While there are many factors, both environmental and genetic, that can increase the risk, it’s important to note from the out-set that everyone with ovaries, every biologically female person, is at risk for developing ovarian cancer.
Taking risk factors out of the equation, around 1 in 70 women will develop the disease during their lifetime, according to the Ovarian Cancer Research Fund. That’s true for women without a family history of ovarian cancer, along with those who’ve never had trouble getting pregnant or used a hormone replacement therapy.
Continue reading about the possibilities of cancer misdiagnosis and filing a lawsuits.
Look at when women are diagnosed with ovarian cancer and it becomes immediately clear that age is a huge risk factor:
|Age Of Patient At Diagnosis||Percentage Of New Patients|
But what’s going on here? We know that women are most likely to develop ovarian cancer after reaching menopause, but why?Researchers aren’t sure yet, but there are two major theories to consider.
Traditional wisdom holds that since cancer is caused by genetic mutations within a patient’s cells, these mutations accumulate over time. At some point, these mutations align in just the right (or wrong) way to produce a cancerous cells, which then begins quickly dividing to produce more cancer cells. From this understanding, the basic formula is that the longer one’s cells are allowed to mutate, the higher one’s likelihood of developing cancer. But recent research out of Colorado has forced scientists to question that time-worn understanding.
James DeGregori, PhD, a professor at the University of Colorado School of Medicine says that if the accumulation of mutations is really driving cancer trends, we’d actually expect more young people to be diagnosed with the disease.
Cellular mutations become less, not more, common as we age. Speaking to ScienceDaily, DeGregori said that mutation rates are highest when we’re in our 20s. “There’s a mismatch,” he noted, “between the mutation curve and the cancer curve.” Plus, lots of healthy tissues are filled with mutations, even ones that we know can cause cancer. In other words, more mutations doesn’t necessarily mean cancer.
Cribbing from evolutionary theory, DeGregori argues that if it’s just these mutations causing cancer, we’d expect natural selection to have figured out some way to weed out cells with cancer-causing mutations. Our immune systems are far more complex, and effective, than those protecting bacteria, but we’re just as bad at preventing genetics mutations as our unicellular forebears.
For DeGregori, it’s not really about what’s inside a cell, but what’s around a cell. Changes in the environment, like structural alterations in body tissues, make it harder for healthy cells to out-compete cancer cells for survival. Healthier cells, ones without mutations, are optimized to live inside healthier body tissues, and that usually means younger body tissues. Once those tissues begin aging, the healthy cells aren’t nearly as fit for their environment as they used to be, opening an opportunity for cancer cells to spread.
Having a child young, under the age of 26, decreases the risk of developing ovarian cancer, and the risk continues to drop with each full-term pregnancy. Women who have never had a child, on the other hand, are at an increased risk. So are women who had their first child after the age of 30.
Lots of other reproductive factors seem to have an effect on ovarian cancers, too. Women who have never taken oral contraceptives are at a higher risk, as are women who began menstruating before the age of 12.
If you’ve noticed a theme here, then you’re not alone. All of these factors have an impact on the number of times a woman ovulates, and some researchers believe that ovulation itself can lead to ovarian cancer in some way. Another theory holds that its actually hormones, increased during pregnancy, that can help stave off the disease. Some support for this idea is found in the fact that women who receive hormone replacement therapies, primarily a combination of estrogen and progestin, increases the risk.
The link between ovarian cancer and obesity, usually measured as a BMI over 30, isn’t as clear as the other risk factors we’ve discussed. Some studies have found a significant correlation, especially for premenopausal women, while others haven’t.
Maybe that confusion is because obesity seems to increase the risk only for certain, and less common, types of ovarian cancer. Unfortunately, that also means that losing weight might not be enough to reduce the risk. Likely confounding the connection is the clear association between obesity and estrogen, a well-supported causal factor in the development of ovarian cancer. Since estrogen levels appear to rise in step with BMI, it may not be obesity specifically, but estrogen, that’s at the root of some cancers.
Obesity also seems to promote the metastasis of ovarian cancers, according to researchers at the University of Notre Dame. Using tissue cultures and mice, researchers analyzed how easy it was for malignant cells to bind themselves to mesothelial cells, the kind that line the inside of your abdomen. This binding process is how most ovarian cancers begin to migrate, and the team found that when mesothelial cells were “loaded” with fats, the cancer cells could more effectively take hold.
Yes, that innocuous white powder sold in almost every grocery or convenience store in America might be causally connected to ovarian cancer.
Actually, there’s a surprisingly robust body of scientific research that suggests a link. One of the first studies on the subject found particles of talc deeply embedded in the tumors of ovarian cancer patients, and subsequent papers have repeatedly confirmed that women who frequently apply baby powders to their perineum or sanitary napkins appear more likely to develop the cancer.
The mechanical theory behind the association is pretty clear, since there’s a continuous conduit from a woman’s vagina, through her uterus and Fallopian tubes to the ovaries. Baby powders, experts theorize, could easily travel by that route after being applied to the genitals. This mechanism has also been proposed as a potential solution to the question of why women who undergo hysterectomy are at a decreased risk for ovarian cancer, because the surgery shut offs the conduit through which harmful environmental factors reach the ovaries.