31st May 2007
by
Dr. George J Georgiou, Ph.D.,N.D.,D.Sc (A.M)
Natural Medicine Practitioner
Director, DaVinci Natural Health Centre, Larnaca, Cyprus
www.naturaltherapycenter.com
drgeorge@avacom.net
Tel: +357 24 82 33 22
CANDIDA ALBICANS : Are You Winning Battles But Losing the War?
WHAT IS IT?
Every person lives in a virtual sea of microorganisms, (bacteria, viruses, fungi, etc.). These microbes can reside in the throat, mouth, nose, intestinal tract, almost anywhere; they are as much a part of our bodies as the food we eat. Usually, these microorganisms do not cause illness, unless our resistance becomes lowered.
Candida albicans is a yeast that lives in the mouth, throat, intestines and genitourinary tract of most humans and is usually considered to be a normal part of the bowel flora (the organisms that coexist with us in our lower digestive tract). It is actually a member of a broader classification of organisms known as fungi.
Traditionally fungi are considered plants, but they contain no chlorophyll and cannot make their own food. Fungi tend to inhabit cool to tropical climates and are found in the air we breathe as well as in moist and shady soil, water, manure, dead leaves, fruit, leftover food, and in a wide variety of places and circumstances.
HOW DO YOU GET IT?
Candida albicans prefers people. Candida enters newborn infants during or shortly after birth. Usually, the growth of the yeast is kept in check by the infant's immune system and thus produces no overt symptoms. But, should the immune response weaken, the condition known as oral thrush can occur as a result. By six months of age, 90% of all babies test positive for Candida . And by adulthood, virtually all humans play host to Candida albicans and are thus engaged in a life-long relationship.
Candida coexists in our bodies with many species of bacteria in a competitive balance. Other bacteria act in part to keep Candida growth in check in our body ecology . . . unless that balance is upset. When health is present, the immune system keeps Candida proliferation under control; but when immune response is weakened, Candida growth can proceed unhindered. It is an "opportunistic organism," one which, when given the opportunity, will attempt to colonize all bodily tissues. The uncontrolled growth of Candida is known as Candida overgrowth or Candidiasis.
Unfortunately, there are many factors in our modern society that can upset the ecological balance of the body, weaken the immune system and thus allow the yeast to overgrow. Of these, the major risk factors which may predispose one to the proliferation of Candida are:
* STEROID HORMONES, IMMUNOSUPPRESSANT DRUGS such as cortisone which treat severe allergic problems by paralyzing the immune system's ability to react
* PREGNANCY, MULTIPLE PREGNANCIES or BIRTH CONTROL PILLS which upset the body's hormonal balance
* DIETS HIGH IN CARBOHYDRATE AND SUGAR INTAKE,
* YEAST AND YEAST PRODUCTS, AS WELL AS MOLDS AND FERMENTED FOODS
* PROLONGED EXPOSURE TO ENVIRONMENTAL MOLDS
* ANTIBIOTICS and SULFA DRUGS Probably the chief culprit of all, antibiotics kill all bacteria . They do not distinguish good bacteria from bad. Antibiotics kill the "good" flora which normally keeps the Candida under control. This allows for the unchecked growth of Candida in the intestinal tract. It is normally difficult to recover a yeast culture from bodily surfaces. However, after 48 hours of taking tetracycline, yeast can be cultured easily from anyone. The prevalence today of Candida may be most directly related to the widespread societal exposure to antibiotics - from prescriptions for colds, infections, acne, and from additional consumption of antibiotic-treated foods such as meats, dairy, poultry and eggs. Notably, antibiotics do not kill viruses; they only destroy bacteria. Yet, they are universally prescribed for all colds, flus and other viral problems. Such indiscriminate and extensive use of antibiotics is not only considered a primary cause of Candida overgrowth, but is recently being found to be responsible for the unbridaled development of "killer bacteria."
The rapid and direct proliferation of the yeast following antibiotic use strongly suggests that the problem of Candida is one which stems from an inner state of imbalance, rather than from an outside attack by a microbe or disease. This is a very important point to understand if one wishes to get rid of an overgrowth problem, suggesting that Candida is not so much a problem as is the body's own failure to control it!
A SERIOUS PROBLEM
Once begun, if not recognized and treated appropriately, Candida overgrowth can result in a self-perpetuating, negative cycle. Large numbers of yeast germs can weaken the immune system, which normally protects the body from harmful invaders. Even though Candida is part of the ecological balance in the body since birth, it is still recognized by the immune system as a foreign body that needs to be controlled. So, when overgrowth occurs, a chronic stimulation to the immune system results -- every second, every minute, every hour, every day, every month, every year -- in an attempt by the immune system to regain control. In time, it is believed that this can exhaust the immune system, predisposing one to more serious degenerative processes. Many believe chronic drains on the immune system such as Candida and parasites can play a direct role in the development of cancer and AIDS. Seen in this light, Candida overgrowth should not be taken lightly.
The immune system may concurrently be also adversely affected by poor nutrition, heavy exposure to molds in the air, as well as an increasing number of chemicals in our food, water and air, including petrochemicals, formaldehyde, perfumes, cleaning fluids, insecticides, tobacco and other indoor and outdoor pollutants. Over 10,000 chemicals have been added to our food supplies alone that were not there just 100 years ago! We do not have the genetic recognition of these substances as foods or as useful additions to our bodies.
Resulting lowered resistance may not only cause an overall sense of ill health, but also may allow for the development of respiratory, digestive and other systemic symptoms. One may also become predisposed to developing sensitivities to foods and chemicals in the environment. Such "allergies" may in turn cause the membranes of the nose, throat, ear, bladder and intestinal tract to swell and develop infection.
Such conditions may lead the physician to prescribe a "broad spectrum" antibiotic . . . which may then further promote the overgrowth of Candida and strengthen the existing negative chain of events, leading to further stress on the immune system and increased Candida-related problems.
WHAT ARE THE SIGNS OF CANDIDA INFECTION?
The result of heightened Candida overgrowth is a list of adverse symptoms of considerable length. Basically, the characteristics of Candida overgrowth fall under three categories, those affecting:
The gastrointestinal and genitourinary tracts
Allergic responses, and Mental/emotional manifestations.
Initially the signs will show near the sights of the original yeast colonies. Most often the first signs are seen in conditions such as nasal congestion and discharge, nasal itching, blisters in the mouth, sore or dry throat, abdominal pain, belching, bloating, heartburn, constipation, diarrhea, rectal burning or itching, vaginal discharge, vaginal itching or burning, increasingly worsening symptoms of PMS, prostatitis, impotence, frequent urination, burning on urination, bladder infections. But, if the immune system remains weak long enough, Candida can spread to all parts of the body causing an additional plethora of problems such as fatigue, drowsiness, uncoordination, lack of concentration, mood swings, dizziness, headaches, bad breath, coughing, wheezing, joint swelling, arthritis, failing vision, spots in front of the eyes, ear pain, deafness, burning or tearing eyes, muscle aches, depression, irritability, sweet cravings, increasing food and chemical sensitivities, numbness and tingling, cold hands and feet, asthma, hay fever, multiple allergies, hives and rashes, eczema, psoriasis, chronic fungal infections like athlete's foot, ringworm and fingernail/ toenail infections.
In addition, 79 different toxic products are known to be released by Candida , which in itself places a considerable burden on the immune system. These get into the bloodstream and travel to all parts of the body where they may give rise to a host of adverse symptoms.
In Candida overgrowth, the yeast colonies can dig deep into intestinal walls, damaging the bowel wall in their colonization.
Candida can also attack the immune system, causing suppressor cell disease, in which the immune system produces antibodies to everything at the slightest provocation, resulting in extreme sensitivities.
Finally, Candida overgrowth can be dangerous if not controlled. The persistent, constant challenge to the immune system by an ever-increasing, long-term overgrowth of Candida can eventually serve to wear down the immune system and cause a seriously weakened capacity for resistance to disease.
Women are more likely to get Candida overgrowth than are men. This is related to the female sex hormone progesterone which is elevated in the last half of the menstrual cycle. Progesterone increases the amount of glycogen (animal starch, easily converted to sugar) in the vaginal tissues which provide an ideal growth medium for Candida. Progesterone levels also elevate during pregnancy. Men are affected less frequently but are by no means invulnerable.
HOW DO YOU KNOW YOU'VE GOT IT?
Currently, diagnosis is primarily clinical. Since almost everyone has Candida in their bodies, tests for its presence are useless; confirmation of overgrowth is very difficult through laboratory tests. And, since what it does is to paralyze the immune system against it, allergy tests to determine the system's reaction to it are also ineffectual.
Furthermore, the results of the yeast imbalance -- the combined effects of different hormones, poisons generated and released by the yeast into the bloodstream, and the confusion created in the immune system -- produces such a wide variety of symptoms and which are seemingly so unrelated (such as wheezing, depression and fungus infection under fingernails) that a definite diagnosis cannot be made from any specific pattern of signs and symptoms.
Conclusive laboratory tests have not yet been developed, even though there are a number of tests that can help in the diagnosis. The patient’s history and symptoms are usually the key to arriving at a diagnosis, and Dr. Crook’s Candida Questionnaire is extremely helpful as it enables the patient to score their symptoms and arrive at a number – anything above 180 for women, and 140 for men is highly significant and represents the majority of symptoms that relate to this condition. There are other testing procedures that I use in clinical practice, mainly bio-dermal screening using the VEGA (see http://www.naturaltherapycenter.com/vega_allergy_testing ). When an ampule of Candida is placed in the honeycomb of the VEGA EXPERT and the probe placed on an acupoint of a finger, it is very clear when a patient “resists” as the conductivity drops. What I have also found time and time again in over 600 Candida patients that I have tested to date is that they all react to yeast, mushrooms, wine and beer as well when tested. In fact, many times I stumble upon Candida while conducting food intolerance testing using the VEGA, and when finding that mushrooms and yeast come out positive, I immediately test for Candida, which is also positive. I personally find the VEGA a very useful diagnostic device that can answer a lot of questions that more traditional laboratory testing cannot.
Another method of testing for Candida is to use a form of Kinesiological muscle testing called AUTONOMIC RESPONSE TESTING (see www.naturaltherapycenter.com/ART ). Autonomic Response Testing (ART) grew out of the importance of detecting and correct problems of the autonomic nervous system. ART allows the doctor to correct the problems of the ANS and to help restore the self regulating mechanism of the body allowing the patient to return to a state of health. ART is a system of evaluation and treatment developed by Dietrich Klinghardt, MD, Ph.D and Lousia Williams, DC, ND. Dr. Klinghardt is a German trained physician who also has a Ph.D in neurology. ART uses Applied Kinesiology, Electroacupuncture (EAV), O-Ring testing, Nogier pulse, Chinese pulse, heart rate variability and other techniques to assess the health or dysfunction of the autonomic nervous system.
Dr. Klinghardt believes that many practitioners using kinesiology or muscle testing in their practice are often getting inaccurate information because the autonomic nervous system is not functioning properly. In ART, this condition is called 'blocked regulation' and refers to the inability of the ANS to self-regulate and is caused by 7 common factors. These include: undiagnosed food allergies, heavy metal toxicity, petroleum chemical toxicity, chronic unresolved infections and scars, temporomandibular joint dysfunction (TMJ), unresolved psychological stress, and electromagnetic stress. Dr. Klinghardt has developed specific tests for these factors and treatments to correct them. ART is also a good way of detecting whether Candida is prevalent, and the effect that it is having on the Autonomic Nervous System and other organ systems of the body.
CASE HISTORIES
There is still a lot of controversy around the topic of Candida, and I am the first to agree that we do not have all the answers. One thing that I have witnessed in clinical practice, however, is the astounding recovery that many of these so-called Candidiasis patients make when placed on a Candida Treatment Protocol. These would include difficult cases that have been through the orthodox medical mill, seeing many different specialties without positive effects. One case that I remember is a 32 year old women who had such a bad case of halitosis that when I approached her to examine her throat I thought that I was surrounded by rotting corpses! Such was the degree of her bad breath that she had NEVER dated in her life for this reason. My mind never even thought of Candidiasis initially. As a staring point, I suggested that she undergo an alkaline detoxification fast with fresh fruit, salads, steamed vegetables, fresh vegetable juices and home-made vegetable soups. This she did for 15 days. During the last day of the fast she went out with her friends to celebrate her birthday, and drank a glass of wine. She phoned me the following morning complaining of a bad headache, muscle pains, bloating, and an irritation in her throat. This is when my thinking began to point towards Candida, as I thought that the yeast in the wine had probably aggravated the condition. I asked her to come in immediately – testing on the VEGA showed a positive reaction to Candida, mushrooms and yeast, and her score on the Crook’s Candida Questionnaire was 356, probably the highest score I have ever seen!
We began Candida treatment, and within 3 months her halitosis had completely cleared, and she had decided to get engaged to a local boy who she had a crush on. It really never ceases to amaze me how Candida can present itself – the symptoms can be strange and varied. Recurrent vaginal infections accompanied by chronic fatigue is often common in women. I have seen a number of cases of infertility with no underlying pathology that was resolved by Candida treatment. Skin problems with no specific diagnosis from dermatologists were Candida related, chronic sinusitis, scleroderma, rheumatoid arthritis, asthma, and many more.
Certainly I am not saying that the common yeast, Candida albicans, is the cause of all these problems. What my experience has shown, however, is that when Candida is one of the underlying causes of these health problems, they are not resolved unless the Candida is eradicated first.
Many physicians now believe that a clinical trial for Candida overgrowth is of so little risk and expense that it should be considered in any chronic illness.
One clinical trial a person may try is to avoid certain foods for five days which are known to facilitate the growth of yeast. Such foods include the following:
* SUGAR and SIMPLE CARBOHYDRATES such as found in all sweetened food including the use of honey, molasses, sorghum, maple syrup, sugar, fructose, maltose, dextrose, corn syrup, etc.
* YEAST PRODUCTS such as beer, wine, yeast leavened bread, natural B vitamins, brewer's yeast
* FERMENTED and MOLD FOODS such as mushrooms, cheese, vinegar, mustard, catsup, relish and other condiments made with vinegar.
After avoiding these foods for 5 days, try adding them back into the diet in large quantities. By observing how one feels while off these foods, in comparison to any adverse affects experienced when going back on the foods, one may get a clue as to any possible yeast involvement as a causative factor for any adverse symptoms.
If adverse symptoms are provoked by a return to the yeast enhancing foods, your physician may feel that there is at least a possible reason to suspect Candida overgrowth, which may then warrant more definitive action.
CANDIDA TREATMENT PROTOCOL
The Candida Treatment Protocol that I have used successfully for a number of years has five basic objectives:
1. First, starve the Candida by eliminating the foods mentioned above that feed it.
2. Second, to kill the Candida through the use of anti-Candida products mentioned below.
3. Repopulate the bowel flora with a high-potency probiotic such as Culturelle which contains 20 billion live bacteria.
4. Regulate the dysbiosis and convert the pathological, mycelial form of Candida back to the normal form by the use of Sanum remedies mentioned below.
5. Restore biochemical balance to the body and strength to the immune system, which will allow the body once again to regain and maintain control over Candida growth by optimizing the diet – this would involve avoiding food intolerances and following the Metabolic Type Diet by Wolcott combined with the Blood Group diet by Dr. Peter D’Adamo.
KILLING CANDIDA
I have found that it is literally impossible to treat Candida if one does not cut out ALL forms of sugar, and that includes fructose from fruit sources. The foods that should be strictly AVOIDED for a 3-month period include:
* SUGAR – and all foods that contain sugar. These include white and brown sugar, honey, syrups, liquors, lactose, fructose, all confectionary and sweet cakes, chocolates, ice-creams, home-made sweets and cakes, biscuits, fizzy beverages, all fruit drinks.
* YEAST – and all foods that contain yeast including breads, vinegar, ketchups, mayonnaise and pickles.
* FRESH AND DRIED FRUIT – all fruit whether fresh, cooked, tinned or dried. These should be avoided for the initial SIX WEEKS ONLY – your health practitioner will advise you when to begin eating fruit again. Obviously this includes fresh fruit juices (vegetable juices are OK), as well as marmalades.
MUSHROOMS – all types, including Chinese mushrooms such as Shitake.
* REFINED FOODS – all white flours, white rice, white pasta products, cornflour, custard and white cereal products, unless they are wholemeal or organic.
FERMENTED PRODUCTS – all alcoholic beverages, vinegar and all vinegar products such as ketchup, mayonnaise and pickles.
* NUTS – all types of nuts that are cleaned and packaged without their shells – these have a tendency to collect fungal spores and moulds from the atmosphere which will antagonize the Candida. Nuts that are fresh with their shells are OK.
Most other foods are allowed. Fruit is cut out of the diet for 6 weeks, and all the other foods mentioned above are disallowed for a period of 12 weeks. In the meantime, there are other nutritional supplements, herbs and homeopathics that are given, as follows (most of these remedies can be found at www.worldwidehealthcenter.net, and some are available from Cyprus):
1. KANDIDAPLEX – a Doctor-formulated compound that contains Berberine, undecylenic acid, biotin, sorbic acid, citrus seed extract and Pau D’Arco - 2 caps x 3 daily
2. KOLOREX – a New Zealand herbal product which contains two powerful anti-fungal agents that have been shown to kill Candida – Winterata colorata and the synergistist herb Aniseed which boosts effectiveness 6 fold – 1 cap of each once daily.
3. CAPRYLIC ACID – a derivative of coconut which stops the Candida reproducing - freely available in most health food stores and pharmacies – 1 tab x 3 daily
4. CANDIDA 30c - homeopathic – freely available in most pharmacies – two pillules or one cap x 3 daily for 2 weeks only. These are stopped just before beginning the Sanum remedies.
5. CULTURELLE - a powerful probiotic containing 20 billion live bacteria, in order to repopulate the ailing flora of the gut.
6. A good-quality multivitamin such as OPTIMUM 6, or VV PACK or similar.
All the above are continued for 3 months, with the exception of the Candida 30c. After two weeks of the anti-Candida diet, certain specialized isopathic remedies are introduced, known as Sanum remedies from Germany, after the work of the famous Prof. Enderlein, as follows:
1. Mucokehl – 1 cap twice weekly
2. Pefrakehl – 1 cap twice weekly
3. Notakehl – 1 cap twice weekly
4. Fortakehl - 1 cap twice weekly
5. Nigersan - 1 cap twice weekly
6. Albicansan – 1 cap every second day
These are continued for about 40 days. As soon as these are completed, fruit is re-introduced back into the diet – this is about 6-7 weeks after the beginning of treatment.
Prof. Enderlein’s Sanum remedies work by changing the harmful microorganisms in the body fluids to non-aggressive forms (pleomorphic changes), which permits gentle healing (isopathy). Harmful bacteria and toxins are broken down and excreted through natural processes. They also help to alleviate the dysbiosis and bring the internal mileau of the intestine back into balance.
HERXHEIMER REACTIONS
Depending on the severity of Candida overgrowth and the amount of the agents taken, the Candida can be killed off in vast numbers in a very short period of time. As they are killed, they release substances which are toxic to the body. If this process occurs more quickly than the toxins can be cleared from the bloodstream and eliminated by the body, a temporary toxic or allergic-type reaction can occur. The technical name for this experience is a Herxheimer reaction ; it is more commonly referred to as "die off."
Usually die off lasts only a few hours, though it can last several days. It can usually be controlled almost entirely by the amount of ingestion of the agent and the rate or frequency it is taken. Signs of Herxheimer reaction can be many and varied but generally involve such discomfort as aching, bloating, dizzines, nausea, and overall "goopy sick" feeling, or a worsening of original symptoms. Fortunately, die off is generally short in duration, and although uncomfortable, is at least a confirmation of the presence of Candida and that something "good" is happening.
Exercise as well as insuring proper, daily bowel evacuation has been reported as being helpful in countering the adversities of die off. Maintaining a high daily intake of pure water is also important to keep the channels of elimination open.
BALANCING BODY CHEMISTRY
It is a commonly recognized and accepted fact that immune system efficiency is highly dependent on the proper biochemical balance in the body . This of course, is dependent on proper and adequate nutrition to supply the body with all the required biochemical constituents (vitamins, minerals, enzymes, intrinsic factors, etc.).
