Sunday, May 22, 2016

Autoimmune Diseases and Treatment Strategies

Immune System Disorders: Autoimmune Diseases

Disorders in the immune system can result in disease, including autoimmune diseases, inflammatory diseases and cancer.
Immunodeficiency diseases occur when the immune system is less active than normal, resulting in recurring and life-threatening infections. Immunodeficiency can either be the result of a genetic disease, such as severe combined immunodeficiency, or be produced by pharmaceuticals or an infection, such as the acquired immune deficiency syndrome (AIDS) that is caused by the retrovirus HIV.
AIDS is a particularly problematic disease for the immune system because the virus actually attacks immune system cells. In particular, it reproduces inside Helper T cells and kills them in the process. Without Helper T cells to orchestrate things, the immune system eventually collapses and the victim dies of some other infection that the immune system would normally be able to handle.
In contrast, autoimmune diseases result from a hyperactive immune system attacking normal tissues as if they were foreign organisms. Common autoimmune diseases include Hashimoto's thyroiditis, rheumatoid arthritis, diabetes mellitus type 1, lupus erythematosus, asthma, familial Mediterranean fever and Crohn's disease (inflammatory bowel disease).

Autoimmune disease refers to a group of more than 80 serious, chronic illnesses including diseases of the nervous, gastrointestinal, and endocrine systems as well as skin and other connective tissues, eyes, blood, and blood vessel.

Autoimmune diseases may manifest in many different places in the body, with many different diagnoses. Their common thread is that the body makes antibodies to its own tissues. The body's immune system becomes misdirected, attacking the very organs it was designed to protect.

Autoimmune diseases are the third most common category of disease in the United States after cancer and heart disease. Conservative estimates indicate that three-quarters of the persons with autoimmune diseases are women.

Autoimmune diseases are the leading cause for death in the United States, especially among women. However, their exact impact is unknown because the National Statistical Center did not include all the diseases in their list of possible causes for death; thus doctors do not list them on the death certificates. At the same time, analysis of the data from the Center of Disease Control from 1995 show that this group of diseases is in the top ten (Am J Public Health, Sep, 2000).

According to the National Health Institute, 23.5 million of Americans suffer from autoimmune diseases; this is 1.5 million more cases than cases of cardio-vascular disease and 14.5 million more cases than cases of cancer. Every year, $100 billion are spent on treating autoimmune conditions. However, financing for autoimmune research is limited and programs for medical students include minimal information.

Autoimmune diseases tend to cluster in families and in individuals – a person with one autoimmune disease is more likely to get another. This indicates that common mechanisms are at work. Studies of the prevalence of autoimmune disease in monozygotic (identical) twins show that genetic as well as environmental factors are necessary for the disease to develop. Also, infections play a big role in the development of autoimmune disease.
Autoimmunity occurs when the immune system for some reason attacks your own body in the same way it would normally attack a germ. Two common diseases are caused by immune system mistakes. Juvenile-onset diabetes is caused by the immune system attacking and eliminating the cells in the pancreas that produce insulin. Rheumatoid arthritis is caused by the immune system attacking tissues inside the joints.
Allergies are another form of immune system error. For some reason, in people with allergies, the immune system strongly reacts to an allergen that should be ignored. The allergen might be a certain food, or a certain type of pollen, or a certain type of animal fur. For example, a person allergic to a certain pollen will get a runny nose, watery eyes, sneezing, etc. This reaction is caused primarily by mast cells in the nasal passages. In reaction to the pollen the mast cells release histamine. Histamine has the effect of causing inflammation, which allows fluid to flow from blood vessels. Histamine also causes itching. To eliminate these symptoms the drug of choice is, of course, an antihistamine.
The effect the immune system has on transplanted tissue is another example of an immune system disorder is . This really isn't a mistake, but it makes organ and tissue transplants nearly impossible. When the foreign tissue is placed inside your body, its cells do not contain the correct identification. Your immune system therefore attacks the tissue. The problem cannot be prevented, but can be diminished by carefully matching the tissue donor with the recipient and by using immunosuppressing drugs to try to prevent an immune system reaction. Of course, by suppressing the immune system these drugs open the patient to opportunistic infections.

List of Autoimmune Diseases/Disorders
The following is a list of the major autoimmune diseases and disorders.
Addison's disease involves dysfunction of the outer portion of the adrenal gland.
Ankylosing spondylitis is a type of arthritis that involves inflammation of the spine and pelvic joints.
Antiphospholipid antibody syndrome (APS) is a condition that affects the blood-clotting process, causing blood clots to form in veins and/or arteries.
Aplastic anemia is a condition whereby the bone marrow does not produce enough blood cells. It is often caused by an autoimmune attack on the bone marrow.
Autoimmune hepatitis involves inflammation of the liver.
Celiac disease is characterized by chronic inflammation of the first third or half of the small intestine, and is caused by exposure to a type of dietary protein called gluten, found in abundance in grains like wheat, oats, barley, and rye.
Crohn's disease involves chronic inflammation of the intestinal tract.
Diabetes Mellitus Type 1 is characterized by low or non-existent production of insulin by the pancreas.
Goodpasture's syndrome involves destruction of kidney tissue and bleeding in the lungs.
Graves' disease is a form of hyperthyroidism.
Guillain-Barré syndrome (GBS) involves inflammation of the peripheral nervous system, and is also called acute inflammatory demyelinating polyneuropathy, acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis and Landry's ascending paralysis.
Hashimoto's disease is a form of hypothyroidism.
Idiopathic thrombocytopenic purpura is characterized by a low platelet count, resulting in easy bleeding.
Systemic lupus erythematosus (SLE) is a chronic autoimmune condition that can involve inflammation in the following areas: skin, joints, heart, lungs, kidneys, and nervous system.
Multiple sclerosis (MS) involves nerve dysfunction due to demyelination of the central nervous system.
Myasthenia gravis involves intermittent weakness and fatigue due to a problem with communication at the junction of nerves and muscles.
Optic neuritis involves inflammation of the nerves that supply your eyes which can cause partial or complete loss of vision.
Pemphigus is characterized by the formation of blisters and raw sores on mucous membranes and skin.
Pernicious Anemia is a form of anemia (inadequate red blood supply/function) that is caused by a problem with absorbing vitamin B12, which is needed to form healthy red blood cells.
Rheumatoid arthritis is characterized by joint pain and inflammation.
Sjögren's syndrome involves destruction of glands that produce saliva and tears.
Takayasu's arteritis is characterized by inflammation that narrows the lumen of arteries.
Temporal arteritis is characterized by inflammation in medium to large-sized arteries, mostly commonly in the head. It is sometimes called giant cell arteritis, and can lead to significant vision loss.
Warm autoimmune hemolytic anemia is characterized by destruction of red blood cells by IgM antibodies.
Wegener's granulomatosis involves inflammation of blood vessels, typically affecting the kidneys and lungs.
The following diagnoses are not universally accepted as being autoimmune in nature, but for all practical purposes, they belong in the same category of health conditions:
Alopecia is characterized by hair loss. Loss of random patches is called alopecia areata, while full body loss of hair is called alopecia universalis.
Endometriosis is characterized by endometrial tissue (tissue found in the uterus) being deposited outside of the uterus, causing pain and sometimes infertility.
Interstitial cystitis is a urinary bladder disease that is characterized by one or more of the following symptoms: intense, intermittent pelvic pain, frequent urination, a sense of urgency to urinate, pain with urination, and pain with sexual intercourse.
Psoriasis is a skin condition that is characterized by patches of rapidly-dividing cells that produce itchy, scaly, and inflamed lesions.
Sarcoidosis is characterized by granuloma formation in the lungs and sometimes throughout the body.
Note: If you have an autoimmune disease, allergies, PCOS, or thyroid issues, get theHow to Treat Autoimmune Diseases, PCOS & Thyroid Issues Naturally ebook. The autoimmune diseases covered in this ebook include: Addison's disease, Celiac disease, Crohn's disease, Graves disease, Hashimoto's Thyroiditis, Lupus, Multiple sclerosis (MS), Rheumatic disease (incl. Rheumatoid arthritis), Sarcoidosis, Sjögren’s syndrome, Type I diabetes and Ulcerative colitis. In addition, this book will discuss allergies and polycystic ovary syndrome (PCOS) even though it is not classified as an autoimmune disease.

