A Reconsideration for Prevention over Treatment

As professionals, we are overwhelmed with the day-to-day medical model diagnosing disease.  We focus instead on rendering the therapeutic option that holds infinitely more benefit than risk.  The traditional “SOAP” note approach mandates reaction to a prior human insult.  We do homage to the preventive side of medicine by administering vaccinations, submitting serum samples when we have a high index of suspicion, and reporting positive cases to government medical officials.  Still, we miss the opportunity to exercise primary prevention in our practices by applying medical knowledge to keep disease at the doorstep.  We must recognize we are treating a developed-status population.  Developed status brings chronic disease such as cancer, which has become our mission.  Recently, ovarian cancer became the ninth in a growing list of obesity-associated cancers. We must reconsider our obligatory role in primary prevention to see how it can improve our therapeutic model, perhaps secondarily augmenting our profitability.

The risk factor of heightened body fat and cancer in certain cancers is nothing new.  Nine cancers have a risk association with body fat, now, according to The American Institute for Cancer Research and the World Cancer Research Fund. Ovarian cancer is the most recent addition.  Previously, it has been known that kidney, pancreas, thyroid, gallbladder, colon and rectum, esophagus, endometrium, and breast cancer in post-menopausal women had direct associations.  We are keenly aware how abdominal body fat affects hormonal and growth factor levels ranging from insulin resistance to chronic hyperinsulinemia, heightened bioavailability of steroid hormones and localized inflammation. This influences dysregulation and activation of cancer cell development.  The obese person, sadly, provides a persistent, low-grade chronic inflammatory state that is fodder for enhanced atypical cellular formation.  According to 2007 USA SEER data (NCI Surveillance, Epidemiology, and End Results) it is thought that approximately 34,000 new cases of cancer in men or 4 percent and 50,500 in women or 7 percent were attributed to obesity.

Body fat, when measured in amounts that are still marginally above 25%, especially displaced about the abdomen, are associated with these findings of increased risk.  This includes well over half of the current population.  Admittedly, the risk factor of obesity, specifically body fat, is marginal at 5% in most of the ten obesity-associated cancers.  Still, when considering the remaining risk factors (usually genetic) are not modifiable, it stands to reason that we should participate in that risk factor that is inherently modifiable.  Additionally, since the public has already accepted the concept of prevention and health as a way of life, our leadership as providers is a natural evolution.

Active Implementation of Further Recommendations

We are quite aware of the recommendations for weight control.  One is suggesting the patient find some form of physical activity for at least 30 minutes a day. We can suggest the patient combine physical activity into the regular functions of the day. Examples might be using the stairs or riding a bicycle instead of the elevator or driving a vehicle so the person benefits without noticing the effort.   The second is to eat a limited calorie diet while avoiding sugar-infused sodas, fast foods, and processed foods that have fat, low fiber or high sugar.  Suggesting the patient eats more fiber, fruits and vegetables are already familiar to the public.  So we can further suggest limiting red meat consumption to 18 ounces a week, avoiding processed meats that are cured, smoked, salted or chemically preserved (ham, bacon, and hot dogs), and replacing this with white meats and fish.  Our endorsement makes it official.

These primary prevention concepts are simple suggestions impartible to our patients with each encounter.  Recently, this education has become a billable and reimbursable event.  In this world where the business of medicine is more business than medicine, it becomes prudent to consider this simple preventive measure to reduce cancer incidence.  There are now many more reasons to add this to our practices.  Simple calculators have become available to identify how participating primary prevention actively can benefit your practice.  It is time we reconsider our essential role in primary prevention, improve our therapeutic model, and protect our profitability.

 

References:

Arab, SJ, Steck SE, Ang A, Fontham ET, Bensen JT, Mohler JL. (2013). Adherence to World Cancer Research Fund/American Institute for Cancer Research lifestyle recommendations reduces prostate cancer aggressiveness among African and Caucasian Americans. Nutr Cancer. 65(5). pp. 633-43. DOI: 10.1080/01635581.2013.789540.

Calle, EE & Kaaks, R. (2004). Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nature Reviews Cancer. 4: 579-91. DOI:10.1038/nrc1408.

Engeland, A, Tretli, S, and Bjørge, T. (2003). Height, Body Mass Index, and Ovarian Cancer: A Follow-Up of 1.1 Million Norwegian Women. JNCI J Natl Cancer Inst. 95(16). pp.1244-48. DOI: 10.1093/jnci/djg010.

Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective, Second Expert Report. (2014). The American Institute for Cancer Research and the World Cancer Research Fund. Retrieved May 5, 2014 from http://www.dietandcancerreport.org/ and http://www.aicr.org/assets/docs/pdf/reports/Second_Expert_Report.pdf.

Obesity and Cancer Risk. (2012). National Cancer Institute at the National Institutes of Health. Retrieved May 5, 2014 from http://www.cancer.gov/cancertopics/factsheet/Risk/obesity.

Ovarian Cancer 2014 Report: Food, Nutrition, Physical Activity, and the Prevention of Ovarian Cancer (2014). The American Institute for Cancer Research and the World Cancer Research Fund. Retrieved May 5, 2014 from http://www.aicr.org/continuous-update-project/reports/ovarian-cancer-2014-report.pdf.

Pizer, ES, Wood, FD, Heine, HS, Romantsev, FE, Pasternack, GR, and Kuhajda, FP. (1996). Inhibition of Fatty Acid Synthesis Delays Disease Progression in a Xenograft Model of Ovarian Cancer. Cancer Res. 56: 1189. Retrieved May 5, 2014 from http://cancerres.aacrjournals.org/content/56/6/1189.full.pdf+html.

Sellers, TA, Gapstur, SM, Potter, JD, Kushi, LH, Bostick, RM, and Folsom, AR. (1993). Association of Body Fat Distribution and Family Histories of Breast and Ovarian Cancer with Risk of Postmenopausal Breast Cancer. Am. J. Epidemiol. 138 (10). pp. 799-803.

 

 

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