Different people require different amounts and balances of nutrients for optimum health . The criteria for the determination of these differing nutritional requirements lies within the definition of one's metabolic type, i.e., the genetically determined metabolic and nutritional parameters that define each person's individuality on every level.
It is precisely because different people have different metabolic types, and therefore different needs for nutrition, that the allopathic, symptom-treatment approach in nutrition is baseless and so often ineffective. This further explains why what (nutritionally) helps make one person better, may have little or no effect on another, or even make a third person worse.
I have not tried to modify this protocol as I have found it to be so successful that I dare not juggle with it in case I lose the effectiveness. I’m sure that it can be improved upon, and would welcome comments from other practitioners working with Candida. It is only through sharing that we will grow and become better practitioners.
Tuesday, July 15, 2008
MONOSODIUM GLUTAMATE: POISON THE BODY TO BETTER THE TASTE
!
6th Oct 2007
INTRODUCTION
Monosodium Glutamate, a food ingredient, was invented in 1908 in Japan, by Kikunae Ikeda. A year later, with a partner, he formed a company, Ajinomoto, to produce the product. The food additive did not appear in the United States to any degree until the late 1940s, following the Second World War. During the war, it had been noted that Japanese soldiers' rations tasted better than the rations used by our soldiers. The difference was believed to be "monosodium glutamate." Today, "monosodium glutamate" or its reactive component, "processed free glutamic acid," is found in almost all of the processed foods that are manufactured in the United States.
ADVERSE EFFECTS OF MSG
In 1957, Lucas and Newhouse found that normal neonatal mice suffered acute degenerative lesions in the inner retina when "monosodium glutamate" was administered by feeding tube.1 In 1968, during a replication of this study at Washington University Medical School, St., Louis, Missouri, Dr. John W. Olney2 noted that, some of the mice had become grotesquely obese. He decided to sacrifice some of the mice to confirm his belief that lesions would be found in the hypothalamus region of the brain. Not only was his suspicion confirmed, but further testing indicated that there were also other neuroendocrine effects from the "monosodium glutamate." His findings were published in 1969.2 Dr. Olney, a National Academy of Science scientist who is credited for the voluntary removal of MSG from baby food in the 1970s, continues to publish research3-5 on the toxicity of glutamic acid, often using "monosodium glutamate."
In 1968, the New England Journal of Medicine published a Letter to the Editor in which Ho Man Kwok, MD, asked for help in determining why he and his friends suffered reactions shortly after eating in some Chinese restaurants, though he never experienced such reactions when he lived in China. The journal titled the letter "Chinese Restaurant Syndrome,"6 and researchers from around the country wrote the journal to suggest that Dr. Kwok and his friends' problem was intolerance to MSG. One letter indicated that 30% of the population reacted to MSG.
In 1969, concerned with the bad reports regarding "monosodium glutamate," the glutamate industry formed a nonprofit organization to defend the safety of MSG, the International Glutamate Technical Committee. Later, in 1977, they increased their efforts with the development of a nonprofit subsidiary, The Glutamate Association, primarily operating as a public relations arm of the glutamate industry. In about 1990, the glutamate industry turned to the International Food Information Council (IFIC), another nonprofit industry-funded organization, to be their spokesman and to promote the safety of MSG along with the other products that they represent.
MSG IS TOXIC TO HUMANS!
The literature is clear in demonstrating that MSG is toxic to humans and that over 25% of the population suffer adverse reactions from MSG7-36. In the opinion of this writer, the subject is only controversial because of the input of the three organizations mentioned above and because of research they have funded to discredit findings of others and to tell the story that the glutamate industry wants told, research that is flawed to the point of being worthless.
"Monosodium glutamate" is approximately 78% processed free glutamic acid and 22% sodium (salt) and moisture, with about 1% contaminants. It is the processed free glutamic acid that causes people to suffer adverse reactions, and, unfortunately, there are over 40 food ingredients other than "monosodium glutamate" that contain processed free glutamic acid in varying amounts.37 Consequently, consumers refer to all processed free glutamic acid as MSG, regardless of the name of the ingredient.
People differ in their tolerances to MSG, but typically always suffer similar reactions each time they ingest amounts of MSG that exceed their tolerances for the substance. Reactions experienced vary dramatically, as if MSG finds the weak link in the body.38 Typically, people will suffer reactions at approximately the same time each time they ingest amounts of MSG that exceed their tolerance levels. However, that time lapse can vary among people from immediately following ingestion of MSG up to 48 hours following ingestion. Use of alcohol or exercise prior to, during or following an MSG-containing meal will exacerbate an MSG reaction in many people. MSG-sensitive people will typically suffer similar reactions to aspartame.
Neuroscientists believe that the young and the elderly are most at risk from MSG. In the young, the blood-brain barrier is not fully developed, exposing the brain to increased levels of MSG that has entered the bloodstream. The elderly are at increased risk because the blood-brain barrier can be damaged by aging, by disease processes, or by injury, including hypertension, diabetes, hypoglycemia, and stroke. Throughout life, the blood-brain barrier is "leaky" at best.
MSG has now been implicated in a number of the neurodegenerative diseases, including ALS (Lou Gehrig's disease), Parkinson's disease, Alzheimer's disease, multiple sclerosis and Huntington's disease39.
In general, the natural glutamic acid found in food does not cause problems, but the synthetic free glutamic acid formed during industrial processing is a toxin. In addition, when MSG is formed using hydrochloric acid the final product includes carcinogens.40
MSG IN INFANT FORMULA: BAD FOR YOUR BABY!
A Canadian Study41 conducted, leaves no room for doubt that ingredients that contain processed free glutamic acid (MSG) and free aspartic acid — known neurotoxins— are used in baby formula. The fact that neurotoxins are present in baby formula is of particular concern since the blood brain barrier is not fully developed in infants, allowing neurotoxins to be more accessible to the brain than is the case in healthy adults.
In studies using experimental animals, neuroscientists have found that glutamic acid and aspartic acid load on the same receptors in the brain, cause identical brain lesions and neuroendocrine disorders, and act in an additive fashion.
You will note that the level of neurotoxins found in the hypoallergenic formula was far greater than the level of neurotoxins found in the other formulas. In reviewing the literature on hypoallergenic formulas, we have found short-term studies that concluded that hypoallergenic formulas are safe because babies tolerated them and gained weight. However, we have not seen any long-term studies on the safety of hypoallergenic formulas. We believe that well designed long term studies would demonstrate that infants raised on hypoallergenic formulas, as compared to infants who are breastfed or fed on non-hypoallergenic formulas, will exhibit more learning disabilities at school age, and/or more endocrine disorders, such as obesity and reproductive disorders, later in life. Long-term studies on the effects of hypoallergenic formulas need to be done42.
To put these figures in perspective, consider that in an FDA-sponsored study dated July, 1992 entitled "Safety of Amino Acids Used in Dietary Supplements," the Federation of American Societies for Experimental Biology concluded, in part, that "...it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children. . . and. . . by women of childbearing age and individuals with affective disorders." (MSG is called glutamic acid or L-glutamic acid when used in supplements.)43
During the 1960s, the food ingredient "monosodium glutamate" was routinely added to baby foods. The industry "voluntarily" ceased the practice after Congressional hearings in which concerned researchers warned of serious adverse effects. However, for some years following the elimination of "monosodium glutamate," hydrolyzed proteins were used in place of "monosodium glutamate." Hydrolyzed proteins always contain MSG.
Many consumers now know to avoid baby foods with hydrolyzed proteins. Yet how many parents realize that MSG lurks in every bottle of formula given to their infants? Babies on hypoallergenic formulas receive about 1 gram of total neurotoxins per day, a level at which many MSG-sensitive individuals experience adverse reactions.
Our advice to you is to do your best to eliminate MSG from your diet. You will feel better. That means avoiding all processed foods. Our advice to investigators of school violence is to investigate the effects of excitotoxins in children's diets. There are high levels of MSG in soy products and seasoning mixes used in school lunch programs, fast foods and snack foods.
Written by Dr. George J Georgiou and Barbara Karafokas
DaVinci Natural Health Centre, Larnaca, Cyprus
drgeorge@avacom.net
www.naturaltherapycenter.com
REFERENCES
1. Lucas, D.R., and Newhouse, J.P. (1957) The toxic effect of sodium L-glutamate on the inner layers of the retina. AMA Arch Ophthal 58: 193-201.
2. Olney, J.W. (1969). Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science 164: 719-721.
3. Olney, J.W. (1993, April). Prepared statement for the public meeting (April 1993) pertaining to adverse reactions to monosodium glutamate (MSG). Presented at a public meeting conducted by the Federation of American Societies for Experimental Biology (FASEB), Bethesda, MD.
4. Olney, J.W. and Price M.T. (1978). Excitotoxic amino acids as neuroendocrine probes. In E.G. McGeer, J.W. Olney, and P.L. McGeer (Eds.), Kainic Acid as a Tool in Neurobiology. New York: Raven.
5. Olney, J.W. and Price, M.T. (1980). Neuroendocrine interactions of excitatory and inhibitory amino acids. Brain Research Bulletin 5: Suppl 2, 361-368.
6. Chinese restaurant syndrome. (1990, January). Mayo Clinic Nutrition Letter.
7. Altman, D.R., Fitzgerald, T. & Chiaramonte, L.T. (1994). Double-blind placebo-controlled challenge (DBPCC) of persons reporting adverse reactions to monosodium glutamate (MSG). J. Allergy and Clinical Immunology Abstracts 93:303 (Abstract 844).
8. Garattini, S. (1979). Evaluation of the neurotoxic effects of glutamic acid. In R.J. Wurtman, & J.J. Wurtman (Eds.), Nutrition and the brain. New York: Raven Press.
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10. Germano, P., Cohen, S.G., Hahn, B., and Metcalfe, D.D. (1991). An evaluation of clinical reactions to monosodium glutamate (MSG) in asthmatics using a blinded, placebo-controlled challenge. J Allergy Clin Immunol Abstracts 87:177 (Abstract 155).
11. Giacometti, T. (1979). Free and bound glutamate in natural products. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
12. Anantharaman, K. (1979). In utero and dietary administration of monosodium L-glutamate to mice: reproductive performance and development in a multigeneration study. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
13. Auer, R.N. (1991). Excitotoxic mechanisms, and age-related susceptibility to brain damage in ischemia, hypoglycemia and toxic mussel poisoning. NeuroToxicology 12:541-546.
14. Bunyan, J., Murrell, E.A., and Shah, P.P. (1976). The induction of obesity in rodents by means of monosodium glutamate. Br J Nutr 35: 25-29.
15. Ebert, A.G. (1970). Chronic toxicity and teratology studies of monosodium L-glutamate and related compounds. Toxicol Appl Pharmacol 17: 274.
16. Federation of American Societies for Experimental Biology (FASEB) (1995). Analysis of adverse reactions to monosodium glutamate (MSG). Bethesda, MD: Life Sciences Research Office, FASEB.
17 Fernstrom, J.D., Cameron, J.L., Fernstrom, M.H., McConaha, C., Weltzin, T.E., and Kaye, W.H. (1996). Short-term neuroendocrine effects of a large, oral dose of monosodium glutamate in fasting male subjects. J Clin Endocrinol Metab 81: 184-191.
18. Filer, L. J. (1993). Public Forum: analysis of adverse reactions to monosodium glutamate. Paper presented at open meeting of the Federation of American Societies for Experimental Biology, April 1993.
19. Kenney, R.A. (1979). Placebo-controlled studies of human reaction to oral monosodium L-glutamate. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
20. Kenney, R.A., and Tidball, C.S. (1972). Human susceptibility to oral monosodium L-glutamate. A J Clin Nutr 25:140-146.
21. Nemeroff, C.B. (1981). Monosodium glutamate-induced neurotoxicity: review of the literature and call for further research. In S.A. Miller (Ed.), Nutrition & behavior. Philadelphia: Franklin Institute Press.
22. Newman, A.J., Heywood, R., Palmer, A.K., Barry, D.H., Edwards, F.P., and Worden, A.N. (1973). The administration of monosodium L-glutamate to neonatal and pregnant rhesus monkeys. Toxicology 1: 197-204.
23. Owen, G., Cherry, C.P., Prentice, D.E., and Worden, A.N. (1978). The feeding of diets containing up to 4% monosodium glutamate to rats for 2 years. Toxicol Lett 1: 221-226.
24. Pulce, C., Vial, T., Verdier, F., et al. (1992). The Chinese restaurant syndrome: a reappraisal of monosodium glutamate's causative role. Adverse Drug Reaction Toxicology Review pp.19-39.
25. Reif-Lehrer, L. (1977). A questionnaire study of the prevalence of Chinese restaurant syndrome. Fed Proc 36:1617-1623.
26. Reynolds, W.A., Butler, V., Lemkey-Johnston, N. (1976). Hypothalamic morphology following ingestion of aspartame or MSG in the neonatal rodent and primate: a preliminary report. J Toxicol environmental Health 2: 471-480.
27. Reynolds, W.A., Filer, L. J., and Stegink, L.D. (1991). Letter to Dr. Kenneth G. Fisher, LSRO, FASEB. May 31, 1991.
28. Reynolds, W.A., Lemkey-Johnston, N., Filer, L.J. Jr., and Pitkin, R.M. (1971). Monosodium glutamate: absence of hypothalamic lesions after ingestion by newborn primates. Science 172: 1342-1344.
29. Samuels, A. (1995). Monosodium L-glutamate: a double-blind study and review. Letter to the editor. Food and Chemical Toxicology. 33: 69-78.
30. Schaumburg, H.H., Byck, R., Gerstl, R. and Mashman, J.H. (1969) Monosodium L-glutamate: its pharmacology and role in the Chinese restaurant syndrome. Science 163: 826-828.
31. Scopp, A.L.(1991). MSG and hydrolyzed vegetable protein induced headache: review and case studies. Headache 31:107-110.
32. Takasaki, Y., Matsuzawa, Y., Iwata, S., O'Hara, Y., Yonetani, S., and Ichimura, M. (1979a). Toxicological studies of monosodium L-glutamate in rodents: relationship between routes of administration and neurotoxicity. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
33 Takasaki, Y., Sekine, S., Matsuzawa, Y., Iwata, S., and Sasaoka, M. (1979b). Effects of parenteral and oral administration of monosodium L-glutamate (MSG) on somatic growth in rats. Toxicol Lett 4: 327-343.
34. Taliferro, P.J. (1995). Monosodium glutamate and the Chinese restaurant syndrome: a review of food additive safety. J. Environmental Health 57: 8-12.
35. Tarasoff, L and Kelly, M.F. (1993). Monosodium L-glutamate: a double-blind study and review. Food Chem Toxic 31:1019-1035.
36. Yang, W.H., Drouin, M.A., Herbert, M., and Mao, Y. (1997). The monosodium glutamate symptom complex: Assessment in a double-blind, placebo-controlled, randomized study. J Allergy Clin Immunol 99: 757-762.
37. Daniels, D.H., Joe, F.L. and Diachenko, G.W. (1995). Determination of free glutamic acid in a variety of foods by high-performance liquid chromatography. Food Additives and Contaminants 12:21-29.
38. Blaylock, R.L. (1994). Excitotoxins: the taste that kills. Santa Fe: Health Press.
39. Taylor, S.L. (1993, April). Possible adverse reactions to hydrolyzed vegetable protein. Paper submitted to the Federation of American Societies for Experimental Biology review panel.
40. Goldschmiedt, M., Redfern, J.S., and Feldman, M. (1990). Food coloring and monosodium glutamate: effects on the cephalic phase of gastric acid secretion and gastrin release in humans. Am J Clin Nutr 51: 794-797.
41. Appreciation to Baby Love Products Inc. of Camrose, Alberta, Canada (www.kidalog.com)
42. Taken from Jack Samuels and his wife, Adrienne Samuels, PhD, who are founders of Truth in Labeling, a nonprofit organization dedicated to accurate labeling of MSG and the removal of MSG from use in agriculture. For further information, see their website at www.truthinlabeling.org.
43. Leibovitz, B. Safety of amino acids used as dietary supplements. Am. J. Clinical Nutrition, Vol. 57, Issue 6, b -946, June 1, 1993
6th Oct 2007
INTRODUCTION
Monosodium Glutamate, a food ingredient, was invented in 1908 in Japan, by Kikunae Ikeda. A year later, with a partner, he formed a company, Ajinomoto, to produce the product. The food additive did not appear in the United States to any degree until the late 1940s, following the Second World War. During the war, it had been noted that Japanese soldiers' rations tasted better than the rations used by our soldiers. The difference was believed to be "monosodium glutamate." Today, "monosodium glutamate" or its reactive component, "processed free glutamic acid," is found in almost all of the processed foods that are manufactured in the United States.
ADVERSE EFFECTS OF MSG
In 1957, Lucas and Newhouse found that normal neonatal mice suffered acute degenerative lesions in the inner retina when "monosodium glutamate" was administered by feeding tube.1 In 1968, during a replication of this study at Washington University Medical School, St., Louis, Missouri, Dr. John W. Olney2 noted that, some of the mice had become grotesquely obese. He decided to sacrifice some of the mice to confirm his belief that lesions would be found in the hypothalamus region of the brain. Not only was his suspicion confirmed, but further testing indicated that there were also other neuroendocrine effects from the "monosodium glutamate." His findings were published in 1969.2 Dr. Olney, a National Academy of Science scientist who is credited for the voluntary removal of MSG from baby food in the 1970s, continues to publish research3-5 on the toxicity of glutamic acid, often using "monosodium glutamate."
In 1968, the New England Journal of Medicine published a Letter to the Editor in which Ho Man Kwok, MD, asked for help in determining why he and his friends suffered reactions shortly after eating in some Chinese restaurants, though he never experienced such reactions when he lived in China. The journal titled the letter "Chinese Restaurant Syndrome,"6 and researchers from around the country wrote the journal to suggest that Dr. Kwok and his friends' problem was intolerance to MSG. One letter indicated that 30% of the population reacted to MSG.
In 1969, concerned with the bad reports regarding "monosodium glutamate," the glutamate industry formed a nonprofit organization to defend the safety of MSG, the International Glutamate Technical Committee. Later, in 1977, they increased their efforts with the development of a nonprofit subsidiary, The Glutamate Association, primarily operating as a public relations arm of the glutamate industry. In about 1990, the glutamate industry turned to the International Food Information Council (IFIC), another nonprofit industry-funded organization, to be their spokesman and to promote the safety of MSG along with the other products that they represent.
MSG IS TOXIC TO HUMANS!
The literature is clear in demonstrating that MSG is toxic to humans and that over 25% of the population suffer adverse reactions from MSG7-36. In the opinion of this writer, the subject is only controversial because of the input of the three organizations mentioned above and because of research they have funded to discredit findings of others and to tell the story that the glutamate industry wants told, research that is flawed to the point of being worthless.
"Monosodium glutamate" is approximately 78% processed free glutamic acid and 22% sodium (salt) and moisture, with about 1% contaminants. It is the processed free glutamic acid that causes people to suffer adverse reactions, and, unfortunately, there are over 40 food ingredients other than "monosodium glutamate" that contain processed free glutamic acid in varying amounts.37 Consequently, consumers refer to all processed free glutamic acid as MSG, regardless of the name of the ingredient.
People differ in their tolerances to MSG, but typically always suffer similar reactions each time they ingest amounts of MSG that exceed their tolerances for the substance. Reactions experienced vary dramatically, as if MSG finds the weak link in the body.38 Typically, people will suffer reactions at approximately the same time each time they ingest amounts of MSG that exceed their tolerance levels. However, that time lapse can vary among people from immediately following ingestion of MSG up to 48 hours following ingestion. Use of alcohol or exercise prior to, during or following an MSG-containing meal will exacerbate an MSG reaction in many people. MSG-sensitive people will typically suffer similar reactions to aspartame.
