Category Archives: Prevention

Can Aspirin Prevent Cancer?

Diana Zuckerman, PhD: Cancer Prevention and Treatment Fund

Many Americans take low-dose aspirin, also called baby aspirin, to prevent cancer and heart disease.  However, by 2019, the latest research suggested that aspirin is not as helpful as many patients believe.

In 2016, the U.S. Preventive Service Task Force (USPSTF), an independent group of medical experts, recommended low-dose aspirin “for the primary prevention of cardiovascular disease (CVD) and colorectal cancer (CRC) in adults aged 50 to 59 years who have a 10% or greater 10-year CVD risk [risk of developing cardiovascular disease], are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years”.1   They did not recommend aspirin to prevent all types of cancer, only colorectal cancer.

Primary prevention means preventing a disease that a person has not yet developed. As you can see above, there were quite a few caveats on who might benefit from “baby” low dose aspirin (typically 81mg).  For example, patients with an increased risk of bleeding due to certain medications, or with a history of other medical conditions such as stomach or intestinal ulcers, kidney disease, or severe liver disease.1

Recommended Guidelines in 2019 from the American College of Cardiology (ACC) and the American Heart Association were not as enthusiastic about aspirin for primary prevention of heart disease, saying that “low-dose aspirin might be considered” for certain patients.2  They did not comment on aspirin to prevent cancer.

Studies  published almost a decade ago had mixed results for cancer prevention. One study suggested that a daily dose of at least 75mg aspirin taken for several years could reduce the risk of developing colorectal cancer or dying from it.3 Other studies suggested that aspirin may reduce mortality from other cancers, as well as reducing the chances of cancer spreading.4,5 However, a 2019 meta-analysis that combined results from several studies found aspirin did not significantly affect cancer mortality.6  One clinical trial known as ASPREE (Aspirin in Reducing Events in the Elderly) found that individuals who took aspirin were more likely to die from cancer.

In conclusion, more research is needed to conclusively determine whether daily baby aspirin can help to prevent cancer.

BottomlineDo I Need Aspirin?

Some patients think they may as well take aspirin, because it might help and won’t harm.  That’s not an accurate assumption.  Aspirin can have risks even at low doses. You should discuss aspirin therapy with your doctor and let him or her know:

  • Your medical history and the medicines you are currently using, whether they are prescription or over-the-counter
  • Any allergies or sensitivities you may have to aspirin
  • Any vitamins or dietary supplements you are currently taking

Other Ways to Prevent Heart Disease and Cancer

To reduce your risk of colorectal cancer, don’t smoke, don’t drink alcohol in excess, have a healthy diet, stay physically active, and maintain a healthy weight.  Being older, and having a family history of colon cancer, Crohn’s disease, or ulcerative colitis are the risk factors you can’t control.7

To reduce your risk of heart disease, don’t smoke, keep your cholesterol and blood pressure under control, and do what you need to do to prevent diabetes.  Being a man and older are risk factors you can’t control.8

All articles on our website have been approved by Dr. Diana Zuckerman and other senior staff.

References:

  1. Final recommendation statement: Aspirin use to prevent cardiovascular disease and colorectal cancer: Preventive Mmedication. U.S. Preventive Services Task Force. 2017.
    https://www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/aspirin-to-prevent-cardiovascular-disease-and-cancer
  2. Donna K. ArnettRoger S. Blumenthal,  Albert MA, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease. Journal of the American College of Cardiology. 2019;17:CIR0000000000000678.   http://www.onlinejacc.org/content/early/2019/03/07/j.jacc.2019.03.010?_ga=2.223365151.502443893.1555427130-1631669420.1554414836
  3. Rothwell PM, Wilson M, Elwin CE, et al.  Long-term effect of aspirin on colorectal cancer incidence and mortality: 20-year follow-up of five randomised trials. Lancet. 2010;376(9754): 1741-50. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)61543-7/fulltext
  4. Rothwell PM, Folkes FG, Belch JF, et al.  Effect of daily aspirin on long-term risk of death due to cancer: Analysis of individual patient data from randomised trials. Lancet. 2011;377(9759): 31-41. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62110-1/fulltext
  5. Rothwell PM, Wilson M, Price JF, et al. Effect of daily aspirin on risk of cancer metastasis: A study of incident cancers during randomised controlled trials. Lancet. 2012;379(9826): 1591-1601.   https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60209-8/fulltext
  6. Zheng SL, Roddick AJ.  Association of aspirin use for primary prevention with cardiovascular events and bleeding events: A systematic review and meta-analysis. JAMA. 2019;321(3):277-287. https://www.ncbi.nlm.nih.gov/pubmed/30667501
  7. Colorectal Cancer Risk Factors. American Cancer Society. https://www.cancer.org/cancer/colon-rectal-cancer/causes-risks-prevention/risk-factors.html
  8. How to Prevent Heart Disease. Medline Plus.  Last reviewed 2015.   https://medlineplus.gov/howtopreventheartdisease.html

The last 50 years of smoking: cigarettes and what we know about them has changed

Anna E. Mazzucco, Ph.D.

The U.S. Surgeon General just released an annual report on the negative health effects of smoking.  But this one marks the 50th anniversary of the very first report on smoking in 1964.  We’ve learned a lot about smoking in 50 years, and unfortunately most of the news is bad.

Many health problems in addition to Lung Cancer

While many people know that smoking comes with serious health risks, such as lung cancer and chronic obstructive pulmonary disease (COPD), the 50th anniversary report warns about less widely known risks. For example, smoking increases the risk of:

  • ectopic pregnancy (this type of pregnancy kills the fetus and the mother can also die or become infertile as a result)
  • birth defects
  • diabetes
  • heart disease
  • stroke
  • rheumatoid arthritis
  • difficulty getting or maintaining an erection (erectile dysfunction or ED).

Smoking also increases your chances of developing cancers. A United Kingdom study involving over 100, 000 women found a significant link between smoking and breast cancer. Over a 7-year period, about 2% of women who ever smoked developed cancer compared to about 1.6% of women who never smoked. This means that smoking causes about 4 in 1000 breast cancers. Even though that number seems small (less than half a percent), it is statistically significant. Starting smoking at a younger age, smoking 15 or more daily cigarettes, and smoking for at least 10 years increase the chances of developing breast cancer. If you smoke, you should talk to your doctor about ways to quit. Quitting decreases the chances of developing breast cancer, but it may take about 20 years to see the full benefits. To read more, click here.

Whether you’re a cancer patient, cancer survivor, or have no known health conditions, smoking puts you at greater risk of dying. Exposure to tobacco smoke while in the womb and smoking in the teenage years have both been shown to cause long-term problems regarding brain development.

 20 Million people have died from smoking since 1964

Although smoking has decreased over the 50 years—from 52% to 25% of adult men, and from 35% to 19% of adult women—the decline has slowed over the last two decades. However, among adults who never completed high school or who have a GED diploma, almost 1 in 2 are smokers.[end Centers for Disease Control and PreventionCurrent Cigarette Smoking Among Adults—United States, 2011. Morbidity and Mortality Weekly Report. 2012; 61(44):889–94 [accessed 2014 Feb 10]  The report estimates that half a million Americans die from smoking every year, and this number has not changed in a decade. Smoking costs the U.S. economy about $100 billion per year, including direct medical costs and the indirect cost of lost productivity from employee sick time due to smoking-related illness.

The Surgeon General cautions that current efforts to reduce smoking are not getting as much support as they need.  While many states have received substantial funds from settlements with tobacco companies which were intended for tobacco control programs, this funding is frequently been spent elsewhere.  In 2013, Alaska was the only state to fund their tobacco control programs at the level recommended by the Centers for Disease Control and Prevention (CDC).

 What more should be done to reduce smoking?

In 2009, the FDA was given much more authority to regulate tobacco products, and in 2010, it made it illegal to sell tobacco products to anyone under 18, banned free samples of cigarettes, and prohibited cigarette brands from sponsoring music and other cultural events. While making public spaces smoke-free and increasing the price of cigarettes and other tobacco products has helped, we need to do more.  Most experts agree that effective tobacco control programs require a combination approach: public health campaigns supplemented by laws that limit where you can smoke, make cigarettes harder to buy, and ensure that programs to help people quit smoking are covered by all health plans.  Under the Affordable Care Act, Medicare, Medicaid and employer-sponsored insurance plans are required to cover medications to help with quitting.  Unfortunately, it is still unclear exactly what will be covered through the state insurance exchanges, even though they are subsidized through the federal government.

Of course, the ideal strategy is to prevent a person from starting to smoke, since tobacco is very addictive.  The Surgeon General’s report says more advertising campaigns targeting young people with anti-smoking messages are needed, since 87% of adult smokers had their first cigarette by age 18.  A study published in 2014 revealed that the nicotine dose from cigarettes increased 15% between 1999 and 2011, making them more addictive without any warning to consumers.[end Land T et al.  Recent Increases in Efficiency in Cigarette Nicotine Delivery: Implications for Tobacco Control.  Nicotine and Tobacco Research. 2014.]  That is only one example of a long history of misleading information from tobacco companies, which is why anti-tobacco ads are so important.  For example, the Surgeon General’s report details how “low-tar” cigarettes, advertised by tobacco companies as safer, were later found to be just as harmful.   In addition, other changes in cigarette design and content have also had unexpected health effects, such as increasing rates of one of the two most common types of smoking-related lung cancer, adenocarcinoma.

Once a person starts to smoke, all doctors and health experts agree: quitting smoking is one of the best things you can do for your health and the health of your loved ones, no matter how long you’ve been smoking.  Studies show that the health benefits of quitting kick in soon after you stop.   Twenty minutes after your last cigarette your high blood pressure will drop; within 3 months your lung function will improve; one year later your risk of heart disease will fall to half of what it was when you were smoking; and five years after your last cigarette your risk of several cancers will drop by half as well.[end S. A. Kenfield, M. J. Stampfer, B. A. Rosner, G. A. Colditz. Smoking and Smoking Cessation in Relation to Mortality in Women. JAMA: The Journal of the American Medical Association, 2008; 299 (17): 2037-2047.],[end Centers for Disease Control and Prevention. 2010 Surgeon General’s Report—How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease. 2010.]  For information on how to quit, see this article.  If you are considering taking medication to help with quitting, check out this article.  And if you are thinking of using e-cigarettes to cut back on regular cigarettes, you should know that there are many unanswered questions about the risks of e-cigarettes and almost no research to support their use in smoking cessation. For more on e-cigarettes, read here.  Many e-cigarette brands are owned by tobacco companies which have been caught lying to the American public about the risks of their products repeatedly.

