Treating the myelin is myopic. Must treat the underlying cause which is gut dysbiosis. I am now very sure of this because I've correlated the pain in my small intestine and later again the traverse colon to the rise in the M.S. effects. And it correlates very well within hours for the small intestine and then again within 2 - 3 days of eating any grains or high Omega-6 meat. Also correlated to when I have loose stools instead of healthy stools.
http://gutcritters.com/part-four-dietary-fat-leaky-gut-endotoxemia-and-heart-disease/Polyunsaturated: These types of fats have two or more double bonds and therefore lack four or more hydrogen atoms. Like monounsaturated fats, these double bonds are kinked so they don’t pack together well making them liquid even when refrigerated. Polyunsaturates can be further classified by the position of their first double bond in relation to their omega end. Polyunsaturated fats are called omega-6 fatty acids when their first double bond is in the sixth position from this position. Vegetable oils are very high in omega 6s.
Polyunsaturates with their first double bond from the third position of the omega end are called omega-3 fatty acids. Fish and flaxseed oils are both omega-3 oils yet differentiated by the length of carbon atoms they contain and their unsaturation.
These types of oils are extremely delicate and prone to oxidation when subjected to heat, light, pressure and free radicals in the body. They should never be used for high temperature cooking. Unfortunately, that is exactly what many vegetable oils are used for. They are routinely utilized in fast-food chains, restaurants and are common in processed foods.
All fats are combinations of different fatty acids. Canola oil, for example, is 62% monounsaturated fat, 6% saturated fat and 32% polyunsaturated fat. Butter fat is 56% saturated fat, 29% monounsaturated fat and 32% polyunsaturated fat.
Trans fats, implicated in both heart disease and cancer, are manufactured fats. They are made from polyunsaturated vegetable oils after the partial addition of hydrogen atoms to empty spots on their carbon chain. Olive oil and lard can also be subjected to partial hydrogenation to extend shelf life. Any lard you see that is not refrigerated is partially hydrogenated. Because hydrogenation straightens out the carbon chain, they have similar physical, although by no means biological, characteristics to natural animal fats. These are true Frankenfoods and should be avoided at all costs if you want to avoid a heart attack or stroke.
Your cells will reflect the type of fat you eat. Lipid peroxidation is the degradation of fats by oxidants leading to their damage and is not something you want happening to fats that are incorporated into your cellular structures. Of the fats mentioned, saturated fats are the least susceptible to this process.
Polyunsaturated oils, however, both omega 6 and omega 3, are particularly prone to lipid peroxidation by virtue of their missing hydrogen atoms. Omega 6 fatty acids are also inflammatory in excess.
While extremely delicate, omega 3 oils reduce inflammatory responses and are good for you as long as inflammatory stress in the liver is not an issue. Omega 3s subjected to oxidation can be very damaging.
How do we know this? Because the fastest way to cause alcohol-induced liver injury in an animal model is to feed them fish oil along with their Hooch. If you are prone to binge drinking, I really do not recommend that you wash down your fish or fish-oil capsules with loads of alcohol.
The history:
https://en.wikipedia.org/wiki/Cottonseed_oil#Economic_HistoryThe by-product of cotton processing, cottonseed was considered virtually worthless before the late 19th century. While cotton production expanded throughout the 17th, 18th, and mid 19th centuries, a largely worthless stock of cottonseed grew. Although some of the seed was used for planting, fertilizer, and animal feed, the majority was left to rot or was illegally dumped into rivers.
In the 1820s and 1830s Europe experienced fats and oils shortages due to rapid population expansion during the Industrial Revolution and the English blockade during the Napoleonic Wars. The increased demand for fats and oils, coupled with a decreasing supply caused prices to rise sharply. Consequently, many Europeans could not afford to buy the fats and oils they had used for cooking and for lighting. Many United States entrepreneurs tried to take advantage of the increasing European demand for oils and America’s increasingly large supply of cottonseed by crushing the seed for oil. But separating the seed hull from the seed meat proved difficult and most of these ventures failed within a few years. This problem was resolved in 1857, when William Fee invented a huller, which effectively separated the tough hulls from the meats of cottonseed. With this new invention, cottonseed oil began to be used for illumination purposes in lamps to supplement increasingly expensive whale oil and lard. But by 1859, this use came to end as the petroleum industry emerged.