Neuroscientists believe that the young and the elderly are most at risk from MSG. In the young, the blood-brain barrier is not fully developed, exposing the brain to increased levels of MSG that has entered the bloodstream. The elderly are at increased risk because the blood-brain barrier can be damaged by aging, by disease processes, or by injury, including hypertension, diabetes, hypoglycemia, and stroke. Throughout life, the blood-brain barrier is "leaky" at best.
MSG has now been implicated in a number of the neurodegenerative diseases, including ALS (Lou Gehrig's disease), Parkinson's disease, Alzheimer's disease, multiple sclerosis and Huntington's disease39.
In general, the natural glutamic acid found in food does not cause problems, but the synthetic free glutamic acid formed during industrial processing is a toxin. In addition, when MSG is formed using hydrochloric acid the final product includes carcinogens.40
MSG IN INFANT FORMULA: BAD FOR YOUR BABY!
A Canadian Study41 conducted, leaves no room for doubt that ingredients that contain processed free glutamic acid (MSG) and free aspartic acid — known neurotoxins— are used in baby formula. The fact that neurotoxins are present in baby formula is of particular concern since the blood brain barrier is not fully developed in infants, allowing neurotoxins to be more accessible to the brain than is the case in healthy adults.
In studies using experimental animals, neuroscientists have found that glutamic acid and aspartic acid load on the same receptors in the brain, cause identical brain lesions and neuroendocrine disorders, and act in an additive fashion.
You will note that the level of neurotoxins found in the hypoallergenic formula was far greater than the level of neurotoxins found in the other formulas. In reviewing the literature on hypoallergenic formulas, we have found short-term studies that concluded that hypoallergenic formulas are safe because babies tolerated them and gained weight. However, we have not seen any long-term studies on the safety of hypoallergenic formulas. We believe that well designed long term studies would demonstrate that infants raised on hypoallergenic formulas, as compared to infants who are breastfed or fed on non-hypoallergenic formulas, will exhibit more learning disabilities at school age, and/or more endocrine disorders, such as obesity and reproductive disorders, later in life. Long-term studies on the effects of hypoallergenic formulas need to be done42.
To put these figures in perspective, consider that in an FDA-sponsored study dated July, 1992 entitled "Safety of Amino Acids Used in Dietary Supplements," the Federation of American Societies for Experimental Biology concluded, in part, that "...it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children. . . and. . . by women of childbearing age and individuals with affective disorders." (MSG is called glutamic acid or L-glutamic acid when used in supplements.)43
During the 1960s, the food ingredient "monosodium glutamate" was routinely added to baby foods. The industry "voluntarily" ceased the practice after Congressional hearings in which concerned researchers warned of serious adverse effects. However, for some years following the elimination of "monosodium glutamate," hydrolyzed proteins were used in place of "monosodium glutamate." Hydrolyzed proteins always contain MSG.
Many consumers now know to avoid baby foods with hydrolyzed proteins. Yet how many parents realize that MSG lurks in every bottle of formula given to their infants? Babies on hypoallergenic formulas receive about 1 gram of total neurotoxins per day, a level at which many MSG-sensitive individuals experience adverse reactions.
Our advice to you is to do your best to eliminate MSG from your diet. You will feel better. That means avoiding all processed foods. Our advice to investigators of school violence is to investigate the effects of excitotoxins in children's diets. There are high levels of MSG in soy products and seasoning mixes used in school lunch programs, fast foods and snack foods.
Written by Dr. George J Georgiou and Barbara Karafokas
DaVinci Natural Health Centre, Larnaca, Cyprus
drgeorge@avacom.net
www.naturaltherapycenter.com
REFERENCES
1. Lucas, D.R., and Newhouse, J.P. (1957) The toxic effect of sodium L-glutamate on the inner layers of the retina. AMA Arch Ophthal 58: 193-201.
2. Olney, J.W. (1969). Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science 164: 719-721.
3. Olney, J.W. (1993, April). Prepared statement for the public meeting (April 1993) pertaining to adverse reactions to monosodium glutamate (MSG). Presented at a public meeting conducted by the Federation of American Societies for Experimental Biology (FASEB), Bethesda, MD.
4. Olney, J.W. and Price M.T. (1978). Excitotoxic amino acids as neuroendocrine probes. In E.G. McGeer, J.W. Olney, and P.L. McGeer (Eds.), Kainic Acid as a Tool in Neurobiology. New York: Raven.
5. Olney, J.W. and Price, M.T. (1980). Neuroendocrine interactions of excitatory and inhibitory amino acids. Brain Research Bulletin 5: Suppl 2, 361-368.
6. Chinese restaurant syndrome. (1990, January). Mayo Clinic Nutrition Letter.
7. Altman, D.R., Fitzgerald, T. & Chiaramonte, L.T. (1994). Double-blind placebo-controlled challenge (DBPCC) of persons reporting adverse reactions to monosodium glutamate (MSG). J. Allergy and Clinical Immunology Abstracts 93:303 (Abstract 844).
8. Garattini, S. (1979). Evaluation of the neurotoxic effects of glutamic acid. In R.J. Wurtman, & J.J. Wurtman (Eds.), Nutrition and the brain. New York: Raven Press.
9. Geha, R., Beiser, A., Ren, C., Patterson, R., Greenberger, P., Grammer, L.C., Ditto, A.M., Harris, K.E., Shaughnessy, M.A., Yarnold, P., Corren, J., Saxon, A. (1998). Multicenter multiphase double blind placebo controlled study to evaluate alleged reactions to monosodium glutamate (MSG). J. Allergy Clin Immunol Abstracts 101:S243 (Abstract 106).
10. Germano, P., Cohen, S.G., Hahn, B., and Metcalfe, D.D. (1991). An evaluation of clinical reactions to monosodium glutamate (MSG) in asthmatics using a blinded, placebo-controlled challenge. J Allergy Clin Immunol Abstracts 87:177 (Abstract 155).
11. Giacometti, T. (1979). Free and bound glutamate in natural products. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
12. Anantharaman, K. (1979). In utero and dietary administration of monosodium L-glutamate to mice: reproductive performance and development in a multigeneration study. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
13. Auer, R.N. (1991). Excitotoxic mechanisms, and age-related susceptibility to brain damage in ischemia, hypoglycemia and toxic mussel poisoning. NeuroToxicology 12:541-546.
14. Bunyan, J., Murrell, E.A., and Shah, P.P. (1976). The induction of obesity in rodents by means of monosodium glutamate. Br J Nutr 35: 25-29.
15. Ebert, A.G. (1970). Chronic toxicity and teratology studies of monosodium L-glutamate and related compounds. Toxicol Appl Pharmacol 17: 274.
16. Federation of American Societies for Experimental Biology (FASEB) (1995). Analysis of adverse reactions to monosodium glutamate (MSG). Bethesda, MD: Life Sciences Research Office, FASEB.
17 Fernstrom, J.D., Cameron, J.L., Fernstrom, M.H., McConaha, C., Weltzin, T.E., and Kaye, W.H. (1996). Short-term neuroendocrine effects of a large, oral dose of monosodium glutamate in fasting male subjects. J Clin Endocrinol Metab 81: 184-191.
18. Filer, L. J. (1993). Public Forum: analysis of adverse reactions to monosodium glutamate. Paper presented at open meeting of the Federation of American Societies for Experimental Biology, April 1993.
19. Kenney, R.A. (1979). Placebo-controlled studies of human reaction to oral monosodium L-glutamate. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
20. Kenney, R.A., and Tidball, C.S. (1972). Human susceptibility to oral monosodium L-glutamate. A J Clin Nutr 25:140-146.
21. Nemeroff, C.B. (1981). Monosodium glutamate-induced neurotoxicity: review of the literature and call for further research. In S.A. Miller (Ed.), Nutrition & behavior. Philadelphia: Franklin Institute Press.
22. Newman, A.J., Heywood, R., Palmer, A.K., Barry, D.H., Edwards, F.P., and Worden, A.N. (1973). The administration of monosodium L-glutamate to neonatal and pregnant rhesus monkeys. Toxicology 1: 197-204.
23. Owen, G., Cherry, C.P., Prentice, D.E., and Worden, A.N. (1978). The feeding of diets containing up to 4% monosodium glutamate to rats for 2 years. Toxicol Lett 1: 221-226.
24. Pulce, C., Vial, T., Verdier, F., et al. (1992). The Chinese restaurant syndrome: a reappraisal of monosodium glutamate's causative role. Adverse Drug Reaction Toxicology Review pp.19-39.
25. Reif-Lehrer, L. (1977). A questionnaire study of the prevalence of Chinese restaurant syndrome. Fed Proc 36:1617-1623.
26. Reynolds, W.A., Butler, V., Lemkey-Johnston, N. (1976). Hypothalamic morphology following ingestion of aspartame or MSG in the neonatal rodent and primate: a preliminary report. J Toxicol environmental Health 2: 471-480.
27. Reynolds, W.A., Filer, L. J., and Stegink, L.D. (1991). Letter to Dr. Kenneth G. Fisher, LSRO, FASEB. May 31, 1991.
28. Reynolds, W.A., Lemkey-Johnston, N., Filer, L.J. Jr., and Pitkin, R.M. (1971). Monosodium glutamate: absence of hypothalamic lesions after ingestion by newborn primates. Science 172: 1342-1344.
29. Samuels, A. (1995). Monosodium L-glutamate: a double-blind study and review. Letter to the editor. Food and Chemical Toxicology. 33: 69-78.
30. Schaumburg, H.H., Byck, R., Gerstl, R. and Mashman, J.H. (1969) Monosodium L-glutamate: its pharmacology and role in the Chinese restaurant syndrome. Science 163: 826-828.
31. Scopp, A.L.(1991). MSG and hydrolyzed vegetable protein induced headache: review and case studies. Headache 31:107-110.
32. Takasaki, Y., Matsuzawa, Y., Iwata, S., O'Hara, Y., Yonetani, S., and Ichimura, M. (1979a). Toxicological studies of monosodium L-glutamate in rodents: relationship between routes of administration and neurotoxicity. In L.J. Filer, Jr., S. Garattini, M.R. Kare, W.A. Reynolds, and R.J. Wurtman, (Eds), Glutamic acid: advances in biochemistry and physiology. New York: Raven.
33 Takasaki, Y., Sekine, S., Matsuzawa, Y., Iwata, S., and Sasaoka, M. (1979b). Effects of parenteral and oral administration of monosodium L-glutamate (MSG) on somatic growth in rats. Toxicol Lett 4: 327-343.
34. Taliferro, P.J. (1995). Monosodium glutamate and the Chinese restaurant syndrome: a review of food additive safety. J. Environmental Health 57: 8-12.
35. Tarasoff, L and Kelly, M.F. (1993). Monosodium L-glutamate: a double-blind study and review. Food Chem Toxic 31:1019-1035.
36. Yang, W.H., Drouin, M.A., Herbert, M., and Mao, Y. (1997). The monosodium glutamate symptom complex: Assessment in a double-blind, placebo-controlled, randomized study. J Allergy Clin Immunol 99: 757-762.
37. Daniels, D.H., Joe, F.L. and Diachenko, G.W. (1995). Determination of free glutamic acid in a variety of foods by high-performance liquid chromatography. Food Additives and Contaminants 12:21-29.
38. Blaylock, R.L. (1994). Excitotoxins: the taste that kills. Santa Fe: Health Press.
39. Taylor, S.L. (1993, April). Possible adverse reactions to hydrolyzed vegetable protein. Paper submitted to the Federation of American Societies for Experimental Biology review panel.
40. Goldschmiedt, M., Redfern, J.S., and Feldman, M. (1990). Food coloring and monosodium glutamate: effects on the cephalic phase of gastric acid secretion and gastrin release in humans. Am J Clin Nutr 51: 794-797.
41. Appreciation to Baby Love Products Inc. of Camrose, Alberta, Canada (www.kidalog.com)
42. Taken from Jack Samuels and his wife, Adrienne Samuels, PhD, who are founders of Truth in Labeling, a nonprofit organization dedicated to accurate labeling of MSG and the removal of MSG from use in agriculture. For further information, see their website at www.truthinlabeling.org.
43. Leibovitz, B. Safety of amino acids used as dietary supplements. Am. J. Clinical Nutrition, Vol. 57, Issue 6, b -946, June 1, 1993
Friday, July 11, 2008
KILLING OURSELVES WITH XENOBIOTICS
27th Aug 2007
by Dr. George J Georgiou, Ph.D.,N.D.,DSc (AM)
Natural Medicine Practitioner, Researcher in Xenobiotics
Email: drgeorge@detoxmetals.com
Web: www.detoxmetals.com
Toxic Chemicals Everywhere
Toxic chemicals, otherwise known as “xenobiotics” (Gk: foreign to life) which are scattered all over our planet from the North Pole to the South Pole, are being constantly researched, and the conclusion is that they are extremely toxic to humans as well as wildlife. Even though some chemicals have been taken off the market, those that remain are even more noxious than the ones already banned. Bioaccumulation in soils, water supplies and the tissues of animals and humans is a real problem which results in these chemicals lingering for many, many years even after they have being banned. DDT, for example, has been banned for more than 25 years in the Western world, yet it is still being found in the tissues of wildlife in the arctic, as well as humans in many different countries.
A recent study noted that only five organochlorine compounds and mercury were found in marine mammals in the 1960s. Today over 265 organic pollutants and 50 inorganic chemicals have been found in these species.1
Recent research has focused on how chemicals affect the thyroid and pituitary systems. Some chemicals have been identified as endocrine disrupters because they can interfere with the body’s own hormones, which are secreted by the endocrine glands.
It is also emerging that endocrine disrupters can have many physiological effects not directly associated with the primary system. For example, the thyroid system is well known to regulate metabolism, but it is also a crucial component in foetal brain development in mammals, and too much or too little thyroid hormone at crucial points can do permanent damage. The immune system is also vulnerable to hormone-mediated disruption. Chemicals can cause neurological problems, reproductive and developmental abnormalities, and cancers as well. And researchers are only just beginning to disentangle the questions about the effects of chronic low-level exposure (as opposed to brief high doses of chemicals), combinations of chemicals, and interactions between chemicals and other physiological and environmental factors.
Let us take a brief look at some of the more common xenobiotics chemicals that that have detrimental effects on humans as well as wildlife.
Perfluorochemicals (PFCs)
These compounds are chains of fully fluorinated carbon atoms of varying lengths, yielding chemicals that are extremely resistant to heat, chemical stress, and that repel both water and oil. Because of these properties PFCs, or chemicals that degrade into PFCs, have been widely used since the 1950s by industry as surfactants and emulsifiers and in commercial products, including stain or water protectors for carpet, textiles, auto interiors, camping gear and leather; food packaging; folding cartons and other paper containers; floor polishes; photographic film; shampoos; dental cleaners; inert pesticide ingredients; and lubricants for bicycles, garden tools and zippers.
Their persistence is extreme, particularly perfluorooctanoic acid (PFOA) - there is no evidence that they ever fully degrade, and they have been found in animals, humans and ecosystems worldwide.
The first public indication that PFOS and PFOA were problematic came on May 16,
2000 when 3M, the primary global manufacturer of many perfluoroalkanesulfonates and
PFOA, announced plans to phase out by the end of 2001 the production of perfluorooctanyl chemistry that underpinned their extremely successful Scotchgard™ and Scotchban™ product lines.2
A 2002 European study of PFCs has detected these compounds in bottlenose, common and striped dolphins, whales, bluefin tuna, swordfish and cormorants in the Mediterranean, and in ringed and grey seals, sea eagles and Atlantic salmon in the
Baltic.3
Other research shows that this chemical is now contaminating many wildlife species around the world, including polar bears in the Arctic, seals in Antarctica, dolphins in the river Ganges in India, albatrosses from Midway Atoll in the Pacific, turtles in the United States, gulls in Korea, cormorants in Canada,4 and fish in Japan.5
Fluorinated telomers are used to keep grease from soaking through fast food containers such as pizza boxes, French fry holders, and food wrapping paper. The digestive system can break telomers down into PFOA and related chemicals. Newly revealed tests conducted by 3M showed that a metabolite specific to the telomers was found in 85 per cent of the children tested.6
Red Cross blood banks, conducted by a team including scientists from the 3M Company, estimated the average concentrations in humans to be 30-40 parts per billion (ppb), with males having higher levels.7 By comparison, levels in wildlife have been measured at 940 ppb in common dolphin liver; 1100 ppb in ringed seals from the Bay of Bothnia; and 270 ppb in long-finned pilot whale liver from the North Thyrrenian Sea.8
Health Effects of Perfluorochemicals (PFCs)
In 1979, 3M administered four doses of PFOS to monkeys and all the monkeys in all treatment groups died within weeks. Typically, when a study like this is conducted, the researchers predict that the lowest dose will not cause any harmful health effects.9
In 1981 both DuPont and 3M reassigned women of childbearing age working in their production plants after they learned that PFOA caused developmental abnormalities in laboratory animals. Within weeks of this discovery, DuPont found PFOA in the women’s blood.
It was known as early as 1975 that fumes from hot pans coated with polytetrafluoroethylene can kill pet birds,10 and broiler chicks have died after exposure to polytetrafluoroethylene-coated light bulbs.11 Laboratory experiments reported in 2003 showed that in rats, PFOS exposure can lead to loss of appetite, interrupted oestrus cycles, and elevated stress hormone levels. PFOS was found to accumulate in brain tissue, particularly the hypothalamus, suggesting that PFOS crosses the blood-brain barrier and may interfere with reproductive hormones through the pituitary-hypothalamus process that stimulates their production.12
Recent laboratory studies with PFOA involving rats show low birth weight, small pituitary gland, altered maternal care behaviour, high pup mortality, and significant changes in the brain, liver, spleen, thymus, adrenal gland, kidney, prostate, testes and epididymides13
Several studies indicate PFOA increases estrogens and leads to testosterone dysfunction in males. There is even more evidence that PFOA as well as chemicals that metabolize to PFOs and PFOA lead to underactive thyroid; thyroid dysfunction during pregnancy can lead to many developmental problems, including faulty brain development and neurological and behavioural problems that affect not only infants and young animals (or humans) but continue into adulthood. The EPA considers both PFOS and PFOA to be a carcinogen in animals, with testicular, pancreatic, mammary, thyroid and liver tumours most frequent in exposed rats.
All studies to date indicate perfluorinated compounds damage the immune system. In one experiment, a chemical very similar to PFOA called PFDA resulted in such atrophy of the thymus gland, (the source of T cells that attack bacteria, viruses and cancer cells) that the gland was undetectable upon clinical examination.
Phthalates
Phthalates are a group of chemicals used as softeners in a variety of plastic products, including the ubiquitous polyvinyl chloride (PVC). Products containing phthalates include medical devices (intravenous tubing, blood bags, masks for sleep apnea devices), building products (insulation of cables and wires, tubes and profiles, flooring, wallpapers, outdoor wall and roof covering, sealants), car products (car under-coating, car seats etc.) and children’s products (teething rings, squeeze toys, clothing and rainwear). They are also used in some lacquers, paints, adhesives, fillers, inks and cosmetics.
The most common phthalate in the environment is di-(2-ethylhexyl)phthalate (DEHP), which comprises half of all phthalates produced in Western Europe, with 450,000 tonnes used per year. Concern about children’s exposure to phthalates prompted the EU to ban six types of phthalate softeners in PVC toys designed to be mouthed by children under three years of age.
Both humans and wildlife may be exposed to various phthalates. For example, a 2003 study of two groups of pregnant women, one in New York City and one in Krakow, Poland, compared the levels of four phthalates in the women’s personal ambient air and measured the levels of the metabolites of these phthalates in the urine of the New York women.14 All four phthalates were present in all the air samples, but air concentrations of DBP, di–isobutyl phthalate and DEHP were higher in Krakow than in New York. The study found that air was a significant source of exposure, that some women receive doses high enough to cause concern, and that there was a correlation between air and urine levels of some phthalates.
