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Inflammatory Joint Diseases / Rheumatic Disorders

- More than 100 different disorders that affect muscles, bones, ligaments, tendons and joints.

Rheumatoid arthritis – it is a systemic inflammatory disorder of the connective tissue/joints characterized by chronicity, remissions and exacerbations.

Systemic Lupus Erythematosus (SLE) – A diffuse connective tissue disease affecting multiple body systems – skin, joints, kidney, serous membrane of heart, lungs, lymph nodes and GI tract.

Scleroderma– is a chronic autoimmune disease characterized by fibrosis or progressive hardening of skin in patches or diffusely with rigidity of underlying tissues. The cause is unknown ,so there is no direct cure for scleroderma.-

Polymyalgia rheumatica (PMR)– is an inflammatory condition of the muscles, which causes pain or stiffness, usually in the neck, shoulders, and hips. The pain can be very sudden, or can occur gradually over a period of time. PMR usually goes away within a year or two after treatment. PMR is usually treated with long courses of oral steroid

Osteoarthritis – is a group of diseases and mechanical abnormalities involving degradation of joints. Clinical manifestations of OA may include joint pain, tenderness, stiffness, creaking, locking of joints. Treatment of OA consists of exercise, manual therapy, lifestyle modification, medication and other interventions to alleviate pain

Ankylosing spondylitis – chronic connective tissue disorder of spine and surrounding cartilaginous joints such as sacroiliac joints and soft tissues around vetebrae. No cure is known for AS, although treatments and medications are available to reduce symptoms and pain

Reiter’s syndrome – is an autoimmune condition that develops in response to an infection in another part of the body. Coming into contact with bacteria and developing an infection can trigger reactive arthritis. The main goal of treatment is to identify the underlying infectious source with the appropriate antibiotics if still present.

Psoriatic arthritis – a skin disease characterized by reddish marinated patches with profuse silvery scaling on extensor surfaces like knees and elbows. Affects around 10-30% of people suffering from the chronic skin condition psoriasis.

Gout – is a medical condition that usually presents with recurrent attacks of acute inflammatory arthritis (red, tender, hot, swollen joint) affects the feet, elbows, ankles and knees. It is caused by elevated levels of uric acid in the blood.

Systemic Lupus Erythematosus SLE - Increased autoantibody production resulting from abnormal suppressor T-cell function.
- Caused by combination of genetic, hormonal and environmental factors.
- Onset often in childbearing years and may be insidious or acute.

Signs and symptoms:

- Arthritis, joint swelling, tenderness and pain.
- Skin lesions and butterfly shaped rash on nose and cheeks.
- Pericarditis and pleural effusions.
- Inflammation of arterioles causing lesions and necrosis.
- Lymphadenopathy: swollen/enlarged lymph nodes
- Behavioral and cognitive changes
- Depression and psychosis
- Fever, fatigue, weight loss
- Can be life threatening
- Control acute exacerbations that may damage organs
- Impaired skin integrity
- Body image disturbance

Rheumatoid Arthritis

- Autoimmune disease
- Result of immune response
- The arthritis of joints known as synovitis, is inflammation of the synovial membrane that lines joints and tendon sheaths. Joints become swollen, tender and warm, and stiffness limits their movement
- Degenerative changes – loss of articular surfaces and joint motion.
- Inflammation involves other areas as well as joints, blood vessels, lungs, heart, kidneys.

Assessment Of Rheumatic Arthritis

- Functional assessment – gait, posture. - Family History – hereditary component

Mb>Signs and symptoms:

- Acute onset of bilateral and symmetric pain, joint swelling, warmth, erythema, loss of function.
- Begins in small joints of hands, wrists, feet.
- Progresses to knees, shoulders, hips, elbows, spine.
- Deformity in hands and feet is common, caused by swelling and joint destruction.
- Rheumatoid nodules (nontender, movable in subcutaneous tissue over bony prominences).
- Raynaud’s phenomenon (cold and stress induced vasospasm in fingers and toes causing cyanosis).

Systemic effects

Fever, weight loss, fatigue, anemia, lymph node enlargement, arteritis, neuropathy, pericarditis, splenomegaly, dry eyes and mucous membranes.


- Degenerative joint disease
- Inflammation and degeneration of cartilage and bone
- Many types, some hereditary, related top obesity, joint trauma, heavy physical activity.

Symptoms of Osteoarthritis

- Pain, stiffness in morning relieved with movement
- Functional impairment
- Occurs most often in weight bearing joints (hips, knee, spine) but dinger joints often involved
- Bony nodules (painless)
- Tender and enlarged joints.
- X-ray: loss of joint cartilage, spurs.
- Blood studies not useful


- Defect in purine metabolism resulting in hyperuricemia
- Oversecretion of uric acid or decreased excretion, or combination
- Urate crystals precipitate within the joint causing inflammatory response
- Repeated attacks cause accumulations of sodium urate crystals (Tophi) to be deposited in greater toe, hands, ear.
- Urate deposits in kidneys cause kidney stones
- Causes : severe diet, starvation, excessive intake of high purine foods (shellfish, organ meats) heredity, leukemia, multiple myeloma, altered renal function (caused by diuretics, ASA, ethanol).

Signs and symptoms of Gout

- Acute gouty arthritis (recurrent, severe attacks of inflammation) triggered by trauma, alcohol ingestion, dieting, medications, stress, illness.
- Abrupt onset at night of severe pain, redness, swelling and warmth.
- Tophi is a deposit of monosodium urate crystals in people with longstanding high levels of uric acid in the blood
- Renal impairment and kidney stones. [back to the top]

Joint inflammation may raise risk of heart disease (Harvard Health Publications)

People coping with rheumatoid arthritis or lupus already have a lot to deal with. Even so, paying attention to heart health may be especially important for this group. The August 2008 issue of the Harvard Heart Letter reports that rheumatoid arthritis doubles a person’s risk of heart attack or cardiac arrest. Heart disease risk is even higher with lupus, and a new study suggests that gout, another common kind of arthritis, is also linked to cardiovascular disease.

Rheumatoid arthritis, lupus, and related autoimmune disorders are caused by a misguided immune system. Certain white blood cells, which ordinarily protect the body from infection, attack its tissues instead. Although no one knows exactly how these conditions are connected to cardiovascular disease, it is possible they all spring from the same source—inflammation.

Inflammation is an essential part of the body’s defenses. In people with rheumatoid arthritis and lupus, though, inflammation turns against the body and damages joints and other tissues. In heart disease, inflammation kicks off artery-clogging atherosclerosis, keeps it smoldering, and influences the formation of clots, the ultimate cause of heart attacks and many strokes.

Controlling rheumatoid arthritis or lupus with medications that calm inflammation may be a good start toward reducing the excess risk of heart disease. Some studies show that using medications like Remicade and Humira reduces the likelihood of having heart attacks. Statins and baby aspirin may also help.

For now, the Harvard Heart Letter suggests that the best way to control heart risk is by paying attention to diet, weight, exercise, blood pressure, and cholesterol. [back to the top]

Does Inflammation Cause Diabetes?

Inactivity and obesity increase the risk for diabetes, but exactly how is unclear. Recent research suggests that inflammation inside the body plays a role in the development of type 2 diabetes.

The good news: An "anti-inflammatory" diet and exercise plan can help prevent and treat type 2 diabetes.

The effects of inflammation are familiar to anyone who has experienced a bug bite, rash, skin infection, or ankle sprain. In those situations, you will see swelling in the affected area.

With type 2 diabetes, inflammation is internal.

How Inflammation Develops

People with type 2 diabetes don't produce enough insulin or their bodies can't use the insulin adequately. Insulin is a hormone that is made by cells in the pancreas. It controls the amount of sugar in the blood.

Insulin may also have an impact on tissue in the body. Its effects on tissue are influenced by many factors, including obesity and the accumulation of fat around the belly and on major organs in the abdomen. The fat cells can produce chemicals that lead to inflammation.

Scientists are only beginning to understand the role this form of internal inflammation may play in the development of chronic diseases like diabetes.

The Role of Inflammatory Chemicals

Decades ago, researchers identified higher levels of inflammation in the bodies of people with type 2 diabetes. The levels of certain inflammatory chemicals called cytokines are often higher in people with type 2 diabetes compared to people without diabetes.

Obesity and inactivity have long been known to be the most important risk factors that drive the development of type 2 diabetes.

How could carrying extra weight and sofa-sitting be connected to higher levels of inflammatory chemicals in the body and the development of diabetes?

Researchers discovered that in people with type 2 diabetes, cytokine levels are elevated inside fat tissue. Their conclusion: Fat causes continuous (chronic), low levels of abnormal inflammation that alters insulin's action and contributes to the disease.

As type 2 diabetes starts to develop, the body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa. Blood sugar levels creep higher and higher, eventually resulting in type 2 diabetes.

Emotional stress can also increase levels of the chemicals of inflammation. It's unknown whether stress by itself can contribute to the development of diabetes, though.

Does inflammation cause diabetes? It's not as simple as that. All researchers know for sure is that inflammation is somehow involved in the development of type 2 diabetes. [back to the top]

Inflammation may help explain depression, diabetes link

(Reuters Health) - People with both depression and diabetes have higher markers of inflammation in their blood than those with diabetes alone, a new study suggests. Researchers have known that people with diabetes have a higher rate of depression than those without the blood sugar disorder. And people with both conditions tend to do worse over the long run than people with diabetes but no depression.

Inflammation is a sign of the body responding to disease, trauma or other stressors. The new study suggests higher inflammation levels may help explain the link between diabetes, depression and worse overall health, researchers said. But it’s still not clear how, exactly.

“We asked, why is depression so bad for diabetes? The study suggests that we have a possible biological explanation,” Dr. Khalida Ismail told Reuters Health.

“Inflammation may be driving a number of different long-term conditions. That’s quite a new way of thinking of the mind and the body,” she said.

Ismail worked on the study at the Institute of Psychiatry at King’s College London in the UK. She and her colleagues examined 1,227 people with newly diagnosed type 2 diabetes.

Those who reported symptoms of depression tended to be younger and heavier. They also had higher rates of heart and circulation problems and higher concentrations of established markers of inflammation in their blood, according to results published in Diabetes Care.

After the researchers took into account other potential differences between study participants, such as their age, sex, amount of body fat and use of certain medications, six of the 12 inflammatory markers they measured were still linked to depression.

More than one in 20 Americans reported depression in 2005-2006, and about one in 12 has diabetes, a major cause of heart disease and stroke, according to the Centers for Disease Control and Prevention.

Death rates are up to twice as high among people with depression and diabetes as those with diabetes alone, Ismail said.

“The conventional wisdom is that this is a consequence of the psychological burden of having diabetes,” she said. “If that’s the case, if you treat the depression, the diabetes control should improve.”

But it does not, Ismail said. So she began to wonder if inflammation, often seen in people with diabetes, could help explain both conditions and the worse outcomes. “It’s a bit like an engine,” Ismail said. “You’re running a bit higher. So there’s this constant low-grade inflammation and that’s causing damage to your brain, your pancreas and to your vascular system.”

Dr. Anne Peters said she often sees patients with diabetes, depression and elevated markers for inflammation. But there are still many questions about how they are related. “The development of depression could in part be triggered by inflammation, but we don’t know what comes first,” she told Reuters Health. “This paper can’t prove causality. The interplay is so complicated.”

Peters directs the University of Southern California Clinical Diabetes Program in Beverly Hills and was not involved in the current study.

“To me, it’s as much a part of diabetes care as looking at blood sugars to screen for and treat depression,” she said. She believes the best way to begin to combat both depression and diabetes is to eat well and exercise. Her own study found that depression scores among people with diabetes dropped when they were physically active. “If you exercise, you feel better, your inflammatory markers improve. It’s all about lifestyle interplaying with your health. We’re just living lives we were not made to live. We sit still too much at work. We’re caged up in a way,” she said.

Peters cited a 2012 study that found that people taking antidepressants were at higher risk for diabetes than non-antidepressant users, even after taking their weight into account. The current study did not examine antidepressant use.

SOURCE: Diabetes Care, online May 19, 2014. [back to the top]

Inflammation and Heart Disease
Massachusetts General Hospital

Heart attacks and strokes may also be caused in part by inflammation.

Atherosclerosis is a condition in which fatty plaques streak the insides of blood vessels and restrict flow. In recent years, doctors have come to appreciate the contribution of inflammation in this artery-clogging process. A high-fat, high-cholesterol diet can induce changes in the architecture of blood vessel walls by increasing the manufacture of a sticky protein called VCAM-1 (vascular cell adhesion molecule-1).

