Friday, May 28, 2010

Weekday Vegetarian: Practicing What I Preach

Most of the CNiC team is pretty good about practicing the cancer prevention tips we offer up, but last week’s "weekday vegetarian" post (link) got me thinking, and this week, I implemented the weekday vegetarian program in my house (well for dinners at least, and my own lunches). For those of you thinking about giving it a try, here’s how we implemented it.

Knowing that a week’s worth of new recipes was a lot of work and a big risk (there is nothing worse than trying a new recipe and having it be a failure and feeling like you’ve wasted all that time and money. Doing that two nights in a row is a non starter). So I pulled out Mark Bittman’s How to Cook Everything Vegetarian knowing that the dinners of Bittman’s that we’ve made from How to Cook Everything are always winners (ditto on his Minimalist column recipes) and grabbed a couple recipes that looked good. I also pulled out one of my “go to” cookbooks with the intention of taking the meat out of a recipe we love. I selected a Giada De Laurentiis’ Everyday Italian, which holds a number of family favorites.

For Monday, I picked a baked rice stuffed tomato from Bittman’s book because I know we’ve had stuffed tomatoes and peppers before – so the concept wasn’t new and I know that my friend Natalie’s beef stuffed peppers are one of my husband’s favorites. The recipe calls for a rice or grain, some grated cheese, onion and garlic. I used a frozen bag of Trader Joe’s brown rice, some grated Gruyere, and added in ½ c of mushrooms hoping that the “meaty” flavor and texture would make the meatlessness of the dish less noticeable.

Verdict: a BIG (huge!) hit. We loved it. The stuffing was flavorful and delicious. I paired it with a simple green salad and that was a full and satisfying meal. Another bonus – I did all of the prep ahead of time – making the filling and stuffing the tomatoes – and threw them in the fridge. The only thing to do at dinner was heat the oven and bake!

On Tuesday, I turned to Everyday Italian and picked a pasta with turkey Italian sausage, mushrooms and peas recipe. It is a family favorite and the simple step of leaving out the sausage makes the dish vegetarian. I wondered if we’d miss it. Leaving out the sausage was easy and the dish came together well. I swapped in whole wheat fusili, because we tend to only use whole wheat and that’s just what we had. I also upped the mushroom content from 10 ounces to about 16.

Verdict: It is still a great pasta dish without the sausage. If I hadn’t known it was a “tweaked” recipe, I wouldn’t have thought twice about it. The sausage definitely adds something extra so I will surely make it that way again (some weekend!), but this is a great (and easy) weeknight dinner.

Wednesday was the day to try out a “classic” vegetarian – black beans and yellow rice. Again, I turned to Bittman’s cookbook for both recipes. I selected his classic yellow rice – substituting short grain brown rice for the white rice. The recipe includes onion, red bell pepper and peas. It also calls for vegetable stock, which we didn’t have. So there was a small cheat – we used homemade chicken stock. Since this meant using all of the chicken we’d had for Sunday dinner a few weeks back, I didn’t feel so “ungreen” by doing this. I went with a beer-based black bean recipe that calls for onion and chili powder. On Tuesday night, I threw the black beans in the slow cooker and they cooked overnight. In the morning, I drained the beans and added them to the onion/beer mix. Once combined, I tossed them in a bowl in the fridge to reheat at dinner.

Verdict: Everyone was decidedly less enthusiastic about this meal. I thought the rice was fantastic, but I had underseasoned the beans and they were bland. I don’t know if everyone was worn out from vegetarian dinners, but the saving grace was pulling out the vanilla ice cream and homemade strawberry sauce at the end of dinner.

Thursday, I’d intended to serve up a lentil and cashew recipe I printed out from somewhere once and had in my recipe binder, but with plenty of leftovers from the pasta and rice and beans, I didn’t need to cook dinner. The real bonus here for me is that the main components of the dish I’d planned all keep for a long time in the pantry so I’ve got a dinner ready to pull together when I need one.

Friday. Friday is Mama’s night off from cooking so this week we ordered pizza – ½ cheese and ½ mushroom. No surprises here – pizza never disappoints. (provided you can find a good New York style pizza, which can be a challenge in the Midwest. Thankfully St. Louis has a couple great places).

Wednesday, May 19, 2010

Workaday Vegetarian: Lower Your Risk with "Weekday Veg"

Related post: Putting "weekday veg" into practice

A lot of us tend to have an all or nothing approach to life, but oftentimes charting a course down the middle can have a lot to offer as well.  In fact, the goal of most public health efforts are modest changes that when spread out over the entire population can actually have huge health benefits (see related post).

In this vein, we want to share this short four minute video from the 2010 TED conference featuring Graham Hill of, who makes a compelling, real-world case for going vegetarian during the work week (video).  From a health standpoint, cutting back on red meat (especially processed meat) can help lower the risk of certain cancers as well as heart disease. And just like you don't need to run marathons to benefit from physical activity, you don't need to subsist totally on nuts and flax to get a health boost from your diet.

Simple, real-world changes can make a real difference, and you'll still have the option to enjoy those weekend barbecues.

Childhood Leukemia: Environmental Toxins and Pesticides in Cancer Risk

Much media attention has focused lately on the links between environmental exposures and cancer risk (see related post), and a new study out this month further confirms the confined effects such exposures seem to have on the risk of cancer.