Other studies in the EU have also raised concerns with regard to current exposure levels. A recent study in Germany, for example, has concluded that exposure to DEHP may be far higher than previously thought. It reported that in 12 per cent of the Germans studied, phthalate levels exceeded the tolerable daily intake (TDI) used by the EU Scientific Committee for Toxicity, Ecotoxicity and the Environment. Exposure to DBP and BBP was also ubiquitous.15
Health Effects of Phthalates
Some phthalates appear to exert endocrine disrupting effects, and can act against the male hormone, androgen, through pathways other than binding to androgen or estrogen receptors. While there is little research on the effects of phthalates on wildlife per se, some studies suggest that there may be serious consequences for both wildlife and humans. Of particular concern is phthalate exposure in pregnant females: some researchers have proposed that the antiandrogenic properties of phthalates might be linked to testicular dysgenesis syndrome, the manifestations of which range from birth defects in males, including undescended testes, to low sperm counts and testicular cancer.16
Numerous Laboratory studies underpin the concern. For example, a study has shown that DEHP, BBP, and DINP administered to pregnant rats induced feminized breasts in the male offspring, as well as other reproductive malformations, including small testes in the case of the DEHP and BBP.17
There are also worries that exposure to manmade chemicals with hormone disrupting properties may be affecting the age of puberty. A study of Puerto Rican girls with premature breast development suggested a possible association with exposure to certain phthalates.18 U.S. researchers recently reported the effects of DEHP on Leydig cells (testosterone-producing cells in the testes) in rats.19 They found that prolonged exposure to DEHP caused the number of Leydig cells to increase by 40 per cent-60 per cent while simultaneously reducing testosterone production. At the same time, blood levels of both testosterone and estrogens increased by 50 per cent. It is known that males with high levels of serum testosterone and luteinizing hormone (a hormone that triggers testosterone production) are at higher risk of early puberty and testicular tumours.
With regard to cancer, a recent study supported other research associating DEHP with liver cancer in rodents.20 A 2003 Harvard study suggested another mechanism for carcinogenic effect of phthalates. The researchers measured levels of eight phthalates in subjects and found an association between monoethyl phthalate (MEP) and increased damage to the DNA in the subjects’ sperm.21 This is the first study showing that phthalates can induce such damage at levels presently found in the environment.
Other studies with phthalates show that additive effects can occur when there is exposure to more than one phthalate.22 This underlines the growing concern with real life exposures to multiple pollutants, and the increasing realisation that current regulatory practices, based on testing chemicals in isolation, may not be protective.
Phenols, Bisphenyl A and Nonylphenol
Evidence for endocrine disruption by the widely used phenol compounds bisphenol A (BPA) and nonylphenol is mounting. BPA is mostly used to make polycarbonate plastic, which has a diverse range of application in making bottles, computer and electronics shells, CDs, crash helmets, and many other consumer products.
Certain compounds that can leach BPA are also used in the plastic linings of food cans
and in dental fillings, through which people can ingest small quantities. In December 2003, concerned about BPA in the plastic linings of food cans, the EU reduced the amount of BPA migration permitted by 80 percent to 0.6 milligrams per kilogram of food.23 However, BPA remains widely distributed in consumer products.
Nonylphenolic compounds have been used in degreasing solutions, and in leather and textile processing, as well as in de-icing fluid, paints, plastics, and pesticides. The EU has imposed restrictions on the marketing and use of nonylphenol and nonylphenol ethoxylates to a certain extent in cleaning products, textile and leather processing, agricultural teat dips, metal working, pulp and paper, cosmetics including shampoos, and personal care products except spermicides.24
Health Effects of Phenols, Bisphenyl A and Nonylphenol
Fish have been shown to be susceptible to the endocrine disrupting effects of both nonylphenol25 and BPA.26 Exposure to either of these chemicals can cause male fish to make vitellogenin (an estrogen-regulated protein produced by female egg-laying vertebrates and not normally produced by males or juveniles), and can also affect the formation of sperm. Before improved regulation, male fish in the river Aire in England were found to be feminised downstream of a wastewater treatment plant discharge containing alkylphenol ethoxylates from the textile industry. Many male fish were found with egg producing cells in their testes, and reduced testis growth rate and size.27,28
Aquatic invertebrates seem particularly sensitive to these chemicals. For example, nonylphenol affects the freshwater algae, Scenedesmus subspicatus at levels of 3.3 micrograms per litre.29 Molluscs in particular have shown effects at very low dose levels. For example, in the mollusc Potamopyrgus antipodarum, BPA and octylphenol, as well as a mixture of these and other chemicals in treated sewage effluent, stimulated egg and embryo production at low doses and inhibited such production at high doses.30
This work supported a 2000 study by some of the same researchers showing that extremely low levels of BPA and octylphenol triggered malformed genitals of female ramshorn (freshwater) snail, Marisa cornuarietis, and the (saltwater) dogwhelk Nucella lapillus.31 In some of the freshwater snails, the excessive growth of the female glands and the egg masses ruptured the egg tube, and the snails died. This syndrome was referred to as superfeminisation. A number of other adverse changes were observed in both species. Another important finding was that in the freshwater snails, the medium doses of octylphenol produced more changes than either the highest or lowest doses.
Other researchers have shown that a single 48-hour exposure to 1 microgram per litre of nonylphenol, comparable to environmental levels, altered the sex ratio of oysters, reduced the survival of offspring, and caused some oysters to become hermaphroditic.32
A 2001 study exposing barnacles to concentrations of nonylphenol similar to those in the environment (0.01-10 micrograms per litre) disrupted the timing of larval development.33 In addition to fish, other vertebrates also show effects when exposed to BPA. For example, in 2003, researchers reported that BPA at environmentally comparable doses resulted in sex reversals and altered gonadal structures in the broad-snouted caiman, an alligator relative native to mid-latitude South America.34 In another study, the offspring of pregnant mice exposed to BPA showed changes in ovarian and mammary gland tissues and disrupted fertility cycles as adults.35 BPA was reported for the first time in 2001 to induce reproductive malformations in birds - specifically, in female quail embryos and male chicken embryos. The female embryos’ oviducts developed abnormally, and the males’ testes were feminized.36
The exact mechanism by which BPA and nonylphenol exert their effects is not clear, but a recent in vitro study demonstrated a molecular mechanism by which BPA and nonylphenol interfere with both the activation and function of cellular androgen receptors.37 In a 2002 study, nonylphenol tested on barnacle larvae induced DNA damage, possibly including mutations, and the authors speculate that this effect may be a mechanism by which higher level reproductive abnormalities are caused.38
Despite evidence from these and other studies, the low dose effects of BPA are still in dispute. Regulators in the EU have been reluctant to act, and further studies have been demanded.
Polybrominated Flame Retardants (BFRs)
Brominated flame retardants (BFRs) in furniture, building material, and clothing have become a serious concern, as their levels are showing sharp increases in living organisms. The first BFRs were taken off the market in the early 1970s after a spill led to poisonings of livestock and farm families in Michigan.39 Three BFRs now dominate the market: TBBPA, the most widely used, primarily in printed circuit boards and in some plastics; HBCD, and the deca-BDEs. The other commercial PBDEs (octa-BDE and penta-BDE) have been banned in the EU as of August 2004,40 and the state of California has taken similar action. However, because of their alarming spread and rate of accumulation in humans and animals, Europe’s ban does not provide complete reassurance, particularly regarding the penta-BDE form used as a flame retardant in polyurethane foam elsewhere in the world.
Researchers recently reported levels of PBDEs in U.S. breast milk.41 Forty-seven Texas women had an average level of 73.9 ng/g lipid; such levels are sharply higher than those found in European studies. There are serious concerns about the transfer of BFRs to nursing infants, and some scientists are worried that BFRs might affect foetal development, including disruption of the thyroid system’s role in foetal brain development.42 In 2003 a WWFUK biomonitoring program found deca-BDE in the blood of seven per cent of those tested.43
New research from Sweden has found high levels of several brominated flame retardants in the eggs of peregrine falcons from 1987-1999. The eggs of falcons living in the wild had significantly higher concentrations of the essentially unregulated deca-BDE than eggs of captive falcons. The fact that deca-BDE was found in eggs demonstrates that the chemical can cross cell membranes, contrary to what scientists had previously thought. The peregrine study represents the first time that the deca formulation has been found in wildlife.44
In 2002, one research team predicted that within 10 to 15 years, concentrations of BFRs in Great Lakes herring gull may be higher than those of PCBs.45 BFRs have also been found in sperm whales,46 ringed seals from the Canadian Arctic,47 mussels and several kinds of fish in Norwegian waters, and harbour seals in San Francisco Bay,48 among other wildlife. Essentially, BFRs are being found wherever we look.
Health Effects of BFRs
Laboratory studies show that certain BFRs are highly toxic to aquatic animals (crustaceans),49 and suggest effects on pubertal development, thyroid and liver in rats, as well as developmental neurotoxicity in mice.50 A recent paper reported behavioural effects in mice pups at a relatively low dose.51 In 1999 Swedish researchers reported that PBDEs and HBCD may have health effects similar to those of DDT and PCBs because of their ability to induce genetic recombination.52
While there are no published epidemiological studies on effects of BFRs on humans, the possible thyroid effects, based on tissue culture and animal studies, are a red flag. As with other chemicals, anything that affects foetal development merits particular study because of the profound, long-term, and often irreversible influence that early exposures have on the entire life of an organism.
What Can We Do To Protect Ourselves?
The answer to this question is two-fold; first we can push for legislation to ban a lot of these harmful chemicals that have been researched and are known to be detrimental to animals and humans. Second, we need to be able to detoxify our bodies in order to eliminate many of these chemicals. Given that we are exposed to these literally daily, this process must be an ongoing one. It is not safe to use chemical chelators on an ongoing basis, but natural ones can be used instead, much like a supplement on a daily basis. HMD™ can be used safely over long periods of time with no side effects – it is presently being tested to see its efficacy in eliminating some of the xenobiotics mentioned in this article.
References
1 O’Shea, T.J., Tanabe, S., Persistent ocean contaminants and marine mammals: a retrospective overview. In: O’Shea, T.J. et al. (Eds.), 1999. Proceedings of the Marine Mammal Commission Workshop Marine Mammals and Persistent Ocean Contaminants, pp 87-92. (cited in Tanabe, S. Contamination and toxic effects of persistent endocrine disrupters in marine mammals and birds. Mar Pollut Bull 2002;45:69-77.)
2 3M. (2000) 3M phasing out some of its specialty materials, May 16, 2000 press release.
3 Kannan, K., Corsolini, S., Falandysz, J., Oehme, G., Focardi, S., Giesy, J.P. Perfluorooctanesulfonate and related fluorinated hydrocarbons in marine mammals, fishes and birds from coasts of the Baltic and MediterraneanSeas. Environ Sci Technol 2002 Aug 1;36(15):3210-6.
4 Geisy J.P. and Kannan K. Global Distribution of Perfluorooctane sulfonate in wildlife.
Env Sci Technol 2001, 35:1339-42.
5 Taniyasu, S., Kannak, K., Horii,Y., Hanari, N.,Yamashita, N. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water, fish, birds and humans from Japan. Environ Sci & Technol 2003, 37:2634-2639.
6 Fields, S. Another fast-food fear. Environ Health Perspect 2003: 111:16:A162.
7 Olsen, G. W., Church, T.R., Miller, J.P., Burris, J.M., Hansen, K.J., Lundberg, J.K., Armitage, J.B., Herron, R.M., Medhdizadehkashi, Z., Nobiletti, J.B., O’Neill, E.M., Mandel, J.H., Zobel, L.R. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Environ Health
Perspect 2003:111:1892-1901. doi.10.1289/ehp.6316 via http://dx.doi.org.
8 Kannan, et al., 2002.
9 Organization for Economic Cooperation and Development (OECD). (2002) Hazard Assessment of perfluorooctane sulfonate (PFOS) and its salts (November, 21 2002). ENV/JM/RD(2002)17/FINAL. Available online at: http://www.oecd.org/dataoecd/23/18/2382880.pdf
10 “PFCs: A Family of Chemicals that Contaminate the Planet,” Part 6: PFCs in Animals Worldwide. Environmental Working Group, 2003.
http://www.ewg.org/reports/pfcworld/part8.php Accessed 3 January 2004.
11 Ibid.
12 Austin, M.E., Kasturi, B.S., Barber, M., Kannan, K., MohanKumar, P.S., MohanKumar, S.M.J. Neuroendocrine effects of perfluorooctane sulfonate in rats.
Environ Health Perspect 2003:111:12:1485-1489.
13 Thayer, K., Klein, J. Gray, S., Houlihan, J.,Wiles, R., Greenleaf, T., PFCs: A Family of Chemicals that Contaminate the Planet. Environmental Working Group 2003.
http://www.ewg.org/reports/pfcworld/part4.php Accessed 5 January 2004.
14. Adibi, J.J., Perera, F.P., Jedrychowski,W., Camann, D.E., Barr, D., Jacek, Ryszard, Whyatt, R.M. Prenatal exposures to phthalates among women in New York City and Krakow, Poland. Environ Health Perspect 2003:111:14:1719-1722.
15 Kock et al, 2003. An estimation of the daily intake of di(2-ethyl) phthalate (DEHP) and other phthalates in the general population. International Journal Hygiene and Environmental Health.
16 Sharpe R.M. (2003). The oestrogen hypothesis – where do we stand now? International Journal of Andrology 26:2-15; Skakkebaek, N.E. et al., (2001) Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects. Human Reproduction 2001:16:5:972-978.
17 Gray, L.E. Jr., Ostby, J., Furr, J., Price, M., Veeramachaneni, D.N., Parks, L. Perinatal exposure to the phthalates DEPH, BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat. Toxicological Sciences 2000:58:350-565.
18 Colón, I., et al., Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development. Environmental Health Perspectives, 2000. 108(9): p. 895-900.
19 Akingbemi, B.T., Ge, R., Klinefelter, G.R., Zirkin, B.R., Hardy, M.P. Phthalate-induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. Proceedings of the NationalAcademy of Sciences 2004 (Early Edition). www.pnas.org/cgi/doi/10.1073/pnas.0305977101 , accessed 31 December 2003.
20 Seo, K.W., Kim, K.B., Kim,Y.J., Choi, J.Y, Lee, K.T., Choi, K.S. Comparison of oxidative stress and changes of xenobiotic metabolizing enzymes induced by phthalates in rats. Food Chem Toxicol. 2004 Jan;42(1):107-14.
21 Duty, S.M., Singh, N.P., Silva, M.J., Barr, D.B., Brock, J.W., Ryan, L., Herrick, R.F., Christiani, D.C., Hauser, R. The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environ Health Perspect 2003 111:9:1164-1169.
http://ehp.niehs.nih.gov/members/2003/5756/5756.html , accessed 6 January 2004.
22 Foster, P M. Turner K J, Barlow N J. Anti-androgenic effects of a phthalate combination on in utero male reproductive development in the Sprague-Dawley rat: additivity of response? Toxicologist 2000 Mar; 66(1-S), 233.
23 Environmental Data Services, Ends Daily 15th Dec 2003.
24 DIRECTIVE 2003/53/EC OF THE EUROPEAN PARLIAMENT AND OF THE COUNCIL of 18 June 2003 amending for the 26th time Council Directive 76/769/EEC relating to restrictions on the marketing and use of certain dangerous substances and preparations (nonylphenol, nonylphenol ethoxylate and cement), Official Journal L 178 17-7-2003
25 Jobling S., Sheahan D., Osborne J., Matthiessen P., Sumpter J. (1996). Inhibition of testicular growth in rainbow Trout (Oncorhynchus mykiss) exposed to oestrogenic alkylphenolic chemicals. Environ. Toxicol. Chem., 15, 194-202.
26 Sohoni et al, Reproductive effects of long term exposure to bisphenol A in the fathead minnow (Pimephales promelas), Environ Sci Technol 2001:35: 2917-2925.
27 Environment Agency of England and Wales 1998; Endocrine Disrupting Substances in the Environment. What Should Be Done? The EA Bristol.
28 Commission of the European Communities. Proposal for a Directive of the European Parliament and of the Council relating to the restrictions on the marketing and use of nonylphenol, nonylphenol ethoxylate and cement. COM (2002) 459, 2002/0206 (COD).
29 Kopf W. Wirkung endokriner stoffe in biotests mit wasserogranismen. In Stoffe mit endokriner wirkung in wasser. Bayerisches landesamt für wasserwirtschaft, Institut für Wasserforschung München (ed) Oldenbourg (1997) (as detailed in the European Union Risk Assessment Report (2002) 4-NONYLPHENOL (BRANCHED) AND NONYLPHENOL, CAS Nos: 84852-15-3 and 25154-52-3 EINECS Nos: 284-325-5 and 246-672-0, Joint Research Centre, European Commission).
30 Jobling, S., Casey, D. Rodgers-Gray, T., Oehlmann, J., Schult-Oehlmann, U., Pawlowski, S., Baunbeck, T., Turner, A.P., Tyler, C.R. comparative responses of molluscs and fish to environmental estrogens and an estrogenic effluent. Aquat Toxicol 2003 Oct 29;65(2):205-20.
31 Oehlmann, J., Schulte-Oehlmann, U., Tillmann, M., Markert, B. Effects of endocrine disruptors on Prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: Bisphenol A and octylphenol as xenoestrogens. Ecotoxicology 2000 9:383-397.
32 Nice, H.E., Morritt, D., Crane, M. Thorndyke, Long-term and transgenerational effects of nonylphenol exposure at a key stage in the development of Crassostrea gigas. Possible endocrine disruption? M. Marine Ecology Progress Series, 2003 256:293-300.
33 Billinghurst, Z., Clare, A.S., Depledge M.H. Effects of 4-n-nonylphenol and 17beta-oestradiol on early development of the barnacle Elminius modestus. J. Exper. Mar. Biol. Ecol. 2001: Mar 15;25(2);255-268.
34 Stoker, C., Rey, F. Rodriguez, H., Ramos, J.G., Sirosky, P., Larriera, A., Luque Munoz-de-Toro, M. Sex reversal effects on Caiman latirostris exposed to environmentally relevant doses of the xenoestrogen bisphenol A. Gen Comp Endocrinol 2003 Oct 1;133(3)287-96.
35 Markey, C.M., Coombs, M.A. Sonnenschein, C., Soto, A.M. Mammalian development in a changing environment: exposure to endocrine disruptors reveals the developmental plasticity of steroid hormone target organs. Evol Dev 2003 Jan-Feb;5(1):67-75.
36 Berg, C., Halldin, K., Brunstrom, B. Effects of bisphenol A and tetrabromobisphenol A on sex organ development in quail and chicken embryos. Environ Toxicol Chem 2001 Dec;20(12):2836-40.
37 Lee, H.J., Chattopadhyay, S., Gong, E-Y, Ahn, R.S, Lee, K. Antiandrogenic effects of bisphenol A and nonylphenol on the function of androgen receptor. Toxicological Sciences 2003 75:, 40-46.
38 Atienzar, F.A., Billinghurst, Z., Depledge, M.H. 4-n-Nonylphenol and 17-beta estradiol may induce common DNA effects in developing barnacle larvae. Environ Pollut 2002;120(3):735-8.
39 Dunckel (cited in Birnbaum, L., Staskal, D.F. Polybrominated flame retardants: cause for concern? Environ Health Perspect 2004:112:9-17. doi10.1289/ehp.6559. available via dx.doi.org. Accessed 5 January 2004.
40 Official Journal of The European Union, L 42/45 Feb. 15, 2003.
41 Schecter, A. Pavuk, M. Papke, O., Ryan, J.J., Birnbaum, L., Rosen, R. Polybrominated diphenyl ethers (PBDEs) in U.S. mothers’ milk. Environ Health Perspect 2003:111:14:1723-1724.
42 http://www.ourstolenfuture.org/NewScience/oncompounds/PBDE/2003/2003-0807schecteretal.htm
Accessed 5 January 2004.
43 http://www.panda.org/about_wwf/where_we_work/europe/what_we_do/policy_and_events/epo/news.cfm?uNewsID=9941 Accessed 8 January 2004.
44 Lindberg, P., Sellström, U., Häggberg, L., and de Wit, C.A. Higher brominated diphenyl ethers and hexabromocyclododecane found in eggs of peregrine falcons (Falco peregrinus) breeding in Sweden. Environ Sci Technol 2004:38;(1): 93-96.