Cottonseed oil then began to be used illegally to fortify animal fats and lards. Initially, meat packers secretly added cottonseed oil to the pure fats, but this practice was uncovered in 1884. Armour and Company, an American meatpacking and food processing company, sought to corner the lard market and realized that it had purchased more lard than the existing hog population could have produced. A congressional investigation followed, and legislation was passed that required products fortified with cottonseed oil to be labeled as ‘‘lard compound.” Similarly, cottonseed oil was often blended with olive oil. Once the practice was exposed, many countries put import tariffs on American olive oil and Italy banned the product completely in 1883. Both of these regulatory schemes depressed cottonseed oil sales and exports, once again creating an oversupply of cottonseed oil, which decreased its value.
It was cottonseeds depressed value that lead a newly formed Procter & Gamble to utilize its oil. The Panic of 1837 caused the two brothers-in-law to merge their candlestick and soap manufacturing businesses in an effort to minimize costs and weather the bear market. Looking for a replacement for expensive animal fats in production, the brothers finally settled on cottonseed oil. Procter & Gamble cornered the cottonseed oil market to circumvent the meat packer's monopoly on the price. But as electricity emerged, the demand for candles decreased. Procter and Gamble then found an edible use for cottonseed oil. Through patented technology, the brothers were able to hydrogenate cottonseed oil and develop a substance that closely resembled lard. In 1911, Procter & Gamble launched an aggressive marketing campaign to publicize its new product, Crisco, a vegetable shortening that could be used in place of lard. Crisco placed ads in major newspapers advertising that the product was "easier on digestion...a healthier alternative to cooking with animal fats. . . and more economical than butter.” The company also gave away free cookbooks, with every recipe calling for Crisco. By the 1920s the company developed cookbooks for specific ethnicities in their native tongues. Additionally, Crisco starting airing radio cooking programs. Similarly, in 1899 David Wesson, a food chemist, developed deodorized cottonseed oil, Wesson cooking oil. Wesson Oil also was marketed heavily and became quite popular too.
Terry Whals protocol is wrong on eating seeds and slightly wrong to emphasize Omega-3 too much, rather should emphasize minimizing Omega-6 and not overdoing protein intake:
http://paleozonenutrition.com/2012/02/08/a-new-experiment-dr-wahls-super-nutrient-paleo-diet-9-cups-veggies-a-day/Part of the nerve cell that is damaged in people with MS is the myelin sheath, a fatty electrically insulating layer along the axon. Myelin is about 70% fatty acids and Omega 3 is a major building block.
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Omega 3 rich foods, ... wild fish and seafood. And you could add fish oil.
Here is why:
http://gutcritters.com/intestinal-alkaline-phosphatase-gut-health/Intestinal alkaline phosphatase (IAP) is a brush-border enzyme expressed by absorptive cells (enterocytes) of the small intestine. It is secreted into both the lumen, or interior, of the digestive tract as well as the basolateral or systemic end.
Unlike gut flora, highest concentrations of IAP are found in the first section of the small intestine (duodenum) and decline the further down the digestive tract you go.
IAP secretion, just like any other small intestinal enzyme, is dependent on the health of enterocytes comprising what is known as the brush border. Intestinal cells that are chronically inflamed are by definition unhealthy, which is a major reason why those battling small intestinal dysbiosis are often deficient in these enzymes.
As you know, inflammation can be due to a number of factors: gluten, acetaldehyde, unsaturated fatty acids, enzyme inhibitors, gut infections, drugs, yeast overgrowth, thin to non-existent mucus layer, viruses, etc.. Whatever the cause, inflammatory cytokines will affect not only the shape of these cells and the tight junction proteins that bind them together, but their ability to properly secrete enzymes.