In a new study published this month in the journal Cancer Causes and Control, researchers report on a very detailed review of the published studies addressing occupational exposure to pesticides and the risk of childhood leukemia (see Van Maele-Fabry et al, 2010).  All studies published through July of 2009 are included in this systematic review of evidence. Established methods are used to combine the results from 25 studies.

From this extensive analysis we see that occupational exposure to pesticides among women increases the risk of childhood leukemia in their children. However, there was no association for exposure of the father and risk of leukemia. Importantly, the report evaluated the timing of exposure specifically addressing exposure before pregnancy, during pregnancy, and after pregnancy. Risk was elevated for exposure both before and during pregnancy. For women, exposure to insecticides, herbicides, and fungicides increased risk. While occupational exposure was associated with risk, a more general classification of "farming" was not related to risk.

These occupational data suggest that the specific exposure to pesticides, rather than merely an assumption from the classification of occupation, is necessary to uncover the relations between exposure to pesticides and risk of childhood leukemia.

Another rigorous study that evaluated the relation between environmental occupational exposures and cancer was reported some five years ago (see Boffetta, 2004). This report also rigorously reviewed the published literature through 2002. Boffetta concluded that approximately 2 percent of cancer is caused by occupational exposures. While much concern in the recent report from the President’s Cancer Panel focused on the fact that the early estimates of the proportion of cancer caused by environmental exposures by Doll and Peto had not been updated since 1980, these two reports exemplify the substantial body of research that has continued to quantify the impact of occupational and environmental exposures on the cancer burden in society.

With these rigorous updates, we are reassured that the estimates continue to support a burden that is in the range of 4 to 6% of cancers caused by occupational and environmental exposures.  This makes such exposures an important cause of cancer, to be sure, but one that is responsible for a much smaller percentage of cancers compared to lifestyle factors like tobacco use and obesity.

Works cited:
Van Maele-Fabry G, Lantin AC, Hoet P, & Lison D (2010). Childhood leukaemia and parental occupational exposure to pesticides: a systematic review and meta-analysis. Cancer causes & control : CCC, 21 (6), 787-809 PMID: 20467891

Boffetta, P. (2004). Epidemiology of environmental and occupational cancer Oncogene, 23 (38), 6392-6403 DOI: 10.1038/sj.onc.1207715

Monday, May 17, 2010

Health Food vs Healthier Food: Trying the White House Fruit and Oat Bars.

I’ve had enough awkward cocktail party conversations by this point in my career to realize that once you say you work in cancer prevention, most people think those of us on this side of things live austerely and subsist on nothing but nuts, twigs and grass. I can’t speak for all prevention researchers, but for me, that doesn’t capture things at all.

Most of the time, I try to eat “well” and prepare “healthy” food for my family. That means lots of fruits and vegetables, not much red meat and using whole grains instead of “white” grains. But everyone in my house enjoys a good dessert, including me.

Usually, when it comes to dessert, my philosophy is to go at the preparation without holding anything back – that means cream and butter when called for and sugar. Because as far as I’m concerned, dessert isn’t dessert without a sugar of some kind (and that includes maple sugar, honey and brown sugar, not just the good ol’ white stuff). And I don’t feel guilty about this because we keep our portions small and dessert is an occasional treat, not a nightly occurrence.

So I was intrigued when reading about the White House Pastry Chef , Bill Yosses, in the New York Times (story/recipe). Yosses has a formidable task as pastry platters seem to be present at every meeting in the White House. And because the White House is home to two VIK’s (Very Important Kids), Yosses tried to create a kid friendly sweet treat to replace cookies. The result is a granola-like fruit and oat bar.

Granola is certainly no health food – it has plenty of sugar on top of the oats and dried fruit. But it is healthier food – an alternative to a cookie or cupcake when you want something sweet with a bit less guilt.

So I decided to give Yosses’ recipe a whirl and have it taste-tested by two very different audiences – my toddler and husband, who are both very traditional when it comes to dessert (i.e. a dessert should clearly be dessert) and a small dinner party of public health professionals.

Yosses’ recipe has several opportunities for adaptation so here’s what I did after prepping my 9 inch square baking pan with oil brushed parchment.

Toasted 2 c of rolled oats with ½ cup of pumpkin and sesame seeds in the oven at 350 for 8 minutes. My seed blend was mostly pumpkin seeds.

Chop up 1 ½ c of dried fruit.

Mine was a mix of apricots


Dried blueberries, dried mission figs and candied ginger

After the oats and seeds were done, I tossed them with the dried fruit and 1 teaspoon of ground cardamom.

Combine in a saucepan ½ c honey, 1/3 c dark brown sugar, 1/3 c maple syrup, pinch of salt and 6 T of canola oil and stir until combined and sugar is dissolved.

Pour over the oat, seed, fruit mix and stir to combine.
Spread in the pan and even the top.

Bake for 25 minutes. Remove from oven and place on rack to cool completely.

 Using paper overhang, remove from pan and cut into bars.

The reviews

The bars were pretty sticky and hard to cut, but the bits that stuck to the paper tasted pretty good. The cardamom flavor was a nice break from the usual granola flavors but a bit strong. When I sampled the final product, I liked it. It certainly isn’t going to bring the same result in a dinner party guest as those whoopie pies I made last month, but these have some redeeming value, and Chef Yosses’ goal wasn’t to make a decadent dessert. I’m sure his whoopie pies would put mine to shame.