 

Ways You Can Cut Your Risk of Breast Cancer

Brandel France de Bravo, MPH and Diana Zuckerman, Ph.D., Cancer Prevention and Treatment Fund

Here’s the good news about how to cut your risk.

1. Lose weight

Numerous studies show that overweight and obese women are more likely to develop breast cancer.1 Estrogen, a female hormone, provides nutrition for most breast cancers. The more fat cells you have, the more estrogen you have circulating in your body. Maintaining a healthy weight is like telling breast cancer cells that the restaurant is closed for business! The healthiest way to lose weight and to keep your weight down is to reduce the number of calories you eat and also to exercise. Regular exercise helps to lower body fat, which keeps estrogen levels down. You don’t need to become a Marion Jones or a Natalie Coughlin. You just need to move! Walk at least part of the way to work, take the stairs instead of the elevator and pump iron (or choose the exercise of your choice) while you’re on the phone.

2. Avoid unnecessary hormones

Hormone therapy increases your risk of breast cancer, so avoid it if you can. If you’re taking hormone therapy, use it at the lowest possible dose for the shortest time – or just get off it as soon as possible. Also reduce your exposure to chemicals that act like hormones. Bisphenol A (BPA) is a chemical used in clear, hard plastic and in the linings of canned foods, canned drinks, disposable cutlery and many other common items, including baby bottles. BPA, phthalates (“Thah-lates”) and other chemicals known as “endocrine disruptors” appear to increase the risk of obesity, diabetes, early puberty in girls, and possibly the risk of breast cancer and prostate cancer. Here are some tips to limit your exposure to BPA:

  • Use frozen or fresh vegetables and fruits instead of canned. Get rid of older canned goods, especially if they contain tomatoes and other acidic fruits since the acid accelerates the leaching of BPA from can linings into the food. If you buy tomato or pasta sauce, look for brands sold in glass jars. Eden is one of the few brands of canned foods that doesn’t use BPA in the linings of its cans (except for its tomato products).
  • Look for drinks sold in glass, plastic bottles (soft plastic bottles like the ones typically used for soft drinks and water don’t have BPA), or cartons like those used for milk. Some of the glass bottles have tops lined with BPA but at least the top is not in constant contact with the beverage. If you carry a reusable water bottle, switch to stainless steel or look for the newer BPA-free sports bottles.
  • Switch to glass, porcelain, or stainless steel containers for hot foods and drinks because the heat is more likely to break down the BPA in the plastic and introduce it into your food or beverage.
  • When you microwave, use glass or ceramic, stoneware, or bone china containers. You can use any kind of non-plastic dishes and bowls as long as they don’t have gold or silver trim. If you need to cover the food to keep it from splattering in the microwave, use another dish or paper towel. Don’t microwave food or beverages in plastic or disposable containers (not even the ones they are sold in), and don’t cover dishes with plastic wrap in the microwave oven. Plastics that contain BPA are usually very hard and may have a triangle on the bottom with “7” inside or may say “PC.” Not all plastics with a Number 7 contain BPA, but all plastics break down when exposed to heat-whether in the microwave or the dishwasher-and strong soaps.

Phthalates, another endocrine disrupting chemical, have been linked to genital abnormalities in boys and men, and to early puberty in girls. While there is no proven link to breast cancer yet, anything that affects hormones has the potential to affect breast cancer. Phthalates are used to soften plastics and add fragrance to personal care products like lotions, shampoos, and make-up. When they aren’t used as part of the fragrance, they are sometimes used to mask the natural smell of the chemicals in a product. Phthalates are everywhere-except on a product’s label. Phthalates are almost never listed as an ingredient if their use is related to the way a product does or doesn’t smell. You can minimize your exposure to phthalates by using shampoos, hair spray, deodorants, lotions, perfumes, make-up and nail polish that are phthalate free. If the product doesn’t state “phthalate-free” (and few do), visit the Environmental Working Group’s Cosmetic Safety Database to find out which of your favorite products are safe. If you are not sure if a product has phthalates, choose the version that says “fragrance-free.”

3. Reduce stress

Reduce stress through regular exercise, meditation, or engaging in hobbies or activities that relax and fulfill you. You’ll never be able to eliminate stress from your life but you can learn to manage it better. If for you de-stressing includes watching television or “screen time,” try not to eat while doing it as people tend to eat more when they’re focused on something other than the food in front of them. If you’re going to snack, choose low-fat, nutrition-dense foods like fruits and low-fat yogurt or cheese and unsalted nuts.

4. Eat the right foods

Some foods have been shown to increase your risk of breast cancer and others appear to help prevent breast cancer (or breast cancer recurrence). Eating more than 3-4 portions of red meat like beef, pork and lamb can increase your risk of several cancers, including breast cancer. So, try to eat those meats less often, and smaller portions. Several studies have found that women who eat lots of fresh fruits and vegetables are at lower risk of breast cancer or breast cancerrecurrence.  A study of post-menopausal women who ate a Mediterranean diet (lots of fresh fruits and vegetables, fish, and olive oil) also found a decrease in breast cancer, especially for women who supplemented their Mediterranean diet with more extra virgin olive oil.2   And a study of premenopausal women found that those who ate a lot fruits and vegetables with carotenoids in them had a lower risk of developing breast cancer. Carotenoid-rich foods are leafy greens like kale, spinach and collard greens and foods that are orange, red and sometimes yellow. They include: carrots, mangoes, apricots, squash, sweet potatoes, and tomatoes. And if you don’t like your veggies plain, you can add cayenne pepper or chili pepper for an extra dose of carotenoid!

It’s too soon to say if walnuts can reduce cancer risks, but one study found that they reduced the frequency and size of breast cancer tumors in mice.

5. Breastfeeding protects

If you are planning to have a child or add to your family, strongly consider breast feeding. Not only is breast milk good food for your baby, but the more you breast feed, the lower your risk of various cancers, including breast cancer. This is especially important if you got a late start on having a family, because delayed childbearing increases your breast cancer risk slightly—unless you have one of the BRCA breast cancer gene mutations. If you have BRCA1 or BRCA2, having children late in life or having no children at all does NOT add to your already elevated risk of breast cancer. Breastfeeding may lower the risk of breast cancer for women with BRCA1, but not for women with BRCA2. To read more about BRCA mutations and breast cancer risk, click here. http://www.ncbi.nlm.nih.gov/pubmed/12133652

6. Don’t smoke (or quit, if you do)

A United Kingdom study involving over 100, 000 women found a significant link between smoking and breast cancer. Over a 7-year period, about 2% of women who ever smoked developed cancer compared to about 1.6% of women who never smoked. This means that smoking causes about 4 in 1000 breast cancers. Even though that number seems small (less than half a percent), it is statistically significant. Starting smoking at a younger age, smoking 15 or more daily cigarettes, and smoking for at least 10 years increase the chances of developing breast cancer. If you smoke, you should talk to your doctor about ways to quit. Quitting decreases the chances of developing breast cancer, but it may take about 20 years to see the full benefits. To read more, click here.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff. 


1 Neuhouser ML, Aragaki AK, Prentice RL, et al. Overweight, Obesity, and Postmenopausal Invasive Breast Cancer Risk: A Secondary Analysis of the Women’s Health Initiative Randomized Clinical Trials. JAMA Oncol. Published online June 11, 2015. http://oncology.jamanetwork.com/article.aspx?articleid=2319235

2 Toledo, Estefanía, et al. Mediterranean Diet and Invasive Breast Cancer Risk Among Women at High Cardiovascular Risk in the PREDIMED Trial A Randomized Clinical Trial. JAMA Intern Med. Published online September 14, 2015. doi:10.1001/jamainternmed.2015.4838. http://archinte.jamanetwork.com/article.aspx?articleID=2434738&utm_source=Silverchair%20Information%20Systems&utm_medium=email&utm_campaign=ArchivesofInternalMedicine:OnlineFirst09/14/2015

3 Jones ME. et al. Smoking and risk of breast cancer in the Generations Study cohort. Breast Cancer Research. 2017;19:118. https://doi.org/10.1186/s13058-017-0908-4

Pancreatic cancer: are you at risk?

Heidi Mallis, Cancer Prevention & Treatment Fund

Pancreatic cancer is the 3rd leading cause of cancer death among women and men in the U.S.[1]

Surprising Facts

  • The five-year survival rate is less than 8%. This figure has improved only slightly since 1975, when it was 3%.[2]
  • There is no reliable screening test for early detection of pancreatic cancer.[3]
  • Only about 2.5% of the National Cancer Institute’s federal research funding is currently allocated to pancreatic cancer.[4]
  • Pancreatic cancer has claimed the lives of several public figures including: actors Patrick Swayze and Alan Rickman, opera tenor Lucianno Pavarotti, and professor and bestselling author Dr. Randy Pausch.[5]

Risk Factors

Every year, more than 50,000 people are diagnosed with pancreatic cancer in the U.S., and more than 40,000 people die from the disease.[6] It is known as a “silent killer” because its symptoms (pain, jaundice, and weight loss) can easily be mistaken for other diseases. Diagnosis is often at an advanced stage when the cancer has spread to other parts of the body, making treatment more difficult. That is why new research is needed to help identify earlier warning signs that could lower the fatality rate for this disease.

Several risk factors are known. Most are common and can’t be changed. The following traits increase your risk of developing pancreatic cancer:

  • 60 years of age or older
  • African American
  • Male
  • Smoking:  Smokers are 2-3 times more likely to develop pancreatic cancer than nonsmokers, and smoking is responsible for 20-30% of all pancreatic cancer cases.
  • Type 2 diabetes:  Several studies show that people with diabetes are more likely to also develop pancreatic cancer and vice versa, but it is unclear whether diabetes causes pancreatic cancer or is caused by pancreatic cancer.[7][8]
  • Family history of pancreatitis (inflammation of the pancreas), ovarian, or colon cancer. If a person has an immediate family member who has any of these types of cancer, his or her chance of developing pancreatic cancer is tripled.[9]

Research has shown that family history or shared genes were a risk factor for pancreatic cancer. In 2009, new light was shed on the role of genes when a study showed that people with blood type O may have a lower risk of pancreatic cancer than those with blood types A, B, or AB. The study was conducted by a group of researchers from several academic institutions that are part of the Pancreatic Cancer Cohort Consortium, which is affiliated with the National Cancer Institute (NCI).[10] The group hopes to further examine genetic risks, and future findings could help increase early detection and prevention of pancreatic cancer.