IAP has some very important functions. First, it’s involved in regulating secretion of bicarbonate in the duodenum.
Bicarbonate helps to neutralize the very acidic semi-digested food (chyme) entering the small intestine after passing through the stomach. Failure to raise pH here can lead to acidified chyme injuring cells lining this part of the digestive tract. That can increase inflammation and intestinal permeability.
But IAP’s most important role is detoxifying lipopolysaccharides (LPSs) derived from the cell wall components of gram-negative gut bacteria. (1) It is therefore an important defense against endotoxemia.
LPSs initiate inflammatory immune responses by binding to proteins known as toll-like receptors (TLRs), and in particular toll-like receptor 4 (TLR4). This in turn induces two separate inflammatory pathways.
The first is nuclear factor kappa B (NF-kB). NF-kB is a protein that regulates inflammatory immune responses, and chronic activation of this pathway has been linked to cancer and autoimmune disorders.
The second pathway initiated by TLR4 activation is release of tumor necrosis factor alpha (TNF-α). As you recall from this post, TNF-α is a very powerful and potentially destructive inflammatory cytokine.
The binding of TLR4 is a necessary condition for immune responses to gram-negative gut bacteria when they come into direct contact with intestinal epithelial cells and the submucosa. This inflammatory cascade is always accompanied by an increase in cortisol generation and synthesis via activation of the hypothalamic-pituitary-adrenal (HPA) axis, and by increasing intracellular expression of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) via the cortisol-cortisone shunt.
Now this immune complex causes the release of IAP as a defensive mechanism. IAP’s ability to detoxify LPSs prevents further immune stimulation. IAP also prevents NF-kB from migrating to the nucleus of enterocytes. So by both detoxifying LPSs and halting NF-kB, IAP serves as a vital anti-inflammatory intestinal enzyme.
Conversely, cytokines like TNF-α and interleukin 1 beta (IL1-β) depress the secretion of IAP from enterocytes. Why this is so no one really knows. However, as mentioned above, oxidative stress no doubt has something to do with it. Very little is more stressful to gut cells than being subjected to the chronic onslaught of inflammatory cytokines.
Therefore as a general rule it’s safe to say that anything that chronically inhibits IAP intestinal expression will increase the risk of LPSs initiating inflammatory immune responses at the gut wall that can result in a leaky gut. In very severe cases sepsis can result should these bacterial components reach systemic circulation in appreciable amounts. At the very least, LPSs reaching the liver will provoke inflammation capable of damaging cells in that organ.
Dietary Fats and Intestinal Alkaline Phosphatase Expression
IAP expression is partly influenced by the type of fatty acids present in the small intestine after a meal. As I covered in this post, unlike short- and medium-chain fatty acids, long-chain fatty acids do not go directly to the liver absent a leaky gut:
“Longer-chain fatty acids…re-form into triacylglycerols within the enterocyte. Together with phospholipids, cholesterol and proteins, they form large particles within the absorptive cell. If there are lipopolysaccharides in the vicinity, these too hitch a ride on the newly formed lipoprotein vehicle or chylomicron.
As I wrote then, chylomicrons and all members of the cholesterol family bind to and inactivate LPSs with varying degrees of efficiency, which is a good thing as Homo Sapiens have been eating long-chain fatty acids for approximately 195,000 years, with most of these lipids coming from animal sources.
However, cholesterol isn’t the only biological substance that defends us against endotoxins. In animal models, IAP secretion has been consistently shown to rise in the presence of saturated fatty acids.
If as a normal consequence of absorbing these fats, LPSs come into direct contact with brush border cells, it’s not at all surprising that this enzyme would be excreted as part of an innate immune defense against these potential troublemakers.
But while saturated fatty acids increase the secretion of this anti-inflammatory enzyme, polyunsaturated fatty acids (PUFAs)–both from omega 6 and omega 3 sources–have been shown in both pigs and rodents to either not provoke IAP release, or actively suppress it.
This is a decidedly undesirable state of affairs.
