A p u b l i c a t i o n o f t h e O N D P G
O N D P G We b s i t e
w w w. o n c o l o g y n u t r i t i o n . o r g
Winter 2010 Volume 18 No. 1
ISSN 1545-9896
With the help of our webmaster, Denise Snyder, MS, RD, CSO, LDN, our website continues to evolve. In the new year look for announcements about a new feature on the public side of our website that can assist the public in identifying oncology dietitians in their area. We also continue to make progress on publishing a hospice resource, in the form of an American Dietetic Association (ADA) Hospice Pocket Guide, authored by Anne Cox, MS, RD, for our members. At the 2009 Food & Nutrition Conference & Expo (FNCE), ON DPG hosted two successful sessions highlighting the importance of the oncology dietitian. Behind the scenes, through the unending efforts of Barbara Grant, MS, RD, CSO, LD and Kathryn Hamilton, MA, RD, CSO, CDN, the value of the Certified Specialist in Oncology (CSO) credential continues to be promoted. Barbara wrote an article for the Association of Community Cancer Centers’ (ACCC) journal “Oncology Issues” describing the CSO and the
requirements for the certification. Rhone Levin, MEd, RD, CSO, LD, past ON DPG chair, and Barbara Grant will both be presenting at the ACCC meeting this year. Newsletter editor, Maureen Leser, MS, RD, LD, CNSD, along with her team of associate editors, smoothly transitioned the newsletter to an electronic format. She continues to find new and exciting features for each issue. The Oncology Toolkit, authored by Laura Elliott, MPH, RD, CSO, LD, and Dianne Kiyomoto, RD, CSO, was field tested and revised late last year. These were the last steps necessary before this tremendous resource for evidence based oncology nutrition practice is available to everyone through the Evidence Analysis Library (EAL) website.
In my last 5 months as chair, I am working on our goals for the next year. We are already planning for our sessions and member reception at FNCE 2010 in Boston.
ON DPG Chair Message:
As I sit here in New Jersey recovering from the last
snowstorm and waiting for the next one, I was
reflecting on the accomplishments of the Executive
Committee of the Oncology Nutrition Dietetic
Practice Group (ON DPG) in my first seven months
as chair. Let me highlight just a few.
Oncology
Nutrition
Connection
IN THIS ISSUE
ON DPG Chair Message
page 1
A Note from the Editor
page 2
Alcohol Consumption and
Breast Cancer Risk
page 3
Professional Update
page 9
Case Study: Gastroesophageal
Cancer and Malnutrition
page 10
Oncology Nutrition News Brief:
Resveratrol and Cancer
page 17
ON DPG Member Spotlight:
Bethany Smith, RD, CSO, LD
page 19
Developing a Research Diet for an
Oncology Nutrition Feeding Trial
page 21
Division of Cancer Prevention,
National Cancer Institute
Fact Sheet
page 23
A Note from the Editor
Maureen Leser, MS, RD, LD, CNSD
[email protected]
In this second decade of the 21st century, the
benefit of oncology nutrition services is being
recognized at a time when competition for health
care dollars is fierce.
Oncology Nutrition Connection
A publication of Oncology Nutrition (ON), a dietetic practice group
of the American Dietetic Association (ADA) ISSN 1545-9896
Visit the ON DPG website at www.oncologynutrition.org
Oncology Nutrition Connection (ONC)(ISSN 1545-9896), the official newsletter of the Oncology Nutrition Dietetic Practice Group (ON DPG), is published quarterly. Each newsletter provides peer reviewed articles and therefore offers 0.5 CPEUs per issue. Members are responsible for recording and tracking their CPEUs in their Professional Development Portfolio (PDP) in accordance with PDP guidelines. Articles published in ONC
highlight specific diseases or areas of practice in oncology nutrition or related interest areas. ONCalso features information on upcoming meetings, book reviews, and special interest topics such as complementary care, hospice, cancer prevention, pediatrics, and survivorship. In 2010 the winter, summer, and fall issues will be distributed electronically only, and the spring issue will be distributed electronically and in print form. Viewpoints and statements in this issue do not necessarily reflect the policies and/or positions of the ADA or the ON DPG. Oncology dietitians are encouraged to review Evidence Analysis Library (EAL) positions of ADA, which provide a summary of the best available research on a variety of topics. The EAL can be accessed via the ADA website and @ http://www.oncologynutrition.org/oncology-resources/evidence-analysis-library. ©2009, Oncology Nutrition, ADA. All rights reserved. Oncology Nutrition Connectionis indexed in the Cumulative Index to Nursing and Allied Health Literature. For inquiries regarding copyright, single issue sales, and previous issues, contact the editor. Individuals interested in submitting a manuscript to Oncology Nutrition Connectionshould contact the editor at the above e-mail address or check the ON website for author guidelines.
