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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

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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

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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.

Is Mesquite Bean Flour Arguably Paleo?

Photo by Robb Hannawacker, while working for Joshua Tree National Park, via Wikimedia Commons

Mesquite is a different subfamily of the “legumes” the Mimosoideae not the fabaceae, and the food part derived from mesquite is not the seed, but rather the pulpy part of the pod wall. Ethnobotanist Richard Felger claimed indigenous populations could obtain their 50g of protein per day from birds, lizards, snakes etc., but preferred the energy for their bodies, provided by the flour milled from the mesquite pods, not seeds. Using a stone gyratory crusher, they would grind off the pulpy mesocarp, moisten the high sugar content flour into “cakes,” and take them on hunting trips. The leathery endocarp containing the hard seed was discarded.

While the article Beans and Legumes: Are They Paleo is very thorough and excellent, the following studies and papers suggest eliminating the seeds eliminates trypsin inhibitors in mesquite bean flour, flatulence producing triglycerides, phytates by ten times less, and a host of other issues that are present in the seeds. Furthermore, carbon 14 data supports mesquite flour consumption approximately 10,000 years before present day.

Felker, Peter, Takeoka, Gary, Dao, Lan. “Pod Mesocarp Flour of North and South American Species of Leguminous Tree Prosopis (Mesquite): Composition and Food Applications.” Food Reviews International 29.1, 49-66, 2013.

Capparelli, Aylen, and Verónica Lema. “Recognition of Post-harvest Processing of Algarrobo (Prosopis Spp.) as Food from Two Sites of Northwestern Argentina: An Ethnobotanical and Experimental Approach for Desiccated Macroremains – Springer.” Archaeological and Anthropological Sciences 3.1 (2011): 71-92.Springer Link. Springer-Verlag, 01 Mar. 2011.

Ortega-Nieblas, Magdalena, Luz Vázquez-Moreno, and María R. Robles-Burgueño. “Protein Quality and Antinutritional Factors of Wild Legume Seeds from the Sonoran Desert.” Journal of Agricultural and Food Chemistry 44.10 (1996): 3130-132. Web.

As part of my Ph.D. in 1977, I worked on the protein and amino acid composition of mesquite pods and seeds and have published more than 100 papers since then, in addition to giving copious talks to international audiences in North and South America, Africa and India/Pakistan.

Takeoka, Gary. “A Review of Flavor, Aroma and Color Enhancement in Gluten Free and Conventional Pastries, Waffles and Dairy Desserts with Mesquite Pod Mesocarp Flour.” Presentation. Institute of Food Technologists (IFT). Western Regional Research Center, ARS, USDA. 13-16 July 2013: Web.

Certainly fresh fruits, veggies and meats are better nutritionally than mesquite flour, but for conventional diets, mesquite is used at only 12-15% to add flavor and aroma in baked goods at low concentrations.

Shouldn’t mesquite bean flour be approved for Paleo Diets?

Thank you for this courtesy,

Peter Felker, Ph.D.

Dr. Cordain’s Response:

Dear Peter,

Many thanks for sending the papers on mesquite beans. You clearly are the international expert on this topic, and I respect your knowledge of a fascinating topic. I appreciate you getting me up to speed on the nutritional aspects of this traditional food which clearly has been consumed in the Americas for tens of thousands of years. I read the papers carefully, and cross checked your voluminous references. Jennie Brand Miller is a close colleague and co-author on a number of papers — she did the glycemic index experiments with this food. Given its reported high sucrose content, I am a bit surprised that it did not have a higher GI.

Clearly, traditional agricultural societies in the Americas and Asian utilized this plant as food on a regular basis, but this evidence does not necessarily mean that habitual consumption is necessarily healthful. I see that the phytic acid concentration is high in mesquite bean flour. This characteristic will necessarily bind (in vivo) all the divalent ions (iron, zinc, calcium, magnesium) you have reported in a dose dependent manner making them of low biological availability in the human gut.

It is also a bit problematic that phytohemoagglutinin (PHA) has been detected in Prosopis species when this lectin is normally only present in Phaseolus species. Hence, I suspect that there likely is a specific lectin, yet to be molecularly classified that is present in Prosopis which agglutinates RBCs but which probably is not PHA. To date, animal experiments have shown that PHA breeches the gut barrier and interacts unfavorably with the immune and GI systems. It would be interesting to determine if the agglutinating factor in Prosopsis also has similar in vivo physiological characteristics as Phaseolus PHA.

Note that heating/cooking does not necessarily destroy all of the antinutrient factors in legumes, particularly saponins. Unless, I missed something, I did not see the saponin content specifically of the pod of Prosopis species reported anywhere in the references you reported. It is almost certain that the saponin content of Prosopsis is high. The combination of lectin, saponin, phytate and trypsin inhibitors is an evolutionary strategy virtually all legumes have evolved to prevent predation by insects, microorganisms and birds and mammals. The degree of toxicity ranges from mild to lethal and generally produce adverse physiological effects in a chronic and dose dependent manner (see Arpad Pustzai’s life’s work).