Researchers think that tiny fat droplets can stimulate inflammation in blood vessels, which prods VCAM-1 production. Fat and other particles cause white blood cells to stick to vessel linings, causing a disturbance in flow. Local disruptions in blood flow can prevent oxygen from reaching vital organs. This can cause heart attacks and strokes, especially at branch points in vessels where the flow is somewhat restricted to begin with.

Another way in which inflammation contributes to heart disease is through the production of so-called foam cells, which are constituents of the fatty plaques in atherosclerosis. Monocytes within blood vessels, which have the ability to ingest various substances, "eat" droplets of cholesterol and turn into foam cells. These cells congregate together to form a plaque, or "lesion." [back to the top]

Chronic inflammation: The new science behind America's deadliest diseases
The Wall Street Journal

What do heart disease, diabetes, Alzheimer's, stroke and cancer have in common? Scientists have linked each of these to a condition known as chronic inflammation, and they are studying how high-fat foods and excess body weight may increase the risk for fatal disorders.

Inflammation is the body's natural response to injury and outside irritants. But when the irritants don't let up, because of a diet of high-fat foods, too much body fat and smoking, for example, the immune system can spiral out of control and increase the risk for disease. Experts say when inflammation becomes chronic it can damage heart valves and brain cells, trigger strokes, and promote resistance to insulin, which leads to diabetes. It also is associated with the development of cancer.

Much of the research on chronic inflammation has focused on fighting it with drugs, such as cholesterol-lowering statins for heart disease. A growing body of research is revealing how abdominal fat and an unhealthy diet can lead to inflammation. Some scientists are investigating how certain components in foods might help. Dietary fiber from whole grains, for instance, may play a protective role against inflammation, a recent study found. And dairy foods may help ease inflammation in patients with a combination of risk factors.

Chronic inflammation is perhaps best understood in its relation to cardiovascular disease. The immune system's white blood cells rush to the arteries when the blood vessels are besieged by low density lipoprotein, or LDL—the "bad" cholesterol. The cells embed themselves in the artery wall and gobble up the invading cholesterol, causing damage to the arteries that can lead to heart attack or stroke.

"You need to have inflammation when you have a wound and the immune system goes in to heal it. Yet we don't want too much inflammation in our system causing damage to our arteries" and other harm, says Wendy Weber, a program director at the National Center for Complementary and Alternative Medicine, part of the National Institutes of Health.

One significant discovery concerns obesity and the ways it promotes inflammation. Fat cells, particularly those in the visceral fat that settles in the belly and around organs, were long thought merely to store excess weight. Instead, fat cells act like small factories to churn out molecules known as cytokines, which set inflammation in motion, says Peter Libby, chief of the division of cardiovascular medicine at Brigham and Women's Hospital in Boston and a professor at Harvard Medical School. [back to the top]

Your sagging skin explained
Gale Benz is an alternative health commentator and blogger. She has interest in Traditional Chinese Medicine and Acupuncture. -

Many people devote themselves to slowing down time, or at least reducing the toll taken on their bodies. Inflammation is believed to be the essential component of aging and age-related disease. This inflammation is present over a broad spectrum that ranges from low to high. On the low side of the spectrum, it takes place on a cellular level and is invisible to the naked eye. It can be discerned only submicroscopically on a molecular level. On the other side of the spectrum, inflammation can be seen as redness and swelling, as seen in a sunburn. The low-grade cellular inflammation eventually explains cell dysfunction that lead to aging and death. The subclinical inflammation is the basis of age-related diseases such as diabetes, different types of cancer, various forms of neurologic diseases, as well as sagging skin.

One of the diseases used as an accelerated aging prototype is diabetes. Studying diabetes has helped us to understand the effects of abnormality in blood sugar level on the making of free radicals which lead to glycation and inflammation. Glycation is an inflammatory biochemical process that takes place when a glucose molecule binds to a protein molecule without the role of enzymes. In scientific terminology, this process is known as AGEs - an appropriate acronym for higher glycation end products. Glycation and AGEs are extremely harmful to all organ systems. AGEs can cause arterial stiffening, cataracts, neurological impairment, diabetic complications, wrinkled skin, and more. The inflammation and glycation observed in diabetics whose disease is poorly managed cause those patients™ aging one-third faster than the normal population.

Uncontrolled diabetes is not the only model for speed-up aging. As we enter a new decade, we are observing a new accelerated aging model. This model has provided us with the information needed for developing effective therapeutic interventions to further slow the aging process and dramatically reduce the development of age-related disease. The culprit is an severe systemic infection called sepsis, which can lead to septic shock. The onset and progression of sepsis very much resemble the changes seen in the aging body. Sepsis results in problems that occur on a cellular level in an a eviated time period, which strongly mimics what occurs to our bodies over a period of years in the normal process of aging.

Understanding how we age on the cellular level gives us the data needed to slow down or even overturn the process. Nutrigenomics is a field that studies how nutrition influences gene expression and how some specific nutrients can turn on the genes that prevent disease and deactivate the genes that cause disease and accelerated aging. The secret of slowing down aging process may be as close as your next meal. In accordance with the above models of accelerated aging, plans of slowing down aging process, such as having specific diet and increasing physical activity, have been developed by different health programs to assist people to look and feel their very best for many decades into the future. In addition, many interventional therapies have been used by these health programs to counteract cellular inflammatory conditions, therefore to improve health and to prolong life. [back to the top]

Aging Process Speeded by Chronic Inflammation

Healthspan: the years of life spent relatively free of disability and serious illness. A study from the Yale School of Medicine released in the October, 2013, issue of Cell Metabolism shows that chronic inflammation can speed the aging process and significantly reduce healthspan.

Chronic inflammation is different from the swelling that occurs with a specific injury, such as a sprained ankle. Acute inflammation can typically be resolved with ice and time. Chronic inflammation is a slowly advancing disturbance that cannot be felt or tested for.

It starts with the immune system, the body’s first line of defense against damage or harm. During the aging process the body’s cells change, causing the immune system to produce low-level, chronic inflammation throughout the body. The Yale research is the first to show that inflammation is directly linked to functional deterioration during aging.

The Yale study has identified an immune sensor, Nlrp3, as the specific trigger of inflammation. Nlrp3 is activated with age and is the common start of inflammation-driven functional decline. This inflammation is associated with many chronic age-related diseases, including gout, arthritis, diabetes, impaired memory, and Alzheimer’s disease.

Mice were tested to determine whether reducing Nlrp3 activity could lower inflammation and age-associated functional decline. Results showed that there were fewer age-related disorders such as bone loss, dementia, cataracts, and glucose intolerance in the mice with lower Nlrp3 activation

Vishwa Deep Dixit, Yale School of Medicine and lead author of the study said the question is whether the trigger for aging that causes low-level inflammation can be switched off to slow the onset of the chronic diseases that occur with age.

If the Nlrp3 immune sensor could be manipulated to reduce or delay the chronic inflammation that speeds the aging process, it could possibly lead to prolonged healthspan, and old age reasonably free of disability or disease.

A study published in the Canadian Medical Association Journal in November, 2013, also said that chronic inflammation is associated with an array of unhealthy aging characteristics, and a likelihood of successful aging that is decreased.

And a study from the Karolinska Institute in Sweden, published in the journal Alzheimer’s & Dementia, shows that Alzheimer’s disease is also associated with inflammation. The problem with Alzheimer’s is that there are not enough of the molecules needed for tissue recovery, so the resolution of the inflammatory process does not happen. The study determined that stimulating the resolution of inflammation may result in less loss of brain function.

Researchers continue to look for therapies or diets that could prevent chronic diseases through reducing excessive inflammation processes. In the meantime there are some tried and true suggestions for improving overall health that may also reduce chronic inflammation.

Control weight: In addition to controlling weight, it is important to pay attention to where the body is putting on fat. Accumulating fat in the waist area can indicate chronic inflammation.

Control stress and get enough sleep: Stress has been found to be related to the accumulation of belly fat. Stress hormones bind to receptors on fat cells, encouraging storage of fat and increasing the number of fat cells. These cells produce more chemicals that increase inflammation.

Exercise: But in moderation. Research suggests that extensive workouts can actually increase inflammation. 60 minutes of activity at one time gives the health benefits needed without risking increased inflammation.

Diet: Follow a Mediterranean-style diet that includes plenty of fruits, nuts, vegetables, olive oil, and fish to protect the heart and lower the levels of chemicals that encourage inflammation. Include antioxidant-rich foods, green tea, and Omega-3 fatty acids (see our Krill Oil).

Floss and brush daily: There is a well-established connection between heart disease and gum disease.

Probiotics (also found in Flamasil): UCLA School of Medicine researchers report that intestinal inflammation could be related to white blood cell damage in other parts of the body, resulting in a whole body inflammatory response.

As the population over 50 increases, doctors are seeing an associated increase in age-related diseases. Researchers now say treating those individual diseases may be wrong, and that they may be more effectively handled by treating the chronic inflammation shown to speed the aging process.

By Beth A. Balen [back to the top]

Understanding Inflammation (by Dermamedics)

Inflammatory skin diseases are the most common problem in dermatology. They come in many forms, from occasional rashes accompanied by skin itching and redness, to chronic conditions such as dermatitis (eczema), rosacea, seborrheic dermatitis, and psoriasis. Skin inflammation can be characterized as acute or chronic. Acute inflammation can result from exposure to UV radiation (UVR), ionizing radiation, allergens, or to contact with chemical irritants (soaps, hair dyes, etc.). This type of inflammation is typically resolved within 1 to 2 weeks with little accompanying tissue destruction. In contrast, chronic inflammation results from a sustained immune cell mediated inflammatory response within the skin itself. This inflammation is long lasting and can cause significant and serious tissue destruction. Inflammatory skin conditions affect over 35 million Americans who annually spend over $2 billion to treat their symptoms.

The process of skin inflammation is complex and is still not completely understood. When the skin is exposed to a “triggering” stimulus, such as UV radiation, an irritant (e.g. soaps or fragrances), or to allergens, the cells in the skin produce a variety of inflammatory "hormones" called cytokines and chemokines. These “inflammatory messengers” bind to specific receptors on target cells and stimulate the production of additional inflammatory signaling "hormones". Some of these cause vasodilation while others activate nerve cells. Still other cytokines cause immune cells to leave the blood and migrate into the skin where they then produce more inflammatory hormones, as well as enzymes, free radicals, and chemicals that damage the skin. The end result of the initial triggering event is the amplification of a large inflammatory response that, while designed to help the skin fight infection from invading bacteria, actually causes considerable damage to the skin.

By far the most effective and commonly used prescription drugs for treating inflammation are the corticosteroids, particularly the glucocorticoid related steroids. They are very effective for many forms of eczema, including atopic dermatitis, allergic contact dermatitis, seborrheic dermatitis (in concert with an anti-fungal agent), and are fairly effective in ameliorating the symptoms of psoriasis. They are not particularly effective, however, in treating acute inflammation, like UVR induced sunburn, which is not primarily an immune cell driven inflammatory response. Corticosteroids can be used topically or orally. Topical corticosteroids have been classified into groups based on potency. For example, the corticosteroid clobetasol proprionate, is ranked as a very potent steroid, while betametasone diproprionate and fluocinolone acetonide can range from potent to moderately potent. OTC topicals containing hydrocortisone are, of course, the least potent. While current treatment regimens for most inflammatory skin diseases are dominated by topical or oral orticosteroids, these are typically used for only short periods of time because they exert some negative side effects on skin, including:

  • Anti-proliferative/thinning effect on the skin.
  • Suppression of the skin’s ability to respond to infection (immunosuppression).
  • Elevation of blood glucose levels (hyperglycemia).
  • Impairment of adrenal gland function.

    By understanding the cellular and biochemical events that are involved in skin inflammation, it has been possible to develop newer and more potent topical and injectable drugs to treat inflammatory skin problems. For example, recently injectable "biological response modifiers" or simply "biologics" have been made available to treat psoriasis and arthritis. Many of these biologics work by targeting and inhibiting the action of an inflammatory cytokine, TNF-alpha, that plays a key role in immune cell recruitment and activation. These immune cells cause many of the symptoms of psoriasis, and thus, by inhibiting these cells, the symptoms are diminished. Similarly, the immune suppressive effects of tacrolimum and pimecrolimus have led to the development of topical dermatologics, such as Protopic and Elidel, to control atopic dermatitis.While effective, these newer drugs can cause serious side effects by virtue of their potent immunosuppressive effects.

