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Here we stand in the middle of this new world with our primitive brain, attuned to the simple cave life, with terrific forces at our disposal, which we are clever enough to release, but whose consequences we cannot comprehend.
–Albert Szent-Gyorgyi
ecause our modern food supply is driven largely by the economics of mass production - and often undergoes historically unprecedented types of industrial processing - it's easy to assume, that most food-based toxins are introduced to our food supply by the hand of man. After all, agricultural pesticides, artificial preservatives, chemical sweeteners, and nutritionally unsound processing methods such as the refining of grain, or the powdering of milk are, of course, the result of human intervention; and it's become well-documented that such practices often compromise the nutritional quality of our foods.
But, as current cultural trends create an ever-larger segment of our population seeking to return to a more "natural" way of eating, it's important not to ignore the potent food-based toxins created by Mother Nature, herself.
All living things possess some mechanisms for ensuring their reproductive capacity in the face of potential predators. An animal, for example, could possess sharp claws, great speed, or the intellect needed to prevent it from becoming the prey of another. But while the defense mechanisms present in the animal kingdom are relatively easy to observe, those of the plant kingdom are often hidden from plain view.
Quite logically, being rooted in the ground doesn't allow plants the luxury of movement as their environment becomes increasingly inhospitable. So, out of necessity, plants have developed a variety of unique mechanisms to increase their chances of reproduction. These run the full gamut from symbiotic - where facilitating plant reproduction is actually beneficial to surrounding animal species (flowers which pollinate with the help of bees are a good example) - to overtly toxic, as evidenced by countless plant-based poisons.
But, for the vast majority of plant species, (including the plants which comprise the majority of human food on the planet) their means of ensuring reproductive capacity can't be categorized in such a black-or-white sense. Many of the substances which plants produce to ward off predators may be toxic in some situations and actually therapeutic in others. The rich history of herbal medicine in cultures throughout the globe illustrates this, as does the fact that so many of our modern pharmaceutical drugs are merely subtle variations of plant-based substances which originally evolved for plant defense.
The plant kingdom has developed so many defensive chemicals, in fact, that some apologists for the usage of chemical pesticides are eager to point out that 99% of the "pesticides" humans consume are those naturally produced by plants for protection. Although true, this fact is not reason to assume that the chemical pesticides added by human intervention are therefore innocuous, but merely reason to look a bit more closely at the effects of plant-based toxins.
Among the most notable of these toxins are protein structures called lectins. It's been postulated that the modern prevalence of food allergy, autoimmune disease, digestive troubles, mental and neurological disorders, obesity (and the related diseases of heart disease, diabetes, and cancer) can be attributed, in part, to the unique lectins in our modern diet. As we examine lectins (and other food-based toxins), we'll see that their biological activity could cause us to significantly alter our conception of what constitutes a healthy diet.
What Are Lectins?
Lectins are carbohydrate-binding proteins found in many foods - most notably, cereal grains (e.g., wheat, rye, barley, oats, corn), beans, oilseeds, and nuts. Lectins are able to bind to micro-organisms and to carbohydrate structures in the tissues of animals; and the often destructive nature of lectins serves to protect plants from things like fungi and insects. Fittingly, the name lectin is derived from the Latin phrase meaning "I choose" - as different lectins possess great specificity as to which carbohydrate structures they bind.
Of course, carbohydrates (and a sub segment of carbohydrates, i.e., sugars) are most commonly known as major "fuel sources" for our bodies. But some carbohydrates also happen to be structural components of our cells. For example, due to its remarkable success as a dietary supplement for joint health, most people recognize the amino-sugar combination known as glucosamine as an integral structural component of connective tissue.
Similarly, in cells throughout our body (and in cells of all living creatures), other sugar-containing molecules (collectively known as glycoconjugates) emanate forth from cell surfaces. These glycoconjugates function not only as structural components, but as essential factors in cellular communication, inflammation, and immune function.
It's precisely these cellular carbohydrate structures to which lectins are able to bind - sometimes wreaking metabolic havoc as a result. As far back as the late 1880's it was known that some proteins of plant origin had the uncanny ability to bind to red blood cells, causing them to clump together (this phenomenon is described in the scientific research, as the agglutination of erythrocytes). Because they caused this "clumping" effect upon red blood cells, lectins of plant origin were often referred to as hemagglutinins or phytoagglutinins.
