthy males.” BMC Endocrine Disorders 9.1 (2009): 3.

[19] Schuenke, Mark D., Richard P. Mikat, and Jeffrey M. McBride. “Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management.” European Journal of Applied Physiology 86.5 (2002): 411-417.

[20] Schuenke, Mark D., Richard P. Mikat, and Jeffrey M. McBride. “Effect of an acute period of resistance exercise on excess post-exercise oxygen consumption: implications for body mass management.” European Journal of Applied Physiology 86.5 (2002): 411-417.

[21] Bahr, Roald, and Ole M. Sejersted. “Effect of intensity of exercise on excess postexercise O 2 consumption.” Metabolism 40.8 (1991): 836-841.

[22] Laforgia, Joseph, et al. “Comparison of energy expenditure elevations after submaximal and supramaximal running.” Journal of Applied Physiology 82.2 (1997): 661-666.

Your Dietary Fix for Stress: Paleo Diet or Nordic Diet | The Paleo Diet

In November of 2014, the International Journal of Obesity published a study conducted by Swedish researchers comparing Paleo-inspired diets with those based on the Nordic Nutrition Recommendations (NNR).1 The NNR are comparable to the USDA’s dietary guidelines, emphasizing low-fat dairy and cereal grains and recommending a macronutrient distribution of 55-60% of calories from carbohydrates, 25-30% from fat, and 15% from protein. The macronutrient distribution used in this study to represent the Paleo diet was 30% carbohydrates, 40% fat, and 30% protein.

The researchers grouped 49 overweight or obese postmenopausal women into the Paleo and NNR groups, tracking their progress over two years. They were primarily serving how these diets influence glucocorticoid metabolism. Glucocorticoids are stress hormones that modulate various metabolic, inflammatory, and cardiovascular processes.2 Abnormal glucocorticoid metabolism is associated with metabolic syndrome and obesity.

Cortisol, the principal active glucocorticoid, is secreted by the adrenal glands and converted to cortisone, the inert form.3 One of the enzymes responsible for this conversion is called 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Obese individuals demonstrate increased activity of 11β-HSD1 in subcutaneous adipose tissue (SAT), which is fatty tissue directly under the skin. The researchers hypothesized that diet-induced weight loss results in decreased expression of 11β-HSD1 in SAT and thus a reversal of the abnormal glucocorticoid metabolism common to obese patients.

The study’s participants were observed at baseline, after 6 months, and after 24 months. Both groups lost weight and decreased BMI, waistline measurements, and total body fat throughout the study. The Paleo group had greater reductions after 6 months, but after 24 months there were no significant differences between the groups. Both groups also demonstrated decreased activity of 11β-HSD1 in SAT. The researchers noted, “We did not find any major difference between diets on glucocorticoid metabolism.”4

So what does this study tell us? The Paleo diet performed better than NNR after 6 months, but after two years, it seems neither diet had any advantages over the other. It’s important, however, to look closer at the structure of the study. Every two months, participants attended sessions with dietitians to ensure compliance with their respective diets. Food journals and urine samples were used for monitoring and measuring food intake. An anomaly, however, pointed out by the researchers, was that urinary nitrogen levels were not higher in the Paleo group (as they should have been) at any time during the study, “indicating that the actual intake of protein was similar in both diet groups.”5 The Paleo group, however, was instructed to eat 30% of calories as protein, double the amount of the NNR group.

Also, Paleo participants were instructed to eat 40% of calories as fat, “with a high proportion of mono- and polyunsaturated fatty acids (MUFAs and PUFAs).” An authentic Paleo diet, however, would have higher proportion of saturated fatty acids and MUFAs, with only very small amounts of PUFAs. So, the “Paleo diet” and the low-fat, high-carb, grain-centric diet fared similarly, but were Paleo participants following an authentic Paleo diet? This seems doubtful. Nevertheless, this study represents an important advance in our understanding of how diets influence stress hormones. Follow-up studies will hopefully ensure greater compliance to authentic Paleo diets.

Christopher James Clark, B.B.A.

@nutrigrail
Nutritional Grail
www.ChristopherJamesClark.com

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

REFERENCES

[1] Stomby, A., et al. (October 2014). Diet-induced weight loss has chronic tissue-specific effects on glucocorticoid metabolism in overweight postmenopausal women. International Journal of Obesity. Retrieved from http://www.nature.com/ijo/journal/vaop/ncurrent/full/ijo2014188a.html

[2] Wang, M. (February 2005). The role of glucocorticoid action in the pathophysiology of the Metabolic Syndrome. Nutrition & Metabolism, 2(3). Retrieved from http://www.nutritionandmetabolism.com/content/2/1/3

[3] Ibid, Wang.

