The medical jury is still out when it comes to exploring the precise role of inflammation in the onset of Polycystic Ovarian Syndrome. But inflammation is increasingly being implicated in such disorders as heart disease and Pre- and Type 2 Diabetes, all of which are often closely linked with PCOS.
Inflammation, a part of the body’s immune system, is the triggering of a defense response to harmful stimuli. The body reacts to injury by sending specialized blood cells to damaged areas where they attack “invaders,” like the renegade molecules called “free radicals,” as well as clean up dead and dying cells.
Is PCOS the Invader Causing Inflammation?
In the case of inflammation and Polycystic Ovarian Syndrome, the “invader” is thought to be excess levels of insulin that can be caused by the imbalance of blood glucose and insulin called Insulin Resistance.
Inflammation can take an external form like the reddened, tender skin that draws attention to a splinter in your finger. Or it can be an unseen, internal process in response to something harmful and long-term like high blood pressure.
To combat internal harm, inflammation produces C-reactive protein (CRP), which, unfortunately, can damage the arteries by forming plaque while attempting to respond to a condition like high blood pressure.
Plaque is a substance that attaches to artery walls, damaging those walls and impairing blood flow, which can eventually lead to a heart attack or stroke. A blood test can measure CRP levels and the higher the level of CRP the higher the risk for cardiovascular disease. There’s contradictory evidence, however, about whether CRP levels and Insulin Resistance are closely linked.
Certain research about inflammation still needs ample verification, but scientists are currently gathering data that inflammation can precede and predict Pre- and Type 2 Diabetes-conditions that PCOS sufferers are prone to developing. Previous research has already linked inflammation to heart disease and obesity, which are both common in women with Polycystic Ovarian Syndrome.
Pre- and Type 2 Diabetes are characterized by high blood-sugar concentrations that result from defects in the body’s use or production of insulin. With Pre-Diabetes, the levels of glucose and insulin are higher than normal but not elevated enough for a diagnosis of Type 2, which is why Pre-Diabetes can be reversible via weight loss as a result of a balanced, nutritious diet and regular exercise.
If neglected, however, Pre-Diabetes can lead to full-blown Type 2 Diabetes, which can only be managed in the vast majority of cases and often requires daily injections of insulin. Type 2 Diabetes itself becomes an increased risk factor for serious complications like heart and kidney disease, declining vision and blindness, and the need for amputation of limbs.
Normally, insulin guides sugar-the body’s basic fuel for energy-from the bloodstream into cells via the cells’ walls. But unbalanced insulin levels, due to insulin de-sensitivity in the cell wall caused by Insulin Resistance, can lead to high concentrations of blood sugar.
Scientists in inflammation research test blood samples not only for insulin and glucose levels but also for a variety of compounds associated with inflammation. Some of these, such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), are cytokines-chemical signals the immune system uses to marshal inflammatory activity.
Others, such as so-called acute-phase proteins made by the liver, rise in response to increased cytokine concentrations. These proteins don’t contribute directly to inflammation but, because they remain detectable in blood longer than cytokines do, they are a convenient measure of it.
The concentrations of cytokines and acute-phase proteins, such as C-reactive protein (CRP), rise at least a hundred-fold when an individual contracts an infection.
By contrast, in most studies linking inflammation to heart disease, these inflammation markers reach only perhaps twice-normal amounts. So it’s not clear whether at such low concentrations the cytokines trigger swelling or other inflammatory responses.
Most of the evidence comes from analyses of blood samples and data collected in studies that have followed the health of large numbers of individuals over several years. These investigations use statistical techniques to take into account various factors, such as obesity, that might confound their results.
Recent support for the CRP-Diabetes link came from a study presented in the October 2001 edition of Diabetes journal. Researchers tracked 5,888 U.S. residents without Diabetes, 65 or older, who got their health care from the a health maintenance organization. Among the quarter of the subjects with the highest CRP blood concentrations at the beginning of the study, twice as many had been diagnosed with Diabetes after 3-4 years, compared to the quarter of the subjects with the lowest CRP concentrations.
Other researchers have looked at both CRP and cytokines. As part of a long-running national study, researchers at Brigham and Women’s Hospital in Boston compared the medical histories of 188 middle-aged women who had Diabetes with the records on 362 women of similar age and weight who didn’t have Diabetes. The quarter of women who had the highest CRP concentrations early in the study were four times as likely to develop Diabetes as the 25 percent of women with the lowest CRP concentrations.
Also, women with the highest IL-6 concentrations were more than twice as likely to develop diabetes as women with the lowest IL-6 concentrations. Finally, those with the highest concentrations of both IL-6 and CRP were six times as likely to develop diabetes over the course of the study as women with low concentrations of the two compounds.
So far, there are no epidemiological studies that prove inflammation causes Diabetes and it’s possible that some unknown factor pre-disposes women with PCOS to the Pre- and Type 2 varieties.
One factor could be obesity. Many women with Polycystic Ovarian Syndrome are overweight or obese, though they do not have a monopoly on this condition. Females of normal weight can suffer from PCOS and so can lean women.
But fat cells are known to produce cytokines, and CRP is typically elevated in individuals who are overweight.
Some studies suggest inflammation causes Insulin Resistance itself. Animals with infections and those with cancer have high concentrations of cytokines, with scientists detecting increased Insulin Resistance in these animals.
Researchers are now examining whether animals without underlying disease but with altered amounts of inflammatory cytokines are vulnerable to Diabetes. For instance, mice lacking the gene for TNF-alpha are less likely to develop obesity-linked Insulin Resistance than are mice with that gene. Recently scientists have shown that TNF-alpha can block insulin from getting into cells.
The general picture is unclear but it’s likely to become much clearer in the not-too-distant future. Nevertheless, women with Polycystic Ovarian Syndrome need to be mindful of how vulnerable their condition can make them to inflammation-linked disorders.
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