    Natural Antioxidant Compounds To Address Skin Problems

    In contrast to the development of synthetic immunosuppressive drugs to fight inflammatory skin diseases, research conducted at the University of Oklahoma Health Sciences Center as well as at other universities has focused on identifying compounds from nature that may have anti-inflammatory benefits without the negative immunosuppressive side effects of potent prescription drugs. Because of the potential benefits of "natural" compounds to address skin problems, a considerable amount of this "botanically-based" research has been funded by the National Institutes of Health, as well as by other government health agencies worldwide. This research has led to the identification of many botanically-derived "antioxidants" that also have significant anti-inflammatory activities. One of the most potent natural anti-inflammatories discovered to date is Curcumin (leading ingredient in Flamasil). This yellow phenolic compound is a constituent of Tumeric and is present curry. Curcumin has been one of the most widely researched natural compounds to date and its anti-inflammatory and anti-cancer effects have led to the development of chemical deriviatives of the compound for use in topical and oral therapeutics. Other botanically-derived compounds that are antioxidants with anti-inflammatory activities include Quercetin (found in apples), Resveratrol (found in wine and in Flamasil), Epigallocatechin Gallate (found in green tea), and Bisabolol (found in Chamomile).

    Key Inflammatory "Mediators" Inhibited by Natural Compounds

    What makes a botanical compound a "good" anti-inflammatory candidate depends primarily on the ability of the compound to block key "inflammatory mediators" produced by skin and immune cells. Two of the most important inflammatory mediators involved in skin disorders are TNF-alpha, as mentioned above, and PGE-2. While TNF-alpha plays a key role in psoriasis, PGE-2 is a major participant in all types of skin inflammation, and is perhaps the most important hormone "mediator" involved in sunburn. Pain, redness and swelling are all due, in part to PGE-2, and studies conducted over many years have implicated PGE-2 as a key participant in the development of skin cancer. Further, PGE-2 suppresses collagen formation in the skin and thus, participates in photoaging. Since PGE-2 is produced in skin cells in response to exposure of the skin to UVR (sunlight) it is no wonder that chronic exposure to the sun can lead to premature aging and skin cancer. Natural anitoxidant compounds that can prevent the production of PGE-2 in skin exposed to sunlight could be extremely useful in preventing skin aging and in reducing the risk of skin cancer.

    Cell and molecular biology research carried out at the University of Oklahoma Heatlh Science Center over the past 12 years has examined the effects of over 200 natural antioxidants on inflammatory pathways that are activated in skin and immune cells by "triggers" such as UVR and chemical irritants. The results of this research have shown that not all "antioxidants" have anti-inflammatory activities, and that some of the weakest anti-oxidants have the best anti-inflammatory and anti-aging effects on human skin cells. In addition to curcumin, bisabolol, quercetin, EGCG, gallic acid, vitamin C and vitamin A derivatives, University of Oklahoma scientists discovered a group of very small, phenolic antioxidants that had wide ranging anti-inflammatory and anti-aging properties. These antioxidants are commonly found in low amounts in basil, nutmeg, bourbon, rum, cheese, and in other foods, and in fact several of these phenolic compounds have been used for many years as food flavoring agents. Interestingly, these compounds were all found to display a very unique "'cell-specific" profile with some compounds being extremely good at blocking inflammation in keratinocytes but poor in preventing inflammation in fibroblasts while others had just the opposite profile. What accounts for these differences in cell specificity is still under investigation. The rights to this "library" of small phenolic anti-inflammatory compounds (SPAC) was transferred to DermaMedics which has been conducting clinical studies in partnership with pharmaceutical companies to determine the efficacy of topical formulations in addressing skin problems. DermaMedics intends to license all or parts of this technology to pharmaceutical partners. [back to the top]

    Food Allergies, Inflammation and Autoimmune Diseases (by Dr. Len Lopez- Christian Post Guest Columnist)

    More than 50 percent of our immune system is found in our digestive tract, which is why it is important to have a properly functioning digestive system. Unfortunately, most doctors don’t recognize how food sensitivities and food allergies can affect those who suffer with irritable bowel, celiac, Crohn’s, rheumatoid arthritis, ulcerative colitis, eczema, psoriases, fibromyalgia, lupus, MS and heart disease.

    People who struggle with bloating, gas, indigestion, reflux and other irritable bowel problems may not realize the root cause may be associated with hidden food allergies. These unknown allergens, if allowed to continue, will trigger inflammation and weaken our immune system. It is this constant exposure to allergens that overworks and confuses our immune system. The ultimate result can be autoimmune and heart diseases.

    Food allergens irritate and inflame our intestinal lining, which compromises our health and digestion. First, they reduce your ability to absorb the nutrients in your food. Just because you ate it, doesn’t mean you absorbed the nutrients in the food. This is a critical step in healing, because the only way to heal and strengthen our body is to nourish it. If our digestive system is compromised, we don’t provide the body with an adequate supply of nutrients.

    Secondly, undigested food particles can leak across the intestinal wall and enter our systemic circulation. This is where the immune problem begins. These undigested food particles are looked upon as ‘foreign invaders’ by our immune fighters. This triggers an antibody and histamine response to fight these foreign invaders. This is why the immune system becomes confused. Our immune fighters – lymphocytes, macrophages and other white blood cells, which attack and destroy harmful invaders, become confused as to which are the harmful, bad guys and which aren’t. These undigested food particles aren’t supposed to be there and are looked upon as the enemy, just as viruses, bacteria and other microbes are.

    Stress contributes to this ‘vicious’ cycle

    Stress triggers cortisol, one of our primary stress hormones, causes erosion of our intestinal lining, which can lead to ulcers. This erosion makes us more susceptible to food allergens and other harmful pathogens such as yeast, fungus, candida and parasites which contributes to the bloating, gas, indigestion, etc. Can you see the ‘vicious’ cycle?

    Constant stress will also interfere with your body’s ability to produce an adequate supply of digestive enzymes and hydrochloric acid (HCL). These two components are extremely important when it comes to good digestion. This is one of the main reasons I recommend a good digestive enzyme with HCL, like ‘Digest-Plus’ for many of my patients who complain of indigestion and other irritable bowel problems. This is especially important for those of us in our 40’s, 50’s and better, because as we age we produce less digestive enzymes and HCL.

    To properly digest our food we also need to be in our “resting-digesting” mode. Unfortunately, most people’s lives are on the fast-track, which puts their bodies in the “fight or flight” mode. When you are constantly running from the ‘saber-tooth tiger’…the last thing your body will do is digest your food. This is why we need to eat our meals in a relaxed state, NOT in the car on the way to a meeting, during rush hour. This should also explain the fact that it’s NOT too much acid that is causing all the digestive problems, but rather the lack of HCL, which is needed to breakdown protein.

    Undigested protein begins to rot and putrefy in your tummy. It is those undigested protein molecules that cross over into your systemic circulation, which causes all the tummy upset many Americans are complaining about. It’s a ‘vicious’ cycle.

    The Inflammation connection

    Heart disease is the number one killer in America. The true cause of heart disease is inflammation. Inflammation also triggers an increase in cholesterol. Unfortunately, just lowering the cholesterol is like closing the barn door after the cows have gotten out. We need to be addressing the cause, which is inflammation. The greatest source of inflammation for most Americans comes from their diet. Improperly digested food irritates and inflames the body. This causes the adrenal glands to produce more cortisol, which is needed to reduce the inflammation. This constant demand on the adrenal glands can easily overwork them and cause adrenal exhaustion and fatigue, which is a primary contributor to so many health problems.

    If you’re suffering from arthritis, fibromyalgia, joint pain along with constant digestive problems, you can easily be causing so much inflammation in your body that your adrenal glands can’t keep it under control. This could then cause an elevation of your cholesterol, as a result of the inflammation. Are you seeing that ‘vicious’ cycle now?

    Don’t forget all the stress triggers increased production of adrenaline, cortisol and norepinephrine, which causes your arteries to constrict, making your blood pressure go up. Additionally, the extra cortisol will trigger an increased production of insulin, which signals your body to start storing calories – NOT burn them! This will than take you down the road of cravings, weight gain, insulin resistance and diabetes.

    Calming down the intestines

    The first step in calming down your inflamed tummy is to stay away from ALL potentially irritating foods. NO dairy, wheat, corn, soy, peanuts, coffee, artificial sweeteners or MSG for 2-4 weeks. You need to remove all of these foods, because if you have more than one offending food and don’t eliminate it from your diet, you may not give your digestive system a true chance to recover and repair. This is not a lifetime ban! In many cases, these foods can be re-introduced after your digestive system has quieted down and healed.

    This elimination diet may cause some people to ask, “what am I supposed to eat, you’ve taken everything out of my diet.” For some people who don’t eat enough fruits, vegetables, nuts and seeds, this elimination diet may make them feel like there aren’t many choices. This is why I recommend the NatraLean Health Bars. They are hypoallergenic and contain NO dairy, wheat, corn, soy, peanuts, artificial sweeteners or trans fatty acids to irritate and inflame your tummy. They come with 8 grams of fiber and 7 grams of mono-unsaturated fats (the good fats), which are key in helping to reduce inflammation.

    Breaking the “vicious” cycle

    The bottom line…Eliminating food allergies can not only help with allergies and sinusitis, but can help with many of the other health complaints including auto immune and heart disease. If you’re looking for a natural approach that targets the cause of your problem. Eliminate those common food allergens, add some digestive enzymes with HCL, fish oils and nutrients to support your adrenal glands such as Adrenal Fuel. You’ll be amazed at how much better your body will begin to feel and function, and the better your body functions the better it runs.

    FYI…One last piece of valuable information – an inflamed intestinal lining also hinders the production of serotonin, which is produced in the gut. Decreased serotonin levels are associated with depression, anxiety, insomnia, PMS, cravings and ADD/ADHD. [back to the top]

    IBS Science- Low-grade Inflammation and IBS

    The times they may be a-changing. Conventional wisdom has always held that there is no inflammation seen in patients with irritable bowel syndrome (IBS). Cutting edge research has begun to find evidence of low-grade inflammation in digestive tract tissue in some IBS patients. Considered very preliminary, these results may pave the way to new and improved treatment options. Here are the things that you need to know in order to have an understanding of the role that inflammation may play in the development and maintenance of IBS.

    Two Necessary Definitions

    Mast cells:

    Mast cells are found in tissue all over the body. They are believed to play an important role in protecting the body from pathogens -- outside agents, such as germs or viruses, that pose a threat to your health. It is thought that mast cells induce a rapid inflammatory response in response to a pathogen. It is thus not surprising that mast cells appear to be highly involved in what we commonly know as allergies.


    Cytokines are proteins that are released by mast cells and other cells associated with the immune response. It is thought that after the quick inflammatory reaction triggered by mast cells, a longer lasting inflammatory process occurs due to the release of certain kinds of cytokines. Cytokines can be pro-inflammatory or anti-inflammatory.

    The Possible Problem

    Imagine that your body gets infected by a nasty stomach virus (gastroenteritis). Mast cells react quickly, followed by cytokines, to fight back against the infection. The release of these substances causes abdominal pain, cramping and diarrhea. In most cases, this inflammatory response is temporary. Once the body senses that the invader has been conquered, the inflammatory process closes down.

    Latest research appears to point to the possibility that, in a small set of IBS patients, this inflammatory process persists after the main infection is gone. And because things are never simple with IBS, it is also entirely possible that there are some individuals who experience this chronic low-grade inflammation without ever experiencing a clear-cut case of gastroenteritis. In any case, the continued activation of mast cells, even on a very mild basis, could contribute to the motility dysfunction that characterizes IBS, particularly in terms of continued episodes of diarrhea. In addition, mast cells can be found very close to nerve cells in the intestines, perhaps contributing to ongoing pain and visceral hypersensitivity that is typical of IBS.

    Potential Risk Factors

    It is not clear why this continued inflammatory process would affect some people and not others. More research is needed to investigate the following possibilities:

    Genetic predisposition Altered state of gut bacteria Food allergies Common allergies The Bottom Line

    Investigation into the role of ongoing inflammation in the development and maintenance of IBS is in a very early stage. What is known is that, in a certain small set of IBS patients, an increase in inflammatory cells has been found in the lining of the large intestine and the ileum part of the small intestine. This inflammation cannot be seen with a microscope as part of an ordinary biopsy procedure, but requires more in-depth examination. Patients whose tissue contains these increased inflammatory substances are more likely to suffer post-infectious IBS (IBS-PI) or diarrhea predominant IBS (IBS-D). Clearly, more research needs to be conducted in order to develop a clearer picture of the role of inflammation in IBS. The hope is that this improved understanding will lead to the development of new treatment options and bring about a relief from suffering.


    Barbara, G., De Giorgio, R., Stangellini, V., Cremon, C. & Corinaldesi, R. “A role for inflammation in irritable bowel syndrome?" Gut 2002 51:i41-i44.