[4] Ibid, Stomby.

[5] Ibid, Stomby.

Millet | The Paleo Diet

Over the past 5-7 years, more and more people worldwide have become aware of the Paleo Diet, which really is not a diet at all, but rather a lifelong way of eating to reduce the risk of chronic disease and maximize health and wellbeing. One of the fundamental principles of The Paleo Diet is to eliminate or drastically reduce consumption of cereal grains, whether they are refined or whole. Currently, 8 cereal grains (wheat, corn, rice, barley, sorghum, oats, rye, and millet) provide 56% of the food energy and 50% of the protein consumed on earth.3 However, from an evolutionary perspective, these foods were rarely or never consumed by our hunter gatherer ancestors.3

When I first made the suggestion that as a species we would be a lot healthier if we reduced or eliminated cereal consumption in 1999,3 I received, and still receive, criticism by some professionals in the nutritional community because they believe that the elimination of an entire food group (cereals) is nutritionally unsound and “will produce numerous dietary deficiencies.” This statement is not supported by any experimental evidence. In fact, the contrary is true. As I have previously pointed out, elimination of cereal grains actually increases the nutrient density of the 13 vitamins and minerals most lacking in the U.S. diet4, 5 – providing cereals are replaced by fresh fruits, vegetables, meats, poultry, fish, seafood and eggs.

Besides this fundamental lack of knowledge concerning the nutrient density of cereal grains, nearly all classically trained nutritionists have little or no appreciation for the antinutrients present in grains. As the name implies, antinutrients are dietary substances which interfere with our normal metabolism and physiology. Cereal grains are generally concentrated sources of numerous antinutrients and may produce undesirable health effects,3 particularly when consumed as daily staples.

In the U.S. “gluten free” foods have become incredibly popular in recent years as many people recognize that they simply feel better by eliminating the 3 gluten containing grains (wheat, rye and barley). Gluten conscious consumers frequently replace wheat, rye and barley with non-gluten containing grains (rice, corn, oats, sorghum and millet) in the mistaken belief that these 5 non-gluten grains are harmless. However, as I have previously pointed out, even the 5 non-gluten containing grains should be avoided for a variety of reasons.3 Specifically, I’ll detail below how millet adversely affects iodine metabolism and may cause goiter (swelling of the neck) when eaten regularly.

The Culprit: Millet

Unless you are a vegan, a vegetarian or are in search of gluten-free grains, most Americans and westerners have never tasted millet. Nevertheless, you don’t have to look very far to find this cereal grain (grass seed) at most health food stores. If you only dine upon millet dishes once in a blue moon, it will have zero repercussions upon your health, but be aware that millet is a nutrient poor, antinutrient laden food – the regular consumption of which may cause multiple dietary deficiencies and nutrient related diseases,3 including impairment of iodine metabolism and risk for goiter.

Millet is not a single plant species (as are most other cereal grains), but rather interpreted broadly may comprise about 500 species of grass seeds worldwide.13 Only a few species of millet are commonly cultivated as food crops. Worldwide, pearl millet (Pennisetum glaucum) is the most widely produced millet15 and is cultivated extensively in Africa and India. Finger millet (Eleusine coracana, proso millet (Panicum miliaceum), fonio millet (Digitaria exilis), and foxtail millet (Setaria italic) are also important crop species in developing countries.13, 15 Nevertheless millet is a minor cereal grain in terms of global economic importance. Worldwide production of millet is about 1% of either wheat or rice.13

Because millets require little water and are highly drought resistant, they grow well in arid and semi arid regions of the world such as in countries surrounding the Sahara desert in Africa and in dry areas in India and Asia. Further, millet is an attractive agricultural crop for farmers in these regions because under good conditions, it can yield two harvests per year13 and is resistant to pests and pathogens.