Although consumption of Prosopsis species products dates back to at least 10,000 years, generally consumption of this legume or any legume cannot be done in their raw state, and requires cooking (eg. the advent of fire production at will). As I have pointed out in an extensive publication, “Ancestral Fire Production: Implications for Contemporary Paleo Diets,” the ability of produce fire is a very recent invention in the 2.5 million history of our genus Homo. Hence, all legumes would not have been a part of the dietary repertoire that shaped the current human genome. Accordingly, humans are not well adapted to legumes, even with cooking.

One of the nutritional obstacles that pre-agricultural people faced was the physiological protein ceiling which our group has extensively described in a paper we published in 2000 in the American Journal of Clinical Nutrition. Basically, protein becomes toxic for a variety of physiological mechanisms when ingested at about 35-40% of the total eucaloric intake. Wild game worldwide is typically very lean, and muscle meat of wild animals averages about 80% protein and 20% fat by energy. Accordingly, if you or any human were only to have wild game muscle meat as your only food source, you would rapidly (within a few days) develop protein toxicity which ultimately causes death — you would be better off starving or fasting. The solution to the physiological protein ceiling (which all pre-agricultural people must have inferred) was to dilute the protein portion of game animals with either fat or carbohydrate. Since animal carcasses only contain tiny amounts of carbohydrate, then you are dealing with a food mixture of protein and fat. But the problem is that wild game have little fat. However, with selective butchering and carcass consumption, the fattier portions (brain, marrow, tongue, perinephral fat, mesenteric fat etc.) can be consumed and the leaner portions eaten at physiologically tolerable levels. A caveat to this problem is that larger mammals contain more body fat than smaller mammals. Hence bison would be preferred to squirrels or field mice to negate the effects of excessive protein.

A final solution is to dilute the high protein content of wild animals with carbohydrate from plant foods. The problem here is that most wild plant foods are generally inedible to humans unless cooked and processed, and most edible plant foods are only edible seasonally. There are obviously notable exceptions, but until the ability to start fire at will was developed, the carbohydrate from plant foods would have contributed only a small percentage of the total yearly diet (see our papers on the topic available at my website for the references)

So how does this concept relate to Prosopis? Any plant food which is a good source of starch, sugar and or fat would have been exploited by indigenous people during the Neolithic or slightly earlier to offset the physiological protein ceiling. By cooking and processing formerly inedible foods (eg. legumes) using recently invented technology (fire production at will) previously unexploited foods could now be consumed. The problem is that cooking and processing still does not fully remove antinutrients. Apparently, more work needs to be done to fully and completely analyze the antinutrients in Prosopis and then do both in vitro and in vivo testing in animal and human models.

There clearly are better food choices from a nutritional perspective, and that is my point. It’s not that we can’t eat cooked Prosopis, but rather fresh meats, fish, seafood, eggs, organ meats, fresh fruits and veggies are better choices to mesquite beans.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

Fire Production | The Paleo Diet
In our world, fire is such a basic element that we almost never give it a second thought. You click upon your gas powered kitchen range and instantly a circular blue flame emerges to fry your eggs, boil your water or steam your veggies. Your summertime barbecue or campfire is lit without a second thought from the cheap butane lighter you bought from the convenience store. If you happen to be a cigarette or pot smoker – who amongst you worries about ignition for your habit – the problem is not fire starting itself, but rather paying for or obtaining tobacco or marijuana. Such is the way of the western world – virtually all of us do not give a second thought about creating fire. We can all do it at anytime we want with no worry whatsoever.

But what if in our contemporary world we didn’t have a butane lighter, matches or other modern procedures to produce fire? How could it be done? Do you know how to start a simple fire without modern technology? Could you create a simple flame to cook, to smoke or for warmth? I am not a betting man, but I can almost guarantee you that for even a hundred or a thousand dollars, none of you could start a fire without modern technology, even if your life depended upon it. The very first friction matches were only invented in 1827 by John Walker2 and the invention of simple butane lighters are even more recent still in the early part of the 20th century. How did humanity create fire before these inventions?

Let’s eventually travel backwards in time and see how fire was created without modern technology, but more importantly, for the Paleo Diet community, let’s examine how the control and production of fire defines the food groups that our ancestors could not have consumed – food groups that have now become arbitrary staples of civilization and which are ironically recommended by governmental and institutional organizations as promoters of good health and well being.

As simple as it seems; knowing, using and producing fire from an evolutionary perspective requires a number of fundamental steps:

  1. Logical identification of the event (fire itself)
  2. Recognition of fire’s benefits
  3. Controlling fire
  4. Producing fire at will4, 15

Virtually all mammals and primates are aware of fire’s dangers and logically flee from it, but none other than our own species identify its potential benefits. The majority of the anthropological community now recognize that fire use by hominids did not appear habitually anywhere in the world except in Europe, sporadically and opportunistically until about 300,000 to 400,000 years ago.9, 11, 14 I quote the most comprehensive recent review of ancient fire use:

“However, surprisingly, evidence for use of fire in the Early and early Middle Pleistocene of Europe is extremely weak. Or, more exactly, it is nonexistent, until ∼300–400 ka.”11