    Delvaux, M. " Role of visceral sensitivity in the pathophysiology of irritable bowel syndrome". Gut 2002 51:i61-i67.

    Liebregts, T., Birgit, A., Bredack, C., Roth, A., Heinzel, S., Lester, S., Downie-Doyle, S., Smith, E., Drew, P., Talley, N. & Holtmann, G. "Immune Activation in Patients With Irritable Bowel Syndrome" Gastroenterology 2007 132:913-920.

    Norton, W. & Drossman, D. “Symposium Summary Report” Digestive Health Matters 2007 16:4-7. [back to the top]

    Chohn's Disease: Learn the facts (Abbvie Inc.)

    Did you know?

    Crohn’s is a chronic disorder. Most experts think Crohn's disease is an abnormal immune response that may result in damaging inflammation of the digestive tract.

    One of the best ways to help manage your Crohn’s disease is to learn more about it. The fact is, Crohn’s is an inflammatory bowel disease (IBD) that causes inflammation of the lining of your digestive tract, which can lead to flare-ups.

    For more than half a million American men and women who have been diagnosed with Crohn’s, inflammation is at the root of their Crohn's disease symptoms.

    While the exact cause of Crohn’s remains unknown, researchers now believe that a combination of genetics, environmental factors, and an abnormal immune response may result in the damaging inflammation of the digestive tract.1 Abdominal pain and cramping are two of the many Crohn's disease symptoms.

    These Crohn’s disease symptoms, which range from mild to severe and vary widely from person to person, may also include:

    - Frequent diarrhea
    - Rectal bleeding
    - Feeling of need to move bowels
    - Constipation

    [back to the top]

    Causes And Triggers Of Asthma: Understanding Inflammation (InteliHealth)

    People with asthma have trouble breathing because the tubes that carry air to and from the lungs (that is, the airways) become inflamed. Inflammation causes mucus to build up in these tubes, cutting down on the space available to move air. Inflammation also stimulates the muscles around these tubes to contract, or go into spasm (bronchospasm), in reaction to minor irritations. Bronchospasm further narrows the tubes and cuts down the airflow.

    For many people, inflammation in the lungs is an allergic reaction. Although the trigger for inflammation in the lungs can be different for different people, some allergy triggers are very common, shared by many people who have asthma.

    Allergy reactions occur in most people who have asthma. When allergy occurs, immune cells within the lungs and airways overreact to foreign substances in the air, such as cat hair, mold, or deposits left by dust mites. Many people with asthma benefit from seeing an allergy specialist who can help manage their condition.

    Once the airways are inflamed, minor irritation can make the airway muscles spasm. Inflamed airways are sensitive to irritants in the air that are not true allergens, such as pollution, cigarette smoke, or sulfite gases (gases from fermentation of some drinks or foods). For many asthmatics cold air can constrict the airways, and this is the cause of exercise-induced asthma. (When you breathe hard during exercise, your nose and throat don't have a chance to warm up each breath before the air is drawn into your lungs).

    Understanding how inflammation causes asthma will bring you one step closer to controlling this disease. That's because stopping or preventing inflammation by avoiding the things that trigger it is key to keeping the airways open, which promotes good airflow and comfortable breathing. Understanding the role that inflammation plays also will help you to understand why you may need to take at least two different drugs — one to control or prevent inflammation and another to quickly open constricted airways.

    Unraveling asthma's link to inflammation has led to huge advances in treating this disease. This work has laid the groundwork for new classes of drugs aimed at controlling or preventing airway inflammation. These new drugs work hand in hand with the old and still important standbys: drugs that relax and open the airway.

    The more you can avoid the things that stir up the inflammatory response, the easier you will breathe. [back to the top]

    Systemic Inflammation in COPD (Alice Huertas MD, Paolo Palange MD)

    Among the numerous extra-pulmonary effects of COPD, systemic inflammation has been widely studied and considered as an important key between the pulmonary disease and the related systemic manifestations. Many studies have reported changes in various inflammatory cells and mediators, including neutrophils, lymphocytes, acute-phase reactants, and cytokines. Gan and colleagues recently performed a meta-analysis that showed systemic inflammation is present during COPD exacerbations and stable phases of the disease: increased numbers of leukocytes, levels of acute-phase response proteins (C-reactive protein and fibrinogen), cytokines such as interleukin (IL)-6, and tumor necrosis factor (TNF)-α are present in the peripheral blood of COPD patients [Gan et al. 2004]. Systemic inflammation has been implicated in the pathogenesis of the majority of COPD systemic effects, including weight loss [Wouters, 2002], skeletal muscle dysfunction [Langen et al. 2001], cardiovascular diseases [Sin and Man, 2003], and osteoporosis [Biskobing, 2002], although it is still controversial whether this socalled low-grade systemic inflammation represents the consequence of pulmonary inflammation into the systemic vascular bed [Agustí et al. 2003], or whether it is a systemic inflammation. Vernooy and colleagues, as well as Hurst and colleagues, failed to show a relationship between TNF-α and IL-8 values in induced sputum and plasma, suggesting that the systemic inflammation in COPD is not linked to the pulmonary inflammation in these patients [Hurst et al. 2005; Vernooy et al. 2002]. Although inflammation is certainly one of the major features of COPD, we still need to understand whether the local inflammation is sufficient to induce systemic effects, or whether a second pathogenetic event is required. Therefore, further studies are needed to elucidate the origin of the systemic inflammation in COPD. [back to the top]

    Chronic inflammation in the brain leads the way to Alzheimer's disease(Biomed Central)

    Research published July 2 in Biomed Central's open access journal Journal of Neuroinflammation suggests that chronic inflammation can predispose the brain to develop Alzheimer's disease.

    To date it has been difficult to pin down the role of inflammation in Alzheimer's disease (AD), especially because trials of NSAIDs appeared to have conflicting results. Although the ADAPT (The Alzheimer`s Disease Anti-inflammatory Prevention Trial) trial was stopped early, recent results suggest that NSAIDs can help people with early stages of AD but that prolonged treatment is necessary to see benefit.

    Researchers from the University of Zurich, in collaboration with colleagues from the ETH Zurich and University of Bern investigated what impact immune system challenges (similar to having a severe viral infection) would have on the development of AD in mice. Results showed that a single infection before birth (during late gestation) was enough to induce long-term neurological changes and significant memory problems at old age.

    These mice had a persistent increase in inflammatory cytokines, increased levels of amyloid precursor protein (APP), and altered cellular localization of Tau. If this immune system challenge was repeated during adulthood the effect was strongly exacerbated, resulting in changes similar to those seen for pathological aging. Dr Irene Knuesel who led this research explained, "The AD-like changes within the brain of these mice occurred without an increase in amyloid β (Aβ). However, in mice genetically modified to produce the human version of Aβ, the viral-like challenge drastically increased the amount of Aβ at precisely the sites of inflammation-induced APP deposits. Based on the similarity between these APP/AƒÒ aggregates in mice and those found in human AD, it seems likely that chronic inflammation due to infection could be an early event in the development of AD. [back to the top]

    Chronic Inflammation and Alzheimer’s (Dharma S Khalsa, MD Health Guide)

    One of the devastating effects of aging is chronic low-level inflammation. Countless studies over the years have proved that unchecked inflammation contributes to the progression of often deadly diseases including cancer, atherosclerosis, high blood pressure, diabetes and even Alzheimer’s. It’s also linked to arthritis, depression and even wrinkling of the skin.

    You can compare chronic inflammation to a smoldering fire that leads to premature aging and disease. So taking steps to extinguish the damaging heat it causes is the healthiest thing you can do.

    Diet is a good place to start. Eliminate trans-fats and refined carbohydrates (white bread, pasta, white rice). These foods fan the flames of inflammation. Replace them with omega-3’s, avocados, coconut oil, olive oil and antioxidant-rich fruits and vegetables.

    Get a good night’s sleep. Believe it or not, scientific studies prove that restful sleep is a natural anti-inflammatory that increases health and wellness.

    Take nutritional supplements that naturally reduce inflammation along with providing other life-extending benefits. One of the best is Turmeric. Curcumin-rich turmeric (main ingredient in Flamasil) has been shown to inhibit the onset of rheumatoid arthritis and stop the production of inflammatory proteins that lead to joint destruction. It also has anti-cancer properties, improves the cardiovascular system, inhibits cataract formation, speeds up diabetic wound healing, and decreases the incidence of Alzheimer’s.

    Did you know that people in India have a 25% less cases of Alzheimer’s? That’s an impressive difference. Well, turmeric is believed to be one of the main reasons of such lower incidence. It’s such a powerful anti-oxidant, and is found in curry, the traditional Indian food.

    If you want to add it to your diet, you can find many easy recipes online. Just remember: it should be cooked, so don’t just use on food raw like salt or pepper. Instead, cook it ahead of time, then keep it handy and yes, you can sprinkle it on your food. Here is an easy recipe to have it handy:

    In a small pot, put one cup of water and bring to a boil. Add 1-2 tablespoons of turmeric and boil for 5 minutes. You may have to add water if it gets too sticky. Then let cool and place in a small sealed container in the refrigerator. Sprinkle on your food as desired.

    As you incorporate these tips into your life, you can be sure you are reducing your risk of Alzheimer’s and other diseases on a daily basis. [back to the top]

    Stopping Chronic Inflammation - An Important Aspect of Cancer Treatment -(Envita)

    Inflammation is the body's response to tissue damage, caused by physical injury, ischemic injury (caused by an insufficient supply of blood to an organ), infection, exposure to toxins, or other types of trauma. The body's inflammatory response causes cellular changes and immune responses that result in repair of the damaged tissue and cellular proliferation at the site of the injured tissue.

    Inflammation can become chronic if the cause of the inflammation persists, or because of deregulation in the control mechanisms responsible for shutting down the inflammation process. When these inflammatory responses become chronic, cell mutation and proliferation can result and often create an environment that is conducive to the development of cancer. This is often referred to as "the perfect storm." Envita has developed several proprietary methods to treat these factors and improve outcomes for cancer patients.

    Epigenetics: Our Genes are influenced and can be changed

    Several Important Strategies for Successful Cancer Treatment

  • Genetically Targeted Chemotherapy
  • Transform the patient’s immune system
  • Natural Killer Cells = Better overall prognosis
  • Changing the cancer environment with intravenous vitamin C

    Inflammation Triggers DNA Damage, Epigenetics and Stage 4 Cancer

    Inflammation triggers an immune response and alerts the body's vasculature to release inflammatory cells into a damaged tissue environment. The cellular activity involved in the inflammatory response can increase the production of reactive oxygen species (ROS), such as free radicals, and reactive nitrogen species (RNS).

    Cells are normally able to defend themselves against these two types of molecules. However, when production of these two types of highly reactive molecules is increased due to chronic inflammation, cells can no longer protect themselves, resulting in extensive damage to the essential enzymes involved in DNA repair, actual cell DNA mutation, and mitochondrial damage. These various insults are linked to causes of cancer and often bring about epigenetic changes.

    Research suggests an emerging link between infection, epigenetics and cancer. Changes catalyzed by pathogenic inflammation can transform cells into cancerous tumors. Many cancers are linked to viruses/bacteria that promote reversible, epigenetic changes in the body's cells that lead to tumors. At minimum, 20 percent or more of cancers are linked to infectious disease according to the Journal of American Medical Associates. Moreover, the global medical community is probably only aware of an estimated 13 percent of infections that exist throughout the world. For this reason, it is likely that we shall find that infections play a far larger role in the cause of cancer than current estimates show.

    The Inflammation Process and Stage 4 Cancer's Microenvironment

    Inflammation is known to cause other such changes in the microenvironment of cells. Cells often undergo adaptive changes to survive stressful or toxic environments. These adaptive changes can include: an increased expression of antioxidant enzymes, increased anaerobic respiration and development of angiogenic factors. This adaptation is usually transient, however, and allows normal cells to survive only until the toxic condition is alleviated.

    Even so, under conditions of prolonged stress, such as chronic inflammation, a mutation may actually "lock" in the cell, making these adaptive changes permanent. Not surprisingly, many of the cells and systems involved in inflammation (including abnormal cellular respiration and angiogenesis) are also found in a variety of tumors. In addition to DNA mutation, injuries to tissue may also cause increased cellular proliferation at the site of the injury. In such circumstances, sustained cellular proliferation may result from resultant chronic inflammation. When combined with the DNA mutations described above, enhanced proliferation can increase the number of cells at risk for mutations, leading to an environment that is conducive to the development of cancer.