45 Norstrom RJ, Simon M, Moisey J,Wakeford B,Weseloh D.V. Geographical distribution (2000) and temporal trends (1981-2000) of brominated diphenyl ethers in Great Lakes herring gull eggs. Environ Sci Technol. 2002 Nov 15;36(22):4783-9.
46 De Boer, J.,Wester, P.G., Klamer, H.J.C., Lewis,W.E., Boon, J.P. Do flame retardants threaten ocean life? Nature 1998:394:28-29; doi:10.1038/27798
47 Ikonomou et al., 2002a (cited in Birnbaum & Staskel, 2004).
48 Birnbaum & Staskal, 2004.
49 Birnbaum & Staskal, 2004.
50 Birnbaum & Staskal, 2004.
51 Darnerud, P.O. Toxic effects of brominated flame retardants in man and in wildlife. Environ Int 2003 Sep;29(6):841.
52 Helleday, T., Tuominen, K.L., Bergman, A., Jenssen, D. Brominated flame retardants induce intragenic recombination in mammalian cells. Mutat Res 1999:Feb 19;439(2):137-47.
Adapted by the article written by the World Wildlife Fund (WWF) entitled “Cause for Concern: Chemicals and Wildlife. http://www.wwf.org.uk
WWF is...
the world's largest and most experienced independent conservation organisation;
a truly global network, working in more than 90 countries;
a challenging, constructive, science-based organisation that addresses issues from the survival of species and habitats to climate change, sustainable business and environmental education;
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by Dr. George J Georgiou, Ph.D.,N.D.,DSc (AM)
Natural Medicine Practitioner, Researcher in Xenobiotics
Email: drgeorge@detoxmetals.com
Web: www.detoxmetals.com
Toxic Chemicals Everywhere
Toxic chemicals, otherwise known as “xenobiotics” (Gk: foreign to life) which are scattered all over our planet from the North Pole to the South Pole, are being constantly researched, and the conclusion is that they are extremely toxic to humans as well as wildlife. Even though some chemicals have been taken off the market, those that remain are even more noxious than the ones already banned. Bioaccumulation in soils, water supplies and the tissues of animals and humans is a real problem which results in these chemicals lingering for many, many years even after they have being banned. DDT, for example, has been banned for more than 25 years in the Western world, yet it is still being found in the tissues of wildlife in the arctic, as well as humans in many different countries.
A recent study noted that only five organochlorine compounds and mercury were found in marine mammals in the 1960s. Today over 265 organic pollutants and 50 inorganic chemicals have been found in these species.1
Recent research has focused on how chemicals affect the thyroid and pituitary systems. Some chemicals have been identified as endocrine disrupters because they can interfere with the body’s own hormones, which are secreted by the endocrine glands.
It is also emerging that endocrine disrupters can have many physiological effects not directly associated with the primary system. For example, the thyroid system is well known to regulate metabolism, but it is also a crucial component in foetal brain development in mammals, and too much or too little thyroid hormone at crucial points can do permanent damage. The immune system is also vulnerable to hormone-mediated disruption. Chemicals can cause neurological problems, reproductive and developmental abnormalities, and cancers as well. And researchers are only just beginning to disentangle the questions about the effects of chronic low-level exposure (as opposed to brief high doses of chemicals), combinations of chemicals, and interactions between chemicals and other physiological and environmental factors.
Let us take a brief look at some of the more common xenobiotics chemicals that that have detrimental effects on humans as well as wildlife.
Perfluorochemicals (PFCs)
These compounds are chains of fully fluorinated carbon atoms of varying lengths, yielding chemicals that are extremely resistant to heat, chemical stress, and that repel both water and oil. Because of these properties PFCs, or chemicals that degrade into PFCs, have been widely used since the 1950s by industry as surfactants and emulsifiers and in commercial products, including stain or water protectors for carpet, textiles, auto interiors, camping gear and leather; food packaging; folding cartons and other paper containers; floor polishes; photographic film; shampoos; dental cleaners; inert pesticide ingredients; and lubricants for bicycles, garden tools and zippers.
Their persistence is extreme, particularly perfluorooctanoic acid (PFOA) - there is no evidence that they ever fully degrade, and they have been found in animals, humans and ecosystems worldwide.
The first public indication that PFOS and PFOA were problematic came on May 16,
2000 when 3M, the primary global manufacturer of many perfluoroalkanesulfonates and
PFOA, announced plans to phase out by the end of 2001 the production of perfluorooctanyl chemistry that underpinned their extremely successful Scotchgard™ and Scotchban™ product lines.2
A 2002 European study of PFCs has detected these compounds in bottlenose, common and striped dolphins, whales, bluefin tuna, swordfish and cormorants in the Mediterranean, and in ringed and grey seals, sea eagles and Atlantic salmon in the
Baltic.3
Other research shows that this chemical is now contaminating many wildlife species around the world, including polar bears in the Arctic, seals in Antarctica, dolphins in the river Ganges in India, albatrosses from Midway Atoll in the Pacific, turtles in the United States, gulls in Korea, cormorants in Canada,4 and fish in Japan.5
Fluorinated telomers are used to keep grease from soaking through fast food containers such as pizza boxes, French fry holders, and food wrapping paper. The digestive system can break telomers down into PFOA and related chemicals. Newly revealed tests conducted by 3M showed that a metabolite specific to the telomers was found in 85 per cent of the children tested.6
Red Cross blood banks, conducted by a team including scientists from the 3M Company, estimated the average concentrations in humans to be 30-40 parts per billion (ppb), with males having higher levels.7 By comparison, levels in wildlife have been measured at 940 ppb in common dolphin liver; 1100 ppb in ringed seals from the Bay of Bothnia; and 270 ppb in long-finned pilot whale liver from the North Thyrrenian Sea.8
Health Effects of Perfluorochemicals (PFCs)
In 1979, 3M administered four doses of PFOS to monkeys and all the monkeys in all treatment groups died within weeks. Typically, when a study like this is conducted, the researchers predict that the lowest dose will not cause any harmful health effects.9
In 1981 both DuPont and 3M reassigned women of childbearing age working in their production plants after they learned that PFOA caused developmental abnormalities in laboratory animals. Within weeks of this discovery, DuPont found PFOA in the women’s blood.
It was known as early as 1975 that fumes from hot pans coated with polytetrafluoroethylene can kill pet birds,10 and broiler chicks have died after exposure to polytetrafluoroethylene-coated light bulbs.11 Laboratory experiments reported in 2003 showed that in rats, PFOS exposure can lead to loss of appetite, interrupted oestrus cycles, and elevated stress hormone levels. PFOS was found to accumulate in brain tissue, particularly the hypothalamus, suggesting that PFOS crosses the blood-brain barrier and may interfere with reproductive hormones through the pituitary-hypothalamus process that stimulates their production.12
Recent laboratory studies with PFOA involving rats show low birth weight, small pituitary gland, altered maternal care behaviour, high pup mortality, and significant changes in the brain, liver, spleen, thymus, adrenal gland, kidney, prostate, testes and epididymides13
Several studies indicate PFOA increases estrogens and leads to testosterone dysfunction in males. There is even more evidence that PFOA as well as chemicals that metabolize to PFOs and PFOA lead to underactive thyroid; thyroid dysfunction during pregnancy can lead to many developmental problems, including faulty brain development and neurological and behavioural problems that affect not only infants and young animals (or humans) but continue into adulthood. The EPA considers both PFOS and PFOA to be a carcinogen in animals, with testicular, pancreatic, mammary, thyroid and liver tumours most frequent in exposed rats.
All studies to date indicate perfluorinated compounds damage the immune system. In one experiment, a chemical very similar to PFOA called PFDA resulted in such atrophy of the thymus gland, (the source of T cells that attack bacteria, viruses and cancer cells) that the gland was undetectable upon clinical examination.
Phthalates
Phthalates are a group of chemicals used as softeners in a variety of plastic products, including the ubiquitous polyvinyl chloride (PVC). Products containing phthalates include medical devices (intravenous tubing, blood bags, masks for sleep apnea devices), building products (insulation of cables and wires, tubes and profiles, flooring, wallpapers, outdoor wall and roof covering, sealants), car products (car under-coating, car seats etc.) and children’s products (teething rings, squeeze toys, clothing and rainwear). They are also used in some lacquers, paints, adhesives, fillers, inks and cosmetics.
The most common phthalate in the environment is di-(2-ethylhexyl)phthalate (DEHP), which comprises half of all phthalates produced in Western Europe, with 450,000 tonnes used per year. Concern about children’s exposure to phthalates prompted the EU to ban six types of phthalate softeners in PVC toys designed to be mouthed by children under three years of age.
Both humans and wildlife may be exposed to various phthalates. For example, a 2003 study of two groups of pregnant women, one in New York City and one in Krakow, Poland, compared the levels of four phthalates in the women’s personal ambient air and measured the levels of the metabolites of these phthalates in the urine of the New York women.14 All four phthalates were present in all the air samples, but air concentrations of DBP, di–isobutyl phthalate and DEHP were higher in Krakow than in New York. The study found that air was a significant source of exposure, that some women receive doses high enough to cause concern, and that there was a correlation between air and urine levels of some phthalates.
Other studies in the EU have also raised concerns with regard to current exposure levels. A recent study in Germany, for example, has concluded that exposure to DEHP may be far higher than previously thought. It reported that in 12 per cent of the Germans studied, phthalate levels exceeded the tolerable daily intake (TDI) used by the EU Scientific Committee for Toxicity, Ecotoxicity and the Environment. Exposure to DBP and BBP was also ubiquitous.15
Health Effects of Phthalates
Some phthalates appear to exert endocrine disrupting effects, and can act against the male hormone, androgen, through pathways other than binding to androgen or estrogen receptors. While there is little research on the effects of phthalates on wildlife per se, some studies suggest that there may be serious consequences for both wildlife and humans. Of particular concern is phthalate exposure in pregnant females: some researchers have proposed that the antiandrogenic properties of phthalates might be linked to testicular dysgenesis syndrome, the manifestations of which range from birth defects in males, including undescended testes, to low sperm counts and testicular cancer.16
Numerous Laboratory studies underpin the concern. For example, a study has shown that DEHP, BBP, and DINP administered to pregnant rats induced feminized breasts in the male offspring, as well as other reproductive malformations, including small testes in the case of the DEHP and BBP.17
There are also worries that exposure to manmade chemicals with hormone disrupting properties may be affecting the age of puberty. A study of Puerto Rican girls with premature breast development suggested a possible association with exposure to certain phthalates.18 U.S. researchers recently reported the effects of DEHP on Leydig cells (testosterone-producing cells in the testes) in rats.19 They found that prolonged exposure to DEHP caused the number of Leydig cells to increase by 40 per cent-60 per cent while simultaneously reducing testosterone production. At the same time, blood levels of both testosterone and estrogens increased by 50 per cent. It is known that males with high levels of serum testosterone and luteinizing hormone (a hormone that triggers testosterone production) are at higher risk of early puberty and testicular tumours.
With regard to cancer, a recent study supported other research associating DEHP with liver cancer in rodents.20 A 2003 Harvard study suggested another mechanism for carcinogenic effect of phthalates. The researchers measured levels of eight phthalates in subjects and found an association between monoethyl phthalate (MEP) and increased damage to the DNA in the subjects’ sperm.21 This is the first study showing that phthalates can induce such damage at levels presently found in the environment.
Other studies with phthalates show that additive effects can occur when there is exposure to more than one phthalate.22 This underlines the growing concern with real life exposures to multiple pollutants, and the increasing realisation that current regulatory practices, based on testing chemicals in isolation, may not be protective.
Phenols, Bisphenyl A and Nonylphenol
Evidence for endocrine disruption by the widely used phenol compounds bisphenol A (BPA) and nonylphenol is mounting. BPA is mostly used to make polycarbonate plastic, which has a diverse range of application in making bottles, computer and electronics shells, CDs, crash helmets, and many other consumer products.
Certain compounds that can leach BPA are also used in the plastic linings of food cans
and in dental fillings, through which people can ingest small quantities. In December 2003, concerned about BPA in the plastic linings of food cans, the EU reduced the amount of BPA migration permitted by 80 percent to 0.6 milligrams per kilogram of food.23 However, BPA remains widely distributed in consumer products.
Nonylphenolic compounds have been used in degreasing solutions, and in leather and textile processing, as well as in de-icing fluid, paints, plastics, and pesticides. The EU has imposed restrictions on the marketing and use of nonylphenol and nonylphenol ethoxylates to a certain extent in cleaning products, textile and leather processing, agricultural teat dips, metal working, pulp and paper, cosmetics including shampoos, and personal care products except spermicides.24
Health Effects of Phenols, Bisphenyl A and Nonylphenol
Fish have been shown to be susceptible to the endocrine disrupting effects of both nonylphenol25 and BPA.26 Exposure to either of these chemicals can cause male fish to make vitellogenin (an estrogen-regulated protein produced by female egg-laying vertebrates and not normally produced by males or juveniles), and can also affect the formation of sperm. Before improved regulation, male fish in the river Aire in England were found to be feminised downstream of a wastewater treatment plant discharge containing alkylphenol ethoxylates from the textile industry. Many male fish were found with egg producing cells in their testes, and reduced testis growth rate and size.27,28
Aquatic invertebrates seem particularly sensitive to these chemicals. For example, nonylphenol affects the freshwater algae, Scenedesmus subspicatus at levels of 3.3 micrograms per litre.29 Molluscs in particular have shown effects at very low dose levels. For example, in the mollusc Potamopyrgus antipodarum, BPA and octylphenol, as well as a mixture of these and other chemicals in treated sewage effluent, stimulated egg and embryo production at low doses and inhibited such production at high doses.30
This work supported a 2000 study by some of the same researchers showing that extremely low levels of BPA and octylphenol triggered malformed genitals of female ramshorn (freshwater) snail, Marisa cornuarietis, and the (saltwater) dogwhelk Nucella lapillus.31 In some of the freshwater snails, the excessive growth of the female glands and the egg masses ruptured the egg tube, and the snails died. This syndrome was referred to as superfeminisation. A number of other adverse changes were observed in both species. Another important finding was that in the freshwater snails, the medium doses of octylphenol produced more changes than either the highest or lowest doses.
Other researchers have shown that a single 48-hour exposure to 1 microgram per litre of nonylphenol, comparable to environmental levels, altered the sex ratio of oysters, reduced the survival of offspring, and caused some oysters to become hermaphroditic.32
A 2001 study exposing barnacles to concentrations of nonylphenol similar to those in the environment (0.01-10 micrograms per litre) disrupted the timing of larval development.33 In addition to fish, other vertebrates also show effects when exposed to BPA. For example, in 2003, researchers reported that BPA at environmentally comparable doses resulted in sex reversals and altered gonadal structures in the broad-snouted caiman, an alligator relative native to mid-latitude South America.34 In another study, the offspring of pregnant mice exposed to BPA showed changes in ovarian and mammary gland tissues and disrupted fertility cycles as adults.35 BPA was reported for the first time in 2001 to induce reproductive malformations in birds - specifically, in female quail embryos and male chicken embryos. The female embryos’ oviducts developed abnormally, and the males’ testes were feminized.36
The exact mechanism by which BPA and nonylphenol exert their effects is not clear, but a recent in vitro study demonstrated a molecular mechanism by which BPA and nonylphenol interfere with both the activation and function of cellular androgen receptors.37 In a 2002 study, nonylphenol tested on barnacle larvae induced DNA damage, possibly including mutations, and the authors speculate that this effect may be a mechanism by which higher level reproductive abnormalities are caused.38
Despite evidence from these and other studies, the low dose effects of BPA are still in dispute. Regulators in the EU have been reluctant to act, and further studies have been demanded.
Polybrominated Flame Retardants (BFRs)
Brominated flame retardants (BFRs) in furniture, building material, and clothing have become a serious concern, as their levels are showing sharp increases in living organisms. The first BFRs were taken off the market in the early 1970s after a spill led to poisonings of livestock and farm families in Michigan.39 Three BFRs now dominate the market: TBBPA, the most widely used, primarily in printed circuit boards and in some plastics; HBCD, and the deca-BDEs. The other commercial PBDEs (octa-BDE and penta-BDE) have been banned in the EU as of August 2004,40 and the state of California has taken similar action. However, because of their alarming spread and rate of accumulation in humans and animals, Europe’s ban does not provide complete reassurance, particularly regarding the penta-BDE form used as a flame retardant in polyurethane foam elsewhere in the world.
Researchers recently reported levels of PBDEs in U.S. breast milk.41 Forty-seven Texas women had an average level of 73.9 ng/g lipid; such levels are sharply higher than those found in European studies. There are serious concerns about the transfer of BFRs to nursing infants, and some scientists are worried that BFRs might affect foetal development, including disruption of the thyroid system’s role in foetal brain development.42 In 2003 a WWFUK biomonitoring program found deca-BDE in the blood of seven per cent of those tested.43
New research from Sweden has found high levels of several brominated flame retardants in the eggs of peregrine falcons from 1987-1999. The eggs of falcons living in the wild had significantly higher concentrations of the essentially unregulated deca-BDE than eggs of captive falcons. The fact that deca-BDE was found in eggs demonstrates that the chemical can cross cell membranes, contrary to what scientists had previously thought. The peregrine study represents the first time that the deca formulation has been found in wildlife.44
In 2002, one research team predicted that within 10 to 15 years, concentrations of BFRs in Great Lakes herring gull may be higher than those of PCBs.45 BFRs have also been found in sperm whales,46 ringed seals from the Canadian Arctic,47 mussels and several kinds of fish in Norwegian waters, and harbour seals in San Francisco Bay,48 among other wildlife. Essentially, BFRs are being found wherever we look.
Health Effects of BFRs
Laboratory studies show that certain BFRs are highly toxic to aquatic animals (crustaceans),49 and suggest effects on pubertal development, thyroid and liver in rats, as well as developmental neurotoxicity in mice.50 A recent paper reported behavioural effects in mice pups at a relatively low dose.51 In 1999 Swedish researchers reported that PBDEs and HBCD may have health effects similar to those of DDT and PCBs because of their ability to induce genetic recombination.52
While there are no published epidemiological studies on effects of BFRs on humans, the possible thyroid effects, based on tissue culture and animal studies, are a red flag. As with other chemicals, anything that affects foetal development merits particular study because of the profound, long-term, and often irreversible influence that early exposures have on the entire life of an organism.
What Can We Do To Protect Ourselves?
The answer to this question is two-fold; first we can push for legislation to ban a lot of these harmful chemicals that have been researched and are known to be detrimental to animals and humans. Second, we need to be able to detoxify our bodies in order to eliminate many of these chemicals. Given that we are exposed to these literally daily, this process must be an ongoing one. It is not safe to use chemical chelators on an ongoing basis, but natural ones can be used instead, much like a supplement on a daily basis. HMD™ can be used safely over long periods of time with no side effects – it is presently being tested to see its efficacy in eliminating some of the xenobiotics mentioned in this article.
References
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2 3M. (2000) 3M phasing out some of its specialty materials, May 16, 2000 press release.
3 Kannan, K., Corsolini, S., Falandysz, J., Oehme, G., Focardi, S., Giesy, J.P. Perfluorooctanesulfonate and related fluorinated hydrocarbons in marine mammals, fishes and birds from coasts of the Baltic and MediterraneanSeas. Environ Sci Technol 2002 Aug 1;36(15):3210-6.
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6 Fields, S. Another fast-food fear. Environ Health Perspect 2003: 111:16:A162.
7 Olsen, G. W., Church, T.R., Miller, J.P., Burris, J.M., Hansen, K.J., Lundberg, J.K., Armitage, J.B., Herron, R.M., Medhdizadehkashi, Z., Nobiletti, J.B., O’Neill, E.M., Mandel, J.H., Zobel, L.R. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Environ Health
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8 Kannan, et al., 2002.
9 Organization for Economic Cooperation and Development (OECD). (2002) Hazard Assessment of perfluorooctane sulfonate (PFOS) and its salts (November, 21 2002). ENV/JM/RD(2002)17/FINAL. Available online at: http://www.oecd.org/dataoecd/23/18/2382880.pdf
10 “PFCs: A Family of Chemicals that Contaminate the Planet,” Part 6: PFCs in Animals Worldwide. Environmental Working Group, 2003.
http://www.ewg.org/reports/pfcworld/part8.php Accessed 3 January 2004.