Regardless of blood type and other risk factors, individuals can reduce their risk of developing pancreatic cancer by lowering controllable risk factors. A study revealed that a diet rich in fresh fruit and vegetables, Vitamin C, and fiber might actually reduce the risk of developing pancreatic cancer.[11] Other risk factors, such as smoking or diabetes related to weight gain, can be reduced by quitting smoking and maintaining a healthy weight, which decreases a person’s risk of many other diseases as well. In addition, one study of 60,000 adults indicates that drinking fewer (non-diet) soft drinks may decrease the risk of pancreatic cancer.[12] The authors suggest that sugary drinks, by increasing insulin levels, help fuel pancreatic cancer cell growth. They also speculate that people who consume more soft drinks tend to be more likely to smoke and to eat red meat, all of which are considered potential risk factors for pancreatic cancer.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. Cancer Treatment Centers of America. (2016, October). What should you know about pancreatic cancer? http://www.cancercenter.com/~/media/Images/Others/Misc/10-2016-pancreatic-infographic.jpg
  2. National Cancer Institute. (2016, April). Cancer Stat Facts: Pancreas Cancer. https://seer.cancer.gov/statfacts/html/pancreas.html
  3. American Cancer Society (2017). Can cancer of the pancreas be found early? https://www.cancer.org/cancer/pancreatic-cancer/detection-diagnosis-staging/detection.html
  4. Office of Budget and Finance. Fiscal year 2015 fact book. National Cancer Institute. https://www.cancer.gov/about-nci/budget/fact-book/data/research-funding
  5. Pancreatic Cancer Action Network (2016). Public figures affected by pancreatic cancer. http://media.pancan.org/pdf/Public-Figures-affected-by-pancreatic-cancer.pdf
  6. American Cancer Society (2017). Key statistics for pancreatic cancer. https://www.cancer.org/cancer/pancreatic-cancer/about/key-statistics.html
  7. Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ (2004). Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults. American Journal of Epidemiology, 159: 1160-1167.
  8. European Cancer Organisation. (2017, January). Diabetes or its rapid deterioration can be an early warning sign for pancreatic cancer. http://www.eccocongress.org/Global/News/ECCO2017-News/2017/01/ECCO2017-NEWS-Diabetes-or-its-rapid-deterioration-can-be-an-early-warning-sign-for-pancreatic-cancer
  9. National Cancer Institute (2017). Pancreatic cancer. U.S. National Institutes of Health. https://www.cancer.gov/types/pancreatic
  10. Amundadottir L, Kraft P, Stolzenberg-Solomon RZ, et al (2009, August 2). Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer. Nature Genetics, September 2009; 41(9): 986-990.
  11. Ghadirian P, Lynch HT, and Krewski D (2003). Epidemiology of pancreatic cancer: an overview. Cancer Detection and Prevention, 27(2): 87-93.
  12. Muelle NT, Odegaard A, Anderson A, Yuan J-M, Koh W-P, Pereira MA. Soft Drink and Juice Consumption and Risk of Pancreatic Cancer: The Singapore Chinese Health Study. Cancer Epidemiology, Biomarkers & Prevention. 2010.19(2);447-455.

 

Ovarian Cancer CA-125 Blood Test: Does It Work?

Stephanie Portes-Antoine, Brandel France de Bravo, MPH, and Laura Gottschalk, PhD, Cancer Prevention and Treatment Fund

Ovarian cancer is a deadly disease because it is rarely diagnosed early. There is not yet an effective, life-saving screening tool for the early diagnosis of ovarian cancer.

When ovarian cancer is diagnosed in the early stage—before the cancer has spread beyond the ovaries—chances of a woman’s survival are very good, with about 93% of women surviving at least 5 years.  Unfortunately, only 15% of cases are caught this early, because the symptoms of ovarian cancer are not obvious. For women diagnosed with advanced ovarian cancer, the chances of 5-year survival drop to less than 30%.[1] Given the dramatic differences in survival outcomes between advanced and early onset diagnosis, it is vitally important to detect ovarian cancer early.

Most women whose ovarian cancer is detected in the late stages will have a relapse (usually many times) following their initial treatment, requiring additional treatment.[2] The most widely used test to screen for the recurrence of ovarian cancer is the CA-125. This blood test measures a protein that tends to be higher in women with ovarian cancer. The test was approved for use on women who have already been diagnosed with ovarian cancer once. In 2008, Dr. Vladimir Nosov from UCLA Medical Center and his co-authors reported that elevated levels of the CA-125 biomarker are found in approximately 83% of women with advanced stage ovarian cancer and 50% of patients with stage I disease.[3]

Is testing for this “biomarker” an effective way to tell early on if a woman’s ovarian cancer has returned? And what about women who have never been diagnosed with ovarian cancer? Why can’t the CA-125 test be used to screen them?

Women with No Symptoms or Who Have Never Been Diagnosed with Ovarian Cancer

Other studies have confirmed that CA-125 by itself is not sensitive enough to diagnose ovarian cancer in the very early stage of the disease, before there are symptoms. Dr. Saundra S. Buys is co-director of the Family Cancer Assessment Clinic at the Huntsman Cancer Institute in Salt Lake City, Utah. According to Dr. Buys, CA125 testing “may be appropriate to screen for ovarian cancer in women who have abdominal symptoms, but for women who have no medical symptoms, doing screening for ovarian cancer results in a lot of false-positives.”[4] False positives are test results that inaccurately show the person might have cancer. Dr. Buys based her conclusions on data for women ages 55 to 75 who were participating in a large study called the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial.[5]

In 2011, Dr. Buys and her colleagues published more results from that trial which involved more than 78,000 women. They concluded that using the CA-125 blood test to screen for ovarian cancer doesn’t prevent women from dying from the disease, it actually is harmful.[6] False positives resulted in many women having unnecessary surgery: 3,285 women received false positives and 1080 of these women underwent biopsy surgery. In 15% of cases, the unnecessary surgery caused serious complications. At the same time, there was no benefit in terms of survival for the women who took the test as compared with those who did not.

Women Who Have Previously Had Ovarian Cancer

CA-125 by itself is clearly not reliable at detecting early ovarian cancer in women of low or average risk—women who have never before been diagnosed with ovarian cancer, and women who have no symptoms. Is it at least effective at detecting a recurrence of ovarian cancer?  In 2010, Dr. Gordon Rustin of the Mount Vernon Cancer Centre in England published the results of a study done with women who had already been diagnosed with and treated for ovarian cancer. He found  that women who started chemotherapy early, based on a CA125 test result indicating relapse of ovarian cancer, did not live any longer than women who did not begin treatment until symptoms of relapse appeared.[7]

The Future of Ovarian Cancer Screening

Research is underway to evaluate whether the CA-125 test can be used more reliably, either by administering it only to women with other biomarkers that indicate increased risk (such as elevated levels of the protein HE4) or combined with other screening tests such as vaginal ultrasound.

Dr. Karen Lu from the MD Anderson Center at the University of Texas has had success correctly identifying postmenopausal women at high risk for ovarian cancer by measuring CA-125 at regular intervals and relying on a mathematical model. Only women whose CA-125 levels went up over time were given a vaginal ultrasound, and only those with suspicious findings on the ultrasound had surgery. This two-staged approach seemed potentially effective .[8] However, when this approach was studied on more than 200,00 women, it did not significantly prevent death from ovarian cancer.[9]

The Bottom Line:

The CA-125 test by itself is not a good screening tool for ovarian cancer. When used alone on women with no symptoms or previous history of ovarian cancer, it leads to many false positives. Among women who have already been treated for ovarian cancer once, it doesn’t seem to matter whether they get treatment for their ovarian cancer recurrence based on CA-125 results or based on their symptoms. Either way, women who relapsed and got treatment lived about the same amount of time.

References:

  1. The National Cancer Institute. Surveillance Epidemiology and End Results. SEER Stat Fact Sheets. Cancer: Ovary. http://seer.cancer.gov/statfacts/html/ovary.html
  2. NCI Cancer Bulletin. Early Chemo to Prevent Ovarian Cancer Recurrence Fails to Increase Survival. June 2, 2009. Volume 6/Number 11. http://www.cancer.gov/ncicancerbulletin/060209/page2
  3. Nosov V., et al. The early detection of ovarian cancer: from traditional methods to proteomics. Can we really do better than serum CA-125? American Journal of Obstetrics and Gynecology. September 2008: 199(3): 215-223.
  4. Reinberg, S. Ovarian screening Methods Inaccurate. National Women’s Health Resource Center. November 7, 2005. http://www.healthywomen.org/resources/womenshealthinthenews/dbhealthnews/ovariancancerscreeningmethodsinaccurate
  5. Buys S.S., et al. Ovarian cancer screening in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial: Findings from the initial screening of a randomized trial. American Journal of Obstetrics and Gynecology. November 2005: 193(5): 1630-1639.
  6. Buys S.S., et al. Effects of Screening on Ovarian Cancer Mortality: The Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Randomized Controlled Trial. The Journal of the American Medical Association. July 2011; 2011 (616):1.
  7. Rustin, G.J. and van der Burg. Early versus delayed treatment of relapsed ovarian cancer (MRC OV05/EORTC 55955): a randomized trial. Lancet. October 2010
  8. Lu, Karen et al. A 2-Stage Ovarian Cancer Screening Strategy Using the Risk of Ovarian Cancer Algorithm (ROCA) Identifies Early-Stage Incident Cancers and Demonstrates High Positive Predictive Value. Cancer. September 2013; 2013 (119):17.
  9. Jacobs  IJ, Menon  U, Ryan  A,  et al.  Ovarian cancer screening and mortality in the UK Collaborative Trial of Ovarian Cancer Screening (UKCTOCS): a randomised controlled trial . Lancet. doi:10.1016/S0140-6736(15)01224-6.

Colon Cancer: Who Is at Risk, and How Can It Be Prevented?

Noy Birger, Brandel France de Bravo, MPH, and Alea Sabry,  Cancer Prevention & Treatment Fund

When cancer begins in the colon (large intestine) or rectum, it is called colorectal cancer or colon cancer.