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Autoimmune Diseases and Glycobiology
Every autoimmune condition has one thing in common - the immune system cannot properly recognize cells of the body, and mistakenly attacks them.
"Autoimmune Diseases" are basically ones in which a person's immune system attacks his or her own tissue.
Every disease expresses a symptom or symptoms to alarm your body that there is a problem. Taking a drug to mask the symptom is not addressing the root cause of the problem.
The solution is to identify what factors are causing your immune system dysfunctions. The medical community is so focused on finding a cure for individual diseases, where maybe there is no magic drug that can cure the human body of disease conditions.
Disease conditions are cellular dysfunctions. Each disease has specific problems or dysfunctions that cause symptoms and the medical community focus on addressing the symptoms of disease even if the treatment for the symptom suppression causes adverse side effects and in some cases do more harm in the long-term treatment of the disorder.
Your body is a biological miracle that is pre-programmed for optimal health. With today's scientific and technical advances, they are able to identify the specific cellular dysfunctions of specific disease conditions. As an example there is a deficiency in one of the complement proteins that can result in an autoimmune disease such as lupus.
Healthy and Unhealthy Cells
Above is a picture of a human cell amplified by a powerful microscope; the cell on the left is what a normal healthy cell should look like covered in glycoforms and complement proteins. The cell on the right has altered glycoforms and missing complement proteins due to specific glycoprotein deficiencies.
All cells have various structures as illustrated below. The green strands are carbohydrate structures (made of various glycoforms).
Various Cell Structures
People with autoimmune conditions have altered carbohydrate and glycoprotein structures as compared to normal healthy cells. 
When your cells have altered carbohydrate structures, your immune system mistakes your cells as enemy cells and launches an attack on itself. This triggers dysfunction at the cellular level which results in specific symptoms like inflammation of the joints, skin rashes, extreme fatigue, etc.
Your body is an extremely intelligent organism, behind the scenes science has been focusing on what does your body's systems require and how do you support your body's systems at the cellular level so that your systems can function the way they were designed to.
Immunologists are identifying the specific dysfunctional cellular process in many disease conditions at the molecular level of human cells.
Immunology is a broad branch of biomedical science that covers study of all aspects of the immune system in all organisms. It deals with, among other things, the physiological functioning of the immune system in states of both health and disease; malfunctions of the immune system in immunological disorders.
Science is finally getting that the immune system is not just a few specialized cells in the body every organ and every tissue is part of your immune system. The immune system is composed of the thymus, spleen, lymph nodes, lymphatic vessels, tonsils and adenoids, and—most important—the bone marrow, which manufactures all the stem cells that eventually develop into T cells, B cells, phagocytes, macrophages, Natural Killer (NK) cells, etc.
All your systems work synergistically together and when there is a dysfunction at the cellular level it begins to effect the other systems of your body.
Why would your own immune system try to defend the body against itself? 
Researchers have found that β cells are merely acting on the orders of a set of glycoproteins called cellular messengers, and when these cellular messengers are missing or altered, the system goes awry.
Once these protein messengers on your cell surface become altered your body’s immune cells mistakenly recognize these cells as foreign cells and launch an attack on your own cells, organs and systems.
The true answer to correcting this disease process is to identify why your cells are missing these cell surface protein glycoforms and what is causing them to become altered in the first place. This is the focus of an emerging field called glycobiology.
As previously mentioned, glycobiology is the study of the structure, biosynthesis, and biology of saccharides (sugar chains or glycans) that are widely distributed in nature. Sugars or saccharides are essential components of all living things and aspects of the various roles they play in biology are researched in various medical, biochemical and biotechnological fields.

Because there are multiple factors causing this disease process to manifest in your body you need to focus on providing what your body’s cells require to function properly.
This can be achieved by providing what your body’s systems require to support a biological process called cellular restoration, utilizing a macro-nutrient/micro-nutrient-balanced plant-based diet.

Treating Autoimmune Diseases                                   

The primary underlying root causes of autoimmune diseases include inflammation, infections, viruses, heavy metals, toxicity, damaged cells, and a weakened (confused) immune system.

Inflammation is the immune system's response for beating back invaders in the body, but inflammation gone awry can lead to many different diseases.

Infections of various types, such as Candida Albicans overgrowth, contribute to auto-immune disorders. Eliminating these chronic infections is essential to successfully fighting and defeating auto-immune disease.

Viruses of any kind can trigger a autoimmune response once an infection has settled in the body and damaged the immune system. Once you have a defective immune system, it will persist until the infection is eliminated.

Heavy metals such as mercury contribute to auto-immune disorders due to the damage they cause to our cells, immune system, and organs.

Other toxins such as pesticides, environmental toxins, and chemicals from processed foods also contribute significantly to auto-immune disease due to the damage they cause to our cells, immune system, and organs.

Other causes include heredity/genetics, stress/anxiety, pregnancy (hormone changes), and a poor diet (full of toxic chemicals) may also contribute to the development of an autoimmune disease.

As a result, a person stricken with an autoimmune disease needs a natural wellness treatment strategy that addresses these root causes in order to effectively fight and defeat the disease, or, at least, get the disease under control so that you can live a higher quality of life.

Note: If you have an autoimmune disease, allergies, PCOS, or thyroid issues, get theHow to Treat Autoimmune Diseases, PCOS & Thyroid Issues Naturally ebook.

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Multiple Sclerosis                                   

Multiple Sclerosis or MS is a condition that affects the nerves in the brain, spinal cord and other parts of the central nervous system. The cause is thought to be due to an abnormality in the functioning of the immune system but the exact mechanism is still uncertain. It is a chronic, progressive disease, and as yet, there is no cure.

A fatty substance known as myelin surrounds our nerve fibers (axons), and acts as an insulator. Myelin helps these nerve fibers to transmit signals from the central nervous system to other parts of the body. When myelin is damaged, it can become inflamed, and the result is the formation of hardened scar tissue (sclerosis), causing nerve function to deteriorate over time, resulting in a number of symptoms, including: muscle weakness; imbalance, or loss of coordination; astigmatism and vision loss; and, tremors.

The body’s own immune cells attack the nervous system, and the spinal cord, brain and optic nerves are all affected – this causes the nerve impulses to slow down. Symptoms of multiple sclerosis vary because different nerves are affected at different times. People suffering from multiple sclerosis may experience episodes of vision loss, weakness in their muscles, numbness and pain.

Sometimes these attacks worsen (exacerbate), improve (remission), recur (relapse) or develop in other areas of the body. Attacks can last days, weeks or months, recurring or showing no symptoms at all. Multiple sclerosis tends to have a slow and insidious onset and can progress silently, without you even being aware that you may have the disease until the damage is quite severe and more obvious symptoms are noted.