11 Ibid.
12 Austin, M.E., Kasturi, B.S., Barber, M., Kannan, K., MohanKumar, P.S., MohanKumar, S.M.J. Neuroendocrine effects of perfluorooctane sulfonate in rats.
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13 Thayer, K., Klein, J. Gray, S., Houlihan, J.,Wiles, R., Greenleaf, T., PFCs: A Family of Chemicals that Contaminate the Planet. Environmental Working Group 2003.
http://www.ewg.org/reports/pfcworld/part4.php Accessed 5 January 2004.
14. Adibi, J.J., Perera, F.P., Jedrychowski,W., Camann, D.E., Barr, D., Jacek, Ryszard, Whyatt, R.M. Prenatal exposures to phthalates among women in New York City and Krakow, Poland. Environ Health Perspect 2003:111:14:1719-1722.
15 Kock et al, 2003. An estimation of the daily intake of di(2-ethyl) phthalate (DEHP) and other phthalates in the general population. International Journal Hygiene and Environmental Health.
16 Sharpe R.M. (2003). The oestrogen hypothesis – where do we stand now? International Journal of Andrology 26:2-15; Skakkebaek, N.E. et al., (2001) Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects. Human Reproduction 2001:16:5:972-978.
17 Gray, L.E. Jr., Ostby, J., Furr, J., Price, M., Veeramachaneni, D.N., Parks, L. Perinatal exposure to the phthalates DEPH, BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat. Toxicological Sciences 2000:58:350-565.
18 Colón, I., et al., Identification of phthalate esters in the serum of young Puerto Rican girls with premature breast development. Environmental Health Perspectives, 2000. 108(9): p. 895-900.
19 Akingbemi, B.T., Ge, R., Klinefelter, G.R., Zirkin, B.R., Hardy, M.P. Phthalate-induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. Proceedings of the NationalAcademy of Sciences 2004 (Early Edition). www.pnas.org/cgi/doi/10.1073/pnas.0305977101 , accessed 31 December 2003.
20 Seo, K.W., Kim, K.B., Kim,Y.J., Choi, J.Y, Lee, K.T., Choi, K.S. Comparison of oxidative stress and changes of xenobiotic metabolizing enzymes induced by phthalates in rats. Food Chem Toxicol. 2004 Jan;42(1):107-14.
21 Duty, S.M., Singh, N.P., Silva, M.J., Barr, D.B., Brock, J.W., Ryan, L., Herrick, R.F., Christiani, D.C., Hauser, R. The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environ Health Perspect 2003 111:9:1164-1169.
http://ehp.niehs.nih.gov/members/2003/5756/5756.html , accessed 6 January 2004.
22 Foster, P M. Turner K J, Barlow N J. Anti-androgenic effects of a phthalate combination on in utero male reproductive development in the Sprague-Dawley rat: additivity of response? Toxicologist 2000 Mar; 66(1-S), 233.
23 Environmental Data Services, Ends Daily 15th Dec 2003.
24 DIRECTIVE 2003/53/EC OF THE EUROPEAN PARLIAMENT AND OF THE COUNCIL of 18 June 2003 amending for the 26th time Council Directive 76/769/EEC relating to restrictions on the marketing and use of certain dangerous substances and preparations (nonylphenol, nonylphenol ethoxylate and cement), Official Journal L 178 17-7-2003
25 Jobling S., Sheahan D., Osborne J., Matthiessen P., Sumpter J. (1996). Inhibition of testicular growth in rainbow Trout (Oncorhynchus mykiss) exposed to oestrogenic alkylphenolic chemicals. Environ. Toxicol. Chem., 15, 194-202.
26 Sohoni et al, Reproductive effects of long term exposure to bisphenol A in the fathead minnow (Pimephales promelas), Environ Sci Technol 2001:35: 2917-2925.
27 Environment Agency of England and Wales 1998; Endocrine Disrupting Substances in the Environment. What Should Be Done? The EA Bristol.
28 Commission of the European Communities. Proposal for a Directive of the European Parliament and of the Council relating to the restrictions on the marketing and use of nonylphenol, nonylphenol ethoxylate and cement. COM (2002) 459, 2002/0206 (COD).
29 Kopf W. Wirkung endokriner stoffe in biotests mit wasserogranismen. In Stoffe mit endokriner wirkung in wasser. Bayerisches landesamt für wasserwirtschaft, Institut für Wasserforschung München (ed) Oldenbourg (1997) (as detailed in the European Union Risk Assessment Report (2002) 4-NONYLPHENOL (BRANCHED) AND NONYLPHENOL, CAS Nos: 84852-15-3 and 25154-52-3 EINECS Nos: 284-325-5 and 246-672-0, Joint Research Centre, European Commission).
30 Jobling, S., Casey, D. Rodgers-Gray, T., Oehlmann, J., Schult-Oehlmann, U., Pawlowski, S., Baunbeck, T., Turner, A.P., Tyler, C.R. comparative responses of molluscs and fish to environmental estrogens and an estrogenic effluent. Aquat Toxicol 2003 Oct 29;65(2):205-20.
31 Oehlmann, J., Schulte-Oehlmann, U., Tillmann, M., Markert, B. Effects of endocrine disruptors on Prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: Bisphenol A and octylphenol as xenoestrogens. Ecotoxicology 2000 9:383-397.
32 Nice, H.E., Morritt, D., Crane, M. Thorndyke, Long-term and transgenerational effects of nonylphenol exposure at a key stage in the development of Crassostrea gigas. Possible endocrine disruption? M. Marine Ecology Progress Series, 2003 256:293-300.
33 Billinghurst, Z., Clare, A.S., Depledge M.H. Effects of 4-n-nonylphenol and 17beta-oestradiol on early development of the barnacle Elminius modestus. J. Exper. Mar. Biol. Ecol. 2001: Mar 15;25(2);255-268.
34 Stoker, C., Rey, F. Rodriguez, H., Ramos, J.G., Sirosky, P., Larriera, A., Luque Munoz-de-Toro, M. Sex reversal effects on Caiman latirostris exposed to environmentally relevant doses of the xenoestrogen bisphenol A. Gen Comp Endocrinol 2003 Oct 1;133(3)287-96.
35 Markey, C.M., Coombs, M.A. Sonnenschein, C., Soto, A.M. Mammalian development in a changing environment: exposure to endocrine disruptors reveals the developmental plasticity of steroid hormone target organs. Evol Dev 2003 Jan-Feb;5(1):67-75.
36 Berg, C., Halldin, K., Brunstrom, B. Effects of bisphenol A and tetrabromobisphenol A on sex organ development in quail and chicken embryos. Environ Toxicol Chem 2001 Dec;20(12):2836-40.
37 Lee, H.J., Chattopadhyay, S., Gong, E-Y, Ahn, R.S, Lee, K. Antiandrogenic effects of bisphenol A and nonylphenol on the function of androgen receptor. Toxicological Sciences 2003 75:, 40-46.
38 Atienzar, F.A., Billinghurst, Z., Depledge, M.H. 4-n-Nonylphenol and 17-beta estradiol may induce common DNA effects in developing barnacle larvae. Environ Pollut 2002;120(3):735-8.
39 Dunckel (cited in Birnbaum, L., Staskal, D.F. Polybrominated flame retardants: cause for concern? Environ Health Perspect 2004:112:9-17. doi10.1289/ehp.6559. available via dx.doi.org. Accessed 5 January 2004.
40 Official Journal of The European Union, L 42/45 Feb. 15, 2003.
41 Schecter, A. Pavuk, M. Papke, O., Ryan, J.J., Birnbaum, L., Rosen, R. Polybrominated diphenyl ethers (PBDEs) in U.S. mothers’ milk. Environ Health Perspect 2003:111:14:1723-1724.
42 http://www.ourstolenfuture.org/NewScience/oncompounds/PBDE/2003/2003-0807schecteretal.htm
Accessed 5 January 2004.
43 http://www.panda.org/about_wwf/where_we_work/europe/what_we_do/policy_and_events/epo/news.cfm?uNewsID=9941 Accessed 8 January 2004.
44 Lindberg, P., Sellström, U., Häggberg, L., and de Wit, C.A. Higher brominated diphenyl ethers and hexabromocyclododecane found in eggs of peregrine falcons (Falco peregrinus) breeding in Sweden. Environ Sci Technol 2004:38;(1): 93-96.
45 Norstrom RJ, Simon M, Moisey J,Wakeford B,Weseloh D.V. Geographical distribution (2000) and temporal trends (1981-2000) of brominated diphenyl ethers in Great Lakes herring gull eggs. Environ Sci Technol. 2002 Nov 15;36(22):4783-9.
46 De Boer, J.,Wester, P.G., Klamer, H.J.C., Lewis,W.E., Boon, J.P. Do flame retardants threaten ocean life? Nature 1998:394:28-29; doi:10.1038/27798
47 Ikonomou et al., 2002a (cited in Birnbaum & Staskel, 2004).
48 Birnbaum & Staskal, 2004.
49 Birnbaum & Staskal, 2004.
50 Birnbaum & Staskal, 2004.
51 Darnerud, P.O. Toxic effects of brominated flame retardants in man and in wildlife. Environ Int 2003 Sep;29(6):841.
52 Helleday, T., Tuominen, K.L., Bergman, A., Jenssen, D. Brominated flame retardants induce intragenic recombination in mammalian cells. Mutat Res 1999:Feb 19;439(2):137-47.
Adapted by the article written by the World Wildlife Fund (WWF) entitled “Cause for Concern: Chemicals and Wildlife. http://www.wwf.org.uk
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MY BABY IS LACTOSE INTOLERANT DOCTOR – SHALL I USE SOY INFANT FORMULA
11th Jul 2007
This is a commonly asked question from parents that come to see me for nutritional counselling in Cyprus where I live and work. I have prepared this document in answer to this question about soy infant substitutes for other lactose-containing powdered milks. It’s still unfortunate that many paediatricians in my vicinity are blindly recommending soy infant formula without even looking at the research in order to make a more objective decision – needless to say the children are the victims, including one of my little girls, before becoming wiser to the dangers of soy infant formula.
THE PITFALLS OF SOY INFANT FORMULA
Soybeans are generally high in protein compared to other legumes but contain potent enzyme inhibitors that block the action of trypsin and other enzymes needed for protein digestion. In test animals, diets high in trypsin inhibitors depress growth and cause enlargement and pathological conditions of the pancreas, including cancer.
SOY PROTEIN ISOLATES & CARCINOGENS
Soy protein isolate, a powder extracted from soybeans, is the main ingredient in soymilk products. This is extracted through a process that involves not only high temperatures but also caustic chemicals. The alkaline soaking solution produces a carcinogen, lysinealine, and reduces the cystine content, which is already low in the soybean. Other carcinogens called nitrosamines are formed during high temperature spray drying.
PHYTIC ACID & MINERAL BLOCKAGE
Soybeans also contain high levels of phytic acid or phytates. This is an organic acid, present in the outer portion of all seeds, which blocks the uptake of essential minerals - calcium, magnesium, iron and especially zinc - in the intestinal tract. Soybeans have very high levels of a form of phytic acid that is particularly difficult to neutralize. As early as 1967, researchers testing soy formula found that it caused negative zinc balance in every infant to whom it was given.
Scientists have found a strong correlation between phytate content in formula and poor growth, even when the diets were additionally supplemented with zinc. High amounts of phytic acid in soy foods and grains have caused retarded growth in children on macrobiotic diets. A reduced rate of growth is especially serious in the infant as it causes a delay in the accumulation of lipids in the myelin, and hence jeopardizes the development of the brain and nervous system.
VITAMIN DEFICIENCIES
Soy formula can also cause vitamin deficiencies. Soy increases the body's requirements for vitamin B12, a nutrient that is absolutely vital for good health. Early studies with soy formula indicated that soy blocks the uptake of fats. This may explain why soy seems to increase the body's requirements for fat-soluble vitamin D.
ALUMINIUM & OTHER TOXINS
Aluminum content of soy formula is 10 times greater than milk based formula, and 100 times greater than unprocessed milk. Aluminum has a toxic effect on the kidneys of infants, and has been implicated as causing Alzheimer's in adults. Soy formulas lack cholesterol, another nutrient that is absolutely essential for the development of the brain and nervous system; they also lack lactose and galactose, which play an equally important role in the development of the nervous system. A number of other substances, which are unnecessary and of questionable safety, are added to soy formulas including carrageenan, guar gum, sodium hydroxide (caustic soda), potassium citrate monohydrate, tricalcium phosphate, dibasic magnesium phosphate trihydrate, BHA and BHT.
What about the claim that soy formula is less allergenic than cows milk formula? Studies indicate that allergies to soy are almost as common as those to milk. Use of soy formula to treat infant diarrhoea has had mixed results, some studies showing improvement with soy formula while others show none at all.
PHYTOESTROGENS & ENDOCRINE DISRUPTORS
The most serious problem with soy formula is the presence of phytoestrogens or isoflavones. While many claims have been made about the health benefits of these estrogens-like compounds, animal studies indicate that they are powerful endocrine disrupters that alter growth patterns and cause sterility.
Toxicologists estimate that an infant exclusively fed soy formula receives the estrogenic equivalent of at least five birth control pills per day! By contrast, almost no phytoestrogens have been detected in dairy-based infant formula or in human milk, even when the mother consumes soy products. A recent study found that babies fed soy-based formula had 13,000 to 22,000 times more isoflavones in their blood than babies fed milk-based formula. Scientists have known for years that isoflavones in soy products can depress thyroid function, causing autoimmune thyroid disease and even cancer of the thyroid. But what are the effects of soy products on the hormonal development of the infant, both male and female?
PATTERNS OF SEXUAL ORIENTATION
Male infants undergo a "testosterone surge" during the first few months of life, when testosterone levels may be as high as those of an adult male. During this period, the infant is programmed to express male characteristics after puberty, not only in the development of his sexual organs and other masculine physical traits, but also in setting patterns in the brain characteristic of male behaviour. In monkeys, deficiency of male hormones impairs learning and the ability to perform visual discrimination tasks-such as would be required for reading-and retards the development of spatial perception, which is normally more acute in men than in women.
PREMATURE DEVELOPMENT
Soy infant feeding - which began in earnest in the early 1970s - cannot be ignored as a probable cause for these tragic developments. As for girls, an alarming number are entering puberty much earlier than normal, according to a recent study reported in the journal Pediatrics. Investigators found that one per cent of all girls now show signs of puberty, such as breast development or pubic hair, before the age of three; by age eight, 14.7 per cent of white girls and almost 50 per cent of African-American girls have one or both of these characteristics.
EARLY SEXUAL DEVELOPMENT
New data indicate that environmental oestrogens such as PCBs and DDE (a breakdown product of DDT) may cause early sexual development in girls. In the 1986 Puerto Rico Premature Thelarche study, the most significant dietary association with premature sexual development was not chicken - as reported in the press - but soy infant formula. The consequences of this truncated childhood are tragic. Young girls with mature bodies must cope with feelings and urges that most children are not well-equipped to handle. And early maturation in girls is frequently a harbinger for problems with the reproductive system later in life, including failure to menstruate, infertility and breast cancer.
It goes without saying that future patterns of sexual orientation may also be influenced by the early hormonal environment. Paediatricians are noticing greater numbers of boys whose physical maturation are delayed, or does not occur at all, including lack of development of the sexual organs. Learning disabilities, especially in male children, have reached epidemic proportions. Soy infant feeding-which floods the bloodstream with female hormones that could inhibit the effects of male hormones-cannot be ignored as a possible cause for these tragic developments.
As for girls, an alarming number are entering puberty much earlier than normal, according to a recent study reported in the journal Pediatrics. Investigators found that one percent of all girls now show signs of puberty, such as breast development or pubic hair, before the age of three; by age eight, 14.7 percent of white girls and a whopping 48.3 percent of African-American girls had one or both of these characteristics. New data indicate that environmental estrogens such as PCBs and DDE (a breakdown product of DDT) may cause early sexual development in girls and a study in Puerto Rico implicated soy feeding as a cause of early menarche. The use of soy formula in the WIC program, which supplies free formula to welfare mothers, may explain the astronomical rates of early menarche in African American girls.
The consequences are tragic. Young girls with mature bodies must cope with feelings and urges that most children are not well-equipped to handle. And early maturation in girls is frequently a harbinger for problems with the reproductive system later in life including failure to menstruate, infertility and breast cancer.
Other problems that have been anecdotally associated with children of both sexes who were fed soy-based formula include extreme emotional behavior, asthma, immune system problems, pituitary insufficiency, thyroid disorders and irritable bowel syndrome.
Concerns about the dangers of soy have prompted consumer groups in New Zealand and Canada to call for a ban on the sale of soy infant formula. Milk-based formula contains a better protein profile and does not flood the infant with anti-nutrients and female hormones. Breast feeding is best IF the mother has consumed a healthy diet, one that is rich in animal proteins and fats, throughout her pregnancy and continues to do so while nursing her infant. Mothers who cannot breast feed, for whatever reason, should prepare homemade formula based on whole milk for their babies. The rare child allergic to whole milk formula should be given a whole foods meat-based formula, not one made of soy protein isolate. Parents who invest time in preparing homemade formula will be well rewarded with the joys of conferring robust good health on their children.
For references and further information on soy foods and soy formula, see www.soyonlineservice.co.nz or send $12 US to Soy Alert!, PMB #106-380, 4200 Wisconsin Avenue, NW, Washington DC 20007.
Adapted from the Weston A. Price Foundation Website - www.westonaprice.org
THE SECRETS OF CURING CANDIDA NATURALLY!
31st May 2007
by
Dr. George J Georgiou, Ph.D.,N.D.,D.Sc (A.M)
Natural Medicine Practitioner
Director, DaVinci Natural Health Centre, Larnaca, Cyprus
www.naturaltherapycenter.com
drgeorge@avacom.net
Tel: +357 24 82 33 22
CANDIDA ALBICANS : Are You Winning Battles But Losing the War?
WHAT IS IT?
Every person lives in a virtual sea of microorganisms, (bacteria, viruses, fungi, etc.). These microbes can reside in the throat, mouth, nose, intestinal tract, almost anywhere; they are as much a part of our bodies as the food we eat. Usually, these microorganisms do not cause illness, unless our resistance becomes lowered.
Candida albicans is a yeast that lives in the mouth, throat, intestines and genitourinary tract of most humans and is usually considered to be a normal part of the bowel flora (the organisms that coexist with us in our lower digestive tract). It is actually a member of a broader classification of organisms known as fungi.
Traditionally fungi are considered plants, but they contain no chlorophyll and cannot make their own food. Fungi tend to inhabit cool to tropical climates and are found in the air we breathe as well as in moist and shady soil, water, manure, dead leaves, fruit, leftover food, and in a wide variety of places and circumstances.
HOW DO YOU GET IT?
Candida albicans prefers people. Candida enters newborn infants during or shortly after birth. Usually, the growth of the yeast is kept in check by the infant's immune system and thus produces no overt symptoms. But, should the immune response weaken, the condition known as oral thrush can occur as a result. By six months of age, 90% of all babies test positive for Candida . And by adulthood, virtually all humans play host to Candida albicans and are thus engaged in a life-long relationship.
Candida coexists in our bodies with many species of bacteria in a competitive balance. Other bacteria act in part to keep Candida growth in check in our body ecology . . . unless that balance is upset. When health is present, the immune system keeps Candida proliferation under control; but when immune response is weakened, Candida growth can proceed unhindered. It is an "opportunistic organism," one which, when given the opportunity, will attempt to colonize all bodily tissues. The uncontrolled growth of Candida is known as Candida overgrowth or Candidiasis.