What does this statement mean? It means that Neanderthals living in Europe 300,000 to 400,000 years ago were the first hominids to:

  1. Logically identify fire
  2. Recognize its benefits
  3. Control it

However, the huge caveat here is that they almost certainly did not have the ability to produce fire at will.12, 13 How do we know this? Archaeological excavations of Neanderthal caves during extended cold periods in Europe show a virtual lack of fire use when the climate worsened and became quite frigid.12, 13 Accordingly, Neanderthals were at the mercy of collecting naturally occurring fire and keeping it alive for extended periods. Clearly, this approach was a “hit and miss” venture at best, as Neanderthals frequently suffered in the bitter cold of their winter caves without fire.12, 13

Controlling Fire vs. Producing Fire

The archaeological record from Europe shows evidence for fire control by about 300,000 to 400,000 years ago, but remember that the ability to control fire is far different than the ability to produce it.9, 11, 14 Naturally occurring fire results from lightening strikes, volcanic eruptions and spontaneous combustion via decaying plant material. Far and away, lightening is responsible for almost all naturally occurring fires. Hence, before humanity had the ability to produce fire, we were generally limited to collecting and preserving lightening caused fires. Apparently, this strategy was opportunistic and occasional at best, based upon the scarcity of fire in the early fossil record.9, 11, 12-14, 18 Because humanity lacked the knowledge and capacity to produce fire wherever and whenever we desired, then this limitation clearly prevented us from regularly consuming entire categories of plant foods (cereal grains, almost all legumes and most tubers and roots) which are normally inedible without cooking. The inability of humanity to produce fire therefore represents a crucial “line drawn in the sand” for defining foods and food groups that should or should not be included in contemporary Paleo Diets.

Producing Fire

As simple as it seems, fire production without modern technology is complicated, requires practice, instruction and dedicated skills.2 Alfred Kroeber, a world famous anthropologist from the University of California at Berkeley who studied the last wild Indian (Ishi) in North America in the early 1900s, simply could not light a fire in front of his University anthropology class when attempting to use Ishi’s hand held fire drill.20

Our genus (Homo) first appeared on earth about 2 million years ago. The most current data suggests that the ability to habitually produce fire by our species occurred only as, “a very late phenomenon restricted to the archaeological record of modern humans at the end of the Pleistocene.”14 This evidence based conclusion12-14 is consistent with the sum of the most recent archaeological data and does not support prior propositions of earlier habitual fire production, but rather opportunistic gathering of naturally occurring fire.1, 3, 18, 19 If we look at the emergence of habitual fire production as an exclusive innovation of modern humans, then you can appreciate how recent this technology really is, particularly from an evolutionary time scale. To put things into a perspective that we can all understand, fire production likely first came into regular play on a 24 hour time clock for all of humanity somewhere between 36 to 48 minutes (75,000 to 100,00 years ago) to midnight. Think about it – our genus (Homo) has existed for more than 2 million years, yet except for the final throes of our evolutionary period on earth did we ever consume any plant foods (cereal grains, legumes and most tuber and roots) that required cooking to make them edible.

One of the questions you certainly must ask, as have numerous people and professional anthropologists have posed before you is this: why did it take so long and why was it so difficult for humanity to produce fire? One of Charles Dickens’ most famous quotes, “It was the best of times; it was the worst of times” sticks in my mind. Good ideas become the “best of times” but only until they surface – before their appearance we must endure the prior status quo with the “worst of times.” Over the course of our species evolution, human technological innovation has moved at a dreadfully slow pace, primarily because prior accomplishments could not be documented or widely distributed until the advent of writing, the printing press and most recently computers and the internet. Nevertheless, the invention of fire production was an innovation that seems to have taken the entire world by storm sometime after modern humans evolved in Africa about 200,000 years ago and then began to colonize the planet about 60,000 years ago.2, 5-9

So just how did our ancestors do it? How did they invent the ability to produce fire whenever and wherever they wanted? The ethnographic literature of hunter gatherer societies universally shows that they utilized two basic means to generate fire:

  1. Wood on wood friction2, 4, 6-8
  2. Stone on stone percussion or friction using flint and iron bearing stones (pyrite or marcasite)10, 14, 15-17

Archaeological evidence from Europe indicates that production of fire via flint and iron stone percussion was rare or virtually absent in pre-agricultural people throughout Europe.14 Hence, it seems likely that the first Europeans to produce fire may have utilized wood on wood friction techniques to start fires.14 This fire starting procedure (wood on wood friction) likely spread rapidly worldwide, and evidence for fire production via this method appears in Australian2, 4 and North American hunter gatherer societies2, 6-8 as humans colonized these continents and elsewhere.2

Fire starting by wood on wood friction can be accomplished by a number of procedures. The most common method by worldwide hunter gatherers is the fire or hand drill (Figure 1 below).2, 4, 6 Other methods include the bow drill, the pump drill, the fire plow, the fire saw and the spear thrower over shield.2 Although the fire drill appears to be an easy and straightforward technique to produce fire, a number of crucial technological nuances virtually prevent unskilled operators from successfully producing fire,2 as was similarly experienced by Professor Kroeber in front of his anthropology class.20 Skilled hunter gatherers under good conditions can ignite fire in less than a minute with a fire drill, whereas the best modern survivalists can do it in 28 seconds.2

Logic dictates that the very first humans to start a fire via the hand drill method certainly did not preconceive this method in its entirety with the intent of producing fire. Rather fire must have accidentally resulted from an entirely separate operation – drilling to produce holes in objects.