The first such lectin was isolated from seeds of the castor tree in 1888 by Peter Hermann Stillmark, and named ricin - a lectin with such toxicity, that it has subsequently been used as an agent of chemical warfare. Some research indicates that ingestion of as few as 4 to 8 castor beans may contain a lethal dose of ricin for an adult:
Study Link - Castor bean poisoning.
Quote from the above study:
The potentially lethal doses reported for children and adults are three beans and four to eight beans respectively.
Of course, nobody in their right mind would knowingly eat castor beans, and food-based lectins don't possess anywhere near the acute toxicity of ricin; but the take-home lesson remains: in the form of lectins, Nature has imbued plant species with powerful weapons to protect themselves (and their offspring - the seed) from ingestion by animals and humans.
Cereal Grains and the Rise of Civilization
It's been commonly noted that one of the major factors responsible for the rise of human civilization was the advent of agricultural societies relying largely on the production of cereal grains. It's thought that prior to this agricultural revolution, and for the majority of human history, a hunter-gatherer lifestyle supplied our prehistoric ancestors with very little, if any, of the wheat, corn, or rice, which are now dietary staples throughout the world. Once these grains began to be cultivated, their predictable growing cycle, and caloric density allowed for a population explosion, and for agrarian societies to eventually thrive into the specialized industrial and technological cultures we know today. It's fair to say that the six, or so, billion inhabitants of the planet earth owe a great debt of gratitude to agriculture, and to cereal grains in particular - feeding our massive global population would simply not be possible without them.
It's also been observed, however, that there often exists a direct correlation between the adoption of an agrarian food supply and the development of what are called "diseases of affluence," including cardiovascular disease, diabetes, autoimmune disease, obesity, and certain types of cancer.
In attempting to explain these diseases of affluence, it's often assumed that agriculture has allowed us to consume greater amounts of food than a hunter-gatherer lifestyle would have. But by most estimates, people in hunter-gatherer societies are said to have consumed, on average, approximately 3,000 calories per day - an amount significantly greater than the current average daily caloric consumption in the US. Even accounting for greater energy expenditure among hunter-gatherers versus modern man, we can see that assessments based merely upon caloric consumption and physical activity don't seem to explain the full gamut of our modern ills. The presence of dietary lectins in cereal grains has been proposed as a critical piece of the overall puzzle. It seems that lectins, acting upon tissues throughout the body, are able to cause exactly the sort of wholesale metabolic disruption which fosters our modern diseases of affluence.
Since industrial processing allows us to form grain-based foods into almost every conceivable shape (commercial breakfast cereals being a prime example), it's easy to lose sight of exactly what we're eating when we eat grains. It's important to realize that when we eat food made from cereal grains, like wheat, rice, barley, corn, or oats, we're actually eating the seed portion of grasses. Where the seed is the reproductive unit of the plant, Nature has built several particularly resilient "defense mechanisms" into them (including lectins) to protect the plant "offspring" from destruction. This same "protect-the-offspring" principle also applies to other lectin-containing "seed" foods such as beans and legumes, as well.
The Biological Effects of Lectins
Lectins can be found in a wide variety of foods, but interestingly, the lectins which are most apt to be problematic to human health happen to come from foods which are also notably allergenic. As examples:
Wheat and other gluten-containing grains Legumes (including beans, soybeans, and peanuts) Nightshades (tomatoes, peppers, eggplant). Shellfish (examples of animal-based lectins)
Some preparation and cooking methods (such as the soaking of beans) are able to reduce the amount of toxic lectins in the prepared food, but merely reducing lectin content and actually eliminating lectins are two different things entirely. And not only do variable amounts of lectins remain in prepared lectin-containing foods, but it has often been shown that certain food lectins are remarkably resistant to the effects of cooking and digestion. One such lectin is a well-studied lectin from wheat, known as wheat germ agglutinin (WGA).
Study Link - Identification of the dietary lectin, wheat germ agglutinin, in human intestinal contents.
Quote from the above study:
These studies demonstrate that wheat germ agglutinin can traverse the human small intestine intact. It is feasible that orally ingested wheat germ agglutinin and other plant lectins which interact with a wide variety of cell membranes may alter intestinal epithelial or bacterial cell function in the human bowel.
Where wheat is the most widely consumed food on the planet, the presence of WGA in dietary staples such as breads, pastas, noodles, and breakfast cereals give the study of its effects pressing real-world significance. And because it's scarcely broken down by cooking or digestion, we know that WGA (and many other lectins from the food we eat) will come in direct contact with cells throughout the gastrointestinal tract.