LPSs carried across the gut wall by long-chain PUFAs are also inactivated once incorporated into chylomicrons. However, the failure to increase IAP secretion when LPSs either reach enterocytes, or slip between them when tight-junction proteins are compromised, inevitably causes immune activation. Couple this with the propensity of these fatty acids to easily oxidize and generate lipid peroxidation byproducts, and the risk of inducing leaky gut and endotoxemia goes through the proverbial roof.
Is it any wonder then that rodents chronically fed alcohol while simultaneously fed PUFAs experienced the liver damage I showed you in this post, while saturated fats were protective under the same chronic alcohol feeding?
In pigs fed either corn oil or beef tallow for four weeks, corn oil feeding consistently decreased a number of brush-border intestinal enzymes (4)
Foods high in Omega 6 to avoid like the plague:
http://www.healthaliciousness.com/articles/high-omega-6-foods.phphttp://authoritynutrition.com/optimize-omega-6-omega-3-ratio/http://www.nutritionj.com/content/9/1/10Omega-3 (n-3) and omega-6 (n-6) fatty acids are two separate distinct families...Table 2 shows significant differences in n-6:n-3 ratios between grass-fed and grain-fed beef, with and overall average of 1.53 and 7.65 for grass-fed and grain-fed, respectively
http://gutcritters.com/part-four-dietary-fat-leaky-gut-endotoxemia-and-heart-disease/In this post, I discussed how unlikely it is that normal digestion of long-chain fatty acids–whether saturated, monounsaturated or polyunsaturated—is the source of the pathogens initiating arterial plaque formation. If anything, I showed how protective chylomicrons are in preventing just that. This then leaves us with increased intestinal permeability as the most likely source of translocating pathogens.
While today’s post will focus on the role of dietary fat in “leaky gut”, I once again need to emphasize that once you have intestinal dysbiosis, ANY food you eat will increase the translocation of bacteria, yeast, larger food molecules, etc. into the bloodstream leading to the liver and to a smaller extent, systemic circulation. The more often you eat, the more frequently this happens.
Since small-gut dysbiosis increases hunger and cravings by its negative effects on gut hormone secretion and nutrient absorption, reigning in overeating can be challenging until dysbiosis is tamed via dietary change and resolution of bacterial and yeast overgrowth.
Increased intestinal permeability will allow long-chain fatty acids, that would normally only be incorporated into chylomicrons, access to the blood flowing to the liver also carrying with them antigens and bacteria that will provoke an immune response. As more fat is now reaching the liver, more cholesterol will be synthesized to export it. As I said, changes in cholesterol levels are a marker of endotoxemia, not the cause of it. I’ll have more to say about this in an upcoming post.
OK, let’s look more closely at the anatomy of the small intestinal gut wall:
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We know that gluten opens these junctions. (2) Plant lectins are also disruptive. (3) Alcohol, especially binge drinking, also compromises intestinal integrity. (4) Small intestinal dysbiosis, and the inflammation that results from such an overgrowth, directly impacts these protein structures for the worse.
All oxidation from gut inflammation has the potential to affect these proteins. Oxidation is a normal process of cells that use oxygen to produce energy from various substrates, including those cells lining the intestinal tract. This process is called oxidative phosphorylation, and it would take an entire book to cover. Should you be interested, this Wikipedia entry is a good place to start. As this article makes clear, the gram-negative pathogen, E. coli, is quite adept at growing in an oxidative environment.
Most oxidation within cells will be harmlessly converted to water but not all. Two very harmful intermediate substances normally produced are superoxide anion and peroxide known collectively as reactive oxygen species or ROS. These are highly unstable agents. They have the potential to damage DNA, proteins, fats and intestinal cells, including those producing protective mucus. There are a number of built-in defenses that cells use to guard themselves against these harmful substances but suffice it to say that these defenses can be overwhelmed in times of intense free radical production as part of an immune response.
Anything that increases oxidation in the intestinal tract will also disrupt beneficial bacterial populations. Especially vulnerable are Lactobacillus species that predominate in the small intestine. These bacteria do not handle oxidation well, certainly not as well as gram-negative pathogens like E. coli. Bifidobacteria species in the colon are also negatively affected.