In the Sudan region (Darfur Province) of Africa, dietary surveys show that millet consumption in three communities (Kas, Tawaila and Nyala) was the primary source of food calories, respectively yielding 73.6%, 66.7%, and 37.1% of total daily energy.20 In this study, the occurrence of goiter was outrageously high – greater than almost anywhere else in the world. The incidence of goiter for girls in these three communities was 75%, 55%, and 13%, respectively; for boys it was 46%, 35%, and 10%, respectively. Similar high rates of goiter and thyroid disorders have been reported for school children in the Gujarat district of Western India where millet is a staple food.2

Millet Consumption, Iodine Deficiency and Goiter

Wherever and whenever millet becomes a staple food worldwide, the incidence of goiter increases and abnormalities of thyroid function and iodine metabolism occur2,7,16-20 Further, animal studies in rats, pet birds, and goats and tissue (in vitro) studies demonstrate unequivocally that this cereal plays a major role in causing goiter, thyroid abnormalities and impairment of iodine metabolism.1, 8, 10-12, 22

Iodine is an essential nutrient for humans, without which we most conspicuously develop goiter (an enlargement of the thyroid gland about the neck). Additionally, lack of iodine in the diet impairs cognitive development in growing infants and children, miscarriage in pregnant women and brain and nervous system dysfunction in adults.24, 25

Originally, it was thought that goiter occurred primarily from a deficiency of iodine in our food supply and water. Accordingly, in the U.S. and elsewhere most dietary salt (NaCl) has been fortified with iodine. An unappreciated aspect of iodine metabolism is that metabolic deficiencies of this nutrient can still occur even when dietary intake of iodine appears to be sufficient.7 Although virtually unknown to most nutritionists, elements found in millet represent powerful antinutrients that impair iodine metabolism and frequently cause goiter and symptoms of iodine deficiency.

Goitrogens in Millet

Goitrogens are dietary substances which impair thyroid and iodine metabolism and may ultimately cause the development of goiter. As I have previously alluded, a few scientists in the nutritional community early on appreciated that high millet diets promoted goiter. However, it was not completely understood how millet produced its goitrogenic effect. Subsequent discoveries and experiments over the past 35 years now show that compounds known as flavonoids in millets are responsible for causing iodine dysfunction and may in turn produce goiter when consumed as staples.6, 7, 21, 23

All millets are concentrated sources of compounds known as polyphenolics, some of which are referred to as flavonoids. Numerous flavonoids have been found in millets including apigenin, luteolin , kaempferol and vitexin; all of which severely impair thyroid function and iodine metabolism6, 10-12, 21, 23 and cause goiter in animal and tissue models.1, 8, 10-12, 22 Although it is not completely understood, flavonoids from millets appear to inhibit iodine uptake by most cells in the body, impair secretion of thyroid hormones, and reduce organification of Iodine by the enzyme thyroperoxidase.6, 7, 10, 23

Additional Antinutrients in Millets

Although a few scientific articles suggest that millets may possess positive health effects,26, 27 these papers and authors seem to be completely unaware of the numerous antinutrients found in millets and their potential for disrupting nutrition and health.

Let’s begin with the mistaken notion that millets are good sources of calcium.26, 27 Upon chemical analysis on paper, this statement may be true, but in the body (in vivo), nothing could be further from the truth. Calcium, along with iron and zinc that may be present in millets are actually poorly absorbed in our bodies because phytates, tannins and other compounds prevent their assimilation.28-32 Accordingly, high cereal grain diets whether millet derived or not, frequently result in multiple nutrient deficiencies including calcium, iron and zinc.3

In addition to their high phytate, flavonoid and polyphenolic contents, millets are also concentrated sources of other antinutrients including protease inhibitors (trypsin, chymotrypsin, alpha amylase and cysteine)33-35 and steroidal saponins.36, 37 Cereal grain protease inhibitors likely elicit adverse effects upon the pancreas when consumed as staple foods,3 and saponins are known to increase intestinal permeability and may contribute to chronic low level systemic inflammation.

Taken in its entirety, an overwhelming scientific literature demonstrates that millets are second rate foods that when consumed regularly may adversely affect iodine metabolism and elicit goiter. I’m not completely sure where the USDA dietitians derived their recommendations for whole grain consumption, but it certainly could not have come from their familiarity with the millet literature.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

 

References

1. Abel Gadir WS, Adam SE. Development of goitre and enterohepatonephropathy in Nubian Goats fed with pearl millet (Pennisetum typhoides). Vet J. 1999 Mar;157(2):178-85.

2. Brahmbhatt S, Brahmbhatt RM, Boyages SC. Thyroid ultrasound is the best prevalence indicator for assessment of iodine deficiency disorders: a study in rural/tribal schoolchildren from Gujarat (Western India). Eur J Endocrinol. 2000 Jul;143(1):37-46.