Fire Production Figure 1

Figure 1. Fire production by the Giwi Hunter Gatherers using fire drills.

Since the appearance of modern humans in Europe more than 40,000 years ago, the fossil record is replete with drilled items – bone and stone necklaces, bone flutes, wooden grommets, and other items which are perforated with holes either drilled or punched into them. Accordingly, the very first fire ever created by any human from the hand drill method must have unexpectedly occurred with the original goal of drilling a hole into a wooden object with a wooden drilling stick. I bring this concept up to provide corroborative evidence that Neanderthals nor any other earlier hominid had the ability to habitually produce fire. Until modern humans arrived on the scene, the fossil record is almost completely devoid of drilled objects. Hence, the technology (drilling) that allowed modern humans to accidentally discover a universal procedure to ignite fire was not part of the technological repertoire of any hominids that came before us.
 
 

Nutritional and Dietary Implications of Fire Production

Before I leave this discussion, the most important consequence of when fire production first occurred in our ancestral past is the nutritional “line in the sand” that I alluded to earlier. As the Paleo Diet becomes more and more popular, its original message has become weakened by so-called experts whose Paleo food recommendations now include legumes, beans, lentils, garbanzo beans, lima beans, green beans, peas, quinoa, chia seeds, amaranth and other foods which are either toxic, indigestible or minimally digestible without cooking.21, 22 Further, these foods contain a variety of antinutrients (phytate, lectins, saponins, protease inhibitors, thaumatin-like proteins, tannins, isoflavones, raffinose oligosaccharides, cyanogenetic glycosides, favism glycosides and others), which in both their uncooked and cooked states impair gut health, immune and hormonal function while impairing nutrient absorption.21, 22

Our species has no nutritional requirement for cereal grains, legumes or tubers. We can obtain all required human vitamins and minerals from fresh vegetables, fruits, meats, fish, shellfish, seafood, eggs and nuts. The archaeological evidence produces a clear factual mandate that no hominids had the ability to habitually produce fire until very recent evolutionary times.11-14 Accordingly, plant foods that required the production of fire and cooking for their digestion and assimilation were not part of our original menu. Incorporation of these foods into contemporary diets is now known to reduce the nutrient density (vitamins and minerals of the 13 nutrients most lacking in the US diet)23, 24 while simultaneously promoting chronic diseases of western civilization.24, 25

The invention of fire was a very good thing. It changed our lives forever. The important message here for the 21st century Paleo Diet movement is to leave the worst of our ancestral world behind us (living in cold caves, etc.) and to adopt the best of their world (fresh living foods, regular exercise and sunlight exposure).

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

1. Berna F, Goldberg P, Horwitz LK, Brink J, Holt S, Bamford M, Chazan M. Microstratigraphic evidence of in situ fire in the Acheulean strata of Wonderwerk Cave, Northern Cape province, South Africa. Proc Natl Acad Sci U S A. 2012 May 15;109(20):E1215-20

2. Blake S, Welch DM. Making Fire. David M. Welch Publisher, Australian Aboriginal Culture Series, 2006.

3. Brain CK, Sillen A. Evidence from the Swartkrans cave for the earliest use of fire. Nature 1988;336:464-466.

4. Davidson DS. Fire making in Australia. Am Anthropologist 1947; 49:426-437.

5. Frazer, SJ. Myths of the Origin of Fire :An Essay. MacMillan Press, London, 1930.

6. Hough W. Aboriginal fire-making. Am Anthropologist 1890;3(4): 359-372.

7. Hough W. Fire as an Agent in Human Culture. Government Printing Office, Washington D.C., 1926.

8. Hough W. Fire making apparatus in the United States National Museum. In: Proc U S Natl Mus, 1928, p. 73.

9. James, SR. Hominid use of fire in the Lower and Middle Pleistocene: a review of the evidence. Curr Anthropol 1989;30: 1-26.

10. Mountford CP, Berndt RM. Making fire by percussion in Australia. Oceania 1941; 11(4): 342-344.

11. Roebroeks W, Villa P. On the earliest evidence for habitual use of fire in Europe. Proc Natl Acad Sci U S A. 2011 Mar 29;108(13):5209-14

12. Sandgathe DM, Dibble HL, Goldberg P, McPherron SP, Turq A, Niven L, Hodgkins J. Timing of the appearance of habitual fire use. Proc Natl Acad Sci U S A. 2011 Jul 19;108(29):E298.

13. Sandgathe DM, Dibble HL, Goldberg P, McPherron SP, Turq A, Niven L, Hodgkins J. On the role of fire in Neandertal adaptations in western Europe: evidence from Pech de l’Aze IV and Roc de Marsal, France. Paleo Anthropology 2011;216-242.