In the early stages, this cancer begins with small polyps, which are shaped like little mushrooms growing on the wall of the colon. Polyps are very common, especially as people get older. Not all polyps develop into cancer but all colorectal cancer begins with polyps. Certain kinds of polyps are more likely to lead to cancer than others, but the doctor can’t tell if a polyp is precancerous just by looking at it. This is why doctors prefer to remove and analyze any polyp found during screening. Polyps can be identified and removed by colonoscopy, in which a small camera on a flexible tube is inserted into the rectum.[1]

Thanks to more screening, the number of people diagnosed with colon cancer has decreased, but it is still the third most common cancer for both men and women.[2][3][4] The death rate is high because many people who are at risk for colon cancer do not get screened for the disease.[5]

A study published in February 2012 in New England Journal of Medicine found that patients who received colonoscopies and had noncancerous or pre-cancerous growths (polyps) removed, were half as likely to die from colon cancer than people in the general population who were not screened or used less effective screening methods. [6]

Men and women are equally likely to die from colon cancer, but men are more likely to be diagnosed with colon cancer than women of the same age.[7][8] Black men and Black women are at higher risk for developing colon cancer and dying from it than are white men and white women of the same age.[9][10] Being overweight or obese increases men’s risk of colon cancer more than it does women’s (see Weight and Cancer: What You Should Know).  In the U.S., nearly one in ten cases of colon cancer is estimated to be caused by excess body fat.[11]

Risk Factors for Developing Colon Cancer

In addition to your sex and race, your age and genes are important risk factors you can’t do anything about. Your chances of developing colon cancer increase as you get older: 90% of cases are in people over 50. Having a family member with colon cancer also increases your chances of developing it. About 20% of people with colon cancer have a first-degree relative (parents, siblings or children) or second-degree relative (aunts, uncles, grandparents, grandchildren, nieces, nephews, or half-siblings) who also had colon cancer. [12]

In addition to people with pre-cancerous polyps, people who suffer from ulcerative colitis or Crohn’s disease are more likely to develop colon cancer.[13] Ulcerative colitis and Crohn’s disease cause inflammation of the colon, which is why they are both also referred to as Inflammatory Bowel Disease (IBD). Chronic inflammations in the body seem to increase the risk of various types of cancer.

Less is known about what you can do to prevent colon cancer. People who eat too much fat in their diet or too little fiber or too little calcium, smoke, drink alcohol, don’t exercise enough, or are overweight are more likely to be diagnosed with colon cancer. However, scientists do not know whether people can lower their risks of getting colon cancer if they change one or more of those behaviors.  For example, several large research studies show that eating a high-fiber diet does not decrease your chances of getting colon cancer.[14][15][16] On the other hand, there is clear evidence that fiber, calcium, exercising, maintaining a healthy weight, and avoiding smoking and alcohol is generally good for your health, whether it reduces your chances of colorectal cancer or not.

So, What Can You Do to Lower Your Risk?

  • Get screened regularly from age 50 to 75. If you have a relative with colon cancer, your doctor may want to screen you earlier than age 50. The recommended screening tests are:
    • High Sensitivity Fecal Occult Blood Test (FOBT), which involves providing stool samples and should be done once every year
    • Colonoscopy (mentioned above), which requires anesthesia and is more expensive, and the doctor can remove polyps if found. It is only needed every 10 years unless a close relative developed colon cancer; and
    • Flexible sigmoidoscopy is similar to a colonoscopy. It can be used to find polyps but not to remove them. It is recommended every 5 years

A “virtual colonoscopy,” which is done with a Computed Tomography (CT) scan, is more expensive than the other screening tools and is not recommended by the U.S. Preventive Services Task Force. As with any CT scan, it exposes you to relatively high levels of radiation (see Everything You Ever Wanted to Know about Radiation and cancer, But Were Afraid to Ask).

The advantage to a regular colonoscopy (not a virtual one) over the other methods is that polyps can be removed during the screening process. The disadvantage is that you need to take a day off from work, fast for about 12 hours and purge with large quantities of an unpleasant laxative drink. The advantage of the FOBT is that it is easier and less expensive. However, the FOBT and CT scan only detect potential problems or polyps – you would still need the colonoscopy to have them removed if the results are abnormal. [17]

  • Quit smoking. Cigarette smoking doubles your chances of getting polyps and long-term smoking increases the risk of colon cancer. It also increases your chances of dying from colon cancer.[18][19][20]
  • Maintain a healthy weight. Extra pounds mean extra risk for all kinds of cancer, including colorectal cancer. Fat cells appear to trigger chronic inflammation of the body, which stresses the immune system.[21]
  • Eat a balanced diet. Be sure to include plenty of fruits and vegetables (especially ones from the cabbage family, like broccoli, cauliflower, cabbage, Brussels sprouts, and collard greens), limit the amount of red meat you eat (particularly well-done) and stay active. At least some of the research supports this kind of diet, and since eating this way offers so many different health benefits, why not try it? [22][23]
  • Get more Vitamin D through sunlight and supplements, since few foods are naturally rich in Vitamin D. Recent studies of doses higher than the 400 IU/day that is in standard multiple vitamins, show that Vitamin D can reduce the risk of colon cancer.[24] Blacks, who are at the highest risk for colon cancer, and people living in the northern half of the U.S., typically have too little Vitamin D in their bodies because they are exposed to less sun, and darker skin benefits less from sunshine.  And since Vitamin D is good for your health in many ways (see http://ods.od.nih.gov/factsheets/vitamind.asp), it makes sense to give this a try if you are concerned about colon cancer.[25] Vitamin D is in milk and fortified breakfast cereals and in fatty fish such as tuna, salmon, and sardines, or you might consider a Vitamin D supplement.  Experts agree that adults can take up to 4,000 IU/day of Vitamin D without harming their health, and they recommend getting 5-30 minutes of sun at least twice a week. This means sun exposure to your face, arms or legs (preferably all three) without sun screen and between 10:00 a.m. to 3:00 p.m. However, too much Vitamin D can be dangerous.  The best way to make sure you are getting enough Vitamin D, but not too much, is to get your Vitamin D levels checked the next time you visit your doctor.
  • Low-dose aspirin. The U.S. Preventive Services Task Force found that taking low-dose aspirin can help prevent colorectal cancer and heart disease in some adults, depending on age and other factors. For more information, see: Aspirin Use for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: Consumer Guide. [PDF-212K]. Despite some early studies, there is no clear evidence that other types of anti-inflammatory products help prevent colorectal cancer, such as ibuprofen or fish oil tablets.
  • Reduce your intake of unnecessary antibiotics. A 2021 study found that people who took unnecessary antibiotics more frequently than others were more likely to develop early-onset colorectal cancer. Researchers believe that altering the gut microbiome structure through antibiotic treatment may increase one’s likelihood of developing colorectal cancer. Despite these findings, more studies are needed to understand the true role of antibiotics in colorectal cancer development, particularly to analyze the long-term effects of antibiotics on gut health.[26]

All articles on our website are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

Related Content:

Have colon cancer? Skip the hot dogs, deli, and burgers
Colon cancer screening
Can aspirin prevent both heart disease and cancer?

References:

1. Basic Information About Colorectal Cancer. Centers for Disease Control and Prevention. http://www.cdc.gov/cancer/colorectal/basic_info/index.htm.

2. “Cancer Among Women.” Centers for Disease Control and Prevention; 2015 http://www.cdc.gov/cancer/dcpc/data/women.htm.

3. American Cancer Society. Key Statistics for Colorectal Cancer. https://www.cancer.org/cancer/colon-rectal-cancer/about/key-statistics.html. January 12, 2021.

4. “Cancer Among Men.” Centers for Disease Control and Prevention; 2015 http://www.cdc.gov/cancer/dcpc/data/men.htm.

5. Swan J, Breen N, Coates RJ, Rimer BK, Lee NC. Progress in cancer screening practices in the United States: results from the National Health Interview Survey.

6. Zauber AG, Winawer SJ, O’Brien M.J, Lansdorp-Vogelaar I, van Ballegooijen M, Hankey BF, et al. Colonoscopic polypectomy and long-term prevention of colorectal-cancer deaths. New  EnglandJournal of Medicine. 2012; 366(8), 687-696.

7. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New England Journal of Medicine. 1999; 340:169-176.

8. Jemal A, Siegal R, Ward E, Hoa Y, Xu J, Thun MJ. Cancer Statistics 2009.  CA:A Cancer Journal for Clinicians.. 2009;59:225-249.

9. Lieberman D, Holub J, Moravec M, Eisen G, Peters D, Morris C. Prevalence of colon polyps detected by colonoscopy screening in asymptomatic black and white patients. Journal of American Medical Association. 2008;300:1417-1422.

10. Colorectal Cancer Rates by Race and Ethnicity. Centers for Disease Control and Prevention. http://www.cdc.gov/cancer/colorectal/statistics/race.htm.

11. American Institute for Cancer Research. Researchers present data linking obesity/overweight to higher cancer risk, poorer cancer survival. November 2009. www.aicr.org.

12. Castels A, Castellvi-Bel S, Balaguer F. Concepts in familial colorectal cancer: where do we stand and what is the future? Gastroenterology. 2009; 137:404-409.

13. Jia Q, Lupton JR, Smith R, Weeks BR, Callaway E, Davidson LA, et al. Reduced Colitis-Associated Colon Cancer in Fat-1 (n-3 Fatty Acid Desaturase) Transgenic Mice. Cancer Research. 2008; 68: (10).

14. Fuchs CS, Giovannucci EL, Colditz GA, et al. Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women. New England Journal of Medicine. 1999; 340:169-176.

15. Park Y, Hunter DJ, Speigelman D, Bergkvist L, Berrino F, van den Brandt PA, et al. Dietary Fiber Intake and Risk of Colorectal Cancer: A Pooled Analysis of Prospective Cohort Studies. Journal of American Medical Association. 2005; 294:2849-2857.

16. Schatzkin A, Mouw T, Park Y, Subar AF, Kipnis V, Hollenbeck A, et al. Dietary fiber and whole-grain consumption in relation to colorectal cancer in the NIH-AARP Diet and Health Study. American Journal of Clinical Nutrition, 2007; 85. 5:1353-1360.

17. Edwards BK, Ward E, Kohler BA, Eheman C, Zauber AG, Anderson RN, Jemal A, Schymura MJ, Lansdorp-Vogelaar I, Seeff LC, van Ballegooijen M, Goede SL, Ries LA. Annual report to the nation on the status of cancer, 1975-2006, featuring colorectal cancer trends and impact of interventions (risk factors, screening, and treatment) to reduce future rates. Cancer 2010;116(3):544-573.