3. Cordain L. (1999). Cereal grains: humanity’s double edged sword. World Review of Nutrition and Dietetics, 84: 19-73.

4. Cordain L. The nutritional characteristics of a contemporary diet based upon Paleolithic food groups. J Am Neutraceut Assoc 2002; 5:15-24.

5. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the western diet: Health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.

6. de Souza Dos Santos MC, Gonçalves CF, Vaisman M, Ferreira AC, de Carvalho DP. Impact of flavonoids on thyroid function. Food Chem Toxicol. 2011 Oct;49(10):2495-502

7. Elnour A, Hambraeus L, Eltom M, Dramaix M, Bourdoux P. Endemic goiter with iodine sufficiency: a possible role for the consumption of pearl millet in the etiology of endemic goiter. Am J Clin Nutr. 2000 Jan;71(1):59-66.

8. Elnour A, Liedén S, Bourdoux P, Eltom M, Khalid SA, Hambraeus L. Traditional fermentation increases goitrogenic activity in pearl millet. Ann Nutr Metab. 1998;42(6):341-9.

9. Elnour A, Liedén S, Bourdoux P, Eltom M, Khalid SA, Hambraeus L. The goitrogenic effect of two Sudanese pearl millet cultivars in rats. Nutr Res 1997; Mar (17): 533–546.

10. Gaitan E, Cooksey RC, Legan J, Lindsay RH. Antithyroid effects in vivo and in vitro of vitexin: a C-glucosylflavone in millet. J Clin Endocrinol Metab. 1995 Apr;80(4):1144-7.

11. Gaitan E, Lindsay RH, Reichert RD, Ingbar SH, Cooksey RC, Legan J, Meydrech EF, Hill J, Kubota K. Antithyroid and goitrogenic effects of millet: role of C-glycosylflavones. J Clin Endocrinol Metab. 1989 Apr;68(4):707-14.

12. Gaitan E, Lindsay RH, Cooksey RC, Hill J, Reichert RD, Ingbar SH. The thyroid effects of C-glycosylflavonoids in millet. Prog Clin Biol Res. 1988;280:349-63

13. Hunt HV, Badakshi F, Romanova O, Howe CJ, Jones MK, Heslop-Harrison JS. Reticulate evolution in Panicum (Poaceae): the origin of tetraploid broomcorn millet, P. miliaceum. J Exp Bot. 2014 Jul;65(12):3165-75.

14. Lu H, Zhang J, Liu KB, Wu N, Li Y, Zhou K, Ye M, Zhang T, Zhang H, Yang X, Shen L, Xu D, Li Q. Earliest domestication of common millet (Panicum miliaceum) in East Asia extended to 10,000 years ago. Proc Natl Acad Sci U S A. 2009 May 5;106(18):7367-72

15. McDonough CM, Rooney LW, Serna-Saldivar SO. (2000). “The Millets”. Food Science and Technology: Handbook of Cereal Science and Technology (CRC Press). 99 2nd ed: 177–210.

16. Medani AM1, Elnour AA, Saeed AM. Endemic goitre in the Sudan despite long-standing programmes for the control of iodine deficiency disorders. Bull World Health Organ. 2011 Feb 1;89(2):121-6.

17. Moreno-Reyes R1, Boelaert M, el Badawi S, Eltom M, Vanderpas JB. Endemic juvenile hypothyroidism in a severe endemic goitre area of Sudan. Clin Endocrinol (Oxf). 1993 Jan;38(1):19-24.

18. [No authors listed] Millet–a possibly goitrogenic cereal. Nutr Rev. 1983 Apr;41(4):113-6.

19. Osman AK, Basu TK, Dickerson JW. A goitrogenic agent from millet (Pennisetum typhoides) in Darfur Province, Western Sudan. Ann Nutr Metab. 1983;27(1):14-8.

20. Osman AK, Fatah AA. Factors other than iodine deficiency contributing to the endemicity of goitre in Darfur Province (Sudan). J Hum Nutr. 1981 Aug;35(4):302-9.

21. Sartelet H, Serghat S, Lobstein A, Ingenbleek Y, Anton R, Petitfrère E, Aguie-Aguie G, Martiny L, Haye B. Flavonoids extracted from fonio millet (Digitaria exilis) reveal potent antithyroid properties. Nutrition. 1996 Feb;12(2):100-6.

22. Schoemaker NJ, Lumeij JT, Dorrestein GM, Beynen AC. Nutrition-related problems in pet birds]. Tijdschr Diergeneeskd. 1999 Jan 15;124(2):39-43.