Multiple sclerosis affects women more than men, particularly Caucasians. The disease typically begins between the ages 20 and 40, but it may also develop in children and the elderly. People with a family history of MS are more susceptible to developing this disease. MS is also more likely to occur in certain geographical areas such as the United States where over 400,000 people are affected, northern Europe, southern Australia and New Zealand.

People suffering from MS have to deal with many obstacles, as well as the uncertainty of the outcome of the disease. If symptoms are detected early, treatment can slow the progress of this disease. Although multiple sclerosis cannot be cured, there are various treatments that can help to ease the symptoms. There are also many techniques and lifestyle changes to help you manage this disease so that those with MS can lead a full and productive life.

MS Treatment
Prednisone is a commonly prescribed corticosteroid (steroid, for short) for people with MS. These drugs have also been called "glucocorticoids" because of their effects on glucose metabolism, causing an increase in blood glucose.People with diabetes receiving steroid treatment should be informed that their blood glucose will increase while they are on the steroid. Doctors should help patients determine what adjustments are needed to keep blood glucose levels within the target range.

Steroid treatment is usually prescribed for short periods of time, so your blood glucose should return to pre-treatment levels a few days after the steroid is stopped.

In addition, people who are not diabetic, but are at risk for developing diabetes, should be informed that a steroid drug such as prednisone can cause Type 2 diabetes!
Some Tips for Managing Your Diabetes while on Prednisone

Nutrition: Eat a plant-based diet with lots of vegetables to better manage your blood glucose levels. Eat lean protein foods such as organic eggs, wild salmon, Greek yogurt, beans, nuts and seeds. Avoid most processed foods, fast foods and sugary foods. You should cut back on sweets even more than you usually do when you are taking a steroid such as prednisone.

Eat smaller meals and eat more frequently to help stabilize your blood glucose levels. Be careful not to miss a meal to avoid the highs and lows that can wreak havoc with your body.

Beverages: Drink more (filtered) water than you usually do. Also, drink raw vegetable juices and green smoothies. Dehydration can make a rise in blood sugar even more dangerous to someone with type 2 diabetes.

Blood Glucose Monitoring: Keep track of your blood sugar levels more frequently than you normally do to stay on top of any extreme changes.

Journaling: Record your blood sugar levels in a journal. While the prednisone is probably going to make these levels increase somewhat, make sure you ask your doctor at what point you need to seek medical attention. For example, if that limit is a blood sugar number over 200, do not take any more prednisone and seek help immediately if you reach that number.

Your Doctor: Talk to your doctor about the risks of taking prednisone when you have type 2 diabetes. Ask about an increase in your dosage of diabetes medication. This may be able to offset the effect of prednisone.
       
In general, be more cautious than usual. It's better to call a doctor one too many times when taking prednisone than not enough times and risking your health.

Note: For more details about MS and how to treat it naturally, get the How to Treat Autoimmune Diseases, PCOS & Thyroid Issues Naturally ebook.

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Inflammatory Bowel Disease (IBD)                            

Inflammatory Bowel Disease (IBD) is a chronic autoimmune disease, which is the name of a group of disorders in which the intestines (small and large intestines or bowels) become inflamed (red and swollen). This inflammation causes symptoms such as severe or chronic pain in the abdomen, diarrhea that may be bloody, weight loss, loss of appetite, bleeding from the rectum, joint pain, fever and skin problems.

Symptoms can range from mild to severe. Also, symptoms can come and go, sometimes going away for months or even years at a time. When people with IBD start to have symptoms again, they are said to be having a relapse or flare-up. When they are not having symptoms, the disease is said to have gone into remission.

The most common forms of IBD include Crohn's disease (Crohn’s) and Ulcerative Colitis (UC). In both Crohn’s and UC, the mucosal inflammation generates large amounts of cytokines such as IFN y and TNF-a, which is why drugs blocking these cytokines have been shown to sometimes be effective in controlling symptoms. The main difference between the two diseases is the parts of the digestive tract they affect. There are about 1.1 million Americans living with IBD.

Crohn's Disease
Crohn's Disease can affect any area of the gastrointestinal tract, but most commonly affects the lower part of the small intestine, the ileum, and the first part of the large intestine and has the characteristic of relapsing inflammatory processes. In Crohn’s disease, inflammation may be patchy and segmental, and typically transmural (all layers of the intestinal wall).

The swelling and scar tissue can thicken the intestinal wall, which narrows the passageway for food that is being digested. The area of the intestine that has narrowed is called a stricture. Also, deep ulcers may turn into tunnels, called fistulas, which connect different parts of the intestine. They may also connect to nearby organs, such as the bladder or vagina, or connect to the skin. And as with ulcerative colitis, ulcers may cause a hole (ulcer) to develop in the wall of the intestine.

When serious damage has been made to the intestine, there may be no other resort, than to surgically remove large portions of the intestine. About 65 to 75 percent of people with Crohn's disease need surgery at some point in their lives. Surgery can relieve symptoms and correct problems like strictures, fistulae, or bleeding in the intestine. Surgery can help relieve Crohn's disease symptoms. But, since Crohn's disease occurs in patches, surgery cannot cure the disease. If a part of the small or large intestine is removed, the inflammation may then affect the part next to the section that was removed. When the large intestine has to be removed, an external pouch is required to collect the waste otherwise known as a colostomy.

While the disease can present itself at any age in a patient, initial incidence is often in the teens and twenties, with another peak incidence in the fifties to seventies. There is evidence of a genetic link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk. It is thought to have a large environmental component as evidenced by a higher incidence in western industrialized nations compared to other parts of the world, although the hygiene hypothesis might explain the industrialized nations distribution.

Males and females are equally affected, while smokers are two times more likely to develop Crohn's disease than nonsmokers. There is no known pharmacological or surgical cure for Crohn’s disease; treatment options are limited to the control of symptoms, maintenance of remission, and prevention of relapse.

Since the etiology of the disease is not completely understood, curative therapies have not yet been developed. Current therapeutic options in the management of patients are symptomatic only. Therapeutic approaches concentrate on suppression of acute flares combined with induction and maintenance of remission to prevent further recurrences.

Standard therapy for the symptomatic treatment of Crohn’s disease may include sulfasalazine, mesalazine, systemic and topical glucocorticoids, immunosuppressants like azathioprine or 6-mercaptopurine, and in severe cases also treatment with anti-TNF-a therapy, methotrexate, or cyclosporine as monotherapy or in combination with other agents. Many patients are ultimately faced with surgery to remove sections of the diseased intestine.

Ulcerative Colitis
Ulcerative colitis affects the top layer of the large intestine, next to where the stool is. The disease causes swelling and tiny open sores, or ulcers, to form on the surface of the lining. The ulcers can bleed and produce pus. In severe cases of ulcerative colitis, ulcers may weaken the intestinal wall so much that a hole develops. Then the contents of the large intestine, including bacteria, spill into the abdominal (belly) cavity or leak into the blood. This causes a serious infection and requires emergency surgery.

Inflammation in the colon also causes the colon to empty frequently, causing diarrhea. When the inflammation occurs in the rectum and lower part of the colon it is called ulcerative proctitis. If the entire colon is affected it is called pancolitis. If only the left side of the colon is affected it is called limited or distal colitis.

Ulcerative colitis can occur in people of any age, but it usually starts between the ages of 15 and 30, and less frequently between 50 and 70 years of age. It affects men and women equally and appears to run in families, with reports of up to 20 percent of people with ulcerative colitis having a family member or relative with ulcerative colitis or Crohn's disease.