18. Botteri E, Iodice S, Raimondi D, Maisonneuve P, Lowenfels AB. Smoking and Adenomatous Polyps: a Meta-analysis. Gastroenterology. 2008;134(2):388-395.e3

19. Hannan LM, Jacobds EJ, Thun MJ. The association between cigarette smoking and risk of colorectal cancer in a large prospective cohort from the United States. Cancer Epidemiology, Biomarkers & Prevention.2009;18(12):3362-3367.

20. Botteri E, Iodice S, Bagnard V, Raimondi S, Lowenfels AB, Maisonneuve P. Smoking and colorectal cancer: a meta-analysis. Journal of American Medical Association.2008;300(23):2765-2778.

21. American Institute for Cancer Research. Researchers present data linking obesity/overweight to higher cancer risk, poorer cancer survival. November 2009. www.aicr.org.

22. Cotterchio M, Boucher BA, Manno M, Gallinger S, Okey AB, Harper PA. Red meat intake, doneness, polymorphisms in genes that encode carcinogen-metabolizing enzymes, and colorectal cancer risk.Cancer Epidemiology, Biomarkers & Prevention. 2008;17:3098-3107.

23. Cheng J, Ogawa K, Kuriki K, Yokoyama Y, Kamiya T, Seno K. Increased intake of n-3 polyunsaturated fatty acids elevates the level of apoptosis in the normal sigmoid colon of patients polypectomized for adenomas/tumors. Cancer Letters, Volume 193, Issue 1,10 April 2003; 1: 17-24

24. “Vitamin D and Cancer Prevention.” National Institutes of Health. National Cancer Institute; 2013 http://www.cancer.gov/about-cancer/causes-prevention/risk/diet/vitamin-d-fact-sheet.

25. “Dietary Supplement Fact Sheet: Vitamin D.” National Institutes of Health. Office of Dietary Supplements. https://ods.od.nih.gov/factsheets/VitaminD-Consumer/ 

26. Bassett, M. Are Antibiotics Linked to Early-Onset Colorectal Cancer?. Medpage Today. July 2021. https://www.medpagetoday.com/meetingcoverage/additionalmeetings/93412?xid=nl_mpt_DHE_2021-07-05&eun=g1146420d0r&utm_source=Sailthru&utm_medium=email&utm_campaign=Daily%20Headlines%20Top%20Cat%20HeC%20%202021-07-05&utm_term=NL_Daily_DHE_dual-gmail-definition

Phthalates and Children’s Products

Paul Brown, Keris Krenn Hrubec, Dana Casciotti, PhD, Brandel France de Bravo, MPH, Stephanie Fox-Rawlings, PhD, Cancer Prevention & Treatment Fund

Phthalates are synthetic chemicals found in every home, in plastic toys, personal care products such as shampoos and lotions, vinyl floors, and shower curtains. They are also found in some medical products, such as saline bags, feeding tubes and catheters. They are used to make plastic flexible and to add fragrances to soap and other personal products.  Unfortunately, these chemicals don’t stay inside the products. Based on recent research on ants, scientists have concluded that the high levels of phthalates in the bodies of insects around the world are the result of phthalates in the air.[1] Because phthalates are released into the air and dust around us, they are found in human urine, blood, and breast milk.[2] Levels are highest in women and children ages 6 to 11. Young children may have higher levels of phthalates in their bodies because their hands find their way into their mouths more frequently: they touch objects made with phthalates and surfaces covered with phthalate dust, and then their hands touch their mouths.

Phthalates are called “endocrine disruptors” because they affect the body’s hormones by mimicking them or blocking them. They interfere with the body’s natural levels of estrogen, testosterone, and other hormones, which is why they are called “disruptors.” Endocrine disruptors are hard to study for several reasons: 1) we are exposed to very small quantities from many different sources every day, 2) researchers have proved that, unlike other chemicals, these appear to have more serious effects at lower levels than at higher levels.[3] Usually, we assume that the higher the dose or exposure, the greater the harm, but endocrine disruptors play by different rules. The director of the National Institute of Environmental Health Sciences, Linda Birnbaum, says that chemical manufacturers are asking “old questions” when they test for safety even though “science has moved on.”[4]

Hormones can increase the risk of some cancers, whether those hormones are natural or synthetic. Too much or too little of a hormone can be harmful. Is a child who is exposed to phthalates more likely to develop cancer as an adult?  No one knows for sure but animals exposed to phthalates are more likely to develop liver cancer, kidney cancer, and male reproductive organ damage.[5]

Phthalates are believed to also affect girls’ hormones, but the health impact is not yet known. Studies also show associations between children’s exposure to phthalates and the risk of asthma, allergies and bronchial obstruction.[6][7][8]

Researchers at Mount Sinai also found a link between obesity and phthalates.[9] They found that among overweight girls ages 6 to 8, the higher the concentration of certain phthalates (including low molecular weight phthalates) in their urine, the higher their body mass index (BMI).  BMI takes height and weight into account when determining if someone is overweight. A study among Danish children ages 4 to 9 found that the higher the concentration of phthalates (all of them), the shorter the child. This was true for girls and boys.[10] More research is needed to determine the impact of phthalates on height and BMI.

Even short-term exposure has now been linked to developmental deficits.[11] Researchers found that children in intensive care units were exposed to the phthalate DEHP through plastic tubing and catheters. The children had 18 times (!)  as much DEHP in their blood compared to children who had not spent time in the ICU. Four years later, the children who had been exposed to DEHP had more problems with attention and motor coordination. The researchers found that the DEHP caused these problems regardless of medical complications or treatments.

Prenatal Exposure to Phthalates

Childhood exposure to phthalates begins in the womb. Several studies that have tested phthalate levels in women in their third trimester of pregnancy have found health effects in the infants, toddlers, and older children of the mothers with the highest levels. There are many different types of phthalates. Most studies look at several types, and the effects tend to vary by type.  A 2011 study found that six-month-old boys whose mothers had the highest phthalate levels scored lower on brain and motor development tests.[12] The same effect was not true for female infants.

Research indicates that boys exposed to phthalates while in the womb may be more likely to develop smaller genitals and incomplete descent of the testicles.[13] Boys who are born with undescended testicles are 2-8 times more likely to develop testicular cancer later on than men born with both testicles descended[14] (their risk is lessened if they get corrective surgery before age 13.[15]). Studies by Harvard researchers have shown phthalates may alter human sperm DNA and semen quality.[16][17][18][19]

Columbia University researchers discovered that three-year olds with high prenatal exposure to two types of phthalates were more likely to have motor delays.[20] They also reported that three phthalates were linked to certain behavior problems in three-year olds, such as social withdrawal.  One phthalate in the study was linked to lower mental development in girls.

Other studies have also linked increased prenatal phthalate exposure to behavior problems. Researchers in Taiwan found an association with aggressive and disobedient behaviors in eight-year-olds of both sexes.[21][22] Similarly, researchers from Icahn School of Medicine at Mount Sinai found that higher levels of exposure to phthalates during gestation were associated with aggression, rule-breaking, and conduct problems for males only.[23]

Researchers at Mount Sinai School of Medicine studied the impact of prenatal exposure to “low molecular weight” phthalates—the kind often found in personal care products and the coatings of some medications—on the social behavior of children ages 7 to 9. Children who were exposed to higher levels of these phthalates, which include DEP and DBP, had worse scores for social learning, communication, and awareness.  This means they were less able to interpret social cues, use language to communicate, and engage in social interactions.[24]

What Is Being Done to Limit Children’s Exposure?

As of February, 2009, children’s toys and child care products sold in the U.S (such as teething rings and plastic books) cannot contain certain phthalates.  The ban on those phthalates is the result of a law passed in 2008, the Consumer Product Safety Improvement Act.  The law permanently bans certain kinds of phthalates (BBP, DBP and DEHP) from toys and child care products, and temporarily bans other phthalates (DIDP, DINP and DnOP) until a scientific board (the Chronic Hazard Advisory Panel) determines for the Consumer Product Safety Commission (CPSC) whether or not they are safe. In 2014 the Chronic Hazard Advisory Panel determined that stricter regulations were appropriate.[25] It stated that the permeant bans should remain on BBP, DBP and DEHP, and that DINP should be added to this list. Furthermore, because a large component of exposure to these chemicals comes from food and other products, it recommended increased regulation. The panel was less concerned about DIDP and DnOP, but recommended additional study. Finally, the panel recommended permanently banning DIBP, DPENP, DHEXP, and DCHP, and putting an interim ban on DIOP.

A few months before the 2008 bill passed, major retailers such as Wal-Mart, Target, and Babies “R” Us promised to remove or severely restrict children’s products containing phthalates by the end of 2008.[26] That provided added incentives for major companies making teething rings and other soft plastic products to stop using phthalates.

The ban in the U.S.followed similar bans in other countries.  In 2006, the European Union banned the use of 6 phthalates in toys that may be placed in the mouth by children younger than 3 years old.[27] The banned phthalates are DINP, DEHP, DBP, DIDP, DNOP, and BBzP.  Fourteen other countries, including Japan, Argentina, and Mexico, had also banned phthalates from children’s toys prior to the U.S.

Phthalate Exposure Continues

A 2014 study looking at data over a ten-year period (2001– 2010) found that exposures to some phthalates have declined while others have increased. Americans’ exposure to three substances permanently banned in toys and children’s products—DEHP, DBP and BBP—has declined. But exposure to other phthalates such as DiNP and DiBP, as measured in urine, has increased. The higher  levels of DiBP and other phthalates “suggest that manufacturers may be using them as substitutes for other phthalates even though the US EPA has expressed concern about their use.”[28] It is surprising that DiNP exposure has gone up since it was banned on an interim basis from children’s toys and children’s products.  Additionally, in 2013, California declared DiNP a carcinogen.[29]

Even with the ban on phthalates in children’s toys, children, and adults, too, continue to be exposed because these chemicals are in many products, including food packaging, pharmaceuticals, medical devices and tubing, soap, lotions, and shampoos.[30] Johnson & Johnson recently reformulated its baby shampoo to remove harmful chemicals,[31] and Proctor & Gamble has promised to eliminate the phthalate DEP from fragrances used in its products by the end of 2014.[32] DEP is used in personal care products  and “reductions in DEP exposures have been the most pronounced,” according to the 2014 study.[33] Ten years ago, more than a thousand companies pledged to remove “chemicals of concern from personal care products,” however, it is unclear how many have done so. The U.S. Food and Drug Administration (FDA) regulates many of these products, including baby shampoo and baby lotion.  If the FDA does not decide to ban phthalates from these products, legislation would be required to do so.