14. Sorensen A, Roebroeks W, van Gijn A. Fire production in the deep past? The expedient strike-a-light model. J Archaeol Sci 2014; 42:476-486.

15. Stapert D, Johansen L. Flint and pyrite: making fire in the Stone Age. Antiquity 1999; 73:765-777.

16. Weiner J. Pyrite vs. marcasite. Or: is everything that glitters pyrite? with a structured bibliography on firemaking through the ages. Bull Cherch Wallonie 1997;37:51-79.

17. Weiner J. Friction vs. percussion. Some comments on firemaking from Old Europe. Bull Primit Technol 2003; 26:10-16.

18. Wrangham R. Catching Fire: How Cooking Made Us Human. Basic Books, New York, 2009.

19. Wrangham R, Carmody R. Human adaptation to the control of fire. Evol Anthropol 2010;19:187-199.

20. Kroeber T. Ishi in Two Worlds, 50th Anniversary Edition: A Biography of the Last Wild Indian in North America. University of California Press, Berkeley, CA, 2011.

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

22. Cordain L. (2012). The trouble with beans. In: Cordain L, The Paleo Answer, John Wiley & Sons, NY, NY, pp 130-147.

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

24. 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.

25. Carrera-Bastos P, Fontes Villalba M, O’Keefe JH, Lindeberg S, Cordain L. The western diet and lifestyle and diseases of civilization. Res Rep Clin Cardiol 2011; 2: 215-235.

Nuts | The Paleo Diet

Do you find yourself having difficulty shedding weight on your Paleo regime? Or perhaps you’re still experiencing GI distress or frequent breakouts even though you’ve cut out the gluten, the dairy and the legumes.

Too many nuts, or the wrong type of nuts could be causing the problem.

Nuts can indeed be a part of the Paleo Diet when eaten in moderation: “in moderation” being the key takeaway message.

Since nuts are high in inflammatory Omega-6 and low in anti-inflammatory Omega-3, they should be regarding more as a garnish than a regular, go-to source of dietary fat.

The fats we should rely on regularly are raw avocados, coconut oil and extra virgin olive oil, as well as the fats we find with our protein sources, like wild salmon or the occasional fattier cut of grass fed meat, like a nice rib-eye.

Are All Nuts Created Equal?

Not at all.

We must factor in not only the type of nut, but also how the nut might be processed.

  • Raw, sprouted nuts are best, whereas you should steer clear of those found in large canisters, roasted in peanut oil. By soaking nuts and allowing them to sprout, we can reduce the amount of phytates we consume when we eat a handful of them with an apple as a snack, for example.
  • Surprisingly, almonds, which we see in abundance in many forms and varieties, have one of the worst Omega 3:6 ratios, with virtually no detectable Omega-3s!
  • Walnuts, Macadamias and Brazil Nuts, however, rank as the top three in their ratio which is more favorable, but still not ideal.

Don’t make the common mistake of buying a huge vat of nuts and bringing them to the office to “snack on” throughout the day. Far too often this ends in too many calories, an unbalanced macronutrient profile and an upset stomach.

How many nuts are too many nuts?

Simply put, if you’re eating any nuts more often than as the occasional garnish, it may be too much. Because they’re easy to purchase, easy to eat and require zero preparation, many people make the mistake of making them their go-to snack for the office or home, and end up consuming hundreds of extra calories each day without even realizing it.

But why are some nuts ok, but not some grains or some legumes?

It comes down to portion sizes and frequency. We’re only meant to be eating a small portion, as a garnish, on occasion, whereas with pasta, bread or bagels, the amount eaten in the typical Standard American Diet is closer to cupfuls.

A good example of how many nuts to eat might include a tablespoon of raw walnuts on a salad or a handful of raw almonds with an apple, some sliced turkey and spinach made into a wrap a couple times per week is the way to go.

Eating a vat of salted nuts, roasted in peanut oil that you purchased on sale at Costco each week is the wrong approach.

Are Nuts for Everyone?

Certain populations may need to be even more careful with nuts, such as those with autoimmune conditions. While some can tolerate nuts and seeds others cannot. The best approach is to go nut-free for a month on top of the standard Paleo Diet and then test to see if you react.

Storing

Because of their high fat content, nuts kept in the freezer can be eaten in that state. They won’t freeze into a rock-solid piece of ice the way a piece of lean chicken or veggies would.

Rather than following the budget friendly strategy of buying in bulk, only to find that two pound bag of organic raw walnuts still sitting in your cupboard two months later and not tasting so great, keeping them in the freezer proves to be cost-effective too, as nothing will spoil and go to waste.

For an easy to make treat, rinse, then freeze some organic grapes or a sliced banana. Paired with a handful of macadamias and topped with a dash of cinnamon and ginger, this makes an incredibly decadent “something sweet” way to finish a meal, far more representative of True Paleo than any treat.

Zero processing and loads of flavor is the way to go.

For a special occasion, create the decadent Raw Chocolate Covered Walnuts with Berries.