23. Schröder-van der Elst JP1, Smit JW, Romijn HA, van der Heide D. Dietary flavonoids and iodine metabolism. Biofactors. 2003;19(3-4):171-6.

24. Zimmermann MB.The role of iodine in human growth and development. Semin Cell Dev Biol. 2011 Aug;22(6):645-52.
25. Taylor PN1, Okosieme OE, Dayan CM, Lazarus JH. Therapy of endocrine disease: Impact of iodine supplementation in mild-to-moderate iodine deficiency: systematic review and meta-analysis. Eur J Endocrinol. 2013 Nov 22;170(1):R1-R15. doi: 10.1530/EJE-13-0651. Print 2014 Jan.

26. Devi PB, Vijayabharathi R, Sathyabama S, Malleshi NG, Priyadarisini VB. Health benefits of finger millet (Eleusine coracana L.) polyphenols and dietary fiber: a review. J Food Sci Technol. 2014 Jun;51(6):1021-40.

27. Shobana S, Krishnaswamy K, Sudha V, Malleshi NG, Anjana RM, Palaniappan L, Mohan V. Finger millet (Ragi, Eleusine coracana L.): a review of its nutritional properties, processing, and plausible health benefits. Adv Food Nutr Res. 2013;69:1-39.

28. Lestienne I, Besançon P, Caporiccio B, Lullien-Péllerin V, Tréche S. Iron and zinc in vitro availability in pearl millet flours (Pennisetum glaucum) with varying phytate, tannin, and fiber contents. J Agric Food Chem. 2005 Apr 20;53(8):3240-7.

29. Lestienne I, Caporiccio B, Besançon P, Rochette I, Trèche S. Relative contribution of phytates, fibers, and tannins to low iron and zinc in vitro solubility in pearl millet (Pennisetum glaucum) flour and grain fractions. J Agric Food Chem. 2005 Oct 19;53(21):8342-8.

30 Udayasekhara Rao P, Deosthale YG. In vitro availability of iron and zinc in white and coloured ragi (Eleusine coracana): role of tannin and phytate. Plant Foods Hum Nutr. 1988;38(1):35-41.

31. Suma PF, Urooj A. Nutrients, antinutrients & bioaccessible mineral content (invitro) of pearl millet as influenced by milling. J Food Sci Technol. 2014 Apr;51(4):756-61.

32. Archana, Sehgal S, Kawatra A. Reduction of polyphenol and phytic acid content of pearl millet grains by malting and blanching. Plant Foods Hum Nutr. 1999;53(2):93-8.

33. Pattabiraman TN. Trypsin/chymotrypsin inhibitors from millets. Adv Exp Med Biol. 1986;199:439-48.

34. Shivaraj B, Pattabiraman TN. Natural plant enzyme inhibitors. Characterization of an unusual alpha-amylase/trypsin inhibitor from ragi (Eleusine coracana Geartn.). Biochem J. 1981 Jan 1;193(1):29-36.

35. Joshi BN, Sainani MN, Bastawade KB, Deshpande VV, Gupta VS, Ranjekar PK.
Pearl millet cysteine protease inhibitor. Evidence for the presence of two distinct sites responsible for anti-fungal and anti-feedent activities. Eur J Biochem. 1999 Oct;265(2):556-63.

36. Lee ST, Mitchell RB, Wang Z, Heiss C, Gardner DR, Azadi P. Isolation, characterization, and quantification of steroidal saponins in switchgrass (Panicum virgatum L.). J Agric Food Chem. 2009 Mar 25;57(6):2599-604.

37. Patamalai B, Hejtmancik E, Bridges CH, Hill DW, Camp BJ. The isolation and identification of steroidal sapogenins in Kleingrass. Vet Hum Toxicol. 1990 Aug;32(4):314-8.

Molecular Biology | The Paleo Diet

Dr. Cordain,

I’ve read your book The Paleo Diet and many, but not all of your posted PDF articles. I find your work and those of your colleagues compelling. There is so much we don’t know in the area you are defining. Yours is very important work.

I’m recuperating on a medical leave from NYU after a successful angioplasty and stent – in the nick of time – that opened a total blockage of my right coronary artery, at the end of January, that was precipitated by excessive use of a snow shovel! Hence, I’m more than interested in the papers on your web site for two important reasons: (1) eating appropriately from this point onward; and (2) introducing some of your material into the metabolism section of our biochemistry course. I also teach the molecular biology section as well. Your book will save and extend many lives.

Prof. Gene C. Lavers, Ph.D.

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