The U.S. Environmental Protection Agency (EPA) developed an “action plan” in 2010 for eight phthalates “because of their toxicity and the evidence of pervasive human and environmental exposure.” [34] The phthalates are being studied for health effects and for alternatives. The EPA developed two new rules for these chemicals. However, the rules were delayed and then withdrawn in 2013.[35] In 2014, seven of these phthalates were included in the Toxic Substances Control Act work plan, because of their potential for harm and the frequency of exposure.[36] The eighth phthalate (DnPP) was not included because it is no longer being used in new products. The chemicals on the work plan are to be assessed for additional study or regulation, but it is unclear when that assessment will occur.

While other government agencies are concerned about phthalates in specific products, the EPA’s job is to focus on the chemicals for use in any kind of product and establish safety standards for each phthalate.  A challenge for the EPA is to set safety standards that make sense given that people may be exposed to several phthalates from many different sources. Teenage girls, for instance, have been found to use up to 17 personal care products a day.[37] Setting safety standards for phthalates individually or for individual products without considering their interactions and cumulative effects could underestimate the real-world risks of phthalates to the health of children and adults.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. Rudel RA, Brody JG, Spengler JD, Vallarino J, Geno PW, Sun G, Yau A (2001). Identification of selected hormonally active agents and animal mammary carcinogens in commercial and residential air and dust samples. Journal of Air and Waste Management Association 51(4):499-513.
  2. Kato K, Silva MJ, Reidy JA, Hurtz D, Malek NA, Needham LL, Nakazawa H, Barr DB, Calafat AM (2003). Mono(2-ethyl-5-hydroxyhexyl) phthalate and mono-(2-ethyl-5-oxhexyl) phthalate as biomarkers for human exposure assessment to di-(2-ethylhexyl) phthalate. Environmental Health Perspectives 112: 327-330.
  3. Vandenberg et al. (2012). Hormones and Endocrine Disrupting Chemicals: Low-dose Effects and Nonmonotonic Dose Responses. Endocrine Reviews.  First published ahead of print March 14, 2012 as doi:10.1210/er.2011-1050.
  4. Cone, Marla and Environmental Health News. Low Doses of Hormone-Like Chemicals May Have Big Effects. Scientific American.march 15, 2012. http://www.scientificamerican.com/article.cfm?id=low-doses-hormone-like-chemicals-may-have-big-effects.
  5. Vastag, B., (2001). CDC Unveils First Report on Toxins in People, JAMA 285(14): 1827-1828.
  6. Jaakkola JJ, Knight TL (2008 July). The Role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis. Environ Health Perspect, 116(7): 845-53.
  7. Kanazawa A, Kishi R (2009 May). Potential risk of indoor semivolatile organic compounds indoors to human health. Nippon Eiseigaku Zasshi, 64(3): 672-82.
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  9. Teitelbaum SL, Mervish N, L Moshier E, Vangeepuram N, Galvez MP, Calafat AM, Silva MJ, L Brenner B, Wolff MS. (2012, January).Associations between phthalate metabolite urinary concentrations and body size measures in New York City children. Environmental Research 112:186-193.
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  11. Verstraete S, Vanhorebeek I, Covaci A, Güiza F, Malarvannan G, Jorens PG, Van den Berghe G. (2016). Circulating phthalates during critical illness in children are associated with long-term attention deficit: a study of a development and a validation cohort. Intensive Care Med 42(3):379-92.
  12. Yeni Kim Y, Eun-Hee Ha, Eui-Jung Kim, et al. (2011). Prenatal Exposure to Phthalates and Infant Development at Six Months: Prospective Mothers and Children’s Environmental Health (MOCEH) Study, Environmental Health Perspectives. 119(10): 1495-500.
  13. Main KM, Skakkebaek NE, Virtanen HE, Toppari J (2010). Genital anomalies in boys and the environment. Best Pract Res Clin Endocrinol Metab.Apr;24(2):279-89.
  14. Toppari J, Kaleva M. Maldescendus testis. Horm Res 1999;51:261-9.
  15. Pettersson A et al. (2007) Age at surgery for undescended testis and risk of testicular cancer. New England Journal of Medicine 356:1835-41.
  16. Duty, S. M., M. J. Silva, et al., (2003). Phthalate exposure and human semen parameters. Epidemiology 14(3): 269-77.
  17. Duty, S. M., N. P. Singh, et al., (2003). The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environ Health Perspect 111(9): 1164-9.
  18. Duty, S. M., A. M. Calafat, et al., (2004). The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. J Androl 25(2): 293-302.
  19. Duty, S. M., A. M. Calafat, et al., (2005). Phthalate exposure and reproductive hormones in adult men. Hum Reprod 20(3): 604-10.
  20. Whyatt RM, Liu X, Rauh, VA, Calafat AM, Just AC, Hoepner L, Diaz D, et al. (2012). Maternal prenatal urinary phthalate metabolite concentrations and child mental, psychomotor and behavioral development at age three years.  Environmental Health Perspectives 120(2):290-5.
  21. Lien YJ, Ku HY, Su PH, Chen SJ, Chen HY, Liao PC, Chen WJ, & Want SL (2015). Prenatal Exposure to Phthalate Esters and Behavioral Syndromes in Children at 8 Years of Age: Taiwan Maternal and Infant Cohort Study. Environ Health Perspect 123(1): 95–100.
  22. Prenatal Phthalate Exposures and Neurobehavioral Development Scores in Boys and Girls at 6–10 Years of Age. Environ Health Perspect 122(5): 521–528.
  23. Kobrosly RW, Evans S, Miodovnik A, Barrett ES, Thurston SW, Calafat AM, & Swan SH (2014).
  24. Miodovnik A, Engel SM, Zhu C, et al. (2011). Endocrine disruptors and childhood social impairment.  Neurotoxicology Mar;32(2):261-7.
  25. CPSC. Chronic Hazard Advisory Panel on Phthalates and Phthalate Alternatives. 2014. http://www.cpsc.gov/PageFiles/169902/CHAP-REPORT-With-Appendices.pdf
  26. Pereira, J. and Stecklow, S. (2008, May). Wal-Mart Raises Bar on Toy-Safety Standards, The Wall Street Journal.
  27. Sathyanarayana S, Swan SH et al., (2008, February). Baby Care Products: Possible Sources of Infant Phthalate Exposure, Pediatrics, Vol. 121, No. 2.
  28. Zota AR, Calafat AM, & Woodruff TJ (Advance on-line publication January 15, 2014) Temporal Trends in Phthalate Exposures: Findings from the National Health and Nutrition Examination Survey, 2001-2010.
  29. Lee SM, (January 15, 2014). Banned chemicals replaced by worrisome ones, UCSF study shows. SFgate.com (San Francisco Chronicle).
  30. U.S. Food and Drug Administration (2008). Phthalates and Cosmetic Products. Retrieved November 4, 2009 at http://www.fda.gov/Cosmetics/ProductandIngredientSafety/SelectedCosmeticIngredients/ucm128250.htm
  31. Thomas K (January 17, 2014). The ‘No More Tears’ Shampoo, Now With No Formaldehyde. The New York Times. http://www.nytimes.com/2014/01/18/business/johnson-johnson-takes-first-step-in-removal-of-questionable-chemicals-from-products.html.
  32. Prcoter & Gamble Web site: What are Phthalates?  Accessed January 22, 2014. http://www.pg.com/en_US/sustainability/safety/ingredients/phthalates.shtml.
  33. Zota AR, Calafat AM, & Woodruff TJ (Advance on-line publication January 15, 2014) Temporal Trends in Phthalate Exposures: Findings from the National Health and Nutrition Examination Survey, 2001-2010.
  34. EPA. Phthalates Action Plan Summary. http://www.epa.gov/assessing-and-managing-chemicals-under-tsca/phthalates.
  35. Sheppard Kate (September 6, 2013). EPA Quietly Withdraws Two Proposed Chemical Safety Rules. Huffington Post. http://www.huffingtonpost.com/2013/09/06/epa-chemical-safety_n_3882262.html.
  36. EPA. TSCA Work Plan for Chemical Assessments: 2014 Update. https://www.epa.gov/sites/production/files/2015-01/documents/tsca_work_plan_chemicals_2014_update-final.pdf
  37. Environmental Working Group. 2008. Sutton R. Adolescent exposures to cosmetic chemicals of concern. http://www.ewg.org/research/teen-girls-body-burden-hormone-altering-cosmetics-chemicals.

Stomach Cancer and Diet: Can Certain Foods Increase Your Risk?

Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

There is growing evidence that the foods we eat can increase the chances of developing certain types of cancer. A report by the World Cancer Research Fund International says that stomach cancer is one of them.

Stomach cancer is the fifth most common cancer worldwide and the third most common cause of death from cancer.[1] Older adults are more at risk to develop stomach cancer with most people in the U.S. being diagnosed over the age of 70.[2] Men are twice as likely to develop stomach cancer compared to women.[2]

You can’t control how old you are or whether you are a man or woman, but what you eat can either increase or decrease your chances of developing stomach cancer. The World Cancer Research Fund looked at all the scientific research that was available discussing diet, weight, physical activity, and the risk of stomach cancer.[3] After looking at 89 studies that examined nearly 77,000 cases of stomach cancer, the report concluded that each of the following can increase a person’s risk for developing stomach cancer.

  • Drinking three or more alcoholic drinks per day.
  • Eating foods preserved by salting, such as pickled vegetables and salted or dried fish, as traditionally prepared in East Asia.
  • Eating processed meats that have been preserved by smoking, curing or salting, or by the addition of preservatives. Examples: ham, bacon, pastrami, salami, hot dogs, and some sausages
  • Being overweight or obese, as measured by body mass index (BMI).

Based on their findings, the WCFR has made several recommendations to reduce your risk of stomach cancer:

  • Maintain a healthy weight
  • Be physically active
  • Eat a healthy diet that avoids processed meat and limits salt
  • Limit your alcohol consumption

These recommendations are good ones for preventing cancer in general, not just stomach cancer.

Still not convinced to give up your 6-packs, kimchi, and bacon just yet? This is just the latest of many studies showing that being overweight and eating processed meats increases your risk of cancer. And, previous research has also shown that drinking more alcohol increases your chances of developing cancer.[4] However, this is probably the most comprehensive study showing the link between a range of eating and drinking habits and stomach cancer.