Kefir Consumption Ill Founded at Best | The Paleo Dit
Hi Dr. Cordain,

Just finished The Paleo Diet for Athletes; I have found it extremely useful so thank you! In the meantime, I noted Chris Kresser has recently been promoting the consumption of Kefir: http://chriskresser.com/kefir-the-not-quite-paleo-superfood

If you are able to comment I would be very interested in your views! I entirely understand if you are unable or unwilling to comment. Suspect you probably get a few emails like this!

Keep up the good work!

Michael

Dr. Cordain’s Response:

Hi Michael,

Good to hear from you and many thanks for your kind words about The Paleo Diet for Athletes.  I note that Chris Kresser has recently become quite a spokesperson for contemporary Paleo Diets, as he recently appeared on the Dr. Oz TV program, espousing the dietary benefits of both dairy products and legumes in contemporary Paleo diets.  A brief check of Chris’s scientific publication record on PubMed for “Paleo Diets,” or any other topic for that matter, comes up with absolutely zilch — zero ! — nothing !  — no publications whatsoever!  This evidence (or lack thereof) lends little credibility to Chris’s claims as an expert in diet, nutrition or anthropology — much less Paleo Diets.  He has simply never put forth his ideas in peer review, scientific journals.  Nevertheless, the presence of scientific publications or advanced degrees don’t always guarantee expert advice; rather good ideas and rationale thought, supported by solid data frequently do.  Chris’s advice that legumes and dairy are indeed “Paleo” foods that should be regularly consumed in contemporary diets mimicking the nutritional characteristics of our pre-agricultural, hunter gatherer ancestors is ill founded at best.

The Paleolithic period or Old Stone Age is generally defined as the time span in which human ancestors first began to manufacture stone tools (about 2.5 million years ago to 3.2 million years ago) until the beginnings of agriculture in the Middle East about 10,000 years.  During this period all humans and our hominid ancestors lived as hunter gatherers and only consumed wild plant and animal foods available in their environments.

Because it is difficult or impossible to milk wild mammals, humans couldn’t have consumed the milk of another species until they were domesticated, beginning about 10,000 years ago.  Even though 10,000 years ago seems to be incredibly distant from a historical perspective; on an evolutionary time scale it only represents about 330 human generations.1 Hence, dairy products (milk, butter, cheese, yogurt, kefir etc.) are very recent introductions into the human diet and never were components of Paleolithic diets.1 In support of this notion is the very recent evolutionary appearance of genes which allow certain human populations on the planet to digest milk without gastro-intestinal upset.2 In fact, about 65 % of the world’s people are lactose intolerant and cannot drink milk without digestive discomfort.  By fermenting dairy products, it is possible to reduce their lactose content, but not all fermented dairy products (yogurt, kumiss, sour milk etc) are completely lactose free.  So the question comes up, should people consuming contemporary Paleo Diets be regularly consuming a food (kefir or for that matter any dairy product) for which our species has scant evolutionary experience? I have fully addressed this issue in an entire chapter in my most recent book, The Paleo Answer.3

It is not the lactose in milk that is the sole reason to avoid dairy.  Except for calcium, milk and dairy products are relative nutritional lightweights in the 13 nutrients most lacking in the U.S. diet.1, 3 Of seven food groups (seafood, meats, fresh vegetables, fresh fruits, milk, whole grains and nuts), milk ranked 5th for the 13 nutrients most deficient in the U.S. diet.  Seafood, meat, fresh vegetables, fresh fruits and nuts provide humans with all known nutritional requirements4 and represent the major food groups that conditioned the human genome for more than 2.5 million years of evolutionary experience.3 No mammal on earth has a nutritional requirement for the milk of another species, nor do we.

Besides its poor nutritional value and indigestibility for 65% of the world’s people, milk and other dairy products may produce a variety of adverse health effects including: 1) a high insulin response and insulin resistance, 2) an increased risk for cardiovascular disease, 3) an increased risk for acne, 4) an increased risk for many autoimmune diseases including multiple sclerosis, rheumatoid arthritis, Crohn’s disease and ulcerative colitis, 5) an increased risk for food allergies,  6) an increased risk for breast, ovarian, prostate and testicular cancers, 7) an increased risk for senile cataracts 8) dairy products’ high calcium content impairs zinc and iron absorption, and finally 9) increased dairy consumption doesn’t reduce the risk for bone fractures – so why consume them?. The mechanisms underlying these adverse health effects are fully outlined in my chapter on the topic, including more than 100 references to support this information.3

If you think milk is just a healthy white liquid that is “Good for Every Body,” think again! The following non-comprehensive list contains hormones and bioactive substances found in cow’s milk which are either known to, or suspected of causing a number of the deleterious health effects associated with milk and dairy consumption.3

Growth Hormones

  • Insulin, Insulin like growth factor 1 (IGF-1), Insulin like growth factor 2 (IGF-2)
  • Insulin like growth factor binding proteins, 1 to 6 (IGFBP-1, 2, 3, 4, 5, 6),
  • Betacellulin (BTC), Growth hormone (GH), Growth hormone releasing factor (GHRF), Transforming growth factor alpha (TGF α), Transforming growth factor beta 1 (TGF-β1), (TGF-β2), Platelet derived growth factor (PDGF)