One substance that can be extremely oxidizing is fructose. Fructose forms half of the sugar molecule and can comprise anywhere from 42% to 90% of high-fructose corn syrup. We are well adapted to handling moderate amounts of it in its natural form where it comes packaged with fiber, antioxidants, vitamins and phytochemicals. Strip it of these protective substances during refining and we become far more prone to its ill effects. In large quantities, fructose produces lots of free radicals in those intestinal cells that are able to metabolize it because of its ability to rapidly degrade ATP to uric acid. (5)
Fructose, gluten, lectins and alcohol are not the only dietary components that increase oxidative stress in intestinal cells. Some fats do too.
You’ve all heard of saturated, monounsaturated, and polyunsaturated fats. The difference between these fats comes down to whether the carbon atoms that compose them contain double bonds.
Saturated: These fats do not have any double bonds between carbon atoms, and are saturated with hydrogen atoms. Saturated fats are very stable and not prone to oxidation when subjected to heat or free radicals in the body. For this reason, they are ideal for high-temperature cooking. Because they are straight in form, saturated-fatty-acid chains pack together readily and are solid or semisolid at room temperature. Saturated fats are found in animal fats and in tropical oils like palm and coconut oil.
Monounsaturated: These fats have one double bond which means two carbon atoms in the chain are double-bonded to each other. For this reason, they lack two hydrogen atoms. At the double-bond, these fats form a kink, so they don’t pack as easily as saturated fats. They are therefore liquid at room temperature although will congeal somewhat when refrigerated. While stable, these oils are more prone to oxidation than saturated fats. Oleic acid is a common form of monounsaturated fat found in our food and is the main component of olive oil. Almond, pecan, cashews, peanuts and avocados are also rich in oleic acid as is lard. Lard is 44% oleic acid, 42% saturated fat and 10% polyunsaturated fat. As fats are typically classified by the predominant fatty acid contained in them, lard should be classified as a monounsaturated fat, not a saturated one.
Polyunsaturated: These types of fats have two or more double bonds and therefore lack four or more hydrogen atoms. Like monounsaturated fats, these double bonds are kinked so they don’t pack together well making them liquid even when refrigerated. Polyunsaturates can be further classified by the position of their first double bond in relation to their omega end. Polyunsaturated fats are called omega-6 fatty acids when their first double bond is in the sixth position from this position. Vegetable oils are very high in omega 6s.
Polyunsaturates with their first double bond from the third position of the omega end are called omega-3 fatty acids. Fish and flaxseed oils are both omega-3 oils yet differentiated by the length of carbon atoms they contain and their unsaturation.
These types of oils are extremely delicate and prone to oxidation when subjected to heat, light, pressure and free radicals in the body. They should never be used for high temperature cooking. Unfortunately, that is exactly what many vegetable oils are used for. They are routinely utilized in fast-food chains, restaurants and are common in processed foods.
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Any fat in the presence of gut wall dysfunction, along with protein and carbohydrate, will cause translocation of gut pathogens. The majority of these pathogens will end up in the liver creating oxidative damage and disease. A small portion will bypass the liver entirely and directly enter the bloodstream. In more advanced cases of “leaky gut” and subsequent hepatic damage, these pathogens will also escape the liver and enter systemic circulation. Cholesterol will try to neutralize these substances and repair the damage they cause in arteries, but along with other responding immune cells, form atheromas and fibrous caps. If unstable, these complexes can rupture producing a heart attack or stroke.
In populations where gut dysbiosis and endotoxemia are rampant, encouraging people to substitute highly reactive and inflammatory omega 6 polyunsaturated fats for saturated fat is nothing short of dietary madness and a denial of the basics of fatty acid structure and biochemistry.