My daughter was very excited that mama was baking, but when I handed her a bite she looked puzzled. While she loves fresh blueberries and will eat close to her body weight in one sitting after a normal sized meal, she has never been a fan of blueberries IN other food – blueberry bagels are not appealing, nor are blueberries in pancakes. She took one look and asked if the bar had blueberries in it. When I confirmed her suspicion, she asked me to remove them. As you can probably guess from the pictures above, that isn’t really feasible. When informed of this, she handed the bar back and went back to her coloring book. My husband had a slightly better response – he at least tried it. His review: “It’s alright. I wouldn’t crave it.” He too found the cardamom flavor a bit strong.

In the interest of allowing my “study participants” to be fully aware of the circumstances, I shared my “experiment” with my dining companions before dessert was served. The assessment of the guests was similar to mine – they liked the flavor combination, but thought it would be better with a bit less cardamom. They, however, thought it was a perfectly good dessert.

The verdict

All in all, I’d say there is no surprise why so many folks are impressed with Mr. Yosses. The bars are a great alternative to cookies and I think would be a great thing to take to a school function where kids and parents have traditionally expected a dessert, but a healthier alternative might be appreciated. I would have been thrilled to get these as our post-game treat during my adolescent soccer career instead of a packaged store cookie, but my husband would probably have picked the chocolate cream sandwich cookie from the store. I think they’d also make a great alternative to the cookie plates that sometimes appear at 3pm meetings and lectures around some hospitals and universities. And I’m sure they’d be a welcome addition to a BBQ or pot-luck, though some folks may choose the slice and bake cookies first.

Wednesday, May 12, 2010

Of Maps and Cancer Clusters: When Good Data Go Bad

Often on CNiC we highlight the power of data and how valuable it can be in providing key information about the causes of cancer and the success, or failure, at interventions designed to prevent or treat it.

This week, New York State released the first set of maps that allow individuals to map cancer cases and align them with various locations, like power plants and waste storage facilities (map). While data and maps can be powerful and fascinating tools (my personal favorite this week is the Die-Hard baseball fan graphic), the New York maps fail to account for some key data points.

In the past, this type of map was used to identify potential locations of “cancer clusters” – areas where people felt the number of cancer cases was particularly high. But, when researchers looked closer, nearly all of these cancer clusters were explained by other factors that also tended to cluster in these areas. For example, cancer is a disease of age – age is one of the strongest risk factors for the most common cancers. As a result, areas where there is a high prevalence of older adults, will have more cases of cancer. Similarly, breast cancer rates are higher in Ashkenazi Jewish women, so a town or county that has a high number of Ashkenazi Jewish women, like certain suburbs of New York City, should be expected to have a higher rate of breast cancer than a town or county further upstate where there are fewer Ashkenazi Jewish women.

Cancer is also a disease that develops over many years, unlike infectious diseases like the flu or acute incidents like salmonella poisoning. Mapping of diseases can be extremely valuable in those instances as it can identify a possible geographic location for the outbreak (i.e., a grocery store selling tainted chicken or the mapping of the 2003 SARS outbreak). But in the case of cancer, the location where an individual lives at the time of diagnosis may have little to do with the relevant exposures or risks for when the cancer developed. As we noted in an earlier CNiC post, we are increasingly finding a role for early life exposures in cancer risk. Cancer maps like those from New York provide little to no context for such risks.

As a result, any mapping of this kind is a useful tool in the context of a much larger and more detailed investigation of cancer rates, but should be used with extreme caution, if at all, otherwise.

For more on this, check out the National Cancer Institute's Cancer Cluster Page

Tuesday, May 11, 2010

Environmental Contaminants: Recent Media Coverage Misleads on Preventability of Cancer

Coverage of the President’s Cancer Panel report this week draws attention to environmental contaminants as a potential cause of cancer (report). While this is an area of much public interest and certainly an important part of comprehensive health policy, it is a strange focus for a report that is meant to influence the nation’s approach to cancer control and prevention. The excitement and fear this report is likely to stir up could direct efforts away from combating known lifestyle factors that have a much larger effect on cancer risk than environmental contaminants (see figure). Current evidence shows that pollutants cause just 1 - 4 percent of all cancer, while obesity and tobacco each cause 20 percent and 30 percent, respectively. Even when occupational exposures are added in, lifestyle factors trump environmental factors by at least a factor of six.

At a time when we know we’re in the midst of an obesity epidemic and we know that we’re not as physically active as we should be and we know that 20 percent of the population still smokes, why focus so much effort exploring a topic we also know has such a modest impact on risk? At its worst, it plays into the hands of tobacco companies and food manufacturers by deflecting discussions of harsher regulations onto other fields. If we acted with passion to remove causes of cancer as is proposed in the report for plastics, then clearly tobacco products would have been banned decades ago.

It’s only natural for humans to search for a magic bullet, that one thing that can easily fix it all – easily erase our cancer risk. Better studying and controlling environmental pollutants is an easy projection for this. But, the evidence clearly shows this would be no magic bullet. More than half of all cancer can be prevented with what we know today, and pollutants make up only a small part of this.

Below we summarize the known causes of cancer.