Steroid Hormones

  • Estrogens (Estrone, Estradiol-17β, Estriol and Estrone sulfate), Progesterone, 20 alpha-dihydropregnenolone, 5α androstanedione, 5 α pregnanedione, 20α- and 20β-dihydroprogesterone, 5α-pregnan-3β-ol-20-one,  5α-androstene-3β17β-diol, 5α-androstan-3β-ol-17-one, androstenedione, testosterone, and DHEA acyl ester

Bioactive Proteins and Peptides

  • Relaxin, Thyrotropin releasing hormone (TRH), Luteinizing hormone releasing hormone (LHRH), Somatostatin (SIH), Gastrin releasing peptide (GRP), Calcitonin, Adrenocorticotropic hormone (ACTH), Prolactin, Thyroid stimulating hormone (TSH), Lysozyme, Lactoperoxidase, Lactoferrin, Transferrin, Immunoglobulins (IgA, IgM, IgG), Proteose-peptone, Glycomacropeptide, Plasmin, α Casein, β Casein, κ Casein, α Lactoglobulin, β Lactoglobulin, Bovine serum albumen (BSA), Gastric inhibitory polypeptide (GIP), Glucagon-like peptide-1 (GLP-1), Antitrypsin, Plasminogen activator inhibitor-1, α(2) antiplasmin , Butyrophilin, Xanthine oxidase, Mucin-1, Mucin-15, Adipohilin, Fatty acid binding protein, CD36, Periodic acid Schiff 6/7

Bioactive Peptides formed in gut from Milk Proteins

  • Casomorphins, α Lactorphin, β Lactorphin, Lactoferroxins, Casoxins, Casokinins, Casoplatelins, Immunopeptides, Phosphopeptides.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

REFERENCES

1. 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.

2. Cordain, L., Hickey, M. , Kim K. Malaria and rickets represent selective forces for the convergent evolution of adult lactase persistence. In: Biodiversity in Agriculture: Domestication, Evolution and Sustainability, Gepts P, Famula T, Bettinger R et al. (Eds.), Cambridge University Press, Cambridge, UK, 2011, pp 299-308.

3. Cordain L. Just say no to the milk mustache.  In: The Paleo Answer, John Wiley & Sons, New York, NY, 2012, pp. 72-103.

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

Are Sprouted Legumes Paleo | The Paleo Diet

Hi Dr. Cordain, the Paleo Diet makes a lot of sense to me and I very much appreciate the research that’s gone into it. However, am I right in thinking that any diet we are adapted to may nevertheless not be an ideal diet? We adapted to a diet that enabled us to be healthy enough to live long enough to reproduce healthy enough offspring.

If I understand correctly, couldn’t certain foods could make that basic diet even healthier? For example, I have The Paleo Diet for Atheletes out from the library right now and I see that you believe that the life of an athlete requires departure from a strict paleolithic diet. Couldn’t properly treated grains and legumes be beneficial additions to the diet? (i.e. soaked or sprouted to reduce/eliminate anti-nutrients?)

I am waiting to receive The Paleo Diet from the library (I’m on a long waiting list, which is good news I guess!) so maybe you address this issue in the book, in which case, I apologize. But if not, I would appreciate knowing your views on soaking/sprouting grains and legumes, and the reasons behind those views.

Thanks so much,
Zena

Maelán Fontes’ Response:

Dear Zena, first of all – thanks for supporting our work.

Lectins, one of the known antinutrients in cereal grains and legumes1, have been demonstrated to exert several deleterious effects upon human physiology1, (especially for those with autoimmune diseases) by increasing intestinal permeability2. Their function is to protect the plant against attacks by plant-eating animals by using several toxic substances, such as lectins3. There is a growing body of evidence showing that both the root and the sprout of wheat kernels have significant amounts of wheat germ agglutinin (WGA), one of the most studied lectins. Indeed, WGA originates in the wheat kernel, especially during germination and growth4, and the highest concentrations are found in young plant roots, seeds, and sprouts.

Lectins are resistant to digestive enzymes, and are found intact in peripheral circulation, as shown by Wang et al (1998)5. Furthermore, they are deposited in the internal organs6.

As stated by Pusztai et al7, lectins are heat stable, and normal cooking does not completely eliminate these toxic compounds unless they are pressure cooked8-11. The best way to reduce lectins’ adverse health effects is to limit their intake.

In addition, saponins – another type of toxic/antinutritive compound – exist in legume sprouts. Saponins have been shown to affect the gut barrier and by extension immune system function12. They may also increase the risk of autoimmune diseases in genetically susceptible individuals13. Soaking, sprouting or cooking legumes, does not reduce their saponin content14, 15.

In addition, a peptide fraction from gluten proteins called gliadin is found in wheat. Gliadin is resistant to digestive enzyme degradation16, arrives intact when it comes into contact with intestinal epithelial cells17, and increases intestinal permeability. Increased intestinal permeability may be at the root of autoimmune diseases such as Celiac Disease and Type 1 Diabetes13.