The cause of heart disease is metabolic endotoxemia. Binge drinking, excess consumption of sugar, trans fats, overeating, omega 6 oils, tooth decay, respiratory infections, gluten, stress, aging, poor anti-oxidant status, cigarette smoking, etc. are all risk factors for cardiovascular disease because they can all negatively impact gut wall integrity and beneficial bacterial populations. Correcting dysbiosis through changes in diet and resolving bacterial and yeast infections while replenishing and maintaining beneficial gut flora populations is the only hope you have for preventing this potentially deadly disease.
http://gutcritters.com/small-intestinal-bacterial-overgrowth-part-seven-the-role-of-plant-lectins/there are two families of lectins that have toxic effects in humans if they appear in our food.
Lectins found in legumes (beans and peanuts) and gluten grains are the most problematical. Whole-gluten grains like whole-wheat is a particularly rich source of a lectin called wheat-germ agglutinin or WGA for short. WGA is found in highest concentration in the germ of the plant. This makes the most evolutionary sense as the seed of the plant contains the genetic material necessary to propagate the species.
Lectins have shown very active biological properties when studied in animals and humans and entire books have been written on the subject. It is not my intention to summarize all these findings here. Rather, I want to concentrate on those factors that are directly relevant to acquiring small intestinal bacterial overgrowth.
But first, let me clear something up. Recently, there has been talk in the “Paleo Diet” and health blogosphere that concerns about lectin toxicity in the diet are overblown and should not unduly worry anyone because cooking inactivates them.
Yes, wet-heat cooking does indeed inactivate these pesticides. Subjecting beans to prolonged, high-heat cooking renders them a harmless and nutritious, albeit fiber-rich and gassy, source of food. And subjecting wheat-based foods to wet heat as in boiling pasta or noodles also inactivates WGA. So far so good.
However, dry-heat cooking methods as exists in baking or breakfast cereal manufacturing does not seem to inactivate them.
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I need to make one other clarification before proceeding. The findings I refer to were conducted in animals using raw bean or wheat lectin which are pretty much interchangeable as they attach to the same gut structures and intestinal flora.
This obviously doesn’t mimic how humans consume these foods in real life. No one is eating uncooked legumes (except for peanuts) or gnawing on a stalk of wheat. If they are they have bigger problems to contend with.
But that doesn’t mean that these research findings are irrelevant. Far from it. While human exposure to these natural pesticides is at far lower concentrations than what was used in animal studies (or at least I hope so), the impact on gut health from low-grade, chronic exposure would be expected to be the same although not manifest as quickly.
In a culture where wheat is the “king” of grains and consumption of processed-wheat products is pervasive, exposure to lectins begins at a very early age and extends for a lifetime in most. Meal after meal, day after day, year after year and the damage begins to pile up.
Lectins, inflammatory gluten peptides, gluten opioids, adenosine and increased zonulin production really make this noxious grain and its siblings a true biohazard of the first order for the gut. Throw in other gut-destroying practices like repeated courses of antibiotics, drugs (both licit and illicit) and alcohol and the negative impact skyrockets.
Lectin’s known effects on gastrointestinal function
Lectins are extremely efficient at attaching themselves to the mucosa of the small intestine. The interior lining of our small intestine is called the sugar coat for a reason. Here, cells and bacteria present a surface coating that consists of sugar molecules attached to either protein (glycoprotein) or fat (glycolipid) creating a kind of “slime” that serves both a protective and attachment function.
In lectin-fed rodents, lectins bind to and strip away the mucous coat exposing the underlying cells to the contents of the lumen. They also inhibit repair by blocking mucus secreting cells from producing this important protective lubricant.
Rodents fed lectins are incapable of properly utilizing the protein content of their diets. If sufficient quantities of lectins are present in their food, the rate of protein breakdown and loss from their body exceeds the amount of protein taken in.
Lectins bind to the epithelial cells of the small intestine resulting in disfigurement and damage to the digestive brush border.
Lectins cause rapid cell division, growth and turnover in the cells lining the small intestine. Because of this, these cells are too immature to properly digest food or maintain proper intestinal barrier function.
In rodents, lectins consistently increase the size of the pancreas.
Lectins bind to and interfere with cells responsible for the production of various gut-satiety hormones. Satiety hormones tell your brain, gee, I’m really full and can’t eat another bite. When they aren’t produced or produced in lower amounts than normal, hunger is a constant companion. I’ll explore this topic in a future series on gut health and weight regulation.