1. Tobacco
Established as the primary cause of cancer-related deaths and considered the single largest preventable cause of cancer in the world (1), the impact of tobacco on international health is hugely detrimental. Tobacco smoking causes bladder, cervical, esophageal, kidney, laryngeal, lung, oral, pancreatic, and stomach cancers and acute myeloid leukaemia (AML) (2). In the United States alone, smoking causes at least 30 per cent of cancer deaths annually; globally tobacco will kill more than five million people. Risk increases with daily consumption as well as duration of smoking. Second hand smoke poses significant risk as well, which makes tobacco the only legal consumer product that can harm everyone exposed to it.

Stopping smoking reduces future risk of cancer. For example, the reduction in risk of lung cancer is rapid with 50 percent risk reduction in less than 10 years (3). After more than 20 years, risk drops to near that of a never smoker.

2. Alcohol consumption
Alcohol is estimated to cause 4 per cent of all cancers in high income countries (4), with a higher burden in men than women, reflecting overall intake. Health risks increase with heavier drinking leading to oral cavity, pharynx, larynx, oesophagus, liver, breast and colorectal cancers (5). Risks increase further when heavy alcohol use is combined with smoking.

3. Physical activity
Globally, inactivity causes close to 2 million deaths each year (6). Lack of activity is linked to most major chronic diseases, including type II diabetes, osteoporosis, stroke, cardiovascular disease, and cancer. Based on a well-designed systematic review of published evidence, the World Cancer Research Fund reports there is “convincing” evidence that physical activity decreases risk for colon cancer, “probable” evidence of a decrease in postmenopausal breast cancer and endometrial cancer, and “suggestive” evidence of an impact on lung, pancreas, and premenopausal breast cancer (5). Growing evidence also points to physical activity substantially lower the risk of premenopausal breast cancer (7, 8) as well as other chronic diseases.

4. Weight control
Obesity is increasing at epidemic rates around the world (9). United States data from 2003-2004 show that 66 percent of adults are overweight or obese (BMI ≥25) and 32 percent of adults are obese (BMI ≥ 30). Since 1988, these rates have been steadily increasing (10).

Historical data from the past 25 years point to obesity as a cause of approximately 14 percent of cancer deaths in men and up to 20 percent of cancer deaths in women (11). These may be conservative estimates as the population has gained substantial weight over this time period, with the prevalence of overweight and obesity increasing from 15 percent in 1980 to 35 percent in 2005. The American Institute for Cancer Research (AICR) and World Cancer Research Fund (WCRF) reported there is convincing evidence for a relation between obesity and esophageal, pancreatic, colorectal, postmenopausal breast, endometrial and kidney cancers with probable evidence for cancer of the gallbladder. In addition, they found probable evidence that fat around the mid section (abdominal adiposity) in particular increases risk of pancreas, endometrial and postmenopausal breast cancer. Finally, emerging evidence suggests that obesity increases the risk of aggressive prostate cancer (12).

Overall, we estimate that overweight and obesity cause approximately 20 percent of all cancer. Previously, Doll and Peto (13) combined “overnutrition” (overweight) with diet and estimated that together they caused 35 percent of all cancer. We break out overweight and obesity from diet and provide updated estimates for the causes of cancer (figure).

The burden of obesity has increased so much that some now estimate that the total health burden of overweight and obesity may exceed that for cigarette smoking (14).

Public health recommendations call for adults to stay within the recommended BMI range (18.5-24.9) and avoid weight gain.

5. Diet and dietary supplementation
aflatoxin and liver cancer, and salt and stomach cancer, while non-starchy vegetables reduce risk of cancers of the mouth, oesophagus, and stomach (5). Because of benefits in preventing other major chronic diseases such as cardiovascular disease and diabetes, it is estimated that a global increase in fruit and vegetable consumption would save 2.7 million lives annually (6).

International recommendations prescribe a diet high in fruits and vegetables (at least 4-13 servings per day) with emphasis placed on nutrient-rich green leafy vegetables, orange vegetables, and legumes. Avoiding certain foods potentially decreases cancer risk, such as salt-preserved meats or other foods, red meat, and very hot food or drinks. The U.S. National Cancer Institute (NCI) recommends that only 20-35 percent of daily calories be from fat; comprised of primarily polyunsaturated or monounsaturated fats in fish, nuts, and vegetable oils, 10 per cent saturated fats, and as little trans fat as possible (15).

Substantial evidence supports a link between vitamin D and reduced incidence of colon cancer – the third most common cancer among both men and women in the United States. Studies show that people with higher circulating vitamin D levels can have as little as half the risk of developing colon cancer as those with lower vitamin D levels (16). This and other possible benefits were reviewed systematically by the International Agency for Research on Cancer (IARC) (16), and led to the recommendation that better understanding of possible adverse health effects of population supplementation, and the possible variation in benefits depending on the baseline serum 25-hydroxyvitamin D level, are necessary before recommending routine vitamin D supplementation for cancer prevention. Further research is needed to define the optimal dose or level of vitamin D, its efficacy in reducing cancer incidence, and the time course for change in risk of cancer after increasing levels.