Unfortunately, there are many factors in our modern society that can upset the ecological balance of the body, weaken the immune system and thus allow the yeast to overgrow. Of these, the major risk factors which may predispose one to the proliferation of Candida are:
* STEROID HORMONES, IMMUNOSUPPRESSANT DRUGS such as cortisone which treat severe allergic problems by paralyzing the immune system's ability to react
* PREGNANCY, MULTIPLE PREGNANCIES or BIRTH CONTROL PILLS which upset the body's hormonal balance
* DIETS HIGH IN CARBOHYDRATE AND SUGAR INTAKE,
* YEAST AND YEAST PRODUCTS, AS WELL AS MOLDS AND FERMENTED FOODS
* PROLONGED EXPOSURE TO ENVIRONMENTAL MOLDS
* ANTIBIOTICS and SULFA DRUGS Probably the chief culprit of all, antibiotics kill all bacteria . They do not distinguish good bacteria from bad. Antibiotics kill the "good" flora which normally keeps the Candida under control. This allows for the unchecked growth of Candida in the intestinal tract. It is normally difficult to recover a yeast culture from bodily surfaces. However, after 48 hours of taking tetracycline, yeast can be cultured easily from anyone. The prevalence today of Candida may be most directly related to the widespread societal exposure to antibiotics - from prescriptions for colds, infections, acne, and from additional consumption of antibiotic-treated foods such as meats, dairy, poultry and eggs. Notably, antibiotics do not kill viruses; they only destroy bacteria. Yet, they are universally prescribed for all colds, flus and other viral problems. Such indiscriminate and extensive use of antibiotics is not only considered a primary cause of Candida overgrowth, but is recently being found to be responsible for the unbridaled development of "killer bacteria."
The rapid and direct proliferation of the yeast following antibiotic use strongly suggests that the problem of Candida is one which stems from an inner state of imbalance, rather than from an outside attack by a microbe or disease. This is a very important point to understand if one wishes to get rid of an overgrowth problem, suggesting that Candida is not so much a problem as is the body's own failure to control it!
A SERIOUS PROBLEM
Once begun, if not recognized and treated appropriately, Candida overgrowth can result in a self-perpetuating, negative cycle. Large numbers of yeast germs can weaken the immune system, which normally protects the body from harmful invaders. Even though Candida is part of the ecological balance in the body since birth, it is still recognized by the immune system as a foreign body that needs to be controlled. So, when overgrowth occurs, a chronic stimulation to the immune system results -- every second, every minute, every hour, every day, every month, every year -- in an attempt by the immune system to regain control. In time, it is believed that this can exhaust the immune system, predisposing one to more serious degenerative processes. Many believe chronic drains on the immune system such as Candida and parasites can play a direct role in the development of cancer and AIDS. Seen in this light, Candida overgrowth should not be taken lightly.
The immune system may concurrently be also adversely affected by poor nutrition, heavy exposure to molds in the air, as well as an increasing number of chemicals in our food, water and air, including petrochemicals, formaldehyde, perfumes, cleaning fluids, insecticides, tobacco and other indoor and outdoor pollutants. Over 10,000 chemicals have been added to our food supplies alone that were not there just 100 years ago! We do not have the genetic recognition of these substances as foods or as useful additions to our bodies.
Resulting lowered resistance may not only cause an overall sense of ill health, but also may allow for the development of respiratory, digestive and other systemic symptoms. One may also become predisposed to developing sensitivities to foods and chemicals in the environment. Such "allergies" may in turn cause the membranes of the nose, throat, ear, bladder and intestinal tract to swell and develop infection.
Such conditions may lead the physician to prescribe a "broad spectrum" antibiotic . . . which may then further promote the overgrowth of Candida and strengthen the existing negative chain of events, leading to further stress on the immune system and increased Candida-related problems.
WHAT ARE THE SIGNS OF CANDIDA INFECTION?
The result of heightened Candida overgrowth is a list of adverse symptoms of considerable length. Basically, the characteristics of Candida overgrowth fall under three categories, those affecting:
The gastrointestinal and genitourinary tracts
Allergic responses, and Mental/emotional manifestations.
Initially the signs will show near the sights of the original yeast colonies. Most often the first signs are seen in conditions such as nasal congestion and discharge, nasal itching, blisters in the mouth, sore or dry throat, abdominal pain, belching, bloating, heartburn, constipation, diarrhea, rectal burning or itching, vaginal discharge, vaginal itching or burning, increasingly worsening symptoms of PMS, prostatitis, impotence, frequent urination, burning on urination, bladder infections. But, if the immune system remains weak long enough, Candida can spread to all parts of the body causing an additional plethora of problems such as fatigue, drowsiness, uncoordination, lack of concentration, mood swings, dizziness, headaches, bad breath, coughing, wheezing, joint swelling, arthritis, failing vision, spots in front of the eyes, ear pain, deafness, burning or tearing eyes, muscle aches, depression, irritability, sweet cravings, increasing food and chemical sensitivities, numbness and tingling, cold hands and feet, asthma, hay fever, multiple allergies, hives and rashes, eczema, psoriasis, chronic fungal infections like athlete's foot, ringworm and fingernail/ toenail infections.
In addition, 79 different toxic products are known to be released by Candida , which in itself places a considerable burden on the immune system. These get into the bloodstream and travel to all parts of the body where they may give rise to a host of adverse symptoms.
In Candida overgrowth, the yeast colonies can dig deep into intestinal walls, damaging the bowel wall in their colonization.
Candida can also attack the immune system, causing suppressor cell disease, in which the immune system produces antibodies to everything at the slightest provocation, resulting in extreme sensitivities.
Finally, Candida overgrowth can be dangerous if not controlled. The persistent, constant challenge to the immune system by an ever-increasing, long-term overgrowth of Candida can eventually serve to wear down the immune system and cause a seriously weakened capacity for resistance to disease.
Women are more likely to get Candida overgrowth than are men. This is related to the female sex hormone progesterone which is elevated in the last half of the menstrual cycle. Progesterone increases the amount of glycogen (animal starch, easily converted to sugar) in the vaginal tissues which provide an ideal growth medium for Candida. Progesterone levels also elevate during pregnancy. Men are affected less frequently but are by no means invulnerable.
HOW DO YOU KNOW YOU'VE GOT IT?
Currently, diagnosis is primarily clinical. Since almost everyone has Candida in their bodies, tests for its presence are useless; confirmation of overgrowth is very difficult through laboratory tests. And, since what it does is to paralyze the immune system against it, allergy tests to determine the system's reaction to it are also ineffectual.
Furthermore, the results of the yeast imbalance -- the combined effects of different hormones, poisons generated and released by the yeast into the bloodstream, and the confusion created in the immune system -- produces such a wide variety of symptoms and which are seemingly so unrelated (such as wheezing, depression and fungus infection under fingernails) that a definite diagnosis cannot be made from any specific pattern of signs and symptoms.
Conclusive laboratory tests have not yet been developed, even though there are a number of tests that can help in the diagnosis. The patient’s history and symptoms are usually the key to arriving at a diagnosis, and Dr. Crook’s Candida Questionnaire is extremely helpful as it enables the patient to score their symptoms and arrive at a number – anything above 180 for women, and 140 for men is highly significant and represents the majority of symptoms that relate to this condition. There are other testing procedures that I use in clinical practice, mainly bio-dermal screening using the VEGA (see http://www.naturaltherapycenter.com/vega_allergy_testing ). When an ampule of Candida is placed in the honeycomb of the VEGA EXPERT and the probe placed on an acupoint of a finger, it is very clear when a patient “resists” as the conductivity drops. What I have also found time and time again in over 600 Candida patients that I have tested to date is that they all react to yeast, mushrooms, wine and beer as well when tested. In fact, many times I stumble upon Candida while conducting food intolerance testing using the VEGA, and when finding that mushrooms and yeast come out positive, I immediately test for Candida, which is also positive. I personally find the VEGA a very useful diagnostic device that can answer a lot of questions that more traditional laboratory testing cannot.
Another method of testing for Candida is to use a form of Kinesiological muscle testing called AUTONOMIC RESPONSE TESTING (see www.naturaltherapycenter.com/ART ). Autonomic Response Testing (ART) grew out of the importance of detecting and correct problems of the autonomic nervous system. ART allows the doctor to correct the problems of the ANS and to help restore the self regulating mechanism of the body allowing the patient to return to a state of health. ART is a system of evaluation and treatment developed by Dietrich Klinghardt, MD, Ph.D and Lousia Williams, DC, ND. Dr. Klinghardt is a German trained physician who also has a Ph.D in neurology. ART uses Applied Kinesiology, Electroacupuncture (EAV), O-Ring testing, Nogier pulse, Chinese pulse, heart rate variability and other techniques to assess the health or dysfunction of the autonomic nervous system.
Dr. Klinghardt believes that many practitioners using kinesiology or muscle testing in their practice are often getting inaccurate information because the autonomic nervous system is not functioning properly. In ART, this condition is called 'blocked regulation' and refers to the inability of the ANS to self-regulate and is caused by 7 common factors. These include: undiagnosed food allergies, heavy metal toxicity, petroleum chemical toxicity, chronic unresolved infections and scars, temporomandibular joint dysfunction (TMJ), unresolved psychological stress, and electromagnetic stress. Dr. Klinghardt has developed specific tests for these factors and treatments to correct them. ART is also a good way of detecting whether Candida is prevalent, and the effect that it is having on the Autonomic Nervous System and other organ systems of the body.
CASE HISTORIES
There is still a lot of controversy around the topic of Candida, and I am the first to agree that we do not have all the answers. One thing that I have witnessed in clinical practice, however, is the astounding recovery that many of these so-called Candidiasis patients make when placed on a Candida Treatment Protocol. These would include difficult cases that have been through the orthodox medical mill, seeing many different specialties without positive effects. One case that I remember is a 32 year old women who had such a bad case of halitosis that when I approached her to examine her throat I thought that I was surrounded by rotting corpses! Such was the degree of her bad breath that she had NEVER dated in her life for this reason. My mind never even thought of Candidiasis initially. As a staring point, I suggested that she undergo an alkaline detoxification fast with fresh fruit, salads, steamed vegetables, fresh vegetable juices and home-made vegetable soups. This she did for 15 days. During the last day of the fast she went out with her friends to celebrate her birthday, and drank a glass of wine. She phoned me the following morning complaining of a bad headache, muscle pains, bloating, and an irritation in her throat. This is when my thinking began to point towards Candida, as I thought that the yeast in the wine had probably aggravated the condition. I asked her to come in immediately – testing on the VEGA showed a positive reaction to Candida, mushrooms and yeast, and her score on the Crook’s Candida Questionnaire was 356, probably the highest score I have ever seen!
We began Candida treatment, and within 3 months her halitosis had completely cleared, and she had decided to get engaged to a local boy who she had a crush on. It really never ceases to amaze me how Candida can present itself – the symptoms can be strange and varied. Recurrent vaginal infections accompanied by chronic fatigue is often common in women. I have seen a number of cases of infertility with no underlying pathology that was resolved by Candida treatment. Skin problems with no specific diagnosis from dermatologists were Candida related, chronic sinusitis, scleroderma, rheumatoid arthritis, asthma, and many more.
Certainly I am not saying that the common yeast, Candida albicans, is the cause of all these problems. What my experience has shown, however, is that when Candida is one of the underlying causes of these health problems, they are not resolved unless the Candida is eradicated first.
Many physicians now believe that a clinical trial for Candida overgrowth is of so little risk and expense that it should be considered in any chronic illness.
One clinical trial a person may try is to avoid certain foods for five days which are known to facilitate the growth of yeast. Such foods include the following:
* SUGAR and SIMPLE CARBOHYDRATES such as found in all sweetened food including the use of honey, molasses, sorghum, maple syrup, sugar, fructose, maltose, dextrose, corn syrup, etc.
* YEAST PRODUCTS such as beer, wine, yeast leavened bread, natural B vitamins, brewer's yeast
* FERMENTED and MOLD FOODS such as mushrooms, cheese, vinegar, mustard, catsup, relish and other condiments made with vinegar.
After avoiding these foods for 5 days, try adding them back into the diet in large quantities. By observing how one feels while off these foods, in comparison to any adverse affects experienced when going back on the foods, one may get a clue as to any possible yeast involvement as a causative factor for any adverse symptoms.
If adverse symptoms are provoked by a return to the yeast enhancing foods, your physician may feel that there is at least a possible reason to suspect Candida overgrowth, which may then warrant more definitive action.
CANDIDA TREATMENT PROTOCOL
The Candida Treatment Protocol that I have used successfully for a number of years has five basic objectives:
1. First, starve the Candida by eliminating the foods mentioned above that feed it.
2. Second, to kill the Candida through the use of anti-Candida products mentioned below.
3. Repopulate the bowel flora with a high-potency probiotic such as Culturelle which contains 20 billion live bacteria.
4. Regulate the dysbiosis and convert the pathological, mycelial form of Candida back to the normal form by the use of Sanum remedies mentioned below.
5. Restore biochemical balance to the body and strength to the immune system, which will allow the body once again to regain and maintain control over Candida growth by optimizing the diet – this would involve avoiding food intolerances and following the Metabolic Type Diet by Wolcott combined with the Blood Group diet by Dr. Peter D’Adamo.
KILLING CANDIDA
I have found that it is literally impossible to treat Candida if one does not cut out ALL forms of sugar, and that includes fructose from fruit sources. The foods that should be strictly AVOIDED for a 3-month period include:
* SUGAR – and all foods that contain sugar. These include white and brown sugar, honey, syrups, liquors, lactose, fructose, all confectionary and sweet cakes, chocolates, ice-creams, home-made sweets and cakes, biscuits, fizzy beverages, all fruit drinks.
* YEAST – and all foods that contain yeast including breads, vinegar, ketchups, mayonnaise and pickles.
* FRESH AND DRIED FRUIT – all fruit whether fresh, cooked, tinned or dried. These should be avoided for the initial SIX WEEKS ONLY – your health practitioner will advise you when to begin eating fruit again. Obviously this includes fresh fruit juices (vegetable juices are OK), as well as marmalades.
MUSHROOMS – all types, including Chinese mushrooms such as Shitake.
* REFINED FOODS – all white flours, white rice, white pasta products, cornflour, custard and white cereal products, unless they are wholemeal or organic.
FERMENTED PRODUCTS – all alcoholic beverages, vinegar and all vinegar products such as ketchup, mayonnaise and pickles.
* NUTS – all types of nuts that are cleaned and packaged without their shells – these have a tendency to collect fungal spores and moulds from the atmosphere which will antagonize the Candida. Nuts that are fresh with their shells are OK.
Most other foods are allowed. Fruit is cut out of the diet for 6 weeks, and all the other foods mentioned above are disallowed for a period of 12 weeks. In the meantime, there are other nutritional supplements, herbs and homeopathics that are given, as follows (most of these remedies can be found at www.worldwidehealthcenter.net, and some are available from Cyprus):
1. KANDIDAPLEX – a Doctor-formulated compound that contains Berberine, undecylenic acid, biotin, sorbic acid, citrus seed extract and Pau D’Arco - 2 caps x 3 daily
2. KOLOREX – a New Zealand herbal product which contains two powerful anti-fungal agents that have been shown to kill Candida – Winterata colorata and the synergistist herb Aniseed which boosts effectiveness 6 fold – 1 cap of each once daily.
3. CAPRYLIC ACID – a derivative of coconut which stops the Candida reproducing - freely available in most health food stores and pharmacies – 1 tab x 3 daily
4. CANDIDA 30c - homeopathic – freely available in most pharmacies – two pillules or one cap x 3 daily for 2 weeks only. These are stopped just before beginning the Sanum remedies.
5. CULTURELLE - a powerful probiotic containing 20 billion live bacteria, in order to repopulate the ailing flora of the gut.
6. A good-quality multivitamin such as OPTIMUM 6, or VV PACK or similar.
All the above are continued for 3 months, with the exception of the Candida 30c. After two weeks of the anti-Candida diet, certain specialized isopathic remedies are introduced, known as Sanum remedies from Germany, after the work of the famous Prof. Enderlein, as follows:
1. Mucokehl – 1 cap twice weekly
2. Pefrakehl – 1 cap twice weekly
3. Notakehl – 1 cap twice weekly
4. Fortakehl - 1 cap twice weekly
5. Nigersan - 1 cap twice weekly
6. Albicansan – 1 cap every second day
These are continued for about 40 days. As soon as these are completed, fruit is re-introduced back into the diet – this is about 6-7 weeks after the beginning of treatment.
Prof. Enderlein’s Sanum remedies work by changing the harmful microorganisms in the body fluids to non-aggressive forms (pleomorphic changes), which permits gentle healing (isopathy). Harmful bacteria and toxins are broken down and excreted through natural processes. They also help to alleviate the dysbiosis and bring the internal mileau of the intestine back into balance.
HERXHEIMER REACTIONS
Depending on the severity of Candida overgrowth and the amount of the agents taken, the Candida can be killed off in vast numbers in a very short period of time. As they are killed, they release substances which are toxic to the body. If this process occurs more quickly than the toxins can be cleared from the bloodstream and eliminated by the body, a temporary toxic or allergic-type reaction can occur. The technical name for this experience is a Herxheimer reaction ; it is more commonly referred to as "die off."
Usually die off lasts only a few hours, though it can last several days. It can usually be controlled almost entirely by the amount of ingestion of the agent and the rate or frequency it is taken. Signs of Herxheimer reaction can be many and varied but generally involve such discomfort as aching, bloating, dizzines, nausea, and overall "goopy sick" feeling, or a worsening of original symptoms. Fortunately, die off is generally short in duration, and although uncomfortable, is at least a confirmation of the presence of Candida and that something "good" is happening.
Exercise as well as insuring proper, daily bowel evacuation has been reported as being helpful in countering the adversities of die off. Maintaining a high daily intake of pure water is also important to keep the channels of elimination open.
BALANCING BODY CHEMISTRY
It is a commonly recognized and accepted fact that immune system efficiency is highly dependent on the proper biochemical balance in the body . This of course, is dependent on proper and adequate nutrition to supply the body with all the required biochemical constituents (vitamins, minerals, enzymes, intrinsic factors, etc.).
Different people require different amounts and balances of nutrients for optimum health . The criteria for the determination of these differing nutritional requirements lies within the definition of one's metabolic type, i.e., the genetically determined metabolic and nutritional parameters that define each person's individuality on every level.
It is precisely because different people have different metabolic types, and therefore different needs for nutrition, that the allopathic, symptom-treatment approach in nutrition is baseless and so often ineffective. This further explains why what (nutritionally) helps make one person better, may have little or no effect on another, or even make a third person worse.
I have not tried to modify this protocol as I have found it to be so successful that I dare not juggle with it in case I lose the effectiveness. I’m sure that it can be improved upon, and would welcome comments from other practitioners working with Candida. It is only through sharing that we will grow and become better practitioners.
Suggested Products
Beta 1,3 D-Glucan 60 caps (100mg), 60 caps (500mg)
Culturelle®, Lactobacillus GG (LGG) 30 caps
Horopito & Aniseed (Kolorex) - 60 Caps
KandidaPlex - 90 Caps
KandidaPlex - 360 Caps
Optimum 6 Multivitamins - 180 Caps
Silver Liquid 500 - 4 fl.oz
View Article List
by
Dr. George J Georgiou, Ph.D.,N.D.,D.Sc (A.M)
Natural Medicine Practitioner
Director, DaVinci Natural Health Centre, Larnaca, Cyprus
www.naturaltherapycenter.com
drgeorge@avacom.net
Tel: +357 24 82 33 22
CANDIDA ALBICANS : Are You Winning Battles But Losing the War?
WHAT IS IT?
Every person lives in a virtual sea of microorganisms, (bacteria, viruses, fungi, etc.). These microbes can reside in the throat, mouth, nose, intestinal tract, almost anywhere; they are as much a part of our bodies as the food we eat. Usually, these microorganisms do not cause illness, unless our resistance becomes lowered.
Candida albicans is a yeast that lives in the mouth, throat, intestines and genitourinary tract of most humans and is usually considered to be a normal part of the bowel flora (the organisms that coexist with us in our lower digestive tract). It is actually a member of a broader classification of organisms known as fungi.
Traditionally fungi are considered plants, but they contain no chlorophyll and cannot make their own food. Fungi tend to inhabit cool to tropical climates and are found in the air we breathe as well as in moist and shady soil, water, manure, dead leaves, fruit, leftover food, and in a wide variety of places and circumstances.