    Inflammation, Progression and Metastasis of Cancer Inflammation is one major fuel that feeds the fire of stage 4 cancer growths and spread. The interaction between viruses, bacteria, environmental toxins (carcinogens) lead to DNA methylation and other changes in cellular metabolism. Inflammations from infections/toxins that can lead to cancer are major contributors in tumor genesis or progression. [back to the top]

    Link Between Chronic Inflammation and Cancer Confirmed
    (Medical News Today)

    According to scientists at the Massachussets Institute of Technology, chronic inflammation of the intestine or stomach has been linked to DNA damage and thus increased cancer risk. These results were released on June 2, 2008 in the Journal of Clinical Investigation (JCI).

    Inflammation can be caused by many factors, including infectious agents such as Helicobacter pylori and Hepatitis C, which are already known to increase cancer risk in the stomach and liver, respectively. The inflammatory response produces cytokines, the chemicals in the immune response that encourage cell proliferation and suppress apoptosis, which can also contribute to an increased risk of cancer. In most normal situations, damage induced to DNA during an inflammatory response is repaired by the cell's internal error correction system -- but if this is not functioning properly, there is a higher chance that mutation will occur, increasing the risk of cancer. Knowing the connection between these factors and cancer can help doctors better guide patients who might be at risk for inflammation induced cancers. "That variation could influence the susceptibility of individuals and how they are going to respond to a chronic inflammation response," said senior author Leona Samson, director of the CEHS.

    By performing two separate studies, the team discovered that chronic inflammation in mice generally increased the development of tumors. This was tested additionally using mice who were already less able to repair DNA damage and thus more susceptible to cancerous mutations. While this was long hypothesized, these studies help confirm the idea that inflammation can be linked to cancer. "It's something that was expected but it was never formally proven," said lead author Lisiane Meira, research scientist in MIT's Center for Environmental Health Sciences (CEHS).

    In the JCI study, colon inflammation was induced using a chemical compound that mimics a human colitis. This induced a higher rate of cancer. According to Meira: "Lo and behold, the DNA repair deficient mice were more susceptible."

    A second study, in collaboration with James Fox, director of the Division of Comparative Medicine at MIT, and one of his students, Chung-Wei Lee, meant to solidify the first. In this, mice were infected with H. pylori, and those lacking the proper DNA repair mechanisms were more likely to have pre-cancerous regions in the stomach. The latter study is further related to another piece published by Fox, which showed that treating infection with this bacterium quicly could prevent cancer development.

    These results indicate that individuals who are less able to perform DNA damage with chronic inflammation, such as ulcerative colitis, are more susceptible to cancer than others, according to Meira. However, there is another effect of inflamation that they postulate might influence this -- during the inflammatory response to infection, immune cells like macrophages and neutrophils excrete oxygen and nitrogen species that might damage DNA.

    DNA damage induced by chronic inflammation contributes to colon carcinogenesis in mice
    Lisiane B. Meira, James M. Bugni, Stephanie L. Green, Chung-Wei Lee, Bo Pang, Diana Borenshtein, Barry H. Rickman, Arlin B. Rogers, Catherine A. Moroski-Erkul, Jose L. McFaline, David B. Schauer, Peter C. Dedon, James G. Fox and Leona D. Samson J. Clin. Invest. doi:10.1172/JCI35073. [back to the top]

    Curcumin/Turmeric (found in Flamasil™) and Arthritis
    (Medical News Today)

    Summary# 44468

    Topic: Curcumin Holds Potential in the Treatment of Arthritis

    Keywords: ARTHRITIS, RHEUMATOID ARTHRITIS - Curcumin, Turmeric, Quercetin, Antioxidants, Crystal-induced Arthritis, Anti-proliferative, Anti-inflammatory, Immunosuppressive

    Reference: "The antioxidants curcumin and quercetin inhibit inflammatory processes associated with arthritis," Jackson JK, Higo T, et al, Inflamm Res, 2006; 55(4): 168-75. (Address: Faculty of Pharmaceutical Sciences, University of British Columbia, 2146 East Mall, Vancouver, B.C., Canada, V6T 1Z3. E-mail: ). Summary: In a study examining the potential effects of the antioxidants curcumin (active agent in turmeric) and quercetin (found in onions, apples, etc.) on the inflammatory aspects of arthritis, curcumin, and to a lesser degree, quercetin was found to inhibit various inflammatory agents implicated in arthritis - particularly crystal-induced arthritis or rheumatoid arthritis. Four assays of inflammatory aspects of arthritis were conducted. Results found that both curcumin and quercetin inhibited neutrophil activation, synoviocyte proliferation and angiogenesis. Only curcumin was found to strongly inhibit collagenase and stromelysin expression at micromolar concentrations, as measured by Northern Blot analysis. The results of this study suggest that curcumin, and to a lesser degree, quercetin, may hold potential as therapeutic agents in the treatment of crystal-induced arthritis and rheumatoid arthritis. [back to the top]

    Osteoarthritis results from inflammatory process, not just wear and tear, study suggests (Stanford Medicine)

    In a study published online Nov. 6 in Nature Medicine, investigators at the Stanford University School of Medicine have shown that the development of osteoarthritis is in great part driven by low-grade inflammatory processes. This is at odds with the prevailing view attributing the condition to a lifetime of wear and tear on long-suffering joints.

    “It’s a paradigm change,” said William Robinson, MD, PhD, the study’s senior author, of the implication of the findings. “People in the field predominantly view osteoarthritis as a matter of simple wear and tear, like tires gradually wearing out on a car.” It also is commonly associated with blow-outs, he added, such as a tear in the meniscus — a cartilage-rich, crescent-shaped pad that serves as a shock-absorber in joints — or some other traumatic damage to a joint.

    But Robinson’s paper suggests a different way of understanding the disease. Its findings offer hope that by targeting the inflammatory processes that occur early on in the development of osteoarthritis — well before it progresses to the point where symptoms appear — the condition might someday be preventable.

    Robinson is an associate professor of immunology and rheumatology at Stanford and a staff physician with the Veterans Affairs Palo Alto Health Care System. The first authorship of the study is shared by research associate Qian Wang, MD, PhD, and Andrew Rozelle, MD, a former Stanford rheumatology fellow now at the Palo Alto Medical Foundation.

    Osteoarthritis is the most common joint disease, afflicting some 27 million people in the United States alone. It is characterized by breakdown of cartilage, most often in the knees, hips, fingers and spine. Drugs commonly used to treat osteoarthritis, such as acetaminophen and ibuprofen, relieve pain but do not slow the disease’s progression.

    It has long been known that osteoarthritic joint tissues host a heightened number of migratory inflammatory cells and of some of the substances these cells secrete — “not nearly as much as in the case of rheumatoid arthritis, which is clearly an autoimmune disease, but enough to make us wonder if inflammation is also a major player in osteoarthritis as well,” Robinson said. His team’s observation of increased numbers of certain specialized inflammatory proteins early in the progress of osteoarthritis, before it becomes symptomatic, suggested that inflammation might be a driver, rather than a secondary consequence, of the disease.

    The new study showed that, indeed, initial damage to the joint sets in motion a chain of molecular events that escalates into an attack upon the damaged joint by one of the body’s key defense systems against bacterial and viral infections, the so-called complement system. This sequence of events involves activation of a chain reaction called the “complement cascade,” and begins early in the development of osteoarthritis.

    The complement system consists of an orchestra of proteins present in blood. Upon activation of the complement cascade — typically, in response to the presence of bacterial or viral infection — these proteins engage in a complex interplay, variously enhancing or inhibiting one another’s actions at certain points and culminating in the activation of a protein cluster called the MAC (for “membrane attack complex”). By punching holes in the membranes of bacterial or virally infected human cells, the MAC helps to clear the body of infections.

    An early clue regarding the complement system’s key role in osteoarthritis came when Robinson and his colleagues, employing advanced lab techniques, compared the levels of large numbers of proteins present in the joint fluid taken from osteoarthritis patients with levels present in fluid from healthy individuals. They found that the patients’ tissues had a relative overabundance of proteins that act as accelerators in the complement cascade, along with a dearth of proteins that act as brakes.

    Robinson’s group also examined the activity level of genes (which are recipes for proteins) in joint-lining tissues of osteoarthritic versus healthy subjects, and observed a similar result: more expression of genes encoding complement-activating and related inflammatory proteins, and less expression of genes encoding complement- and inflammation-inhibiting ones, in the osteoarthritic patients’ joint tissues.

    To further explore the complement system’s role in osteoarthritis, the researchers induced the equivalent of meniscal tears or removal in mice who (like humans) are much more prone to getting osteoarthritis in joints that have suffered such damage. The procedure was performed on normal mice and on three separate strains of bioengineered lab mice, each strain missing a different protein component of the complement system. In two cases, the missing protein was one that ordinarily acts as an accelerator within the complement cascade, and in the third case one that acts as a brake.

    The normal mice developed osteoarthritis as expected. But in comparison with these mice, the two strains of bioengineered mice lacking a complement-cascade-accelerating protein developed less-severe arthritis, while the mice lacking the complement-inhibiting protein got worse, faster. Thus, mice with impaired complement activation were protected against the development of osteoarthritis in response to meniscal damage.

    Next, Robinson’s team asked how complement was causing osteoarthritis. Further experiments in mice and with human tissue showed that the MAC, the heavy artillery of the complement system, was damaging joint-tissue cells, but not by punching holes in them. Instead, it was binding to cartilage-producing cells in these tissues and causing them to secrete, on their own, still more complement-component proteins as well as other inflammatory chemicals, and other specialized proteins, or enzymes, that chew up the matrix of cartilage occupying the spaces between cells. They demonstrated that breakdown products of cartilage destruction, including one called fibromodulin, can directly activate the complement system, fostering a continuing cycle of joint-tissue damage.

    Finally, the investigators showed that all these insults inflicted by the complement system — measured by microscopic examination of mouse joints — were mirrored by functional impairment. Bioengineered mice lacking a key complement-component protein, without which the complement system fails to activate, maintained their ability to walk normally, while normal mice developed a hindered gait due to severe osteoarthritis following meniscal injury.

    “Recent findings suggest that low-grade complement activation contributes to the development of degenerative diseases including Alzheimer’s disease and macular degeneration. Our results suggest that osteoarthritis can be added to this list of diseases,” said Robinson.

    Drugs that target the complement system may someday prove useful in preventing the onset of osteoarthritis in people who have suffered joint injuries, Robinson said, though he cautioned that this system is so crucial to our defense against microbial infection that systemic delivery of complement inhibitors would likely not be safe. But it is possible that a brief period of local administration of a complement inhibitor might provide benefit to patients developing osteoarthritis, while minimizing their risk for the development of infections.

    “Right now we don’t have anything to offer osteoarthritis patients to treat their underlying disease,” Robinson said. “It would be incredible, for the one-third of humans over 60 who have it, to find a way to slow it down.”

    The work was funded by the VA Palo Alto Health Care System and the National Heart, Lung and Blood Institute. Additional Stanford co-authors were Medical Scientist Training Program student Christin Lepus; postdoctoral scholars Inyong Hwang, MD, and Jason Song, MD; visiting scientist Tamsin Lindstrom, PhD; research assistant Heidi Wong; director of Stanford’s Behavioral and Functional Neuroscience laboratory Mehrdad Shamloo, PhD; professor of orthopedic surgery Stuart Goodman, MD, PhD; and associate professor of neurology and neurological sciences Tony Wyss-Coray, PhD. [back to the top]

    The Role of Probiotic Bacteria

    The Experts Speak -- Probiotic Bacteria and the Gastrointestinal Tract -- Stig Bengmark, M.D. -- Lund University

    "Ecological Control of the Gastrointestinal Tract: The Role of Probiotic Bacteria," Gut, 1998;42:2-7. - Online July 2000, Published in "Clinical Pearls 1998 with The Experts Speak"

    Kirk Hamilton: What is your educational background and current position®

    Stig Bengmark: I received my M.D. in 1956 and my Ph.D in 1958. Since 1985, I have been active with research in the field of probiotics and functional food. I was chairman and professor of surgery at Lund University from 1970 to 1994, when I retired.

    KH: How long have you been studying the role of gut flora in its relationship to acute and chronic disease®

    SB: During my surgical career, I have specialized in surgery of the liver and pancreas. This surgeries have, at that time and I am sure still have, an unacceptably high morbidity -- approximately 35 percent. Most of the complications are due to infections. Almost every second liver transplant patient gets septic complications following surgery. The morbidity seems to be similar at all leading surgical centers around the world. I had during almost two decades as a standard prescription, that all the patients should be protected by an umbrella of broad-spectrum antibiotics during the five to seven days after surgery. I did in 1985 ask a resident to help me make a follow-up study of our last 81 cases of liver resection. He reported back to me, that due to negligence of staff, one third of the patients never received the intended prophylactic antibiotic treatment, interestingly, there were no infections in the non-antibiotic treated patients. All the infections were in the two-thirds of patents, who had been receiving postoperative antibiotics. This made me think about the commensal flora. It is calculated that the human body under normal circumstances harbors a flora of almost three pounds, of which more than two are to be found in the large intestine (we have 10 times more bacteria in the gut than eukaryotic cells in the body). I decided to start a research program with the aim to develop methods to recondition the gut with new bacteria, surfactants, mucus, etc. At that time, I could not anticipate, that with the expanding problems of antibiotic-resistant bugs, probiotics would one day offer an alternative to antibiotics, and offer the possibility of serving as carriers of luminal vaccines.

