The Genetically Modified Food Connection with Invisible Illness

IIllnesTHE CONNECTION BETWEEN GENETICALLY MODIFIED FOODS AND FOODBORNE ILLNESS

What are Foodborne Diseases?

Organisms or harmful chemicals in the food we eat and drink cause Foodborne illnesses. Most of these illnesses are caused when certain bacteria, viruses or parasites contaminate food. Others occur when harmful chemicals or toxins contaminate food. Many of these toxic chemicals are naturally occurring. Indeed, researchers speculate that many apparent causes of bacterial food poisoning may actually be lectin poisoning. Nevertheless, occasional outbreaks of food poisoning due to the lectins of uncooked or part-cooked beans are reported. The average American consumes around 200 mg of lectin per year from tomatoes alone, and many other salad ingredients are rich in lectins.

Plant defense against Plant Eaters (Insects, Herbivores and Omnivores)

Plants invest energy into the production of seed. Plants have evolved to encourage consumption of the fruit or vegetable for seed dispersal but also evolved mechanisms to decrease consumption of fruits when unripe or vegetables when ripe and from non-seed dispersing enemies. Plants use several strategies to defend against damage caused by plant eaters. Many plants produce toxic chemicals that influence the behavior, growth, or survival of plant eating enemies. These chemical defenses can act as repellents or toxins to plant eaters, or reduce plant digestibility. While most plant defenses are directed against insects, other defenses have evolved that are aimed at vertebrate herbivores (birds and mammals) and omnivores (humans). These natural plant defenses become our edible enemies.

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Plant regulation of Fruit Consumption

Plants invest energy into the production of fruits. Plants have evolved to encourage fruit eaters to consume their fruit for seed dispersal but also evolved mechanisms to decrease consumption of fruits when unripe and from non-seed dispersing predators. Plants have physical and chemical adaptations.

Physical deterrents:

  • Cryptic coloration (e.g. green fruits blend in with the plant leaves)
  • Unpalatable textures (e.g. thick skins made of anti-nutritive substances)
  • Resins and saps (e.g. prevent animals from swallowing)
  • Repellent substances, hard outer coats, spines, thorns.

Chemical deterrents:

When immature, the seed, grain, vegetable or fruit are protected by chemical deterrents such as lectins to keep themselves from being eaten to extinction. Chemical deterrents in plants are called secondary metabolites, i.e. trypsin inhibitor, chymotrypsin inhibitor, α-amylase inhibitor, phytohemagluttinin (lectin), phytic acid, oxalic acid, nitrate and nitrite, L-mimosine, canavanine, L-DOPA, glucosinolates, cyanogenic glucosides/cyanogens, tannins, gossypol, chlorogenic acid, saponins, phorbol esters and alkaloids.

The production of lectins and alkaloids are a defense mechanism to protect them from consumption before the seeds are ready for dispersal. The majority of lectins are of plant origins that are specifically found in plant seeds.  It is thought that lectins concentrated in seeds may be toxic to animals that ingest seeds, and hence, serve as a deterrent to ingestion.  After being eaten lectins are known to cause immune stimulation, inflammation and uncontrolled cell growth.

Secondary metabolites are compounds produced by the plant that are not essential for the primary processes such as growth and reproduction. These toxins might have evolved to prevent consumption by animals that disperse seeds into unsuitable habitats, to prevent too many fruits from being eaten per feeding bout by preventing too many seeds being deposited in one site, or to prevent digestion of the seeds in the gut of the animal.

Traditional herbal remedies are a result of understanding the affects of secondary metabolites, i.e. resveratrol, antioxidants, cannabis. Many currently available pharmaceuticals are derived from the secondary metabolites plants use to protect themselves, including opium, aspirin, cocaine, and atropine. These chemicals have evolved to affect the biochemistry of insects in very specific ways. However, many of these biochemical pathways are active in vertebrates, including humans, and the chemicals act on human biochemistry in ways similar to that of insects.