Phytate, the main form of phosphorus storage in many plants (especially bran and seeds) is classified as an antinutrient because is a chelator of iron, magnesium, calcium and zinc1. Phytate ingestion inhibits the intestinal absorption of those minerals. Phosphorus from phytate is unavailable to humans, as we do not produce the phytase enzyme necessary to break down phytate – unlike ruminants, who do produce phytase, and are able to digest phytate18. Yeast fermentation in bread reduces phytate content19. Furthermore, addition of ascorbic acid counteracts the inhibitory effects of phytate upon iron absorption20. Soaking and fermentation reduces the phytate content of grains and legumes as indicated in several studies21, 22, 23, 24.

Having said that, Dr. Cordain in his first book talks about the 85:15 rule, where he explains that 85% of caloric intake from modern paleolithic-like foods is still more healthy than the typical western diet, where more than 70% of caloric intake comes from foods introduced in the human food chain after the agricultural revolution25.

The bottom line is that our metabolism is perfectly adapted to the nutrition that shaped our genome during million of years of evolution. Therefore, any nutrient introduced after the agricultural revolution may not be compatible with our ancient genome. We believe that anyone engaged in athletic activities could do very well on a diet based on 85% paleolithic nutrients, which are preferable to the nutrients found in the typical western diet.

I hope this is helpful.
Maelán Fontes, MS, Ph.D. candidate in Medical Sciences at Lund University, Sweden; International College of Human Nutrition and Functional Medicine

References:

    1. Cordain L. Cereal Grains: Humanity’s Double-Edged Sword. World Rev Nutr Diet. Basel, Karger,
      1999, vol 84, pp 19–73.
    2. Cordain L. et al. Modulation of immune function by dietary lectins in rheumatoid arthritis. British
      Journal of Nutrition (2000), 83, 207–217.
    3. Chrispeels, M.J. & Raikel, N.V. (1991) Lectins, lectin genes, and their role in plant defense. Plant Cell 3, 1-9.
    4. Miller, R., & Bowles, D. (1982). A comparative study of the localization of wheat-germ agglutinin
      and its potential receptors in wheat grains. Biochem. J., 206, 571-576.
    5. Wang Q, Yu LG, Campbell BJ, Milton JD, Rhodes, JM. Identification of intact peanut lectin in peripheral
      venous blood. Lancet 1998;352:1831-32.
    6. Caron, M. & Steve, A.P. (2000) Lectins and Pathology, Taylor & Francis, London.
    7. Pusztai A and Grant G. Assessment of lectin inactivation by heat and digestion. From Methods
      in Molecular Medicine. Vol 9 Lectin methods and protocols. Edited by J M Rhodes and J D Milton Humana
      Press Inc. Totowa, NJ.
    8. 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.
    9. Boufassa C, Lafont J, Rouanet J M, Besancon P 1986 Thermal inactivation of lectins (PHA)isolated
      from Phaseolus vulgaris. Food Chem 20 295-304.
    10. 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.
    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. Patel B, Rober S, Sporns P, et al. potato glycoalkaloid adversely affect intestinal permeability
      and aggravate inflammatory bowel disease.
    13. Visser J, Rozing J, Sapone A et al. Tight junctions, Intestinal permeability and Autoimmunity.
      Ann. N. Y. Acad. Sci. 1165: 195-205 (2009).
    14. Ruiz RG, Price K, Rose M, Rhodes M, Fenwick R. A preliminary study on the effect of germination
      on saponin content and composition of lentils and chickpeas. Z Lebensm Unters Forsch 1996;203:366-369.
    15. Ruiz RG, Price KR, Arthur AE, Rose ME, Rhodes MJ, Fenwick RG. Effect of soaking and cooking on
      the saponin content and composition of chickpeas (Cicer arietinum) and lentils (Lens culinaris).
      J Agric Food Chem 1996;44:1526-1530.
    16. Shan L, Qiao SW, Arentz-Hansen H, et al. Identification and Analysis of Multivalent Proteolytically
      Resistant Peptides from Gluten: Implications for Celiac Sprue. J Proteome Res. 2005 ; 4(5): 1732–1741.
    17. Drago S, Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac
      intestinal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology,
      2006; 41:408/419.
    18. Klopfenstein, TJ et al. “Animal Diet Modification to Decrease the Potential for Nitrogen and
      Phosphorus Pollution”. Council for Agricultural Science and Technology 21.
    19. Reinhold JG. Phytate destruction by yeast fermentation in whole wheat meals. J Am Diet Assoc 1975;66:38-41.
    20. Hallberg L, Brune M, Rossander L. Iron absorption in man: ascorbic acid and dose-dependent inhibition
      by phytate. Am J Clin Nutr 1989;49:140-4.
    21. Chen LH, Pan SH. Decrease of phytates during germination of pea seeds (Pisium Sativa). Nutr Rept Int.
      1977;16: 125-131.
    22. Walker KA. Changes in phytic acid and phytase during early development of phaseoleus vulgaris beans.
      Planta 1974;116:91-98
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      for the 21st century. Am J Clin Nutr 2005;81:341–54.

 

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