The medical therapies available to Crohn's patients are also applicable to patients with ulcerative colitis, and about 25 to 40 percent of people with ulcerative colitis need surgery at some point in their lives. Surgery that removes the entire large intestine can completely cure ulcerative colitis.

Natural Treatment Strategy
It's important to self-manage Crohn's and ulcerative colitis with healthy lifestyle habits and a nutrient-rich diet. Paying attention to your nutrition is especially important with GI diseases because the symptoms of diarrhea and bleeding can lead to dehydration, electrolyte imbalance, and loss of essential nutrients. That can lead to a host of problems such as fatigue, weakness, and anemia.
Eating should be based on a well-balanced diet that's high in protein, complex carbohydrates, some organic whole grains, and good fats. Such a diet will provide you with energy and keep you well. Your diet may include meat, fish, poultry, and dairy products (if you don't have lactose intolerance); breads and cereals; fruits and vegetables; and plant oils.
If you are a vegetarian with ulcerative colitis, dairy products and plant proteins -- such as soy products -- can provide the nutritional elements found in meat, fish, and poultry.
According to the Crohn's and Colitis Foundation of America, diet is not a major factor in the inflammatory process. However, if you find that certain foods trigger your bowel symptoms, then you may want to avoid these foods to reduce your symptoms and self-manage your illness.

For example, some people find that coffee or caffeine exacerbates diarrhea and cramping. Other people complain that raw vegetables or high-fiber foods cause their GI symptoms.
Some people periodically follow a low-residue diet or low-fiber diet, getting about 10-15 grams of fiber a day. That helps reduce the frequency of bowel movements and prolongs intestinal transit time.
Learning to avoid food triggers may give you better control of your disease and allow you greater freedom to enjoy an active life. Despite the fact there is no scientific proof, many people have found that one or more of the following foods can trigger their GI symptoms:
  • alcohol
  • caffeine
  • carbonated beverages
  • dairy products, if lactose intolerant
  • dried beans, peas, and legumes
  • dried fruits, berries, fruits with pulp or seeds
  • foods containing sulfur or sulfate
  • foods high in fiber, including whole-grain products
  • hot sauce, pepper
  • meats
  • nuts, crunchy nut butters
  • popcorn
  • products containing sorbitol (sugar-free gum and candies)
  • raw vegetables
  • refined sugar
  • seeds
  • spicy foods, sauces
Consider using a food diary or journal to track what you eat and drink eery day; and, track any "suspect" foods and beverages that seem to aggravate your  symptoms.

Note: For more details about IBD, Crohn's and UC and how to treat them naturally, get the How to Treat Autoimmune Diseases, PCOS & Thyroid Issues Naturally ebook.
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Vaccinations                                                                 

There are many diseases that, if you catch them once, you will never catch again. Measles is a good example, as is chicken pox. What happens with these diseases is that they make it into your body and start reproducing. The immune system gears up to eliminate them.
In your body you already have B cells that can recognize the virus and produce antibodies for it. However, there are only a few of these cells for each antibody. Once a particular disease is recognized by these few specific B cells, the B cells turn into plasma cells, clone themselves and start pumping out antibodies. This process takes time, but the disease runs it course and is eventually eliminated. However, while it is being eliminated, other B cells for the disease clone themselves but do not generate antibodies. This second set of B cells remains in your body for years, so if the disease reappears your body is able to eliminate it immediately before it can do anything to you.
A vaccine is a weakened form of a disease. It is either a killed form of the disease, or it is a similar but less virulent strain. Once inside your body your immune system mounts the same defense, but because the disease is different or weaker you get few or no symptoms of the disease. Now, when the real disease invades your body, your body is able to eliminate it immediately.
Vaccines exist for all sorts of diseases, both viral and bacterial: measles, mumps, whooping cough, tuberculosis, smallpox, polio, typhoid, etc.
Many diseases cannot be cured by vaccines, however. The common cold and Influenza are two good examples. These diseases either mutate so quickly or have so many different strains in the wild that it is impossible to inject all of them into your body. Each time you get the flu, for example, you are getting a different strain of the same disease.

Why Flu Vaccines Don't Work for Everyone!

Why don't flu vaccines work for some of us? First of all, flu vaccines don't really give you protection against the intended viruses, because these viruses change over time; and, the flu vaccines only contain 2 or 3 of the hundreds of possible viral strains being targeted for that year. In addition, the vaccine may not give your immune system enough stimulation to build enough TK cells to fight off the disease. Also, according to some reports, flu shots contain heavy metals and other toxins that weaken the immune system.
Every year studies are conducted evaluating the effectiveness of flu vaccines. Every few years the Cochrane Collaboration reviews the scientific literature on the effectiveness of flu vaccines. And every review shows that flu vaccines are relatively ineffective. Despite these findings, vaccine manufacturers and government committees continue to recommend flu vaccines for the entire population.

The July 2010 Cochrane Database Review of 50 studies of flu vaccine use in healthy adults showed once again that these vaccines are not effective for those adults (Jefferson 2010). This confirms a previous review from 2007. That review looked at 274 studies. Both these reviews revealed that flu vaccine had no effect on complications such as pneumonia or on hospital admissions. And flu vaccine reduced the symptoms of illness by only a modest one percent.

The authors of these reviews make an interesting observation. Industry-funded studies were more likely to be cited by other articles and the media. And publicly-funded studies were much less likely to show results favorable to vaccines. Don't forget that if a vaccine manufacturer study does not show the results that the industry wants, they will discard the study.

The authors also note widespread misrepresentation of the conclusions that were reached in these reviews. They berate official government articles that misquote their findings to justify actions previously taken to recommend flu vaccines. Articles from the Centers for Disease Control that quote the Cochrane reviews misrepresent the efficacy of the flu vaccine to serve an agenda that promotes the use of these vaccines. Their conclusion: "The CDC authors clearly do not weight interpretation by quality of the evidence, but quote anything that supports their theory."

The final conclusion of these authors is that their results should discourage the use of flu vaccine in healthy adults as a routine health measure.

Previous reviews of other age groups have shown similar ineffectiveness of the flu vaccine. The vaccine is ineffective in babies and in the elderly. The Cochrane review of flu vaccines in children less than two years of age showed the vaccine had no protective effect compared to placebo (Jefferson 2008). Similarly in the elderly, who are more susceptible to complications of the flu, studies were unable to show effectiveness (Rivetti 2006).

Finally, the flu vaccine itself causes notable adverse effects. For example the swine flu vaccine campaign of 1976 was halted because of a significant incidence of paralysis as a direct effect of the vaccine. This was an H1N1 vaccine similar to the swine flu H1N1 vaccine that is included in this year's flu shots. And the new H1N1 vaccine is showing similar problems.