6. Sun Exposure
The sun, as the primary source of ultraviolet radiation, poses a significant risk of skin cancer particularly in fair-skinned individuals. Internationally, nearly 60,000 deaths are attributed to over-exposure leading to malignant melanomas and skin cancer annually (17). Observing trends of increasing rates of skin cancer, the U.S. National Cancer Institute reports 60,000 new cases in 2007 in the United States alone (15). Prevention recommendations as simple as avoiding the sun in peak hours (approximately 10 am to 3 pm), covering skin whenever possible, protecting exposed skin with sunscreen, and avoiding tanning booths are effective in reducing skin cancer incidence if these lifestyle changes are adopted, particularly, at an early age.

7. Infections
Some 18 per cent of cancers worldwide can be linked to chronic infections due to agents such as Helicobacter pylori, human papillomaviruses (HPV), Hepatitis B, Hepatitis C, Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), human herpes virus 8 (HHV-8), and Schistosoma haematobium (18), with the proportion of all cancer due to infections being much higher in developing countries (26 per cent, compared to 7.7 per cent in developed countries). The current burden of cancer in the developing world is dominated by infection, once smoking is accounted for. (See related post) .

8. Environmental and occupational exposures
Environmental exposures account for 1-4 percent of cancers. Occupational exposures such as asbestos, arsenic in drinking water, food contaminants such as aflatoxins and pesticides, and radiation exposure are classified as environmental carcinogens, but in countries with established market economies, exposure is now largely limited by regulation to reduce harm. International agencies have responded by identifying carcinogens (e.g., IARC classification of carcinogenic compounds) and regulating use, exposure, and protection for employees in the case of occupational hazards.

As better regulations of contaminants have been put into place in the most developed countries, production has been exported, in some cases, to countries with more lenient requirements for environmental exposure and contaminants thereby not eliminating, but shifting, the cancer risk from an international scope. Despite regulatory changes in many countries, exposure to asbestos, for example, continues through occupations such as construction, ship work, and asbestos mining. Given the long lag between exposure and lung and pleural cancers, mortality from asbestos-related disease is estimated to remain at 90,000 per year (19).

Successful enforcement of approaches to reduce exposure to known carcinogens in both the work place and the home is necessary to achieve successful cancer prevention.

9. Medications
Medication use is widespread in high income countries and limited in low and middle income countries. Strong evidence supports several medications as either causing cancer – for example, postmenopausal hormone therapy with estrogen plus progestin (20) - or reducing cancer - for example, oral contraceptives and ovarian cancer (21), and aspirin and colon cancer (22).

For combination estrogen plus progestin, the IARC has now classified this combination therapy as carcinogenic in humans (23) and estimates indicate that the reduction in use of hormones after the widespread publicity of the results of the Women’s Health Initiative (stopped early due to excess breast cancer) accounts for approximately a 10 percent decline in incidence among women 40 - 70 years of age (20). Thus for this combination therapy, evidence shows that risk rises with duration of use and that acting as a late promoter, removal of the drug leads to a rapid decline in incidence (20), though among women with longer durations of use risk may not return to that of women who have never used combination therapy (24). Other less widespread drugs may also contribute to cancer risk (such, DES), but the population impact will be substantially smaller because of their relatively low use in the population.

For some medications that reduce risk, the benefits have been limited to date to those who have had specific indications for use of the medication. Broader population strategies may be developed for more widespread protection, such as could be achieved if all women took oral contraceptives as a chemopreventive for a minimum of 5-years

Related CNiC posts:

Literature cited:
1. Peto, R., et al., Mortality from smoking worldwide. Br Med Bull, 1996. 52(1): p. 12-21.

2. U.S. Department of Health and Human Services, The health consequences of smoking: a report of the Surgeon General. 2004, Centers for Disease Control and Prevention: Washington, DC.

3. Kenfield, S.A., et al., Smoking and smoking cessation in relation to mortality in women. Jama, 2008. 299(17): p. 2037-47.

4. Danaei, G., et al., Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors. Lancet, 2005. 366(9499): p. 1784-93.

5. World Cancer Research Fund, Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. 2007, Washington, DC: AICR.

6. Ezzati, M., et al., Selected major risk factors and global and regional burden of disease. Lancet, 2002. 360(9343): p. 1347-60.

7. Bernstein, L., et al., Physical exercise and reduced risk of breast cancer in young women. J Natl Cancer Inst, 1994. 86(18): p. 1403-8.

8. Maruti, S.S., et al., A prospective study of age-specific physical activity and premenopausal breast cancer. J Natl Cancer Inst, 2008. 100(10): p. 728-37.

9. International Agency for Research on Cancer, Weight Control and Physical Activity. IARC Handbook on Cancer Prevention. Vol. 6. 2002, Lyon: International Agency for Research on Cancer. 315.

10. Ogden, C.L., et al., Prevalence of overweight and obesity in the United States, 1999-2004. JAMA, 2006. 295(13): p. 1549-55.

11. Calle, E.E., et al., Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med, 2003. 348(17): p. 1625-38.

12. Freedland, S.J. and E.A. Platz, Obesity and prostate cancer: making sense out of apparently conflicting data. Epidemiol Rev, 2007. 29: p. 88-97.

13. Doll, R. and R. Peto, The Causes of Cancer: Quantitative Estimates of Avoidable Risks of Cancer in the United States Today. 1981, New York: Oxford University Press.