In addition to what you eat, there are other aspects of your life that increase the risk of stomach cancer.

  • Smoking: It is estimated that 11% of stomach cancer cases are due to smoking.
  • Infection: A bacteria called pylori is known to cause chronic inflammation of the stomach which can lead to stomach cancer. Fortunately, food sanitation in developed countries dramatically cuts down on risk of infection.
  • Industrial chemicals: Exposure to dust and high-temperature environments in the workplace increases the risk of stomach cancer.

If you can’t reduce the risks of smoking, infection or industrial chemicals, changing your diet is the best option for reducing your chances of stomach cancer. Eating fresh vegetables and meats is better than preserved and processed ones. That doesn’t mean you should never eat another hot dog or slice of bacon, but it does mean trying to eat them only rarely. As with most things, moderation is key. Try and balance your diet:  don’t just decrease the amount of unhealthy foods you eat, but also increase the amount of healthy foods. Studies have shown that eating lots of fresh fruits and vegetables, especially citrus fruit,[5] may even reduce your chances of developing stomach cancer![3]

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

References

  1. end Centers for Disease Control and Prevention. “Global Cancer Statistics.”  Department of Health and Human Services. 02 Feb. 2015. Accessed: 05/04/2016. http://www.cdc.gov/cancer/international/statistics.htm
  2. end National Cancer Institute. “What you need to know about stomach cancer.” NIH Publication No. 09-1554. Printed September 2009. Brochure.
  3. end World Cancer Research Fund International/American Institute for Cancer Research. Continuous “Update Project Report: Diet, Nutrition, Physical Activity and Stomach Cancer.” 2016. Available at: wcrf.org/stomach-cancer-2016.
  4. end IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. “Personal habits and indoor combustions. Volume 100 E. A review of human carcinogens. Exit Disclaimer.” IARC Monographs on the Evaluation of Carcinogenic Risks in Humans. 2012: 100(Pt E):373-472.
  5. end Bae JM, Lee EJ, et al. “Citrus fruit intake and stomach cancer risk: a quantitative systematic review.” Gastric Cancer. 2008;11(1):23-32.

Are E-Cigarettes Safer Than Regular Cigarettes?

Brandel France De Bravo, MPH, Sarah Miller, Jessica Becker, and Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

Electronic cigarettes, or e-cigarettes, are being marketed as the “safe” new alternative to conventional cigarettes. But are e-cigarettes safe?  What does the FDA think about them?  Are e-cigarettes going to reverse the decline in smoking—giving new life to an old habit—or can they help people quit smoking? Here is what you need to know before picking up an e-cigarette.

What Are E-Cigarettes?

E-cigarettes are battery-operated devices shaped like cigarettes that provide a way to get nicotine. Nicotine is an addictive drug (it stimulates and relaxes) that is naturally found in tobacco. The most popular way for people to take in nicotine is to inhale it by smoking cigarettes. E-cigarettes also allow nicotine to be inhaled, but they work by heating a liquid cartridge containing nicotine, flavors, and other chemicals into a vapor. Because e-cigarettes heat a liquid instead of tobacco, what is released is considered smokeless.[1]

Are E-Cigarettes Safer Than Traditional Cigarettes?

The key difference between traditional cigarettes and e-cigarettes is that e-cigarettes don’t contain tobacco.  But, it isn’t just the tobacco in cigarettes that causes cancer. Traditional cigarettes contain a laundry list of chemicals that are proven harmful, and e-cigarettes have some of these same chemicals.

Since 2009, FDA has pointed out that e-cigarettes contain “detectable levels of known carcinogens and toxic chemicals to which users could be exposed.”[2] For example, in e-cigarette cartridges marketed as “tobacco-free,” the FDA detected a toxic compound found in antifreeze, tobacco-specific compounds that have been shown to cause cancer in humans, and other toxic tobacco-specific impurities.[3] Another study looked at 42 of these liquid cartridges and determined that they contained formaldehyde,  a chemical known to cause cancer in humans.[4] Formaldehyde was found in several of the cartridges at levels much higher than the maximum EPA recommends for humans.

The body’s reaction to many of the chemicals in traditional cigarette smoke causes long-lasting inflammation, which in turn leads to chronic diseases like bronchitis, emphysema, and heart disease.[5f] Since e-cigarettes also contain many of the same toxic chemicals, there is no reason to believe that they will significantly reduce the risks for these diseases.

There are no long-term studies to back up claims that the vapor from e-cigarettes is less harmful than conventional smoke. Cancer takes years to develop, and e-cigarettes were only very recently introduced to the United States. It is almost impossible to determine if a product increases a person’s risk of cancer or not until the product has been around for at least 15-20 years. Despite positive reviews from e-cigarette users who enjoy being able to smoke them where regular cigarettes are prohibited, very little is known about their safety and long-term health effects.

Can E-Cigarettes Be Used to Cut down or Quit Smoking Regular Cigarettes?

If a company makes a claim that its product can be used to treat a disease or addiction, like nicotine addiction, it must provide studies to the FDA showing that its product is safe and effective for that use. On the basis of those studies, the FDA approves or doesn’t approve the product. So far, there are no large, high-quality studies looking at whether e-cigarettes can be used to cut down or quit smoking long-term. Most of the studies have been either very short term (6 months or less) or the participants were not randomly assigned to different methods to quit smoking, including e-cigarettes. Many of the studies are based on self-reported use of e-cigarettes. For example, a study done in four countries found that e-cigarette users were no more likely to quit than regular smokers even though 85% of them said they were using them to quit.[6] Another year-long study, this one in the U.S., had similar findings.[7] People may believe they are smoking e-cigarettes to help them quit,  but 6-12 months after being first interviewed, nearly all of them are still smoking regular cigarettes.

Until there are results from well-conducted studies, the FDA has not approved e-cigarettes for use in quitting smoking.[8]

Teenagers, Children, and E-Cigarettes

The percentage of teenagers who have tried e-cigarettes has almost quadrupled in just four years, from 5% in 2011 to 19% in 2015.  Three million U.S. students in middle school and high school tried e-cigarettes in 2015, according to the National Youth Tobacco Survey.  And, 1 in 5 middle schoolers who said they had tried e-cigarettes also said they had never smoked conventional cigarettes.[9]

E-cigarette use by young people is worrisome for a number of reasons:

1) The younger people are when they begin smoking, the more likely it is they will develop the habit: nearly 9 out of 10 smokers started before they were 18.[10]

2) Nicotine and other chemicals found in e-cigarettes might harm brain development in younger people.[11]

3) E-cigarettes may introduce many more young people to smoking who might otherwise never have tried it, and once they are addicted to nicotine, some may decide to get their “fix” from regular cigarettes. Whether e-cigarettes end up being a “gateway” to regular cigarettes or not, young people who use them risk becoming addicted to nicotine and exposing their lungs to harmful chemicals.

The sharp rise in young e-cigarette users highlights the need to stop manufacturers from targeting teenagers with candy-like flavors and advertising campaigns.

Even children who are too young to smoke have been harmed by e-cigarettes. The liquid used in e-cigarettes is highly concentrated, so absorbing it through the skin or swallowing it is far more likely to require an emergency room visit than eating or swallowing regular cigarettes. In 2012, less than 50 kids under the age of six were reported to poison control hotlines per month because of e-cigarettes. In 2015, that number had skyrocketed to about 200 children a month, almost half of which were under the age of two![12]

How Are E-Cigarettes Regulated?

The FDA was given the power to regulate the manufacturing, labeling, distribution and marketing of all tobacco products in 2009 when President Obama signed into law the Family Smoking Prevention and Tobacco Control Act and in 2010 a court ruled that the FDA could regulate e-cigarettes as tobacco products.[13]

It wasn’t until 2016 that the FDA finally announced a rule to regulate e-cigarettes.[14] Under the final rule, the FDA plans to ban the sale of e-cigarettes to anyone under the age of 18.  The rule also requires all makers of e-cigarettes sold after February 15, 2007 to go through a “premarket review.” This is the process that the FDA uses to determine whether potentially risky products are safe. However, companies are allowed to have anywhere from 18 months to two years to prepare their applications. And it will take another year for the FDA to actually approve these applications. So don’t expect e-cigarettes currently on the market to be officially allowed to be sold by the FDA for another couple of years.

In the meantime, individual states have always had the power to pass laws restricting the sale and use of e-cigarettes. For example, in May 2013, the California state senate proposed a law making all e-cigarettes subject to the same regulations and restrictions as traditional cigarettes and tobacco products.  However, that did not become law.

The Bottom Line

E-cigarettes have not been around long enough to determine if they are harmful to users in the long run.  Unfortunately, many people, including teenagers, are under the impression that e-cigarettes are safe or that they are effective in helping people quit smoking regular cigarettes.  Neither of these assumptions has yet been proven. Studies by the FDA show that e-cigarettes contain some of the same toxic chemicals as regular cigarettes, even though they don’t have tobacco.  The big three tobacco companies—Lorillard, Reynolds American, and Altria Group—all have their own e-cigarette brands, so it’s not surprising that e-cigarettes are being marketed and advertised much the way regular cigarettes used to be.  Here are the 7 Ways E-Cigarette Companies Are Copying Big Tobacco’s Playbook.

Unless you want to be a guinea pig, hold off on e-cigarettes until more safety information is available.  And if you need help quitting or reducing the number of cigarettes you are smoking, check out the smokefree.gov website.

Related Content:

Quitting smoking: women and men may do it differently
Third-hand smoke
Smoking cessation products

All articles on our website have been approved by Dr. Diana Zuckerman and other senior staff. 