There are much more effective ways to prevent the flu. Taking immune system enhancers such as vitamins A and D3 supplements and medicinal mushrooms like cordyceps, reishi and shiitake, as well as lactoferrin and immunoglobulins contained in whey powder or colostrum, will maintain a strong immune system. All of these supplements are available at most health food stores. There are also excellent natural treatments for the flu (Neustaedter 2005).
The Science Behind Why Most Flu Shots Don't Work
The Centers for Disease Control (CDC) continues to look at whether or not the flu vaccine is effective. Preliminary results indicate you'll get just as sick (with colds, flu, flu-like illnesses) if you got the vaccine than if you didn't. Why doesn't the vaccine work? In order to understand the answer, you'll need to understand some specifics about the flu vaccine and a bit about how immunity works.
Flu Vaccine Facts
There is no single virus that causes the flu; there is no one flu vaccine that protects against all of them. A flu vaccine is designed to confer immunity against the strains of flu that are expected to be most common and most serious. The vaccine is a sort of one-size-fits-all solution, even though there are more types of flu than covered by the vaccine and the flu types vary according to region. It takes time to produce vaccines, so a new vaccine can't be instantly produced when a new type of flu starts to cause problems.
The Vaccine and Immunity
The flu vaccine gives your body parts of inactivated flu viruses. These virus parts correspond to parts of proteins floating around in your body. When the virus part contacts a chemical 'match', it stimulates the body to produce the cells and antibodies that can remove this particular intruder. Antibodies are proteins that float in body fluids and can bind to specific chemical markers. When an antibody binds to a substance, it essentially marks it for destruction by other cells. However, an antibody for one type of flu won't necessarily bind to a virus part from another type of flu. You don't get protection against other viruses. A flu vaccine can only stimulate your immune system to protect you against the viruses in the vaccine, with some lesser protection against very similar ones.
Incomplete Protection Against Intended Targets
You may not even get protection against the intended virus. Why? First, because viruses change over time. The piece that was in the vaccine may not 'look' the same (chemically) as the real thing (months later, after all!). Second, the vaccine may not have given you enough stimulation to fight off the disease.
Let's review what's happened so far: the inactivated virus piece has found a chemical match in your body. This causes an immune response, so your body has started to gear up its production of antibodies and similar markers on cells that can mark the virus for destruction or kill it outright. It's like calling up an army for a battle. Will your body win the fight when the real virus comes to call? Yes, if you have enough defenses built up. However, you will still get the flu if:
  • your body isn't fast enough producing a response
    • get the vaccine and get exposed to the flu too soon (less than 2 weeks)
    • too much time between vaccination and exposure (loses its effectiveness over time)
  • you don't produce enough of a response
    • overwhelmed by exposure to a high level of the virus
    • your body couldn't recognize the initial virus piece (determined by genetics)
    • your body didn't make enough antibodies/cells (common in older people or people with suppressed immune systems)
  • the virus as changed beyond your body's ability to recognize it
  • the part of the virus that was in the vaccine can't be detected by the body in the intact virus
Waste of Time?
Yes and no... the flu vaccine may be more effective some years than others. The CDC predicted that the vaccine developed for the winter of 2003/2004 wasn't going to be effective against most cases of the flu because the strains covered by the vaccine weren't the same as the strains that were common. Highly targeted vaccines work, but only against their targets! There's no point in accepting the risks of a vaccine for a disease you can't get. When the flu vaccine is on-target, it's more effective. Even then, the vaccine isn't perfect because it uses inactivated virus. Is that bad? No. A live vaccine is more effective, but much more risky.
Bottom line: The flu vaccine varies in effectiveness from year-to-year. Even in a best-case scenario, it won't always protect against the flu. The CDC study didn't say that the vaccine didn't work; it says the vaccine didn't protect people from getting sick. Even with imperfect effectiveness, the vaccine is indicated for certain people. Instead of focusing on a flu vaccine, all of us should eat better and strengthen our immune system!
How Antibiotics Work
Sometimes your immune system is not able to activate itself quickly enough to outpace the reproductive rate of a certain bacteria, or the bacteria is producing a toxin so quickly that it will cause permanent damage before the immune system can eliminate the bacteria. In these cases it would be nice to help the immune system by killing the offending bacteria directly.
Antibiotics work on bacterial infections. Antibiotics are chemicals that kill the bacteria cells but do not affect the cells that make up your body. For example, many antibiotics interrupt the machinery inside bacterial cells that builds the cell wall. Human cells do not contain this machinery, so they are unaffected. Different antibiotics work on different parts of bacterial machinery, so each one is more or less effective on specific types of bacteria. You can see that, because a virus is not alive, antibiotics have no effect on a virus.

One problem with antibiotics is that they lose effectiveness over time. If you take an antibiotic it will normally kill all of the bacteria it targets over the course of a week or 10 days. You will feel better very quickly (in just a day or two) because the antibiotic kills the majority of the targeted bacteria very quickly. However, on occasion one of the bacterial offspring will contain a mutation that is able to survive the specific antibiotic. This bacteria will then reproduce and the whole disease mutates. Eventually the new strain is infecting everyone and the old antibiotic has no effect on it. This process has become more and more of a problem over time and has become a significant concern in the medical community.