    KH: What are the major dietary differences between Western society and our prehistoric ancestors that have altered our bacterial flora in an adverse way® What role does refined carbohydrate play in this®

    SB: We eat, compared to our Paleolithic forefathers, far too much fat, cholesterol, sugar, sodium (salt) and also too much processed, refined, industry-modified (and partly destroyed), cooked and fried food and too little fresh fruit, vegetables, pulses, tubers and most often non-refined cereals, at least whole meal (bran). But more than anything, our ancestors ate billions of times more probiotic bacteria, especially of the species Lactobacillus plantarum. This bacterium has the ability to eliminate or reduce most other bacteria and fungi as it is the dominating habitat of all sorts of naturally-fermented foods, varying from silage given to domestic animals and human fermented foods such as fermented vegetables and sauerkraut. Our ancestors, as a matter of fact, had only two methods available for food preservation: drying (which unfortunately destroys many sensitive and important nutrients) and fermentation (which seems to maintain most of the essential nutrients). Furthermore, they had no weapons for hunting. Most of their meat came from dead animals, which most often was half rotten when found. They learned that if the meat was kept in the soil for some time it became edible and also tasted good. We know today, that even if thousands of species of bacteria and fungi are present on the meat at the beginning, if the meat is kept under anaerobic conditions, after some time most bacteria and fungi will have disappeared and mainly one remains -- Lb plantarum. This method was used for all sorts of foods and by this they learned to produce a great variety of fermented foods: meat, fish, vegetables, wine and beer, etc. This capacity of Lb plantarum to eliminate other bacteria has been used by the food industry and families around the world to preserve food. One such example is the dish tempeh, based on cooked soya beans, and kept from decaying by adding Lb plantarum or Lb plantarum-fermented sauerkraut. Refined carbohydrates are absorbed in the upper part of the small intestine and gives rise to high blood glucose and insulin levels with all its negative consequences (this type of foods are called high glycemic index foods). Another negative consequence with eating refined carbohydrates is that too little of the eaten carbohydrates reaches the large intestine and can be processed by the bacteria and also be food for bacteria. It is estimated that approximately ten percent of the consumed calories, or 20 percent of the food weight (remember, fiber foods contain only one to two calories per gram, compared to sugar at four calories per gram and fat at nine calories per gram), should be complex carbohydrates, so called fibers, food for the large intestine (colonic food), food which no small intestine enzyme can metabolize, but reaches the large intestine intact, where it is broken down by intestinal bacteria. I have more extensively developed this concept in two chapters for an issue of the journal Nutrition, which is to come out August 1998.

    KH: What byproducts of fermented food are beneficial to the gastrointestinal tract®

    SB: Short chain fatty acids (SCFAs), amino acids, fatty acids, growth factors, polyamines, vitamins, lectins, phytoestrogens, etc. Furthermore, consumed lactobacilli and bifidobacter are also known to stimulate (upregulate) the immune system -- macrophages, T-cells, B-cells, etc, most likely though production of NO and cytokine-like molecules (bacteriokines). This might be the mechanisms by which the commensal flora has protective and therapeutic effects against Western diseases -- arteriosclerosis, coronary heart, stroke, cancer, rheumatoid arthritis, psoriasis, ulcerative colitis, atopic diseases such as asthma and autoimmune diseases in general.

    KH: Is there any evidence that the increased incidence of allergies and infection in Western societies are related to abnormal gastrointestinal flora®

    SB: There is an increasing amount of work published indicating that allergies, as well as some infections, which are more common in Western countries, relate to GI flora, a condition called dysbacteriosis. As an example, Estonian and Polish children have four to eight times less of atopic diseases, despite the fact that they have more of so called classical risk factors. It has been shown that they have a much "richer" commensal flora. It is especially a Swedish pediatrician, Bengt Bjorksten, and his team, who has presented some interesting data supporting such a concept.

    KH: How vast is the surface area of the gastrointestinal mucosa compared to other areas in the body and approximately how many organisms reside there®

    SB: Skin 1.5 to 2.0 sqm (holds approximately 200 g bacteria), gastrointestinal tract 3 to 400 sqm (holds approximately 1,000 g bacteria), respiratory tract about 6,000 square feet (holds approximately 20 g bacteria). Numerically, a human being is 90 percent bacteria and ten percent eukaryotic cells -- 1014 bacteria cells and 1013 eukaryotic cells, a fact largely neglected by modern medicine. Strong pharmaceutical drugs, such as antibiotics and chemotherapeutics, stress, etc, can reduce the commensal flora, a fact largely unknown to most physicians.

    KH: How does modern medicine and pharmaceutical therapies adversely affect the gastrointestinal tract and what relationship does this have to systemic or acute illness®

    SB: Gastrointestinal epithelial cells have a high rate of regeneration, most of the mucosa cells are replaced every third day, a process easily disturbed by supply of drugs and bad eating. Many pharmaceuticals have a strong inhibitory effect not only on secretion of saliva, but also on other gastrointestinal secretions. Furthermore, supplied drugs often inhibit mucus production and flora. Saliva, and most other gastrointestinal secretions, are very rich in antiinfectious, mucosa- protective ingredients plus important growth factors. Comparisons have been made with the effects of mothers' milk. Most of the studies presented are performed in experimental animals, clinical studies are to a large extent lacking. It is clear that lack of saliva in experimental animals leads to ulcers in esophagus, stomach and small intestinal ulcers do not heal adequately in the absence of salivary IgA. Also, liver regeneration is retarded. It is also evident, that some drugs induce increased microbial translocation (leakage of pathogenic bacteria and toxins from the intestine and into the body) and thereby sometimes promote infections. Examples of such drugs are cytostatic/cytotoxic drugs, antibiotics, heavy psychiatric drug, but also drugs inhibiting gastric secretions like H2- blockers.

    KH: Are nosocomial infections in the hospital related to altered gastrointestinal flora®

    SB: That is what is suspected. It is clear that the flora of hospital patients often is deranged. This is particularly often seen in settings such as intensive care units. In the ICU not only patients, but also hospital employees, show a deranged flora (higher counts of Klebsiella). Especially the sickest have defects in their protective flora, parallel to increased amounts of pathogens. The protective flora is very sensitive to ecological challenges including stress. It has been reported that astronauts on returning have lost most of their intestinal protective flora and acquired high counts of pathogens in their gastrointestinal tract.

    KH: You state that the mortality from gram-negative bacteria has remained between 20 percent and 40 percent even though we have more advanced intensive care technology in using antibiotics. How can this be so®

    SB: It is of course hard to prove. It is the impression that one gets from reading the literature. Microbs are more adaptable to circumstances than are humans, and seem to win with time. History shows that. Microbs have existed on earth much longer than humans and have always resisted and overwon all human attempts to reduce and eliminate them. It is clear that we deal with other microbs today than 40 to 50 years ago. One example today is antibiotic-resistant Enterococcus faecium, second to E. coli, the most frequent microb seen in intensive care patients. The mortality from this particular infection is about 40 percent. This type of antibiotic- resistant bacteria was unknown as late as 10 to 20 years ago.

    KH: How does one choose an appropriate lactobacilli to reinoculate the gastrointestinal tract and how many of these organisms need to be consumed to bypass the digestive process®

    SB: It is not easy to tell. Our knowledge is still in its infancy. Replacement therapy should most likely be complex. There are indications that the different microorganisms function in consortia, as a large orchestra, are dependent on each other and complimenting each other. As one example, if one supplies L plantarum it seems to automatically increase the content of bifidobacter in the intestine up to about ten times. One thing seems to be clear, and that is that bacteria with adhesive properties have much stronger potential health effects. Most probiotic bacteria do not seem to have ability to adhere to the human mucosa. So far adhesion properties have only been documented for a handful of lactobacilli. The strongest adhesion so far is shown for L plantarum, which is one of many reasons why my colleagues and I have chosen to work with L plantarum. Other lactobacilli with adhesive properties are L rhamnosus and L reuteri, but yogurt bacteria, most acidophilus and most bifidobacter have not any documented adhesive abilities. I have no data to tell the optimal amount of bacteria for effective substitution, but the risk of over-supply is minimal.

    KH: With appropriate intestinal flora, how does this positively affect the immune system®

    SB: Few data are available on the effects in individuals with an appropriate normal intestinal flora. From what is available it appears, however, as if a "booster dose" from outside in these individuals will have a stimulatory effect on GI immune system. Such a dose has an upregulatory effect on the immune system, changes the immune cells and influences production of cytokines and nitric oxide (an important signal substance in the body). This is also what our prehistoric ancestors got from every day eating of large amounts of fermented bacteria-containing foods. This is also seen in rural areas of Africa and Asia, where the normal diet to a large extent is based on fermented food. It has as an example been described that persons living in rural areas, eating large amounts of lactobacilli and fibers, have longer coagulation times and softer jelly-like clots compared to those living in urban areas like the city of Madras. One can not exclude that this could be one of the reasons why coronary infarctions are so rare in such regions. Studies published in Lancet some 20 to 25 years ago support that fiber consumption reduces the incidence of thrombosis.

    KH: With abnormal flora due to low fiber diets, increased sugar intake and medications including antibiotics, how has this affected the relationship to hormone related diseases such as breast cancer, prostate cancer and others, and the appropriate metabolism of hormones®

    SB: Several experimental and clinical publications indicate, that regular supply of lactobacillus containing foods, and fiber, especially cruciferous vegetables (indoles), soya and rye (isoflavones/phytoestrogens) not only reduces the incidence of breast and colon cancer, but also retards the growth of the tumors and reduces the rate of recurrence after surgical treatment. Data regarding prostate cancer are unfortunately not available to the same extent, but one can speculate that the effects are the same. There are many theories trying to explain such effects. Apart from a direct immunostimulatory effect are also discussed inhibitory effects induced by tumor growth promoting enzymes like proteases, and by receptor-blocking effects of the benign tamoxifen-like estrogens, called phytoestrogens (plant estrogens).

    KH: Do you believe that we could cut health care cost if appropriate probiotic substances were used in the hospital settings®

    SB: I have the impression that as we get more and more effective pharmaceuticals we also see more and more side effects. It has been mentioned in the media that only in the US do more than 100,000 die each year from side effects of drugs (as many as from traffic accidents), and many more certainly get sick. One should also remember that drugs are becoming increasingly expensive and unreachable for large portions of the people living on earth. Nature is complexed, and health is undoubtedly based on interaction in our body between hundreds of thousands, if not millions, of substances and microorganisms, most of them provided by our diet. Of the carotenoids, there are about 600 different variations, and many of them, if not most are essential to us. There is no substitution for regular fresh food. It seems in many cases to be a sign of too simple thinking that supply of one particular chemical substance -- and probably for that sake also probiotic bacteria -- should completely solve a problem of unhealth. This seems also increasingly to be understood by pharmaceutical industry. While for 15 years none of the 250 largest companies showed an interest in natural products, now according to a survey performed three years ago, at least two-thirds of pharmaceutical companies have a division for natural products. The food industry also seems to be showing an interest in natural products, functional foods, designer foods, nutraceuticals. I have no data to support, but believe that adjustments in lifestyle and recognition of ecological principles in medical care will have a dramatic influence on health costs. Use of probiotics as prevention and treatment will also lead to large hospital savings. [back to the top]

    Psoriasis Strongly Linked With Several Comorbid Conditions

    Summary# 42484
    Keywords: PSORIASIS - Coronary Heart Disease, Diabetes Mellitus, Hyperlipoproteinemia, Hypertension, Metabolic Syndrome
    Reference: "Psoriasis Strongly Linked With Several Comorbid Conditions," Bates B, Family Practice News, December 1, 2004:34.