It just so happens that these cells lining the intestines are particularly rich in the types of cellular sugars to which lectins can easily bind. Remember that these cellular sugar-containing structures are intimately involved in the immune system, inflammation, and cellular communication. When latched on to by certain dietary lectins, the result is often intestinal inflammation and a dramatic increase in the permeability of the intestines (we've written in previous Integrated Supplements Newsletters [July 2008] about the role increased intestinal permeability, or a "leaky gut," can play in exacerbating nearly every manifestation of aging and degenerative disease). In the presence of a leaky gut, toxic intestinal bacteria can enter the blood stream, thus taxing the liver, and compromising the immune system amidst a whirlwind of systemic inflammation.
Dietary lectins, including wheat germ agglutinin, have been shown to directly increase intestinal inflammation, intestinal hyperplastic and hypertrophic growth (thought to be implicated in the development of cancer) and intestinal permeability:
Study Link - The effect of concanavalin A and wheat germ agglutinin on the ultrastructure and permeability of rat intestine. A possible model for an intestinal allergic reaction.
Quote from the above study:
These observations suggest that lectins can affect both the ultrastructure and the permeability of the intestine, in a way assumed to mimic allergic reactions to food constituents.
The delicate cells lining our intestines can grow rapidly and have several mechanisms ensuring their repair when damaged. But lectins have been shown to actually disable the repair mechanisms of intestinal cells - an action which the authors of the following study propose constitutes a unique type of food poisoning:
Study Link - Lectin-based food poisoning: a new mechanism of protein toxicity.
Quote from the above study:
Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning.
In addition, some evidence suggests that certain dietary lectins may not only increase intestinal permeability, but may also alter the bacterial population of the intestines towards an abundance of the more harmful types of micro-organisms.
As an example, the following study found that a lectin from kidney beans, called phytohemagglutinin, or PHA, caused damage to the intestinal lining. This damaged tissue subsequently led to the overgrowth of the opportunistic E. coli bacteria in the intestines:
Study Link - Kidney bean lectin-induced Escherichia coli overgrowth in the small intestine is blocked by GNA, a mannose-specific lectin.
Quote from the above study:
These new a-linked mannosyl terminals, particularly of the damaged epithelium, facilitated the preferential adherence of opportunistic Escherichia coli with mannose-sensitive Type 1 fimbriae, and other coliforms, to the glycocalyx. Accordingly, the growth of the gut was accompanied by a reversible and PHA dose-dependent overgrowth with E.coli.
Note: in the above study, GNA, or the "snowdrop lectin" was able to hinder the growth of E. Coli which was stimulated by PHA, but it, too, caused damage to the GI tract.
Some other studies have shown that even the administration of certain probiotics, the beneficial intestinal bacteria which are often protective of gastrointestinal health, failed to protect against the overgrowth of E. coli in the intestines when PHA was administered:
Study Link - Probiotic Lactobacillus plantarum 299v Does Not Counteract Unfavorable Phytohemagglutinin-Induced Changes in the Rat Intestinal Microbiota.
Considering the fact that many food-based lectins are known to be resistant to digestion, and considering that they may cause dramatic increases in the permeability of the GI tract, it's not surprising that many dietary lectins are able to enter general circulation intact. When absorbed into circulation, lectins have been show to cause even more metabolic disruption, including enlargement of the pancreas and atrophy of the thymus gland. Lectins, including WGA, have also been shown to be deposited in blood vessels and lymphatic tissue.
Study Link - Antinutritive effects of wheat-germ agglutinin and other N-acetylglucosamine-specific lectins.
Quote from the above study:
As a result of their binding and endocytosis by the epithelial cells of the small intestine, all three lectins were growth factors for the gut and interfered with its metabolism and function to varying degrees. WGA was particularly effective; it induced extensive polyamine-dependent hyperplastic and hypertrophic growth of the small bowel by increasing its content of proteins, RNA and DNA. Furthermore, an appreciable portion of the endocytosed WGA was transported across the gut wall into the systemic circulation, where it was deposited in the walls of the blood and lymphatic vessels. WGA also induced the hypertrophic growth of the pancreas and caused thymus atrophy.
Similarly, even low doses of lectins from peanuts and mushrooms have been shown to cause pancreatic growth in the rat - a finding which the researchers warn may have implications for the development of pancreatic cancer in humans:
Study Link - Dietary lectins can stimulate pancreatic growth in the rat.