References
  1. Friedlander, Mark P., and Terry Phillips. Winning the War Within. Emmaus, PA: Rodale Press, Inc., 1986.
  2. Heumer, Richard P. The Roots of Molecular Medicine. New York: W.H. Freeman & Company, 1986.
  3. Principles of Molecular Medicine (Hardcover), by Marschall S. Runge (Editor), Cam Patterson (Editor)
  4. Marchetti, Albert, M.D. Beating the Odds. New York: St. Martin’s Press, 1988.
  5. Wade, Carlson. Immune Power Boosters. West Nyack, New York: Parker Publishing Company, 1990.
  6. a b c Beck, Gregory; Gail S. Habicht (November 1996). "Immunity and the Invertebrates"(PDF). Scientific American: 60–66.http://www.scs.carleton.ca/~soma/biosec/readings/sharkimmu-sciam-Nov1996.pdf. Retrieved 1 January 2007.
  7. ^ "Inflammatory Cells and Cancer", Lisa M. Coussens and Zena Werb, Journal of Experimental Medicine, March 19, 2001, vol. 193, no. 6, pages F23-26, Retrieved Aug 13, 2010
  8. ^ "Chronic Immune Activation and Inflammation as the Cause of Malignancy", K.J. O'Byrne and A.G. Dalgleish, British Journal of Cancer, August 2001, vol. 85, no. 4, pages 473-483, Retrieved Aug 13, 2010
  9. ^ Retief FP, Cilliers L (January 1998). "The epidemic of Athens, 430-426 BC". South African Medical Journal 88 (1): 50–3. PMID 9539938.
  10. ^ Ostoya P (1954). "Maupertuis et la biologie"Revue d'histoire des sciences et de leurs applications 7 (1): 60–78. doi:10.3406/rhs.1954.3379.http://www.persee.fr/web/revues/home/prescript/article/rhs_0048-7996_1954_num_7_1_3379.
  11. ^ Plotkin SA (April 2005). "Vaccines: past, present and future". Nature Medicine 11 (4 Suppl): S5–11. doi:10.1038/nm1209PMID 15812490.
  12. ^ The Nobel Prize in Physiology or Medicine 1905 Nobelprize.org Accessed 8 January 2007.
  13. ^ Major Walter Reed, Medical Corps, U.S. Army Walter Reed Army Medical Center. Accessed 8 January 2007.
  14. ^ Metchnikoff, Elie; Translated by F.G. Binnie. (1905) (Full Text Version: Google Books).Immunity in Infective Diseases. Cambridge University Press. ISBN 68025143.http://books.google.com/?id=ywKp9YhK5t0C&printsec=titlepage&vq=Ehrlich&dq=history+of+humoral+immunity.
  15. ^ The Nobel Prize in Physiology or Medicine 1908 Nobelprize.org Accessed 8 January 2007
  16. a b Litman GW, Cannon JP, Dishaw LJ (November 2005). "Reconstructing immune phylogeny: new perspectives". Nature Reviews. Immunology 5 (11): 866–79.doi:10.1038/nri1712PMID 16261174.
  17. a b c Mayer, Gene (2006). "Immunology - Chapter One: Innate (non-specific) Immunity".Microbiology and Immunology On-Line Textbook. USC School of Medicine.http://pathmicro.med.sc.edu/ghaffar/innate.htm. Retrieved 1 January 2007.
  18. ^ Smith A.D. (Ed) Oxford dictionary of biochemistry and molecular biology.ISBN 0-19-854768-4 (1997) Oxford University Press.
  19. a b c d e f g h i Alberts, Bruce; Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walters (2002). Molecular Biology of the Cell; Fourth Edition. New York and London: Garland Science. ISBN 0-8153-3218-1http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=mboc4.TOC&depth=2.
  20. ^ Zhang, YH; Liu, YL; Yan, SC (1991). "Effect of Polyporus umbellatus polysaccharide on function of macrophages in the peritoneal cavities of mice with liver lesions". Zhong xi yi jie he za zhi 11 (4): 225–6, 198. PMID 1773459.
  21. ^ Lin, YF; Wu, GL (1988). "Protective effect of Polyporus umbellatus polysaccharide on toxic hepatitis in mice". Zhongguo yao li xue bao 9 (4): 345–8. PMID 3195347.
  22. ^ Esteban, Carlos Illana (2009). "Interés medicinal de Poria cocos (= Wolfiporia extensa) [Medicinal interest of Poria cocos (= Wolfiporia extensa)]" (in Spanish). Revista Iberoamericana de Micología 26 (2): 103–7. doi:10.1016/S1130-1406(09)70019-1PMID 19631158.
  23. ^ Mantovani G, Bianchi A, Curreli L, Ghiani M, Astara G, Lampis B et al. (1997). "Clinical and immunological evaluation of schizophyllan (SPG) in combination with standard chemotherapy in patients with head and neck squamous cell carcinoma.". Int J Oncol 10 (1): 213–21.PMID 21533366.
  24. ^ Khamaisie, H; Sussan, S; Tal, M; Najajreh, Y; Ruthardt, M; Mahajna, J (2011). "Oleic acid is the active component in the mushroom Daedalea gibbosa inhibiting Bcr-Abl kinase autophosphorylation activity". Anticancer research 31 (1): 177–83. PMID 21273596.
  25. ^ Hetland, G.; Johnson, E.; Lyberg, T.; Bernardshaw, S.; Tryggestad, A. M. A.; Grinde, B. (2008). "Effects of the Medicinal Mushroom Agaricus blazei Murill on Immunity, Infection and Cancer". Scandinavian Journal of Immunology 68 (4): 363–70. doi:10.1111/j.1365-3083.2008.02156.xPMID 18782264.
  26. ^ Ji Y, Zheng MF, Ye SG, Wu XB, Chen JY (2012). "Agrocybe aegerita polysaccharide combined with chemotherapy improves tumor necrosis factor-α and interferon-γ levels in rat esophageal carcinoma."Dis Esophagusdoi:10.1111/j.1442-2050.2012.01397.xPMID 22947091.
  27. ^ Takeujchi, H; He, P; Mooi, LY (2004). "Reductive effect of hot-water extracts from woody ear (Auricularia auricula-judae Quel.) on food intake and blood glucose concentration in genetically diabetic KK-Ay mice". Journal of nutritional science and vitaminology 50 (4): 300–4. PMID 15527075.
  28. ^ Misaki, A; Kakuta, M; Sasaki, T; Tanaka, M; Miyaji, H (1981). "Studies on interrelation of structure and antitumor effects of polysaccharides: Antitumor action of periodate-modified, branched (1 goes to 3)-beta-D-glucan of Auricularia auricula-judae, and other polysaccharides containing (1 goes to 3)-glycosidic linkages". Carbohydrate research 92 (1): 115–29.doi:10.1016/S0008-6215(00)85986-8PMID 7196285.
  29. ^ Song G, Du Q (2010). "Isolation of a polysaccharide with anticancer activity from Auricularia polytricha using high-speed countercurrent chromatography with an aqueous two-phase system."J Chromatogr A 1217 (38): 5930–4. doi:10.1016/j.chroma.2010.07.036.PMID 20719324.
  30. ^ Textbook of therapeutics : drug and disease management (8. ed.). Philadelphia, Pa. [u.a.]: Lippincott Williams & Wilkins. 2006. pp. 1882. ISBN 9780781757348.
  31. ^ al.], edited by Helga Rübsamen-Waigmann ... [et (2003). Viral Infections and Treatment.. Hoboken: Informa Healthcare. pp. 111. ISBN 9780824756413.
  32. ^ Heikkinen T, Järvinen A (January 2003). "The common cold". Lancet 361 (9351): 51–9.doi:10.1016/S0140-6736(03)12162-9PMID 12517470.
  33. ^ Goldsobel AB, Chipps BE (March 2010). "Cough in the pediatric population". J. Pediatr. 156(3): 352–358.e1. doi:10.1016/j.jpeds.2009.12.004PMID 20176183.
  34. ^ Palmenberg AC, Spiro D, Kuzmickas R, Wang S, Djikeng A, Rathe JA, Fraser-Liggett CM, Liggett SB (2009). "Sequencing and Analyses of All Known Human Rhinovirus Genomes Reveals Structure and Evolution". Science 324 (5923): 55–9. doi:10.1126/science.1165557.PMID 19213880.
  35. ^ Eccles Pg.77
  36. a b c "Common Cold"National Institute of Allergy and Infectious Diseases. 27 November 2006. Retrieved 11 June 2007.
  37. ^ Eccles Pg.107
  38. a b c editors, Ronald Eccles, Olaf Weber, (2009). Common cold (Online-Ausg. ed.). Basel: Birkhäuser. pp. 197. ISBN 978-3-7643-9894-1.
  39. a b Eccles Pg.211
  40. a b c d al.], edited by Arie J. Zuckerman ... [et (2007). Principles and practice of clinical virology (6th ed.). Hoboken, N.J.: Wiley. pp. 496. ISBN 978-0-470-51799-4.
  41. ^ Gwaltney JM Jr, Halstead SB. "Contagiousness of the common cold". Invited letter in"Questions and answers"Journal of the American Medical Association 278 (3): 256–257. 16 July 1997. doi:10.1001/jama.1997.03550030096050. Retrieved 16 September 2011.
  42. a b c d "Influenza: Viral Infections: Merck Manual Home Edition". Merck. Retrieved 15 March 2008.
  43. a b c Eccles, R (2005). "Understanding the symptoms of the common cold and influenza".Lancet Infect Dis 5 (11): 718–25. doi:10.1016/S1473-3099(05)70270-XPMID 16253889.