References

  1. Richard J. O’Connor Non-cigarette tobacco products: What have we learned and where are we headed? Tob Control. Author manuscript; available in PMC 2013 July 19. Published in final edited form as: Tob Control. 2012 March; 21(2): 181–190. doi: 10.1136/tobaccocontrol-2011-050281.
  2. “Summary of Results: Laboratory Analysis of Electronic Cigarettes Conducted By FDA.” FDA News & Events. FDA, 22 July 2009. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm173146.htm.
  3. “Summary of Results: Laboratory Analysis of Electronic Cigarettes Conducted By FDA.” FDA News & Events. FDA, 22 July 2009. Web. 09 Aug. 2013. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm173146.htm.
  4. Varlet et al. (2015) Toxicity of refill liquids for electronic cigarettes. International Journal for Environmental Research and Public Health. 12:4796-4815.
  5. Stoller, JK & Juvelekian, G; Chronic Obstructive Pulmonary Disease; 2010 Cleveland Clinic Center for Continuing Education. https://my.clevelandclinic.org/departments/respiratory/depts/chronic-obstructive-pulmonary-disease.
  6. Adkison SE, O’Connor RJ, Bansal-Travers M, et al. Electronic nicotine delivery systems: international tobacco control four-country survey. Am J Prev Med. 2013;44(3):207-215.
  7. Grana RA, Popova L, Ling PM. A Longitudinal Analysis of Electronic Cigarette Use and Smoking Cessation. JAMA Internal Medicine, published online March 24, 2014
  8. “Electronic Cigarettes” FDA News & Events. FDA, 25 July 2013. http://www.fda.gov/newsevents/publichealthfocus/ucm172906.htm
  9. Singh T, Arrazola RA, Corey CG, et al. Tobacco Use Among Middle and High School Students – United States, 2011-2015. CDC Morbidity and Mortality Weekly Report. April 15, 2016. 65(14);361-367.
  10. Centers for Disease Control and Prevention. Fact sheets: Youth and tobacco use.  http://www.cdc.gov/tobacco/data_statistics/fact_sheets/youth_data/tobacco_use/.
  11. US Department of Health and Human Services. Preventing tobacco use among youth and young adults. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. http://www.cdc.gov/tobacco/data_statistics/sgr/2012/index.htm.
  12. Kamboj A, Spiller HA, Casavant MJ, et al. Pediatric Exposure to E-Cigarettes, Nicotine, and Tobacco Products in the United States. Pediatrics. May 2016. In Press.
  13. “Regulation of E-Cigarettes and Other Tobacco Products.” FDA News & Events. FDA, April 25, 2011. http://www.fda.gov/newsevents/publichealthfocus/ucm252360.htm.
  14. Deeming Tobacco Products To Be Subject to the Federal Food, Drug, and Cosmetic Act, as Amended by the Family Smoking Prevention and Tobacco Control Act; Restrictions on the Sale and Distribution of Tobacco Products and Required Warning Statements for Tobacco Products. 21 CFR Parts 1100, 1140, and 1143 (2016).
  15. Vaping Could Up Risks for Asthma, COPD and Other Lung Diseases. Dec 16, 2019. (HealthDay) Newshttps://consumer.healthday.com/cancer-information-5/electronic-cigarettes-970/vaping-could-up-risks-for-asthma-copd-and-other-lung-diseases-753003.html

Prostate Cancer: Diet and Dietary Supplements

Brandel France de Bravo, MPH, Caitlin Kennedy, PhD, Anna E. Mazzucco, PhD, and Laura Gottschalk, PhD, Cancer Prevention & Treatment Fund

Prostate cancer is the second most common cancer among American men, and the second leading cause of cancer deaths among them as well. The American Cancer Society estimates almost 192,000 new diagnoses of prostate cancer in 2020, and more than 33,000 prostate cancer related deaths.[1] 

Compared to most cancers, prostate cancer usually progresses very slowly, and many men live with it for years and even decades. Once diagnosed, some men decide to undergo treatment to halt the progression of the disease, and others refrain from treatment, preferring instead to closely monitor the cancer’s progression. Those who choose “active surveillance” do this because the medical and surgical treatments for prostate cancer often cause very undesirable side effects, and because most men with prostate cancer will die from something else. This strategy is especially likely for older men in the earliest stage of the disease.

At one time, it was unheard of to suggest that diet might have a role to play in battling prostate cancer. But there is now evidence that certain foods and dietary supplements have an impact on prostate health—both positive and negative. Some foods or supplements appear to promote prostate health and prevent cancer cells from developing, but others should not necessarily be taken by men who already have prostate cancer.

The role of diet drew researchers’ attention when they noticed that prostate cancer rates vary greatly from one country to another, with the highest rates appearing in countries where people tend to eat a lot of fat. Studies also show that men who are obese or have a high fat diet are more likely to have prostate cancer.[2] Diets high in saturated fats, such as the animal fats found in red meat, may pose the greatest risk. The lowest rates of prostate cancer are found in Asian countries where men eat a lot of soy foods, a rich source of naturally occurring phytoestrogens. It was hoped that by increasing men’s intake of phytoestrogens, they might reduce their risk of prostate cancer, slow its progression, or reduce the risk of prostate cancer recurring, but at least three studies have failed to find any protective benefit from phytoestrogens.[4][5][6]

Dietary Supplements

As more and more people take dietary supplements containing antioxidants, studies have been conducted to determine their effect on reducing the risk and growth of cancers, including prostate cancer. Three antioxidants that have received attention with regard to prostate health are vitamin E, selenium, and vitamin D.

Studies comparing men who live in areas of the country with high levels of selenium to men in areas with low levels suggest that this mineral protects against prostate cancer. Selenium was believed to reduce the risk of developing prostate cancer because it keeps cells from proliferating or dying off in a rapid or unusual way. An analysis in 2002 of the Nutritional Prevention of Cancer Trial revealed that the men who took selenium supplements daily were half as likely to be diagnosed with prostate cancer.[7] However, a 2014 report based on the Selenium and Vitamin E Cancer Prevention Trial (SELECT) indicated that selenium supplements increased the risk of prostate cancer by 91% and taking vitamin E supplements increased the risk of prostate cancer by 17%.[8] This result led the researchers to discourage men over 55 from taking amounts of vitamin E higher than the recommended dietary allowance (RDA), which is 15 mg of alpha-tocopherol.  Moreover, a 2009 study found that higher selenium levels in the blood may worsen prostate cancer in many men who already have the disease.[9] As a result of this trial, the researchers have encouraged men over 55 to limit their intake of selenium to the recommended dietary allowance (RDA) of 55 mcgs.

The SELECT findings on selenium don’t mean that antioxidants have no role to play in preventing cancer or slowing its spread. Some antioxidants may be helpful but some may encourage small cancers to grow larger.  A 2014 study by researchers in the U.K. tested the effect of Pomi-T, a supplement that contains broccoli, pomegranate, green tea, and turmeric on the health of men with prostate cancer. After six months, they found that the men taking Pomi-T had a smaller increase in PSA, a protein that becomes elevated with prostate cancer, as compared to men with prostate cancer who didn’t take Pomi-T. The researchers suggest that the unique blend of polyphenols and antioxidants in the supplement had a beneficial effect on health of these prostate cancer patients.[10]

A study published in 2016 brought yet another antioxidant, vitamin D, into the prostate cancer discussion. Vitamin D is well known for its role in helping build strong bones and teeth, but it may also contribute to the fight against cancer (read more here AND here). The prostate cancer study looked at the levels of vitamin D in men who had their prostates removed due to cancer. They found that men who had the most aggressive forms of prostate cancer had lower levels of vitamin D in their blood compared to men with less aggressive forms of cancer.[11] It is not yet known whether higher levels of vitamin D prevent more aggressive forms of prostate cancer or if aggressive prostate cancer lowers levels of vitamin D. Since it is impossible to know if low levels of vitamin D is a cause or effect of aggressive prostate cancer, and since high levels of vitamin D can be dangerous, more research is needed before experts will know if men diagnosed with prostate cancer should try to take more vitamin D.

Bottom Line: We need studies to determine exactly how diet and dietary supplements can be used to prevent prostate cancer and slow its spread. Meanwhile, men should reduce saturated fats as much as possible. While the jury is still out on phytoestrogens, men may benefit from eating more soy products—especially if they are eating them in place of red meat!

For more on cancer and antioxidants, read here.

All articles are reviewed and approved by Dr. Diana Zuckerman and other senior staff.

  1. American Cancer Society. Key Statistics for Prostate Cancer. Cancer.org. https://www.cancer.org/cancer/prostate-cancer/about/key-statistics.html. Updated 2020.
  2. Narita, S., Nara, T., Sato, H., Koizumi, A., Huang, M., Inoue, T., & Habuchi, T. (2019). Research evidence on high-fat diet-induced prostate cancer development and progression. Journal of clinical medicine, 8(5), 597.
  3. Ma R, Chapman K. A systematic review of the effect of diet in prostate cancer prevention and treatment. Journal of Human Nutrition and Dietetics. Vol (22)2009:187-199.
  4. Ganry O. Phytoestrogens and prostate cancer risk. Preventive Medicine. Vol (41) 2005:1-6.
  5. Ward H, Chapelais G, Kuhnle GC, Luben R, Khaw KT, Bingham S. Lack of Prospective Associations between Plasma and Urinary Phytoestrogens and Risk of Prostate or Colorectal Cancer in the European Prospective into Cancer-Norfolk Study. Cancer Epidemiology Biomarkers & Prevention Vol (17) 2008: 2891-2894.5
  6. Bosland MC, Kato I, Zeleniuch-Jacquotte A, Schmoll J, Rueter EE, Melamed J, Kong MX, Macias V, Kajdacsy-Balla A, Lumey LH, Xie H, Gao W, Walden P, Lepor H, Taneja SS, Randolph C, Schlicht MJ, Meserve-Watanabe H, Deaton RJ, & Davies JA. Effect of soy protein isolate supplementation on biochemical recurrence of prostate cancer after radical prostatectomy. JAMA 2013; 310(2): 170-178. doi: 10.1001/jama.2013.7842
  7. Duffield-Lillico AJ, et al. Baseline characteristics and the effect of selenium supplementation on cancer incidence in a randomized clinical trial: A summary report of the Nutritional Prevention of Cancer Trial.Cancer Epidemiology, Biomarkers, and Prevention. Vol (11) 2002: 630-639.
  8. Kristal AR, et al., Baseline Selenium Status and Effects of Selenium and Vitamin E Supplementation on Prostate Cancer Risk.  Journal of the National Cancer Institute, 2014.
  9. Chan JM et al. Plasma Selenium, Manganese Superoxide Dismutase, and Intermediate-or High-Risk Prostate Cancer. Journal of Clinical Oncology. Vol (27) 2009: 3577-3583.
  10. Thomas, R., Williams, M., Sharma, H., Chaudry, A., & Bellamy, P. (2014). A double-blind, placebo-controlled randomised trial evaluating the effect of a polyphenol-rich whole food supplement on PSA progression in men with prostate cancer—the UK NCRN Pomi-T study. Prostate Cancer and Prostatic Diseases, 17(2), 180-186.
  11. Nyame Ya, et al. Associations between serum vitamin D and adverse pathology in men undergoing radical prostatectomy. J Clin Oncol. 2016 Feb 22.