14. Stewart, S.T., D.M. Cutler, and A.B. Rosen, Forecasting the effects of obesity and smoking on U.S. life expectancy. N Engl J Med, 2009. 361(23): p. 2252-60.

15. National Cancer Institute, Cancer Trends Progress Report – 2007 Update. 2007, NIH, DHHS: Bethesda, MD.

16. International Agency for Research on Cancer, Vitamin D and Cancer. 2008, International Agency for Research on Cancer: Lyon.

17. World Health Organization, The World Health Organization's Fight Against Cancer: Strategies that prevent, cure, and care. 2007, World Health Organization: Geneva.

18. Parkin, D.M., The global health burden of infection-associated cancers in the year 2002. Int J Cancer, 2006. 118(12): p. 3030-44.

19. World Health Organization, Elimination of Asbestos-related Disease, in Public Health and the Environment. 2006, World Health Organization: Geneva.

20. Colditz, G.A., Decline in breast cancer incidence due to removal of promoter: combination estrogen plus progestin. Breast Cancer Res, 2007. 9(4): p. 108.

21. Collaborative Group on Epidemiological Studies of Ovarian, C., et al., Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23,257 women with ovarian cancer and 87,303 controls. Lancet, 2008. 371(9609): p. 303-14.

22. Chan, A.T., et al., Long-term use of aspirin and nonsteroidal anti-inflammatory drugs and risk of colorectal cancer. JAMA, 2005. 294(8): p. 914-23.

23. International Agency for Research on Cancer, Combined estrogen-progestogen contraceptives and combined estrogen-progestogen menopausal therapy. IARC Monogr Eval Carcinog Risks Hum, 2007. 91: p. 1-528.

24. Colditz, G.A. and B. Rosner, Cumulative risk of breast cancer to age 70 years according to risk factor status: data from the Nurses' Health Study. Am J Epidemiol, 2000. 152(10): p. 950-64.

Monday, May 10, 2010

Quick Facts About Soy and Health

Soy foods have been studied a great deal for their potential protection against a range of chronic conditions, including breast and prostate cancer, heart disease, osteoporosis, and menopausal symptoms.

It’s not known exactly how a diet rich in soy results in such benefits. It could be due to some of the individual components of soy, such as isoflavones which have some qualities similar to naturally occurring hormones. Or it could be the collective make up of soy, all its components together, which have the beneficial effects.

Because most pre-menopausal symptoms are linked to dropping levels of the hormone estrogen, it’s been considered that soy, and the insoflavones it contains, could help mimic natural estrogen and therefore quell things like hot flashes. Current evidence, though, suggests that soy intake actually has little impact on hormone levels. Still, research also suggest that a diet rich in soy may reduce menopausal symptoms (1).

The potential cardiovascular benefits from higher soy intake may be due to soy’s being a healthier replacement for some higher fat choices. Soy has only about 20 percent of its calories from fat, which is predominantly “healthy” polyunsaturated fat (2), whereas chicken can have nearly half of its calories from fat, and beef can have as much as 80 percent of its calories from fat, much of it in the form of “unhealthy” saturated fat. Studies looking at the relationship between soy intake and heart disease suggest that a diet rich in soy can improve blood pressure, blood cholesterol, and insulin levels (3).

Much of the interest in the links between soy intake and cancer risk is motivated by the historically low breast and prostate cancer risk among Asians, whose diets are traditionally high in soy. Detailed reviews by Wu and colleagues shows that at high intakes typical of Asian diets, soy is significantly related to a reduced risk for breast cancer, and the effect may be strongest for high intake in childhood and adolescence. A meta-analysis found that diets with high amounts of soy (20 mg per day of isoflavone) in Asian women was associated with a decreased risk for breast cancer, compared to Asian women consuming lower amounts (5 mg daily) (4). What this means for most American women is unclear. Studies in the US have typically not found a link between soy intake and breast cancer, but this could largely be due to widely different diets between the two regions. The highest intake in the US is typically 80 percent below the lowest intake in Asia (0.3 mg isoflavones/day in the US versus 25-50 mg isoflavones/day in Asia, which is equivalent to 1 g of soy food versus 80-160 g of soy food). Should diets shift to resemble those of Asia, it’s more than likely that studies would begin to reveal breast cancer benefits with soy as well.

Looking at the data on soy and prostate cancer, a number of studies show benefits from a higher intake of soy and soy-products. Soy milk intake was shown to be inversely related to risk of prostate cancer among US men in the Seventh Day Adventist Cohort study (5). As soy milk consumption went up, the risk of prostate cancer went down. A similar relationship has been seen between total soy intake and the risk of prostate cancer in other cohort and case-control studies (6), even though the amount of the effect on risk varied a bit from study to study. The only potential evidence that soy might increase the risk of prostate cancer comes from research of fermented soy (Miso), which has been positively related to risk in some studies.

Overall, there is currently little evidence that a diet high in soy is bad for health, and a growing body of evidence that it could have substantial health benefits. Realizing such potential benefits though, would likely take intake levels beyond what most people in the US typically eat.