  44. ^ Seasonal Flu vs. Stomach Flu by Kristina Duda, R.N.; Retrieved 12 March 2007 (Website: "About, Inc., A part of The New York Times Company")
  45. ^ Ballinger, MN; Standiford, TJ (Sep 2010). "Postinfluenza bacterial pneumonia: host defenses gone awry". J Interferon Cytokine Res 30 (9): 643–52. doi:10.1089/jir.2010.0049.PMID 20726789.
  46. a b Hospitalized Patients with 2009 H1N1 Influenza in the United States, April–June 2009, New England Journal of Medicine, Jain, Kamimoto, et al., 12 November 2009.
  47. a b c Transcript of virtual press conference with Gregory Hartl, Spokesperson for H1N1, and Dr Nikki Shindo, Medical Officer, Global Influenza Programme, World Health Organization, 12 November 2009.
  48. a b Report Finds Swine Flu Has Killed 36 Children, New York Times, DENISE GRADY, 3 September 2009.
  49. a b Brankston G, Gitterman L, Hirji Z, Lemieux C, Gardam M (April 2007). "Transmission of influenza A in human beings". Lancet Infect Dis 7 (4): 257–65. doi:10.1016/S1473-3099(07)70029-4PMID 17376383.
  50. ^ Suarez, D; Spackman E, Senne D, Bulaga L, Welsch A, Froberg K (2003). "The effect of various disinfectants on detection of avian influenza virus by real time RT-PCR". Avian Dis 47(3 Suppl): 1091–5. doi:10.1637/0005-2086-47.s3.1091PMID 14575118.
  51. ^ Avian Influenza (Bird Flu): Implications for Human Disease. Physical characteristics of influenza A viruses. UMN CIDRAP.
  52. ^ Jefferson T, Del Mar CB, Dooley L, et al. (2011). "Physical interventions to interrupt or reduce the spread of respiratory viruses". Cochrane Database Syst Rev (7): CD006207.doi:10.1002/14651858.CD006207.pub4PMID 21735402.
  53. ^ Influenza (Seasonal)World Health Organization, April 2009. Retrieved 13 February 2010.
  54. ^ "Avian influenza ("bird flu") fact sheet". WHO. February 2006. Retrieved 20 October 2006.
  55. ^ World Health Organization. World now at the start of 2009 influenza pandemic.http://www.who.int/mediacentre/news/statements/2009/h1n1_pandemic_phase6_20090611/en/index.html
  56. ^ WHO position paper: influenza vaccines WHO weekly Epidemiological Record 19 August 2005, vol. 80, 33, pp. 277–288.
References (Crohn's)
  1. a b c d e f g h i j k l m n o Baumgart, Daniel C; Sandborn, William J (2012). "Crohn's disease". The Lancet 380 (9853): 1590–605. doi:10.1016/S0140-6736(12)60026-9.PMID 22914295.
  2. ^ Crohn's Disease Mayo Clinic[full citation needed]
  3. ^ Crohn's Disease National Digestive Diseases Information Clearinghouse
  4. ^ Cho, Judy H.; Brant, Steven R. (2011). "Recent Insights into the Genetics of Inflammatory Bowel Disease". Gastroenterology 140 (6): 1704–12. doi:10.1053/j.gastro.2011.02.046.PMID 21530736.
  5. a b c Dessein, Rodrigue; Chamaillard, Mathias; Danese, Silvio (2008). "Innate Immunity in Crohnʼs Disease". Journal of Clinical Gastroenterology 42: S144–7.doi:10.1097/MCG.0b013e3181662c90PMID 18806708.
  6. ^ Stefanelli, Tommaso; Malesci, Alberto; Repici, Alessandro; Vetrano, Stefania; Danese, Silvio (2008). "New Insights into Inflammatory Bowel Disease Pathophysiology: Paving the Way for Novel Therapeutic Targets". Current Drug Targets 9 (5): 413–8.doi:10.2174/138945008784221170PMID 18473770.
  7. a b Marks, DJ; Rahman, FZ; Sewell, GW; Segal, AW (2010). "Crohn's disease: An immune deficiency state". Clinical reviews in allergy & immunology 38 (1): 20–31. doi:10.1007/s12016-009-8133-2PMID 19437144.
  8. ^ Lalande, JD; Behr, MA (2010). "Mycobacteria in Crohn's disease: How innate immune deficiency may result in chronic inflammation". Expert review of clinical immunology 6 (4): 633–41. doi:10.1586/eci.10.29PMID 20594136.
  9. ^ Yamamoto-Furusho, Jesus K; Korzenik, Joshua R (2006). "Crohn's disease: Innate immunodeficiency?"World Journal of Gastroenterology 12 (42): 6751–5. PMID 17106921.
  10. ^ http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2810%2960282-6/fulltextWhat's in a name? The (mis)labelling of Crohn's as an autoimmune disease
  11. ^ Defective IL-1A expression in patients with Crohn's disease is related to attenuated MAP3K4 signaling.http://www.ncbi.nlm.nih.gov/pubmed/22732089
  12. ^ Revisiting Crohn's disease as a primary immunodeficiency of macrophageshttp://jem.rupress.org/content/206/9/1839.full
  13. a b Cosnes, Jacques (2004). "Tobacco and IBD: Relevance in the understanding of disease mechanisms and clinical practice". Best Practice & Research Clinical Gastroenterology 18 (3): 481–96. doi:10.1016/j.bpg.2003.12.003PMID 15157822.
  14. ^ Loftus, E. V.; Schoenfeld, P.; Sandborn, W. J. (2002). "The epidemiology and natural history of Crohn's disease in population-based patient cohorts from North America: A systematic review". Alimentary Pharmacology and Therapeutics 16 (1): 51–60. doi:10.1046/j.1365-2036.2002.01140.xPMID 11856078.
  15. a b Bernstein, Charles N.; Wajda, Andre; Svenson, Lawrence W.; MacKenzie, Adrian; Koehoorn, Mieke; Jackson, Maureen; Fedorak, Richard; Israel, David et al. (2006). "The Epidemiology of Inflammatory Bowel Disease in Canada: A Population-Based Study". The American Journal of Gastroenterology 101 (7): 1559–68. doi:10.1111/j.1572-0241.2006.00603.xPMID 16863561. |displayauthors= suggested (help)
  16. a b c d e f g h i Crohn Disease at eMedicine
  17. a b Crohn, BB; Ginzburg, L; Oppenheimer, GD (2000). "Regional ileitis: A pathologic and clinical entity. 1932". The Mount Sinai journal of medicine, New York 67 (3): 263–8.PMID 10828911.
  18. a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
  19. a b c d e Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American Journal of Gastroenterology 96 (3): 635–43.doi:10.1111/j.1572-0241.2001.03671.xPMID 11280528. Retrieved 2009-11-07.
  20. a b Pimentel, Mark; Chang, Michael; Chow, Evelyn J.; Tabibzadeh, Siamak; Kirit-Kiriak, Viorelia; Targan, Stephan R.; Lin, Henry C. (2000). "Identification of a prodromal period in Crohn's disease but not ulcerative colitis". The American Journal of Gastroenterology 95 (12): 3458–62. doi:10.1111/j.1572-0241.2000.03361.xPMID 11151877.
  21. ^ Crohn's Disease Overview
  22. a b Zieve, David; George F Longstreth (October 18, 2009). "Crohn's Disease". ADAM Health Illustrated Encyclopedia. Retrieved 2010-08-16.[verification needed]
  23. a b c d Podolsky, Daniel K. (2002). "Inflammatory Bowel Disease". New England Journal of Medicine 347 (6): 417–29. doi:10.1056/NEJMra020831PMID 12167685.
  24. ^ Mueller, M. H.; Kreis, M. E.; Gross, M. L.; Becker, H. D.; Zittel, T. T.; Jehle, E. C. (2002). "Anorectal functional disorders in the absence of anorectal inflammation in patients with Crohn's disease". British Journal of Surgery 89 (8): 1027–31. doi:10.1046/j.1365-2168.2002.02173.x.PMID 12153630.
  25. ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (July 30, 2004). "The Gastrointestinal Tract".Robbins and Cotran: Pathologic Basis of Disease (7th ed.). Philadelphia, Pennsylvania: Elsevier Saunders. p. 847. ISBN 0-7216-0187-1.
  26. ^ Taylor, B. A.; Williams, G. T.; Hughes, L. E.; Rhodes, J. (1989). "The histology of anal skin tags in Crohn's disease: An aid to confirmation of the diagnosis". International Journal of Colorectal Disease 4 (3): 197–9. doi:10.1007/BF01649703PMID 2769004.
  27. ^ Fix, Oren K.; Soto, Jorge A.; Andrews, Charles W.; Farraye, Francis A. (2004). "Gastroduodenal Crohn's disease". Gastrointestinal Endoscopy 60 (6): 985. doi:10.1016/S0016-5107(04)02200-XPMID 15605018.
  28. a b Beattie, R M; Croft, NM; Fell, JM; Afzal, NA; Heuschkel, RB (2006). "Inflammatory bowel disease"Archives of Disease in Childhood 91 (5): 426–32.doi:10.1136/adc.2005.080481PMC 2082730PMID 16632672.
  29. ^ Büller, H (1997). "Problems in diagnosis of IBD in children". The Netherlands Journal of Medicine 50 (2): S8–11. doi:10.1016/S0300-2977(96)00064-2PMID 9050326.