    Summary: In a study comparing comorbid conditions in 581 hospitalized patients for severe psoriasis compared with 2 control groups (one composed of 1,024 hospitalized patients for other skin conditions and another community cohort of 4,705 nonhospitalized adults), it was found that patients with psoriasis were nearly 4 times more likely than hospitalized patients and nearly 8 times more likely than nonhospitalized adults to have type 1 diabetes and more than twice as likely as either group to have type 2 diabetes. There were significant associations between psoriasis and arterial hypertension, hyperlipoproteinemia, coronary heart disease, metabolic syndrome, cigarette smoking and alcoholism. Heavy drinking was associated with psoriasis, with an odds ratio of 8.5, compared with nonhospitalized adults. The age-related prevalence of arterial hypertension was 3.27 times greater among patients with psoriasis than other adults. In a retrospective chart review of 200 consecutive patients hospitalized for severe manifestations of psoriasis, it was found that 4.5% were on beta-blockers at the time of their hospitalizations and 8.5% were on ACE inhibitors, some of which can trigger psoriasis flares. Seventy percent of the patients that were included in this chart review were taking at least 1 systemic medication for a comorbid condition and 23% were on 5 or more different systemic medications for conditions other than psoriasis, which puts these patients at high risk for drug interactions. [back to the top]

    The Gall Bladder is NOT just "another" organ

    Since we provide nutritional counseling and support for our patients in the office, we run across our fair share of organ issues. One of the most common, especially dealing with the pregnant patient is gallbladder issues. Almost everyone knows someone (or is that someone) who had had gallbladder attacks and many unfortunately have had to have their gallbladder removed. So why does this happen?? Are there any natural alternatives to surgery and gallbladder attacks?? What’s so special about the gallbladder anyway? Can’t I live without one?

    Let’s start with what the gallbladder really does for us. Medicine has deemed the gallbladder an expendable organ an routinely removes them (even on 33 week pregnant moms!!). But the gallbladder is not just an extra organ, it has some very important roles in the body.

    One of the biggest misconceptions/scams of our time has been the whole cholesterol issue. “Good” cholesterol vs “Bad” cholesterol and what that means for heart disease and stroke has created an entire generation of drugs and of people who stay away from much needed fats in their diet thinking that will prevent cholesterol build-up in the body. Contrary to this theory, fats are very VERY necessary in the body and for normal function and healing in the nervous system. Interestingly enough, one of the organs in the body most responsible for allowing our bodies to absorb fats out of our diet…..the gallbladder. In digestion what happens is that when you eat fats (like some coconut oil for example), the fat is not broken down at all until it gets to your small intestine. It actually skips the mouth and the stomach and goes straight to the small intestines. When it gets there it causes the release of a hormone called Cholecystokinin. The job of this hormone is 2 fold: 1. Close the pyloric sphincter to the stomach to basically prevent some of the fats from re-entering the stomach once they are in the intestines and then keeping more stuff from joining them and 2. Signaling the gallbladder to release bile to help with fat breakdown. Once the bile is released it helps to emulsify the fats or really to spread them out so that we can absorb them through the lining in the small intestines (the site for which most of everything we absorb in the body is absorbed). Without the gallbladder we would have no way of prepping the fats we eat for absorption and would be deficient in these healing fats. Also, if you can’t absorb your fats correctly, then you will become deficient in fat soluble vitamins like Vitamin A, K, E, and D (makes you wonder if the Vitamin D deficiency in our country is really a fat deficiency doesn’t it??). The bile your gallbladder produces is also a powerful antioxidant for the liver, helping to remove toxins from the organ.

    So what causes the gallbladder to become congested and to begin malfunctioning?? Here’s a list of many of the things that can lead to gallbladder problems:

  • Overweight
  • Rapid weight loss
  • Estrogen intake and birth control pills(estrogen increases the concentration of cholesterol in the bile)
  • Hypothyroidism
  • Hashimoto’s Thyroid Disease
  • Over age 40 and increase in risk as one ages
  • Female especially those who have had children
  • Ethnicity (Pima Indians and Mexican-Americans)
  • High triglycerides, high LDL cholesterol, decreased HDL cholesterol, (look at ratio, not levels)
  • Alcohol intake
  • Family history of gallbladder disease (Heredity)
  • Cholesterol-lowering drugs, immunosuppressive drugs and others
  • Very Low Calorie Diets
  • Diet high in saturated fats (not good animal fats, bad fats from fried foods, etc.)
  • Diet high in refined foods and sugars
  • Diet low in fiber (which is what the refined diets are) and not enough vegetables
  • Non-fat diets (diets of no fat at all will create pressure in the gallbladder)
  • Low-fat diets
  • Constipation
  • Diabetes
  • Diseases such as chronic inflammatory bowel disease, chrons disease (ulcerative colitis is controversial) Hemolytic anemias

    So the biggest issues out of that list that I see in the office are overweight, estrogen dominance (due to either birth control pills, hormone replacement, or general estrogen dominance due to environment), horrible diets (no fats or bad fats), and major stress for years.

    So what exactly happens to cause the gallbladder to become congested or go into an attack anyway??

    Well, over long periods of time with either bad diet, stress, or lack of function and circulation, the flow of bile becomes sluggish and gallstones are formed, known as Cholelithiasis. Gallstones are made up of calcium, cholesterol, and bilirubin. As the size and amount of gallstones increases over time, the main bile duct that the gallbladder uses to transport bile to the intestines can become blocked causing inflammation to the bile duct (Choleangitis) or inflammation in the gallbladder (Cholecystitis).

    Well, interestingly enough, most of the gallbladder issues I’ve uncovered in the office came in complaining of back pain!! That’s right. There’s a neurological phenomenon that occurs with organs called “referral pain”. Basically, every organ has a site that it will refer pain to if in trouble. The gallbladder will refer pain under the right shoulder blade. The pain is an intense, cramping pain that patients describe as feeling like someone is driving a spear straight through from the front to the back. So with the back pain you could experience associated pain in the abdomen on the right side, just under your rib cage, in the area of the gallbladder. Other symptoms include intense itching all over the body, jaundice or yellowing of the skin due to stress on the liver, fatty stools and clotting problems in the blood.

    Unfortunately, most people will have some congestion in their gallbladder just from years of living. But you don’t have to have major symptoms to be having some issues with the organ. The best way to know is to have it tested, either by your chiropractor (we do a specific pressure test for it), or an ultrasound by your primary doc to see if you have any stones forming at all.

    Hopefully that clears up some of the misconceptions about the “extra organ” commonly referred to as the Gallbladder. We need this organ so much so at all cost you want to heal and preserve yours!!

    Dr. JB [back to the top]

    How Inflammation Affects Insulin Resistance

    Inflammation is a familiar phenomenon. Here's what happens beneath the surface: Imagine cutting your fingertip with a dirty knife. Bacteria from the blade enter the wound, where they run into special "sentinel" immune cells that act as watchdogs in the body. The cells are covered with sensitive receptors that recognize an invading cell, like a bacterium, and call for help.

    That's when the immune system swings into action. The signs of battle are visible from outside the body: The finger turns red, swollen, and warm; there may even be a little bit of pus. The inflammation is a sign your immune cells are responding aggressively to the infection. "From being harmless sentinel cells, they become specialized warriors," says Mario Kratz, PhD, a researcher at the Fred Hutchinson Cancer Research Center in Seattle. "It's a well-organized, cool process that tends to be strong—and limited in its time frame."

    Once the invader is defeated, in other words, the active immune cells are replaced by passive guardians, ready for the next attack. But not always. With the help of a grant from the American Diabetes Association, Kratz is studying the links between inflammation and diabetes. In the past six or seven years, research in mice has demonstrated a strange phenomenon. In obese mice, scientists have found an unusually high concentration of immune cells in fat tissue. "It's almost as if there was an infectious agent in fat tissue that triggers the same response as if you had cut your finger," Kratz says.

    Unlike with an infected cut, though, a chronic, low-grade inflammation appears even when there's no underlying infection and no sickness, like a cold or flu, to prompt a typical immune response. "It's associated particularly with obesity and seems to play a role in all of the major diseases—heart disease, diabetes, and certain cancers," says Kratz.

    Stranger still, the immune cells aren't just watching; they're activated, ready to take on an invader that isn't there. Just as in humans, the obese mice with chronic inflammation were more likely to become insulin resistant. Insulin resistance is a key component in the development of type 2 diabetes; if the body's cells don't respond to insulin by absorbing sugar, or glucose, from the blood, the consequences can be disastrous.

    But the initial mouse experiments left a major question unanswered: Was inflammation causing the insulin resistance, or was it the other way around? To find out, researchers bred mice that lacked the ability to make certain immune cells. Such mice wouldn't survive long outside a sterile lab, but when they were fed a special diet designed to make them obese, they had no signs of inflammation—and no insulin resistance or diabetes. "That strongly suggests it's the inflammation response that causes insulin resistance, not just the fat itself," Kratz says. "It's totally a paradigm shift. Now it seems pretty clear that inflammation plays a major role in the development of insulin resistance."

    For researchers, the connection between insulin resistance and inflammation has made the past few years a veritable roller-coaster ride. "There's a game-changing paper coming out every month or so," Kratz says. "But 95 percent of the work has been done in mouse models." While rodents are a time-honored test bed for new observations and theories, it's not always clear that what happens in mice holds true for humans.

    That's why Kratz is working to test the connection between inflammation and insulin resistance in people. In a series of pilot studies, he took fat samples from just underneath the skin of volunteers. Using a sophisticated machine called a flow cytometer that can separate and identify individual cells, he did a sort of cell census, counting how many of each cell type were in the samples.

    The results were promising. "We got a wealth of data that tells us how many of each cell is in each person's fat tissue," Kratz says. "It gives us insight into whether there is inflammation, and which cells are the major players."

    In particular, Kratz paid attention to the immune-system watchdog warriors, called macrophages. He discovered that the presence of a certain macrophage was a red flag. "If there are a lot of a very specific type of macrophage, then people are insulin resistant, and if there are relatively few of these cells, then they're insulin sensitive—no matter how much fat they have in their body," says Kratz.

    Now, Kratz is taking his study a step further. People with fat deep inside the body tend to have more serious problems with insulin resistance than people whose fat is concentrated closer to their skin. Working with surgeons to collect fat samples from the abdomens of people undergoing weight-loss surgery, he'll see if there's a change in inflammation levels as patients lose weight after surgery. That will bring Kratz a step closer to unraveling the connection between inflammation and insulin resistance—and, perhaps, a step closer to preventing the onset of type 2 diabetes. [back to the top]

    How Inflammation Affects Type 2 Diabetes Risk

    Summary# 44517
    Topic: Low-Grade Systemic Inflammation May Increase Risk of Type 2 Diabetes in Obese Children and Adolescents
    Reference: "Low-grade systemic inflammation and the risk of type 2 diabetes in obese children and adolescents," Syrenicz A, Garanty-Bogacka B, et al, Neuro Endocrinol Lett., 2006 Aug 5;27(4): [Epub ahead of print]. (Address: Department of Endocrinology, Arterial Hypertension and Metabolic Diseases, Pomeranian Medical University

    Summary: In a study involving 281 obese children and adolescents, significant correlations were found between the markers of inflammation with most factors implicated in the development of type 2 diabetes. Fasting levels of the inflammation markers, C-reactive protein (CRP), fibrinogen (FB), interleukin-6 (IL-6), interleukin 1-beta (IL-1beta), along with glucose, insulin, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, white blood cell count (WBC) and the ratio of fasting glucose/insulin (FGIR), were measured in the participants. Analysis using Pearson's correlation showed that the markers of inflammation were significantly correlated with insulin resistance indices, HbA1c, lipid profile, hypertension, positive family history of diabetes, low physical fitness, and high-fat/high-carbohydrate diet (known risk factors of type 2 diabetes). Thus, the findings of this study suggest that low-grade systemic inflammation may be associated with an increased risk of type 2 diabetes in obese children and adolescents. [back to the top]

    Gout and your increased risk of mortality

    Gout and mortality.
    Kim SY1, De Vera MA, Choi HK. -- Author information

    This review provides an update on the most recent data on mortality in people with gout. A large prospective study among men found that those with gout have a higher risk of death from all causes. Among men who did not have pre-existing coronary heart disease, the increased mortality risk is due primarily to an elevated risk of cardiovascular death, particularly from coronary heart disease. Also, an extension study of a large clinical trial among men with above-average risk for coronary heart disease found that a diagnosis of gout accompanied by an elevated uric acid level is associated with increased long-term (approximately 17 years) risk of all-cause mortality that arises largely from an increased risk of cardiovascular disease (CVD) mortality. Although limited, these emerging data suggest that men with gout have a higher risk of death from all causes and the increased mortality risk is primarily due to an elevated risk of CVD death. These findings would provide support for the aggressive management of cardiovascular risk factors in men with gout. More data that adjust comprehensively for various associated CVD markers are needed to reinforce this concept. Furthermore, given apparent potential sex differences in gout epidemiology and its risk factors, prospective studies specifically among women would be valuable. [back to the top]

    Dairy Saturated Fats Lower Type 2 Diabetes Risk
    Kathleen Louden

    The odds of incident type 2 diabetes is lower in people who have high plasma levels of odd-chain saturated fatty acids that come primarily from dairy fats, compared with people who did not have these biomarkers, a large, prospective multicenter study finds.