Lectins bind to and interfere with the gut-associated lymphoid tissue or GALT system. This is the gut’s immune system that protects against infections from pathogens.
Finally, lectins have been shown to directly disturb gut flora populations in animals.
I want to put forward the hypothesis that lectins are uniquely toxic to our beneficial gut flora. As disturbed gut flora seems to be a necessary condition for the initiation of infection in the small intestine, this is not a minor issue.
This theory revolves around the fact that lectins, like WGA, have a high affinity for gram-positive bacteria. Beneficial Lactobacillus and Bifodobacterium species are of this type.
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Bean lectins like phytohaemagglutinin or PHA which is found in red kidney beans and wheat germ agglutinin found in gluten grains are specifically designed to attach to cellular structures that express N-acetyglucosamine. If this name sounds familiar, it’s because the word glucosamine is part of it. Glucosamine is what a lot of you take to treat your aching joints.
Because peptidoglycan has two sugar components with one of them being N-acetyglucosamine, these lectins attach to it rather readily. Because the peptidoglycan area of gram-positive bacteria is large and exposed, it can be said that these types of lectins have a high affinity for them.
Conversely, because the peptidoglycan membrane in gram-negative bacteria is thinner and protected behind an outer lipopolysaccharide layer, these lectins do not bind to them or disturb them in any way.
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The bad news is that these lectins are also harmful to beneficial gut flora.
Because gram-negative bacteria are not affected by these lectins, they are more likely to proliferate when beneficial gram-positive gut flora populations are reduced or absent.
In the book Plant Lectins we learn:
“Food and some of its components, particularly the lectins, may directly interact with the bacterial flora or, alternatively, they may indirectly affect bacterial proliferation in the small intestine through interference with the binding of selected species to epithelial tissues. Whichever of these two mechanisms operates, the end result is the potential inducement of selective proliferation of some species of bacteria in the digestive tract, including the small intestine.”
And in animals fed red kidney bean lectin:
“…concurrent with increased toxicity, there is a dramatic overgrowth of Escherichia coli in the small intestine of conventional rats fed on PHA-containing diets…Similar studies with other animal species have fully confirmed the existence of this causative relationship between the presence of PHA in the diet, E. coli overgrowth and toxicity. Although the mechanism of the selective overgrowth and how this affects nutritional efficiency is not clear, one possible mechanism is that the lectin-induced virulence of coliforms [gram-negative pathogens] in the small intestine of kidney bean-fed rats is the result of the elimination of competing species.”
I reiterate again that this is only a hypothesis and has yet to be proven true in humans because no one that I’m aware of has subjected this to clinical investigation.
If beans are a large part of your diet, make sure they are cooked at high temperatures for a sufficient length of time. Many people have been made ill eating undercooked red kidney beans. Don’t be one of them.
I don’t eat beans in restaurants or out of a can because I have no way of knowing how thoroughly they were cooked. The only beans I eat are those I cook myself, and I would recommend you do the same.
Avoid peanuts as they are high in lectins and dry roasting them does not inactivate these toxins.
As for wheat germ agglutinin, make sure your gluten-food product is subjected to wet-heat cooking. Ready-made processed gluten foods are best avoided. Hell, I think gluten grains are best avoided which is why I don’t eat them whether sprouted or fermented.
It is possible that sourdough fermentation may neutralize WGA but I haven’t read anything in the literature to that effect. If anyone out there has info on this, please share.
To counter the negative effects of lectins in the diet, consider supplementing with prebiotics and probiotics found in food or supplements.
Also consider taking a glucosamine pill with every meal containing beans or gluten grains. This will act as a decoy and bind lectins before they can do any damage to your mucosa, digestive cells, and friendly gut flora.
Edit: I think drastically increasing my cayenne pepper consumption is also a significant factor in being able to correct my gut dysbiosys:
http://www.globalhealingcenter.com/natural-health/benefits-of-cayenne-pepper/