References (Ulcerative Colitis)
  1. ^ Danese, S. & Fiocci, C. (2011). Ulcerative colitis. The New England Journal of Medicine, 365:1713-1725.
  2. ^ Kim, IK; Park, KJ; Kang, GH; Im, JP; Kim, SG; Jung, HC; Song, IS; Kim, JS (2012 Oct). "Risk factors for complications after total colectomy in ulcerative colitis". The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology 23 (5): Isayfa–Ssafya. PMID 23161324.
  3. a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.
  4. a b c d Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American Journal of Gastroenterology 96 (3): 635–43.doi:10.1111/j.1572-0241.2001.03671.xPMID 11280528. Retrieved 2009-11-07.
  5. a b Hanauer SB; Hanauer, Stephen B. (1996). "Inflammatory bowel disease". N. Engl. J. Med. 334 (13): 841–8. doi:10.1056/NEJM199603283341307PMID 8596552.
  6. a b c d e f g Kornbluth A, Sachar DB (2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee". Am. J. Gastroenterol. 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.xPMID 15233681.
  7. ^ Langan, RC; Gotsch, PB, Krafczyk, MA, Skillinge, DD (November 2007). "Ulcerative colitis: diagnosis and treatment"American family physician 76 (9): 1323–30. PMID 18019875.
  8. ^ Orholm M, Binder V, Sørensen TI, Rasmussen LP, Kyvik KO (2000). "Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study". Scand. J. Gastroenterol. 35 (10): 1075–81. doi:10.1080/003655200451207PMID 11099061.
  9. ^ Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B (1988). "Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking"Gut 29 (7): 990–996. doi:10.1136/gut.29.7.990PMC 1433769.PMID 3396969.
  10. a b c Baumgart DC, Carding SR (2007). "Inflammatory bowel disease: cause and immunobiology". The Lancet 369 (9573): 1627–1640. doi:10.1016/S0140-6736(07)60750-8.PMID 17499605.
  11. ^ Cho JH, Nicolae DL, Ramos R et al. (2000). "Linkage and linkage disequilibrium in chromosome band 1p36 in American Chaldeans with inflammatory bowel disease"Hum. Mol. Genet. 9 (9): 1425–32. doi:10.1093/hmg/9.9.1425PMID 10814724.
  12. ^ Järnerot G, Järnmark I, Nilsson K (1983). "Consumption of refined sugar by patients with Crohn's disease, ulcerative colitis, or irritable bowel syndrome". Scand. J. Gastroenterol. 18(8): 999–1002. doi:10.3109/00365528309181832PMID 6673083.
  13. ^ Geerling, BJ; Dagnelie, PC; Badart-Smook, A; Russel, MG; Stockbrügger, RW; Brummer, RJ (2000 Apr). "Diet as a risk factor for the development of ulcerative colitis". The American journal of gastroenterology 95 (4): 1008–13. doi:10.1111/j.1572-0241.2000.01942.x.PMID 10763951.
  14. ^ Jowett, SL; Seal, CJ; Pearce, MS; Phillips, E; Gregory, W; Barton, JR; Welfare, MR (2004 Oct). "Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study"Gut 53 (10): 1479–84. doi:10.1136/gut.2003.024828PMC 1774231.PMID 15361498.
  15. ^ Andersen, V; Olsen, A; Carbonnel, F; Tjønneland, A; Vogel, U (2012 Mar). "Diet and risk of inflammatory bowel disease". Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 44 (3): 185–94.doi:10.1016/j.dld.2011.10.001PMID 22055893.
  16. ^ Tilg, H; Kaser, A (1 October 2004). "Diet and relapsing ulcerative colitis: take off the meat?"Gut 53 (10): 1399–1401. doi:10.1136/gut.2003.035287PMC 1774255.PMID 15361484.
  17. ^ Moore, J; Babidge, W; Millard, S; Roediger, W (1998 Jan). "Colonic luminal hydrogen sulfide is not elevated in ulcerative colitis". Digestive diseases and sciences 43 (1): 162–5.doi:10.1023/A:1018848709769PMID 9508519.
  18. ^ Jørgensen, J; Mortensen, PB (2001 Aug). "Hydrogen sulfide and colonic epithelial metabolism: implications for ulcerative colitis". Digestive diseases and sciences 46 (8): 1722–32. doi:10.1023/A:1010661706385PMID 11508674.
  19. ^ Picton, R; Eggo, MC; Langman, MJ; Singh, S (2007 Feb). "Impaired detoxication of hydrogen sulfide in ulcerative colitis?". Digestive diseases and sciences 52 (2): 373–8.doi:10.1007/s10620-006-9529-yPMID 17216575.
  20. ^ Corrao G, Tragnone A, Caprilli R et al. (1998). "Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC)"Int J Epidemiol 27 (3): 397–404. doi:10.1093/ije/27.3.397PMID 9698126.
  21. ^ Voreacos, David (29 May 2007). "Roche Found Liable in First Of 400 Suits Over Accutane".The Washington Post. Retrieved 26 May 2010.
  22. ^ Reddy D, Siegel CA, Sands BE, Kane S (2006). "Possible association between isotretinoin and inflammatory bowel disease". Am. J. Gastroenterol. 101 (7): 1569–73. doi:10.1111/j.1572-0241.2006.00632.xPMID 16863562.
  23. ^ Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C (2004). "[Isotretinoin and ulcerous colitis]". An Sist Sanit Navar (in Spanish; Castilian) 27 (2): 241–3.doi:10.4321/S1137-66272004000300009PMID 15381956.
  24. ^ Reniers DE, Howard JM (2001). "Isotretinoin-induced inflammatory bowel disease in an adolescent". Ann Pharmacother 35 (10): 1214–6. doi:10.1345/aph.10368PMID 11675849.
  25. ^ Heather WonTesoriero (23 April 2008). "Jury Awards $10.5 Million Over Accutane"The Wall Street Journal.
  26. ^ Ko, et al, In Kap. "Targeting Improves MSC Treatment of Inflammatory Bowel Disease". NCBI, National Institutes of Health. PMC 2911249. Missing or empty |url= (help)
  27. a b Fauci et al. Harrison's Internal Medicine, 17th ed. New York: McGraw-Hill Medical, 2008.ISBN 978-0-07-159991-7
  28. a b c d Kornbluth, Asher; David B. Sachar (July 2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee".American Journal of Gastroenterology 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x.PMID 15233681Archived from the original on April 6, 2008. Retrieved 2009-11-07.
  29. ^ Crohn's Disease Overview
  30. a b Roediger WE, Moore J, Babidge W (1997). "Colonic sulfide in pathogenesis and treatment of ulcerative colitis"Dig. Dis. Sci. 42 (8): 1571–9. doi:10.1023/A:1018851723920.PMID 9286219.

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