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


Cherries


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.

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

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.