Literature cited:

  1. Kurzer, M.S., Soy consumption for reduction of menopausal symptoms. Inflammopharmacology, 2008. 16(5): p. 227-9.
  2. van Ee, J.H., Soy constituents: modes of action in low-density lipoprotein management. Nutr Rev, 2009. 67(4): p. 222-34.
  3. Carlson, S., et al., Effects of botanical dietary supplements on cardiovascular, cognitive, and metabolic function in males and females. Gend Med, 2008. 5 Suppl A: p. S76-90.
  4. Wu, A.H., et al., Epidemiology of soy exposures and breast cancer risk. Br J Cancer, 2008. 98(1): p. 9-14.
  5. Jacobsen, B.K., S.F. Knutsen, and G.E. Fraser, Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States). Cancer Causes Control, 1998. 9(6): p. 553-557.
  6. Jian, L., Soy, isoflavones, and prostate cancer. Mol Nutr Food Res, 2009. 53(2): p. 217-26.

Sunday, May 9, 2010

Oral Contraceptives – 50 Years of Progress in Women’s Health

Numerous recent media reports highlight the historic progress in women's health with development and marketing of oral contraceptives. As Collins reported in the New York Times (column), we celebrate the 50th anniversary of the birth control pill. She notes the need for information on contraception and the challenges women had historically obtaining accurate data. Over the past 50 years much research has focused on contraceptives methods their risks and benefits. As we have noted previously, benefits of oral contraceptives can be substantial. Media attention, however, often focuses on potential adverse effects such as venous thrombosis and pulmonary embolism, the benefits of prevention are not identified at the individual level and hence often ignored.

Contraception avoids not only unintended pregnancies, but also millions of abortions and many pregnancy related deaths. These global benefits are detailed in a report from the Alan Guttmacher Institute in New York. (report). US data indicate that among women 15 to 49 years of age 72.8% are using a method of contraception, 21.2 % repot female sterilization, 9.7% male partner sterilization, and 18% are using contraceptive pills (report).

A rigorous systematic review of contraceptive methods and effectiveness shows that failure varies by approach and by the level of adherence to “perfect use” (review). Combining data from epidemiologic studies show significant reduction in risk of ovarian cancer, endometrial cancer and colon cancer as well as dysfunctional uterine bleeding, and ovarian cysts.

Risk of ovarian cancer is reduced by 20 percent for each 5 years of use. After 15 years of use a woman’s risk is half that of what it would be if she had never user the contraceptive pill. The benefit of reduced ovarian cancer persists after stopping use.

The combined evidence shows without doubt that the pill is safe and has major benefits including a reduction in the level of cancer among users. Like many other prevention benefits, particularly those for cancer, the time course is long and the beneficiaries are largely unknown. This time to benefit clearly contrasts with the immediate benefit related to the indication for using the pill - avoidance of conception – a benefit that is observed each month.  

Wednesday, May 5, 2010

Harnessing the Power of Data

The New York Times this weekend (story) featured a fascinating article on the role that data and monitoring are increasingly playing in our lives. Among other things, people routinely harness technology to monitor their own physical activity, daily schedules, and diets as well as to identify missed opportunities and potential causes of desirable outcomes. Research has shown that monitoring behaviors can help sustain those behaviors over time, something we discussed in a related post earlier this month (post). The New York Times, though, came at monitoring in a different way, showing how individuals also use monitoring to identify patterns or cause-and-effect relations in their lives - for example, one person used his own productivity data to show that, despite his assumptions, drinking coffee didn’t actually boost his productivity at work.

However people use it, one thing is clear: Data is powerful. This isn’t news. But the ways that data are collected and by whom is important. And although there are myriad minefields to avoid these days as our personal lives play out in an increasingly monitored world, the data that good monitoring provides can also prove invaluable to improving the health and well-being of the nation.

As noted by Dr. Howard Koh, Assistant Secretary of Health and Human Services, in this week’s New England Journal of Medicine, now is a great time to think about data (article). The federal government is about to set forth its own update of health indicators for the nation – something it has done every 10 years since 1979 in the form of the Healthy People initiative – called Healthy People 2020 (official site). Healthy People isn’t just data – it is about setting goals and monitoring our progress toward them using data.

The data show progress, or not, and help identify priority areas. In some ways, the lapses in progress have been one of the most important features – identifying how, despite numerous efforts across public and private, professional and grass-roots organizations, we haven’t made the progress we’d like.

Dr. Koh notes that we made progress toward the earlier Healthy People 2010 goals in just over half of the measureable objectives, and actually met the goal less than 20 percent of the time. This knowledge provides a new starting point – a way to identify a need for better coordination and cooperation among groups to leverage our limited public health resources in cost effective, scientifically effective, and efficient ways.

As Dr. Koh points out, improving health involves intersecting with many different segments of the population. In thinking about data, this means that key data for health might come from groups and sources that ostensibly have little to do with health indicators – for example, crime rates are often used in studies of physical activity because if an individual’s neighborhood has high rates of personal violent crimes, that individual is less inclined to go out for a walk after dinner.

Understanding these data is key to successfully measuring and intervening on health. They can show us not only where we’ve been but also where we need to go, and often how to get there.

The Skinny on Esophageal Cancer: Obesity, Tobacco, and Screening

While the rates of many cancers have remained stable over the past decade, the rate of some esophageal cancers has been rising, and the main culprit is likely the epidemic of overweight and obesity.