HOW DO YOU GET IT?
Candida albicans prefers people. Candida enters newborn infants during or shortly after birth. Usually, the growth of the yeast is kept in check by the infant's immune system and thus produces no overt symptoms. But, should the immune response weaken, the condition known as oral thrush can occur as a result. By six months of age, 90% of all babies test positive for Candida . And by adulthood, virtually all humans play host to Candida albicans and are thus engaged in a life-long relationship.
Candida coexists in our bodies with many species of bacteria in a competitive balance. Other bacteria act in part to keep Candida growth in check in our body ecology . . . unless that balance is upset. When health is present, the immune system keeps Candida proliferation under control; but when immune response is weakened, Candida growth can proceed unhindered. It is an "opportunistic organism," one which, when given the opportunity, will attempt to colonize all bodily tissues. The uncontrolled growth of Candida is known as Candida overgrowth or Candidiasis.
Unfortunately, there are many factors in our modern society that can upset the ecological balance of the body, weaken the immune system and thus allow the yeast to overgrow. Of these, the major risk factors which may predispose one to the proliferation of Candida are:
* STEROID HORMONES, IMMUNOSUPPRESSANT DRUGS such as cortisone which treat severe allergic problems by paralyzing the immune system's ability to react
* PREGNANCY, MULTIPLE PREGNANCIES or BIRTH CONTROL PILLS which upset the body's hormonal balance
* DIETS HIGH IN CARBOHYDRATE AND SUGAR INTAKE,
* YEAST AND YEAST PRODUCTS, AS WELL AS MOLDS AND FERMENTED FOODS
* PROLONGED EXPOSURE TO ENVIRONMENTAL MOLDS
* ANTIBIOTICS and SULFA DRUGS Probably the chief culprit of all, antibiotics kill all bacteria . They do not distinguish good bacteria from bad. Antibiotics kill the "good" flora which normally keeps the Candida under control. This allows for the unchecked growth of Candida in the intestinal tract. It is normally difficult to recover a yeast culture from bodily surfaces. However, after 48 hours of taking tetracycline, yeast can be cultured easily from anyone. The prevalence today of Candida may be most directly related to the widespread societal exposure to antibiotics - from prescriptions for colds, infections, acne, and from additional consumption of antibiotic-treated foods such as meats, dairy, poultry and eggs. Notably, antibiotics do not kill viruses; they only destroy bacteria. Yet, they are universally prescribed for all colds, flus and other viral problems. Such indiscriminate and extensive use of antibiotics is not only considered a primary cause of Candida overgrowth, but is recently being found to be responsible for the unbridaled development of "killer bacteria."
The rapid and direct proliferation of the yeast following antibiotic use strongly suggests that the problem of Candida is one which stems from an inner state of imbalance, rather than from an outside attack by a microbe or disease. This is a very important point to understand if one wishes to get rid of an overgrowth problem, suggesting that Candida is not so much a problem as is the body's own failure to control it!
A SERIOUS PROBLEM
Once begun, if not recognized and treated appropriately, Candida overgrowth can result in a self-perpetuating, negative cycle. Large numbers of yeast germs can weaken the immune system, which normally protects the body from harmful invaders. Even though Candida is part of the ecological balance in the body since birth, it is still recognized by the immune system as a foreign body that needs to be controlled. So, when overgrowth occurs, a chronic stimulation to the immune system results -- every second, every minute, every hour, every day, every month, every year -- in an attempt by the immune system to regain control. In time, it is believed that this can exhaust the immune system, predisposing one to more serious degenerative processes. Many believe chronic drains on the immune system such as Candida and parasites can play a direct role in the development of cancer and AIDS. Seen in this light, Candida overgrowth should not be taken lightly.
The immune system may concurrently be also adversely affected by poor nutrition, heavy exposure to molds in the air, as well as an increasing number of chemicals in our food, water and air, including petrochemicals, formaldehyde, perfumes, cleaning fluids, insecticides, tobacco and other indoor and outdoor pollutants. Over 10,000 chemicals have been added to our food supplies alone that were not there just 100 years ago! We do not have the genetic recognition of these substances as foods or as useful additions to our bodies.
Resulting lowered resistance may not only cause an overall sense of ill health, but also may allow for the development of respiratory, digestive and other systemic symptoms. One may also become predisposed to developing sensitivities to foods and chemicals in the environment. Such "allergies" may in turn cause the membranes of the nose, throat, ear, bladder and intestinal tract to swell and develop infection.
Such conditions may lead the physician to prescribe a "broad spectrum" antibiotic . . . which may then further promote the overgrowth of Candida and strengthen the existing negative chain of events, leading to further stress on the immune system and increased Candida-related problems.
WHAT ARE THE SIGNS OF CANDIDA INFECTION?
The result of heightened Candida overgrowth is a list of adverse symptoms of considerable length. Basically, the characteristics of Candida overgrowth fall under three categories, those affecting:
The gastrointestinal and genitourinary tracts
Allergic responses, and Mental/emotional manifestations.
Initially the signs will show near the sights of the original yeast colonies. Most often the first signs are seen in conditions such as nasal congestion and discharge, nasal itching, blisters in the mouth, sore or dry throat, abdominal pain, belching, bloating, heartburn, constipation, diarrhea, rectal burning or itching, vaginal discharge, vaginal itching or burning, increasingly worsening symptoms of PMS, prostatitis, impotence, frequent urination, burning on urination, bladder infections. But, if the immune system remains weak long enough, Candida can spread to all parts of the body causing an additional plethora of problems such as fatigue, drowsiness, uncoordination, lack of concentration, mood swings, dizziness, headaches, bad breath, coughing, wheezing, joint swelling, arthritis, failing vision, spots in front of the eyes, ear pain, deafness, burning or tearing eyes, muscle aches, depression, irritability, sweet cravings, increasing food and chemical sensitivities, numbness and tingling, cold hands and feet, asthma, hay fever, multiple allergies, hives and rashes, eczema, psoriasis, chronic fungal infections like athlete's foot, ringworm and fingernail/ toenail infections.
In addition, 79 different toxic products are known to be released by Candida , which in itself places a considerable burden on the immune system. These get into the bloodstream and travel to all parts of the body where they may give rise to a host of adverse symptoms.
In Candida overgrowth, the yeast colonies can dig deep into intestinal walls, damaging the bowel wall in their colonization.
Candida can also attack the immune system, causing suppressor cell disease, in which the immune system produces antibodies to everything at the slightest provocation, resulting in extreme sensitivities.
Finally, Candida overgrowth can be dangerous if not controlled. The persistent, constant challenge to the immune system by an ever-increasing, long-term overgrowth of Candida can eventually serve to wear down the immune system and cause a seriously weakened capacity for resistance to disease.
Women are more likely to get Candida overgrowth than are men. This is related to the female sex hormone progesterone which is elevated in the last half of the menstrual cycle. Progesterone increases the amount of glycogen (animal starch, easily converted to sugar) in the vaginal tissues which provide an ideal growth medium for Candida. Progesterone levels also elevate during pregnancy. Men are affected less frequently but are by no means invulnerable.
HOW DO YOU KNOW YOU'VE GOT IT?
Currently, diagnosis is primarily clinical. Since almost everyone has Candida in their bodies, tests for its presence are useless; confirmation of overgrowth is very difficult through laboratory tests. And, since what it does is to paralyze the immune system against it, allergy tests to determine the system's reaction to it are also ineffectual.
Furthermore, the results of the yeast imbalance -- the combined effects of different hormones, poisons generated and released by the yeast into the bloodstream, and the confusion created in the immune system -- produces such a wide variety of symptoms and which are seemingly so unrelated (such as wheezing, depression and fungus infection under fingernails) that a definite diagnosis cannot be made from any specific pattern of signs and symptoms.
Conclusive laboratory tests have not yet been developed, even though there are a number of tests that can help in the diagnosis. The patient’s history and symptoms are usually the key to arriving at a diagnosis, and Dr. Crook’s Candida Questionnaire is extremely helpful as it enables the patient to score their symptoms and arrive at a number – anything above 180 for women, and 140 for men is highly significant and represents the majority of symptoms that relate to this condition. There are other testing procedures that I use in clinical practice, mainly bio-dermal screening using the VEGA (see http://www.naturaltherapycenter.com/vega_allergy_testing ). When an ampule of Candida is placed in the honeycomb of the VEGA EXPERT and the probe placed on an acupoint of a finger, it is very clear when a patient “resists” as the conductivity drops. What I have also found time and time again in over 600 Candida patients that I have tested to date is that they all react to yeast, mushrooms, wine and beer as well when tested. In fact, many times I stumble upon Candida while conducting food intolerance testing using the VEGA, and when finding that mushrooms and yeast come out positive, I immediately test for Candida, which is also positive. I personally find the VEGA a very useful diagnostic device that can answer a lot of questions that more traditional laboratory testing cannot.
Another method of testing for Candida is to use a form of Kinesiological muscle testing called AUTONOMIC RESPONSE TESTING (see www.naturaltherapycenter.com/ART ). Autonomic Response Testing (ART) grew out of the importance of detecting and correct problems of the autonomic nervous system. ART allows the doctor to correct the problems of the ANS and to help restore the self regulating mechanism of the body allowing the patient to return to a state of health. ART is a system of evaluation and treatment developed by Dietrich Klinghardt, MD, Ph.D and Lousia Williams, DC, ND. Dr. Klinghardt is a German trained physician who also has a Ph.D in neurology. ART uses Applied Kinesiology, Electroacupuncture (EAV), O-Ring testing, Nogier pulse, Chinese pulse, heart rate variability and other techniques to assess the health or dysfunction of the autonomic nervous system.
Dr. Klinghardt believes that many practitioners using kinesiology or muscle testing in their practice are often getting inaccurate information because the autonomic nervous system is not functioning properly. In ART, this condition is called 'blocked regulation' and refers to the inability of the ANS to self-regulate and is caused by 7 common factors. These include: undiagnosed food allergies, heavy metal toxicity, petroleum chemical toxicity, chronic unresolved infections and scars, temporomandibular joint dysfunction (TMJ), unresolved psychological stress, and electromagnetic stress. Dr. Klinghardt has developed specific tests for these factors and treatments to correct them. ART is also a good way of detecting whether Candida is prevalent, and the effect that it is having on the Autonomic Nervous System and other organ systems of the body.
CASE HISTORIES
There is still a lot of controversy around the topic of Candida, and I am the first to agree that we do not have all the answers. One thing that I have witnessed in clinical practice, however, is the astounding recovery that many of these so-called Candidiasis patients make when placed on a Candida Treatment Protocol. These would include difficult cases that have been through the orthodox medical mill, seeing many different specialties without positive effects. One case that I remember is a 32 year old women who had such a bad case of halitosis that when I approached her to examine her throat I thought that I was surrounded by rotting corpses! Such was the degree of her bad breath that she had NEVER dated in her life for this reason. My mind never even thought of Candidiasis initially. As a staring point, I suggested that she undergo an alkaline detoxification fast with fresh fruit, salads, steamed vegetables, fresh vegetable juices and home-made vegetable soups. This she did for 15 days. During the last day of the fast she went out with her friends to celebrate her birthday, and drank a glass of wine. She phoned me the following morning complaining of a bad headache, muscle pains, bloating, and an irritation in her throat. This is when my thinking began to point towards Candida, as I thought that the yeast in the wine had probably aggravated the condition. I asked her to come in immediately – testing on the VEGA showed a positive reaction to Candida, mushrooms and yeast, and her score on the Crook’s Candida Questionnaire was 356, probably the highest score I have ever seen!
We began Candida treatment, and within 3 months her halitosis had completely cleared, and she had decided to get engaged to a local boy who she had a crush on. It really never ceases to amaze me how Candida can present itself – the symptoms can be strange and varied. Recurrent vaginal infections accompanied by chronic fatigue is often common in women. I have seen a number of cases of infertility with no underlying pathology that was resolved by Candida treatment. Skin problems with no specific diagnosis from dermatologists were Candida related, chronic sinusitis, scleroderma, rheumatoid arthritis, asthma, and many more.
Certainly I am not saying that the common yeast, Candida albicans, is the cause of all these problems. What my experience has shown, however, is that when Candida is one of the underlying causes of these health problems, they are not resolved unless the Candida is eradicated first.
Many physicians now believe that a clinical trial for Candida overgrowth is of so little risk and expense that it should be considered in any chronic illness.
One clinical trial a person may try is to avoid certain foods for five days which are known to facilitate the growth of yeast. Such foods include the following:
* SUGAR and SIMPLE CARBOHYDRATES such as found in all sweetened food including the use of honey, molasses, sorghum, maple syrup, sugar, fructose, maltose, dextrose, corn syrup, etc.
* YEAST PRODUCTS such as beer, wine, yeast leavened bread, natural B vitamins, brewer's yeast
* FERMENTED and MOLD FOODS such as mushrooms, cheese, vinegar, mustard, catsup, relish and other condiments made with vinegar.
After avoiding these foods for 5 days, try adding them back into the diet in large quantities. By observing how one feels while off these foods, in comparison to any adverse affects experienced when going back on the foods, one may get a clue as to any possible yeast involvement as a causative factor for any adverse symptoms.
If adverse symptoms are provoked by a return to the yeast enhancing foods, your physician may feel that there is at least a possible reason to suspect Candida overgrowth, which may then warrant more definitive action.
CANDIDA TREATMENT PROTOCOL
The Candida Treatment Protocol that I have used successfully for a number of years has five basic objectives:
1. First, starve the Candida by eliminating the foods mentioned above that feed it.
2. Second, to kill the Candida through the use of anti-Candida products mentioned below.
3. Repopulate the bowel flora with a high-potency probiotic such as Culturelle which contains 20 billion live bacteria.
4. Regulate the dysbiosis and convert the pathological, mycelial form of Candida back to the normal form by the use of Sanum remedies mentioned below.
5. Restore biochemical balance to the body and strength to the immune system, which will allow the body once again to regain and maintain control over Candida growth by optimizing the diet – this would involve avoiding food intolerances and following the Metabolic Type Diet by Wolcott combined with the Blood Group diet by Dr. Peter D’Adamo.
KILLING CANDIDA
I have found that it is literally impossible to treat Candida if one does not cut out ALL forms of sugar, and that includes fructose from fruit sources. The foods that should be strictly AVOIDED for a 3-month period include:
* SUGAR – and all foods that contain sugar. These include white and brown sugar, honey, syrups, liquors, lactose, fructose, all confectionary and sweet cakes, chocolates, ice-creams, home-made sweets and cakes, biscuits, fizzy beverages, all fruit drinks.
* YEAST – and all foods that contain yeast including breads, vinegar, ketchups, mayonnaise and pickles.
* FRESH AND DRIED FRUIT – all fruit whether fresh, cooked, tinned or dried. These should be avoided for the initial SIX WEEKS ONLY – your health practitioner will advise you when to begin eating fruit again. Obviously this includes fresh fruit juices (vegetable juices are OK), as well as marmalades.
MUSHROOMS – all types, including Chinese mushrooms such as Shitake.
* REFINED FOODS – all white flours, white rice, white pasta products, cornflour, custard and white cereal products, unless they are wholemeal or organic.
FERMENTED PRODUCTS – all alcoholic beverages, vinegar and all vinegar products such as ketchup, mayonnaise and pickles.
* NUTS – all types of nuts that are cleaned and packaged without their shells – these have a tendency to collect fungal spores and moulds from the atmosphere which will antagonize the Candida. Nuts that are fresh with their shells are OK.
Most other foods are allowed. Fruit is cut out of the diet for 6 weeks, and all the other foods mentioned above are disallowed for a period of 12 weeks. In the meantime, there are other nutritional supplements, herbs and homeopathics that are given, as follows (most of these remedies can be found at www.worldwidehealthcenter.net, and some are available from Cyprus):
1. KANDIDAPLEX – a Doctor-formulated compound that contains Berberine, undecylenic acid, biotin, sorbic acid, citrus seed extract and Pau D’Arco - 2 caps x 3 daily
2. KOLOREX – a New Zealand herbal product which contains two powerful anti-fungal agents that have been shown to kill Candida – Winterata colorata and the synergistist herb Aniseed which boosts effectiveness 6 fold – 1 cap of each once daily.
3. CAPRYLIC ACID – a derivative of coconut which stops the Candida reproducing - freely available in most health food stores and pharmacies – 1 tab x 3 daily
4. CANDIDA 30c - homeopathic – freely available in most pharmacies – two pillules or one cap x 3 daily for 2 weeks only. These are stopped just before beginning the Sanum remedies.
5. CULTURELLE - a powerful probiotic containing 20 billion live bacteria, in order to repopulate the ailing flora of the gut.
6. A good-quality multivitamin such as OPTIMUM 6, or VV PACK or similar.
All the above are continued for 3 months, with the exception of the Candida 30c. After two weeks of the anti-Candida diet, certain specialized isopathic remedies are introduced, known as Sanum remedies from Germany, after the work of the famous Prof. Enderlein, as follows:
1. Mucokehl – 1 cap twice weekly
2. Pefrakehl – 1 cap twice weekly
3. Notakehl – 1 cap twice weekly
4. Fortakehl - 1 cap twice weekly
5. Nigersan - 1 cap twice weekly
6. Albicansan – 1 cap every second day
These are continued for about 40 days. As soon as these are completed, fruit is re-introduced back into the diet – this is about 6-7 weeks after the beginning of treatment.
Prof. Enderlein’s Sanum remedies work by changing the harmful microorganisms in the body fluids to non-aggressive forms (pleomorphic changes), which permits gentle healing (isopathy). Harmful bacteria and toxins are broken down and excreted through natural processes. They also help to alleviate the dysbiosis and bring the internal mileau of the intestine back into balance.
HERXHEIMER REACTIONS
Depending on the severity of Candida overgrowth and the amount of the agents taken, the Candida can be killed off in vast numbers in a very short period of time. As they are killed, they release substances which are toxic to the body. If this process occurs more quickly than the toxins can be cleared from the bloodstream and eliminated by the body, a temporary toxic or allergic-type reaction can occur. The technical name for this experience is a Herxheimer reaction ; it is more commonly referred to as "die off."
Usually die off lasts only a few hours, though it can last several days. It can usually be controlled almost entirely by the amount of ingestion of the agent and the rate or frequency it is taken. Signs of Herxheimer reaction can be many and varied but generally involve such discomfort as aching, bloating, dizzines, nausea, and overall "goopy sick" feeling, or a worsening of original symptoms. Fortunately, die off is generally short in duration, and although uncomfortable, is at least a confirmation of the presence of Candida and that something "good" is happening.
Exercise as well as insuring proper, daily bowel evacuation has been reported as being helpful in countering the adversities of die off. Maintaining a high daily intake of pure water is also important to keep the channels of elimination open.
BALANCING BODY CHEMISTRY
It is a commonly recognized and accepted fact that immune system efficiency is highly dependent on the proper biochemical balance in the body . This of course, is dependent on proper and adequate nutrition to supply the body with all the required biochemical constituents (vitamins, minerals, enzymes, intrinsic factors, etc.).
Different people require different amounts and balances of nutrients for optimum health . The criteria for the determination of these differing nutritional requirements lies within the definition of one's metabolic type, i.e., the genetically determined metabolic and nutritional parameters that define each person's individuality on every level.
It is precisely because different people have different metabolic types, and therefore different needs for nutrition, that the allopathic, symptom-treatment approach in nutrition is baseless and so often ineffective. This further explains why what (nutritionally) helps make one person better, may have little or no effect on another, or even make a third person worse.
I have not tried to modify this protocol as I have found it to be so successful that I dare not juggle with it in case I lose the effectiveness. I’m sure that it can be improved upon, and would welcome comments from other practitioners working with Candida. It is only through sharing that we will grow and become better practitioners.
Suggested Products
Beta 1,3 D-Glucan 60 caps (100mg), 60 caps (500mg)
Culturelle®, Lactobacillus GG (LGG) 30 caps
Horopito & Aniseed (Kolorex) - 60 Caps
KandidaPlex - 90 Caps
KandidaPlex - 360 Caps
Optimum 6 Multivitamins - 180 Caps
Silver Liquid 500 - 4 fl.oz
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