Plants evolved dangerous anti-nutrients to attack the digestive systems of the animals that fed on them.  These anti-nutrients are essentially low-grade toxins – not powerful enough to kill instantly, they are more of a passive-aggressive defense. Lectins when consumed at low levels are slightly irritating, but when eaten in moderate quantities become more damaging.

The Genetically Modified Foods Connection

Researchers have been experimenting with inserting the gene for certain lectins normally found in one species of plant into other species as way of increasing their resistance to pests or disease. Splicing lectins from one plant or animal to another genetically modifies food plants. Lectins are chosen for their naturally toxic characteristics. This is how pest resistance is transferred, by splicing a lectin from a pest-resistant species into one that is not. Lectins are transferred to a food plant that’s normally healthy for you. This adds additional lectins to the number of naturally occurring lectins in the food plant. This contributes to the bad effects Genetically Modified Foods (GMO) have with human consumption. Obviously, the risk of eating plants with unknown numbers of lectins is significant.

Editorials discussing GMO foods are frequently published in reputable journals while papers about the safety of GMO foods are surprisingly very rare. If information on the toxicity of GMO foods have been obtained, these have not been reported in scientific journals and subjected to the scientific judgment. Because of the importance of inherent plant toxins and anti-nutrients on nutritional safety, consistent lists of genetically modified organisms (GMO) and clear criteria for mandatory declarations are necessary.

What Do Lectins Do To The Body?

When the contents of the gut cross the gut barrier, they stimulate the production of antibodies or inflammatory cytokines. Protection is supplied by a number of mechanisms making up the intestinal barrier variables including: mucosa, intestinal secretions, primarily mucus and secretory immunoglobulin (IgA), and lymphocytes in the gut lining.

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Under normal circumstances in a healthy person, the intestinal immune system mounts rapid and potent immune responses to prevent invasion by pathogenic viruses and bacteria.

Healthy, functionally intact intestinal epithelial mucosa cells normally do not allow passage of more than small amounts, approximately 2% of intact dietary proteins. However, translocation of viable bacteria from the gastrointestinal tract to extra-intestinal sites, i.e. mesenteric lymph nodes, liver, spleen, kidney and blood has been shown to occur under three circumstances: disruption of ecological equilibrium which allows intestinal bacterial overgrowth, deficiencies in host immune defenses, and increased permeability of the intestinal barrier.

Poorly digested dietary protein have been shown to enter circulation in the blood, particularly when intestinal permeability is increased by disease, non-steroidal anti-inflammatory drugs, ethanol, acetic acid and dietary lectins derived from legumes and cereal grains.

Under normal circumstances, when the concentration of intact dietary proteins in the gut contents is low, absorbed proteins generally elicit a minimal allergic response because of the limiting influence of T-suppressor cells. Because of their resistance to digestive breakdown, the concentration of dietary lectins can be quite high, consequently their transport through the gut wall can exceed that of other dietary antigens by several orders of magnitude, and absorbed dietary lectins will stimulate a response from the immune system.

Lectins binding with the gastrointestinal lining, particularly the villi, of the small intestine causing intestinal damage with impaired cellular repair potential and cellular death. Since this compromises the intestinal villi, the absorption of other nutrients such as minerals and protein is reduced. With the damaged gut lining, there is limited space for beneficial bacteria to attach. This reduces the good bacteria, which allows certain harmful bacterial strains like E. coli to run rampant. Because the body is now responding full time to the needs of the injured gut lining, proteins and other resources are redirected from other basic growth and repair processes.

Perhaps the most insidious affect lectins can leave in their wake is leaky gut. Leaky gut is a term used for the breach of multiple layers of the Barrier Variables of the intestinal lining produced by lectins hand in hand with physical triggers and other anti-nutrients. Once the intestinal breach exists, lectins and other particles (like partially digested food, toxins, etc.) can “leak” into the bloodstream and provoke an inflammatory cytokine response.