Quote from the above study:
The aim of the present study was to investigate the long-term actions of low doses of lectins on the rat intestine and pancreas. A long-term carcinogenesis study was performed using low levels (40 micro g/rat/day) of peanut (PNA) or mushroom lectin (ABA) which bind to O-linked (mucin-type) oligosaccharides in the gut¿The weight of the pancreas was significantly greater (by 18 and 23%) in both lectin treated groups (P < 0.03/0.001). The weights of the acini and septal tissue were also increased by 39-46% in PNA and ABA fed animals, respectively (P < 0.002); there was no significant change in the endocrine pancreas. In conclusion, long-term feeding of low doses of lectin can influence pancreatic growth, and this trophic action may have potential adverse implications for the development of pancreatic cancer in humans.
All told, this reseach makes it clear that lectins possess the unique ability to foster widespread gastrointestinal, immunologic, and vascular damage.
Lectins and Gluten
It has been proposed that wheat germ agglutinin is, in fact, the lectin contained in the wheat-protein, gluten, which is responsible for many of the inflammatory intestinal and systemic effects of wheat consumption in people with gluten intolerance, or celiac disease:
Study Link - Lectin activity of gluten identified as wheat germ agglutinin.
Quote from the above study:
Our results indicate that the lectin properties of gluten are due to traces of WGA. This finding is relevant for theories about the pathogenesis of coeliac disease.
Those with celiac disease have a strong sensitivity to gluten, making strict avoidance of gluten-containing foods a necessity. But studies have shown that gluten is able to induce pathological changes in the gastrointestinal tract, even in healthy people without celiac disease:
Study Link - Gluten-induced mucosal changes in subjects without overt small-bowel disease.
Quote from the above study:
Administration of the high gluten diet produced significant architectural changes in the jejunal mucosa of both the normal relatives of coeliac patients and the patients with altered immunity (p less than 0.01). In some cases changes amounted to severe partial villous atrophy. A significant increase in intraepithelial lymphocytes was also observed in the normal relatives of coeliac patients and in the normal volunteers (p less than 0.05)¿These findings indicate that excessive gluten intake can induce changes in the jejunal mucosal architecture in susceptible individuals who do not have overt coeliac disease.
Given the general biological effects of gluten and WGA, even many people who don't suffer from celiac disease, per se, are beginning to consciously eliminate wheat and gluten from their diet both as a preventative measure, and as a possible therapeutic intervention. Digestive disorders such as heartburn, ulcers, irritable bowel syndrome, Crohn's disease, and colitis, as well as disorders such as autism, lupus, rheumatoid arthritis, and multiple sclerosis are often significantly improved by a gluten-free diet. Conceptually, if the avoidance of wheat lectins is a reason why, then the avoidance of not just gluten, but many high-lectin foods can be entertained as a viable option for these disorders. To put it another way, even many "gluten-free" foods contain unique lectins of their own, each imparting a potentially similar toxic burden.
To understand how lectins as a group may be responsible for such far reaching biological mayhem, it will help to take a closer look at the common thread running through many of the above listed disorders.
Lectins in Autoimmune Disease
Celiac disease is not, in fact, a food allergy as many people seem to think. It's more correctly classified as a type of autoimmune disorder - where the bodies' immune system attacks structures of the body itself, as if they were foreign or harmful. Examples of common autoimmune disorders include rheumatoid arthritis, dermatitis herpetiformis (which, like celiac disease, is symptomatically rectified by the strict avoidance of gluten), insulin-dependent diabetes mellitus (aka Type-1 diabetes), Sjögren's syndrome, multiple sclerosis, and lupus.
Exactly why the body turns on itself in autoimmune disease is still somewhat of a mystery. Genetic susceptibilities are known to be involved, but increasingly, researchers have begun to look at other, more controllable factors. The research on rheumatoid arthritis in particular, often offers a clear illustration of the dietary and environmental factors which may underlie the development of many autoimmune disorders.
For starters, intestinal inflammation and increased intestinal permeability (like that caused by lectins) have repeatedly been shown to be directly related to joint inflammation:
Study Link - Importance of intestinal mucosal immunity and luminal bacterial cell wall polymers in the aetiology of inflammatory joint diseases.
Quote from the above study:
Occult intestinal inflammation, which may be related to non-steroidal anti-inflammatory drugs or may be disease-associated, occurs in approximately two thirds of patients with rheumatoid arthritis, idiopathic reactive arthritis and ankylosing spondylitis. Enhanced mucosal permeability to macromolecules occurs in rheumatoid arthritis, enteric infections and idiopathic inflammatory bowel disease.