    In contrast, even-chain saturated fatty acids, such as those that come from consuming alcohol, soft drinks, or margarine, were associated with a greater likelihood of diabetes in the study, published online August 6 in Lancet Diabetes & Endocrinology. These fatty acids include palmitic acid, the most common saturated fatty acid in the US diet.

    The findings suggest that saturated fatty acids are not homogeneous in their effects and "emphasize the importance of the recognition of subtypes of these fatty acids," say Nita Forouhi, FFPHM, from the Medical Research Council (MRC) Epidemiology Unit at the University of Cambridge, United Kingdom, and colleagues in their paper.

    "The message from this study is that saturated fatty acids are not only different but have opposite relationships with diabetes risk," Dariush Mozaffarian, MD, DrPH, dean of the Friedman School of Nutrition Science and Policy at Tufts University, in Boston, Massachusetts, told Medscape Medical News.

    Dr. Mozaffarian is the author of a commentary that accompanies the research. "These results add to growing evidence that dairy fat might reduce insulin resistance and type 2 diabetes; benefits that might be greatest for cheese and yogurt," he writes.

    Diabetes Risk Varies by Fatty-Acid Carbon Chain

    In their paper, Dr. Forouhi and colleagues explain that saturated fatty acids are generally thought to have a detrimental impact on health, but little evidence exists to support the adverse effects of high saturated fatty-acid intake on the risk for type 2 diabetes.

    In this longitudinal case-cohort analysis, they aimed to investigate the prospective associations between objectively measured levels of 9 saturated fatty acids in the plasma and incident type 2 diabetes in participants from the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct study.

    They identified 12,132 verified cases of type 2 diabetes and 15,919 subcohort participants (including an "overlap" of 755 incident cases of type 2 diabetes, a feature of case-cohort studies). They used gas chromatography to measure the distribution of fatty acids in plasma phospholipids.

    The investigators found that saturated fatty acids with an odd number of carbon atoms in their chain—15:0 and 17:0—were associated with a lower risk of type 2 diabetes, whereas even-chain saturated fatty acids—14:0, 16:0, and 18:0—were associated with a higher risk.

    Longer-chain saturated fatty acids—20:0, 22:0, 23:0, and 24:0—also were found to be inversely associated with incident type 2 diabetes.

    These associations held true for each saturated fatty acid individually and when combined by carbon-chain group (even, odd, or longer).

    Hazard Ratio for Type 2 Diabetes by Saturated Fatty-Acid Carbon-Chain Group

    Saturated fatty-acid carbon-chain group Fatty acids measured Hazard ratio 95% Confidence Interval Even chain Myristic, palmitic, and stearic acids 1.43 1.29–1.58 Odd chain Pentadecanoic and heptadecanoic acids 0.70 0.66–0.74 Longer chain Arachidic, behenic, tricosanoic, and lignoceric acids 0.70 0.59–0.84

    The presence of odd-chain saturated fatty acids are well-established markers for eating dairy fat, according to the authors. The other saturated fatty acids can be exogenous or endogenous. [back to the top]

    The effect of Curcumin (found in Flamasil) on Gall Bladder Function
    Kathleen Louden

    Summary# 34700

    Keywords: GALLBLADDER - Curcumin

    Reference: "The Effect of Curcumin and Placebo on Human Gall-Bladder Function: An Ultrasound Study," Rasyid A, Lelo A, Aliment Pharmacol Ther, February, 1999;13(2):245-249.

    Summary: In a randomized, double-blind, crossover trial of 12 healthy volunteers (7 males and 5 females), subjects received 20 mg of curcumin or placebo. Results showed that fasting gallbladder volumes were 15.74 ml on curcumin and 15.98 ml on placebo. The gallbladder volume was reduced within the period after curcumin administration. Curcumin appears to induce contraction of the human gallbladder. [back to the top]

    Systemic Inflammation and Cardiovascular Disease in Chronic Kidney Disease
    Denise Mafra, Julie C Lobo, Amanda F Barros, Laetitia Koppe, Nosratola D Vaziri, Denis Fouque Disclosures Future Microbiol. 2014;9(3):399-410.


    The normal intestinal microbiota plays a major role in the maintenance of health and disease prevention. In fact, the alteration of the intestinal microbiota has been shown to contribute to the pathogenesis of several pathological conditions, including obesity and insulin resistance, among others. Recent studies have revealed profound alterations of the gut microbial flora in patients and animals with chronic kidney disease (CKD). Alterations in the composition of the microbiome in CKD may contribute to the systemic inflammation and accumulation of gut-derived uremic toxins, which play a central role in the pathogenesis of accelerated cardiovascular disease and numerous other CKD-associated complications. This review is intended to provide a concise description of the potential role of the CKD-associated changes in the gut microbiome and its potential role the pathogenesis of inflammation and uremic toxicity. In addition, the potential efficacy of pre- and pro-biotics in the restoration of the microbiome is briefly described.


    Chronic kidney disease (CKD) patients have several risk factors for cardiovascular disease (CVD), and the rate of cardiovascular mortality is extremely high in these patients. In addition to traditional risk factors (obesity, hypertension, diabetes and dyslipidemia, among others) and situations specific to kidney disease (hypervolemia, electrolyte disorders, anemia, changes in calcium-phosphorus metabolism and dyslipidemia), CKD patients have a high prevalence of so-called 'emerging risk factors', including hyperhomocysteinemia, increased lipoprotein(a), oxidative stress and inflammation.

    Recent studies have identified intestinal microbiota imbalance as a new factor that may contribute to inflammation and CVD. Indeed, the microbial inhabitants of the gut may affect the body's metabolic processes and should be considered an environmental factor that contributes to obesity and its comorbidities (insulin resistance, diabetes and cardiovascular disease). In this context, until recently, little was known about the gut microbiota in CKD.

    In a recent study, Vaziri et al. demonstrated that uremia profoundly alters the composition of the intestinal microbiota in humans and experimental animals. These changes may result in the production and absorption of noxious byproducts that can contribute to uremic toxicity, inflammation, malnutrition and other morbidities in uremic patients. Moreover, the authors demonstrated that uremia results in the depletion of key protein constituents in the colonic epithelial tight junction in experimental animals, which is a phenomenon that can account for the impaired intestinal barrier structure and function in uremia.[9] Together, the alteration of the intestinal microbiome and impaired intestinal epithelial barrier structure and function can lead to endotoxemia and the accumulation of the gut-derived uremic toxin(s)/metabolite(s). This accumulation contributes to the metabolic perturbation, systemic inflammation and increased cardiovascular risk in CKD patients. Therefore, the metabolic crosstalk between the microbiota and the development of cardiovascular disease appears to be a new challenge in the studies on CKD patients. This review provides a brief overview of the function of the microbiota and the possible role of its alteration in systemic inflammation and cardiovascular disease, with a particular emphasis on CKD patients.


    The human gut contains approximately 10–100 trillion microorganisms and houses the largest and most diverse ecosystem of microbes in the human body, consisting of more than 400 species of bacteria.[10] Five bacterial phyla are present in the human gut (Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria and Verrucomicrobia), of which, two are dominant: Bacteroidetes (Bacteroides, Prevotella and Xylanibacter) and Firmicutes (Ruminococcus, Clostridium, Lactobacillus, Eubacterium, Faecalibacterium and Roseburia).

    The human microbiota plays an important role in the biochemical activities of the human body including the production of vitamins and other essential nutrients and the regulation of many aspects of immunity. Through their constituent enzymes, the intestinal microbial flora participate in the fermentation of the ingested nutrients and the metabolism of bile acid. The latter leads to the conversion of the primary bile acids into secondary bile acids, which act as signaling molecules by binding to cellular receptors implicated in the modulation of lipids and glucose metabolism.

    The composition of the diet can have a marked impact on the gut environment, including gut transit time, pH and available substrates that bacteria can use. Consequently, changes in the intakes of the three main macronutrients (proteins, lipids, and digestible and nondigestible complex carbohydrates) significantly affect the composition of the gut microbiota.

    Effects of Probiotics (ingredient in Flamasil)

    By modulating the composition of the intestinal microbiota, the use of probiotics could potentially minimize the deleterious effects of its imbalance, thereby improving the health of the gastrointestinal tract, strengthening the immune system, restoring the bioavailability of micronutrients, exerting antidiabetic actions, improving dyslipidemia and allergic disorders, and reducing the risk of certain cancers.

    The mechanism by which probiotics exert their favorable effects seems to include changes in intestinal pH, suppression of pathogens (through the production of antibacterial compounds, competitive exclusion of pathogens in receptor binding sites and competition for available nutrients), suppression of mutagenic and carcinogenic processes and protection of the intestinal barrier.

    Previous studies have demonstrated the immune modulatory and anti-inflammatory effects of probiotics, leading to a reduction in the influx of LPS into the systemic circulation, the attenuation of the TLR-4 mediated activation of NF-κB, the formation of proinflammatory cytokines, reductions in systolic blood pressure and fibrinogen levels, and interactions with immune cells, leading to improvements in intestinal integrity. In addition, the use of probiotics may confer cardioprotective effects, including the prevention and attenuation of ischemic heart disease and the reduction of serum cholesterol.


    In conclusion, the gut microbiota plays an important role in health, and changes in its composition can contribute to systemic inflammation and the generation of uremic toxins, both of which have been linked to cardiovascular mortality in dialysis patients. The potential efficacy of pro- or pre-biotics in attenuating CKD-associated inflammation and CVD in humans with CKD is unknown and awaits future investigation. [back to the top]

    Gout Linked to Increased Vascular Disease Risk
    Laurie Barclay, MD - August 29, 2014

    Patients with gout, particularly women, have increased risk for vascular disease, according to findings of a study published online August 27 in the Annals of Rheumatic Diseases. "Hyperuricaemia, the biochemical precursor to gout, has been linked with an increased incidence of, and mortality from, both [coronary heart disease (CHD)] and stroke," write Lorna E. Clarson, MBChB, from the Research Institute for Primary Care & Health Sciences at Keele University in the United Kingdom, and colleagues. "Although gout is traditionally thought of as an intermittent inflammatory condition, recent ultrasound studies have identified persistent subclinical inflammation in the intercritical period between acute attacks. It has been hypothesised that the combination of persistent inflammation and hyperuricaemia may potentiate or synergise CHD development."

    Dr. Clarson and colleagues examined the association of gout with incident CHD, cerebrovascular disease (CVD), and peripheral vascular disease (PVD) in a large cohort of primary care patients with gout.

    They identified 8386 patients with gout who were enrolled in the Clinical Practice Research Datalink and matched them on the basis of age, sex, and registered general practice, with 39,766 control participants. All patients and matched participants were older than 50 years and had no previous vascular history. Multivariable Cox regression allowed estimation of hazard ratios (HRs) in the 10 years after incidence of gout or matched index date (baseline), using covariates of sex, baseline age, body mass index, smoking, alcohol drinking, Charlson comorbidity index, history of hypertension, hyperlipidemia, chronic kidney disease, statin use, and aspirin use.

    Men with gout had a small but significantly elevated risk for any vascular event (hazard ratio [HR], 1.06; 95% confidence interval [CI], 1.01 - 1.12) compared with men without gout. Similarly, men with gout had a greater risk for any CHD (HR, 1.08; 95% CI, 1.01 - 1.15) and PVD (HR, 1.18; 95% CI, 1.01 - 1.38).

    Among women with gout, the risk for any vascular event was 25% higher than among women without gout (HR, 1.25; 95% CI, 1.15 - 1.35). Their risk for any CHD (HR, 1.25; 95% CI, 1.12 - 1.39) and PVD (1.89; 95% CI, 1.50 - 2.38) was also higher, but the researchers found no difference for risk for any CVD.

    In addition, women with gout, but not men with gout, were at increased risk for angina, transient ischemic attack, and stroke.

    "In this cohort of over 50s with gout, female patients with gout were at greatest risk of incident vascular events, even after adjustment for vascular risk factors, despite a higher prevalence of both gout and vascular disease in men," the study authors write.

    Limitations of this study include possible misclassification bias from the use of diagnostic codes, possible residual confounding, and inability to adjust for hyperuricemia.

    "Further work is required to establish the effect of optimum management of both vascular risk factors and gout itself on the long-term health of gout patients, clarify the nature of the relationship between gout and PVD, and the mechanism by which women are at greatest risk," the study authors conclude. [back to the top]