Normal repair of these cell surface disruptions allows the wounded cell to survive while failure results in necrotic cell death. Lectins inhibit membrane repair and are toxic to wounded cells. At least one form of muscular dystrophy is caused by a failure in the membrane repair mechanism.

Lectins interfere with membrane repair (mucus secretion) and potently block repair. Lectins are toxic when present in the GI tract based on two, interrelated effects. First, barrier variable failure occurs within the GI tract cells before now exposed to troublesome levels of mechanical stress (gas, bloating, constipation, diarrhea), leading to death of the cells of the gut lining. The second lectin-induced effect is a reduction of the protective mucus that is secreted by the GI tract cells. This a consequent increase in the incidence of irritation and inflammation as lectins adhere to the gut lining. Based on the damage they do to the lining of the GI tract, lectins and their hypertrophic effect have been implicated in celiac disease and cancer.

Knowledge of this interference may have implications beyond lectin food poisoning. Many suffer from an invisible illness. There is very little information on the effects lectins have on the body. Healthcare providers are taught the basics of the immune system and rarely look deeper. The use of the Neuroscience NEI Gold test opened my eyes and gave me a eureka moment in working with invisible illness.

Cytokine Induced Sickness Behavior AKA The Invisible Illness

After Cytokine Induced Sickness has started, dietary changes alone will not reverse this invisible illness. The immune status of each individual is critical to improvement and recovery.

During inflammation brought on by lectin exposure and other physical triggers, there is increased production of certain cytokines and chemokines (small messenger proteins) by white blood cells and other cell types. When cytokines and chemokines are released into the circulation, systemic symptoms such as fever, nausea, chills, low blood pressure, racing heart or palpitations, loss of feeling, headache, rash, scratchy throat, and trouble breathing can result. Pro-inflammatory cytokines acting in the brain cause sickness behaviors. This can affect neurological and hormone functions in a number of ways, including the litany of symptoms described above termed Cytokine Induced Sickness Behavior (CISB).

CISB individuals have little motivation to eat, are listless, complain of fatigue and malaise, loose interest in social activities and have significant changes in sleep patterns. They have an inability to experience pleasure, and may have exaggerated responses to pain and fail to concentrate.

Determining the Immune Status Is An Essential First Step.

CISB is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation.

Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, racing heart, digestive issues, hot flashes, sore throat with (neuro)inflammation and (neuro)degenerative processes following less well defined triggers.

Those suffering from CISB are complicated cases often diagnosed as depression or bi-polar. They must be treated low and slow to not provoke any pro-inflammatory immune or excitatory neurotransmitter response. Most all suffer from a neurotransmitter imbalance along with a cytokine imbalance. A Lectin Free Diet is an essential first step. Many with CISB find themselves having adverse reaction to supplements.

Measuring the Immune Status and Intestinal Permeability

Using the NEI Gold Stimulated Cytokine and Neurotransmitter testing, it became apparent that lectins were a problem with autoimmune patients. Most patients were eating a “healthy” diet of legumes, beans and raw vegetables. Most had tried to determine their immune status with the TH1/TH2 challenge with confusing results. They endured months of cleanses and detoxes without any significant improvement.

High levels of PHA (lectin) stimulation were a common finding in many of the NEI Gold reports. This was especially true for those with conditions that were responding poorly to treatment. A review of food allergy results saw many patients with lima and navy bean sensitivities. Who eats lima and navy beans in today’s diet (both of which happen to be major lectins)? As an experiment, staff members and several patients were asked to avoid lectins in their diet. As a result, all patients reported less gastrointestinal symptoms, improved GI function, moods, energy, etc.

It is now possible to develop clinical supplement protocols that are aimed at blocking cytokine production or action, reducing the production of second messengers or deactivating glial cells that produce excessive quantities of proinflammatory cytokines. If you are looking good but feeling rotten – suffering invisibly. We can help you.

How to Talk to Your Friends and Family About Your Invisible Illness. Read More

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