As such, with regard to autoimmunity, the predominant thinking has been that the bacterial burden introduced into the blood stream via this inflamed, leaky gut serves to activate the immune system inappropriately. On a molecular level, many of the protein fragments from gut bacteria bear a striking resemblance to certain proteins contained in joint tissue.
The immune system attempts to clear up the harmful bacteria by, in essence, taking an immunological "snapshot" of it, thus allowing immune cells to identify and destroy the troublemakers. But if these trouble-making bacterial fragments are similar enough in structure to the proteins of the joint matrix, the immune system is unable to distinguish one from another. In rheumatoid arthritis, this may be a major reason why the immune system begins attacking the joint tissue. Similar phenomena are now thought to occur in many other autoimmune disorders, including multiple sclerosis, where several viral, bacterial, and food-based peptides contain amino acid sequences similar to those found in the myelin sheath.
As relates to rheumatoid arthritis, research has shown that injections of cell-wall fragments of Eubacterium aerofaciens (a major component of human intestinal flora) can lead to both acute and chronic arthritis in rats:
Study Link - Are intestinal bacteria involved in the etiology of rheumatoid arthritis?
Quote from the above study:
We feel that the immunoreaction against PG peptides [from intestinal bacteria] plays a pivotal role in experimental and human arthritis of an unknown etiology.
And antibiotics, which, logically, serve to kill bacteria, have been shown to exert beneficial effects upon the symptoms of rheumatoid arthritis.
Study Link - Antibiotic therapy for rheumatoid arthritis. Scientific and anecdotal appraisals.
Quote from the above study:
Minocycline is arguably the most interesting new drug for rheumatoid arthritis since the development of methotrexate. Tetracycline compounds have long been used by rheumatologists who were considered mavericks by their peers, and recent controlled studies have demonstrated their antirheumatic activity. The reason that minocycline works is unclear, and their niche in the treatment of rheumatoid arthritis remains to be established. Nonetheless, it is clear that some patients with rheumatoid arthritis respond favorably to this form of treatment.
Interestingly, many autoimmune disorders have been observed to occur following viral infections such as influenza. It just so happens that the influenza virus serves to disable a major line of defense against lectins by stripping away protective sialic acid molecules from intestinal glycoconjugates - thus exposing the delicate intestinal cells to the destructive actions of lectins.
Because our bodies are particularly susceptible to the harmful effect of dietary lectins when we are under viral attack, some researchers have noted that the folk wisdom advising to "starve a fever" may have a legitimate scientific basis:
Study Link - Proposed biomolecular theory of fasting during fevers due to infection.
Quote from the above study:
The folk admonition to starve a fever may have a scientific basis. Fevers due to infectious organisms that produce neuraminidase (sialidase) may contribute to the pathophysiology of autoimmune conditions. Neuraminidase unmasks host cellular lectins that interact with food lectins and can induce human leukocyte antigen type II (HLA II) expression. HLA II can then bind food lectins and serve as targets for antibody production. Some of these antibodies can then cross-react and attack healthy tissue, inducing disease.
Do Lectins Cause Weight Gain?
Although the increasing prevalence of autoimmune disorders is likely to be a significant result of our modern grain-based and lectin-rich diet, there is perhaps no greater health threat posed by our modern diet than its uncanny ability to steadily expand our waistlines. In recent years, several biological mechanisms have been uncovered by which certain dietary lectins may contribute to our modern epidemics of overweight and obesity.
In keeping with their actions as potent disruptors of animal and human metabolism, many dietary lectins possess the ability to interfere with the proper actions of metabolic hormones. For example, several lectins, including, and especially wheat germ agglutinin, exhibit insulin-like actions on adipocytes (fat cells) - causing these cells to take up glucose from the bloodstream, and to subsequently convert any excess into fat. But unlike insulin itself, dietary lectins seem reluctant to "let go" of the insulin receptor once the job of lowering blood sugar is accomplished. For this reason, lectins have been found to send a nearly constant message to the adipocytes to produce fat:
Study Link - Bound lectins that mimic insulin produce persistent insulin-like activities.
Quote from the above study:
Short preincubation of rat adipocytes with wheat germ agglutinin, followed by removal of unbound lectin, resulted in persistent activation of lipogenesis [the production of fat], which lasted at least 3 h¿The property of producing persistent bioactivation is not shared by insulin itself, since removal of the unbound hormone results in termination of bioactivation.