Squamous cell cancers of the esophogous , a cancer type largely caused by smoking, have remained stable. But adenocarcinomas of the esophagus (including the gastric-cardia) have been rising steeply in recent years, and aside from tobacco use, most of its main risk factors are tied directly or indirectly to weight .
Directly, obesity can induce inflammation throughout the body as well as increase levels of insulin and related hormones, both of which have been linked to an increased risk of cancer. Indirectly, obesity, is also closely tied to severe acid reflux (also known as GERD) and Barrett’s esophagus, a condition where the make-up of the cell lining of the esophagus changes. Obesity increases pressure on the abdomen and stomach, which may be part of the process by which it increases risk of reflux (see figure), which in turn can increase the risk of Barrett’s esophagus.

Adenocarcinoma of the esophagus generally arises from the changes that mark Barrett’s esophagus. Yet , only a relatively few individuals with reflux or Barrett’s esophagus go on to develop cancer. This points to a role for both lifestyle and genetic factors in the transition from Barrett’s esophagus to esophageal cancer. At present, we don’t have good indicators of who will progress from Barrett’s esophagus to esophageal cancer.

Currently, screening with endoscopy (a lighted tube inserted into the esophagus) is often recommended for those with sever reflux or Barrett’s esophagus to try to catch cancers early when they’re most treatable, or even find pre-cancers that can be removed before they turn into cancer. Unfortunately, such tests have yet to be shown to be effective. Individuals with Barrett’s esophagus who have regular endoscopies don’t live longer than those who do not have regular endoscopies. In part, this is because the test isn’t as precise as we’d like. Estimates are that only 10 percent of those with suspicious test results in a high risk population (like those with reflux) actually have cancer.

Even though the science of screening for esophageal cancer is still developing, there are important steps we can take right now that can reduce the risk of the disease, and they are increasingly important as rates of the disease overall keep increasing and more than half of all cases are diagnosed at a late stage. The most promising approach is to keep acting on what we already know: Continue to combat tobacco use and take steps to stem the national (and worldwide) epidemic of overweight and obesity.

Tuesday, May 4, 2010

Vaccination Against Hepatitis B Prevents Liver Cancer

As reported in the New York Times, San Francisco has launched an important public health campaign to promote vaccination against the hepatitis B virus which causes liver disease and liver cancer (story). This campaign is important for several reasons. Infection is usually silent and the impact on disease is many years after initial infection.

Prevention programs for cancer take different durations for the benefit to be observed. Vaccination programs offer one insight to the time frame of intervention and the ultimate reduction in cancer incidence. For cervical cancer prevention with human papilloma virus (HPV) vaccine, the current U.S. Center for Disease Control (CDC) recommends vaccination for women between ages 13 and 26; the benefit of this prevention will be observed many years hence. Hepatitis vaccination programs in Africa and Asia offer further illustration of these points. In the Gambia, a program launched in 1986 aims to evaluate the effectiveness of childhood vaccination with hepatitis B and current estimates are that the final outcome of reduced hepatocellular carcinoma in adults should be measurable from 2017 onwards. In Asia with nationwide hepatitis B vaccination implemented in Taiwan in 1984, results at 10 years show significant reduction in hepatocellular carcinoma in children. Clearly many years of follow-up are required to demonstrate protection of adults, though this outcome is implied by results to date.

The etiology of some 18 per cent of cancers worldwide can be linked to chronic infections due to agents such as Helicobacter pylori, human papillomaviruses (HPV), Hepatitis B, Hepatitis C, Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), human herpes virus 8 (HHV-8), and Schistosoma haematobium, with the proportion of all cancer due to infections being much higher in developing countries (26 per cent, compared to 7.7 per cent in developed countries). The current burden of cancer in the developing world is dominated by infection, once smoking is accounted for. Of 10.8 million new cases of cancer worldwide (2002 figures), those caused by infectious agents are estimated as: H. pylori 5.5 per cent (mainly stomach, and lymphoma); HPV 5.2 per cent (mainly cervix, and ano-genital, mouth, pharynx); HBV and HBC 4.9 per cent (liver); EBV 1.0 per cent (nasopharynx, Hodgkin lymphoma and Burkitt lymphoma), HIV and HHV-8 0.9 per cent (Kaposi sarcoma, non-Hodgkin lymphoma) and other less common agents including schistosomes, HTLV-1, and liver flukes, less than 0.5 per cent. More than 25 per cent of cancer incidence in developing countries could be avoided if infectious causes of cancer were prevented. Successful vaccination programs have the potential to reduce cancer incidence and mortality; for example, Taiwan’s HBV vaccination program was initiated in 1984, and impressively high coverage rates (up to 97 per cent in 2004) have led to a consistent decline in hepatocellular cancer rates. However, a recent study by Chang et al. underscores the importance of a multi-pronged approach. Though Taiwan has seen a decrease in the incidence of hepatocellular cancer in children since initiation of the vaccination program (from 0.54 to 0.20 per 100,000 before and after the program), vertical transmission, vaccine failure, and the lack of hepatitis B immunoglobulin injection has affected program effectiveness and public health impact.

Given the burden of infection with the virus in Asian Americans in California, estimated at 10% it is not too early to begin a major campaign such as that instituted in San Francisco.

Monday, May 3, 2010

Video - "Workplace Wellness: Good for Business, Great for You"

On his recent trip to Syndney, CNiC's Graham Colditz, MD, Dr PH, spent some time at the Cancer Council discussing the benefits of workplace wellness and some strategies that can make such programs successful (video).