In previous newsletters, we've pointed out that body fat isn't the inert storehouse of energy which many people assume it to be - it's actually a remarkably active endocrine organ which constantly emits various systemic inflammatory and hormonal signals. Not surprisingly, the greater the amount of body fat we carry, the more inefficient and pathological these signaling functions become.
One important adipose-derived hormone is called leptin. Under ideal situations, in the presence of adequate or excessive food intake, leptin is released from fat cells as a signal to the brain to reduce hunger. When first discovered, some researchers hoped that leptin injections could be used profitably to counter the obesity epidemic. But most obese people, it was found, already have high levels of leptin (and leptin injections don't seem to be at all effective in reducing appetite or weight in humans).
Research quickly showed that it doesn't seem to be a lack of leptin which is responsible for excessive weight gain in humans. It's now thought that in overweight and obese individuals, the brain doesn't seem to receive leptin's message properly - even though there's a ton of it floating around in the bloodstream. Scientists have coined this phenomenon leptin resistance, and have begun to seek out, on a molecular level, the factors which may block leptin signaling.
Though the research is far from conclusive, it seems that wheat germ agglutinin may be a common dietary substance capable of blocking the binding of leptin to its receptor:
Study Link - Contribution of leptin receptor N-linked glycans to leptin binding.
Quote from the above study:
We found that a mammalian cell-expressed sOb-R (soluble Ob-R)[leptin receptor] fragment (residues 22-839 of the extracellular domain) bound leptin with a dissociation constant of 1.8 nM. This binding was inhibited by Con A (concanavalin A) or wheatgerm agglutinin.
Cellular receptors like the insulin receptor and the leptin receptor always contain glycoconjugates, and are therefore always susceptible to binding by dietary lectins (the glycoconjugates of these receptors are often so general, that some scientists have noted that the term "receptor" is misleading because it gives the impression that each is specific to one substance).
Though not the only factor leading to weight gain in our modern culture, the actions of lectins on the insulin receptor may provide an interesting answer to the puzzle of why some people gain weight (or fail to lose weight) even on relatively low caloric intakes. Similarly, the actions of lectins on the leptin receptor may help to explain the oftentimes seemingly addictive nature of grain-based foods - the more of these foods we eat, the more we may incapacitate our bodies' innate ability to regulate hunger.
If lectin-containing foods such as grains do inhibit weight loss, this could give an interesting perspective on the success of many of the recently-popular "low-carb" diets. It may be that it's not carbohydrates and sugars, per se, that are leading to weight gain in our modern societies, but, instead, the unprecedented consumption of particularly disruptive lectins. Low carbohydrate diets are necessarily low-grain, low lectin diets, which would largely account for their success, but perhaps these diets could be tweaked a bit so as not to be so restrictive.
It's likely that the prehistoric diet which fulfilled the high energetic demands and gave rise to the large brains of humans is one that we should probably try to emulate as best we can in our modern world. Although nutritional anthropologists continually debate over exactly what the diet of our prehistoric ancestors was actually like, we can use the biological effects of food components (like lectins) as clues to guide our choices. In all probability, we'll want to seek out a moderate carbohydrate diet, which specifically avoids high-lectin foods, such as cereal grains and beans. A modest amount of carbohydrates in the form of ripe fruits and possibly some root foods is advisable, as many of these contain relatively low levels of harmful lectins and other anti-nutrients. Leafy vegetables and (uncontaminated) meat and fish represent important sources of nutrients as well.
Of course, completely avoiding grain-based foods, or lectins in general, may not be possible, or even advisable. Several well-conducted epidemiological studies do show the consumption of whole grains to be associated with health benefits:
Study Link - Whole-grain consumption and chronic disease: protective mechanisms.
Quote from the above study:
Epidemiologic studies support the belief that whole grains are protective against cancers, especially gastrointestinal cancers such as gastric and colonic, and cardiovascular disease.
But it's important that the downside of grains and their lectins not be ignored either. The task, therefore, becomes to reduce lectin-induced damage as much as possible, while still benefiting from the nutrients (vitamins, minerals, fiber, phytonutrients) contained in lectin-containing foods. Fortunately, several nutritional strategies exist which may allow us to do just that - by specifically binding and, in essence, deactivating dietary lectins before they exert their damaging effects on our bodies' cells. These strategies will be the focus of the next Integrated Supplements Newsletter.
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