Individuals who are ineligible for ADA membership can order yearly subscriptions to Oncology Nutrition Connectionfor $35.00 (domestic fee) and $40.00 (international fee), payable to ADA/ON DPG. Institutions can subscribe to Oncology Nutrition Connectionfor $50.00 (domestic yearly fee) and $65.00 (international yearly fee). ON DPG members have access to archived back issues in pdf format. Printed copies of back issues can also be ordered. Cost is $5.00 each for domestic ON DPG members ($10.00 if mailed internationally) and $10.00 each for domestic non-members ($15.00 each if mailed internationally), pending their availability. Send requests for subscriptions or back issues to the editor at the above address. All ON DPG member address changes should be sent to the ADA using the address change card in the Journal of the American Dietetic Association or at www.eatright.org in the members-only section.
In May, the Executive Committee of ON DPG will meet to discuss future projects. If you have suggestions or ideas that you feel would improve our practice group, please let us know. As always, if you are interested in becoming more involved in ON DPG contact me directly at
Thank you.
Maureen Huhmann, DCN, RD, CSO ON DPG Chair 2009-2010 Editor Maureen Leser, MS, RD, LD, CNSD 56 Boston Drive Berlin, Maryland 21811 [email protected] Associate Editors
Daria Pori, RD, CSO, LD [email protected]
Kimberlee Taylor, MS, RD, CSO, LD, CNSD [email protected]
These circumstances challenge oncology RDs to broaden their knowledge base and skills, and to demonstrate the benefit of their services through outcomes-based research. This issue of Oncology Nutrition Connection (ONC)provides several features that support the learning needs of oncology dietitians and demonstrates the need for oncology nutrition services.
In the United States (U.S.), the National Cancer Institute (NCI) expected about 192,000 new cases of breast cancer in women and 1,900 cases in men in 2009, with 40,000 deaths from this disease. A higher alcohol intake has been associated with increased risk of breast cancer, but does that
association pertain to all types of alcohol and any amount? And does wine’s phytochemical (including resveratrol) content exempt it from this association? Those questions are addressed in this issue of ONC. The winter 2010 issue also brings you a member spotlight and a Division of Cancer Prevention, NCI, fact sheet on vitamin D and cancer. But one of the main highlights of this issue is a case study submitted by a dietetic intern. Many of us can remember a patient or a challenge that inspired us to specialize in oncology. This intern’s case study dramatically demonstrates the need for nutrition screening and assessment in all health care settings, and the importance of nutrition intervention during chemoradiation therapy.
A new year frequently inspires contemplation; have you thought about want you want to accomplish in the field of oncology nutrition? Let ONChelp you achieve your professional goals. Share your learning needs. Tell us if you want more case studies, review articles, or news briefs. We also encourage you to share your knowledge with your colleagues
by writing articles and submitting case studies, and thank those RDs (and Dietetic Interns) who have already taken that step.
This issue of ONCoffers 0.5 CPEUs. Members are responsible for recording and tracking their CPEUs in their Professional Development Portfolio (PDP) in accordance with PDP guidelines.
Thanks!
ON DPG Chair Message:
What is an alcoholic drink?
One of the confounding factors encountered while reviewing the literature was lack of standardization on what constitutes a serving of an alcoholic beverage. The term alcohol refers to ethanol, which represents a family of alcohols produced by the fermentation process. While the most common alcoholic beverages include beers, wines and spirits, or liquor, other types include locally produced products such as fermented milks, fermented honey-water (mead), fermented apples (cider) and the
illegally produced “moonshine” (3). The alcohol content of all these beverages varies considerably. For the purposes of this review, the discussion is limited to beers, wines, and spirits/liquor. Table 1 lists the alcohol content, source of sugars used to produce the alcohol, and the recommended portion size of common alcoholic beverages.
Most research studies define the grams of alcohol that may constitute a serving of alcohol in their study, while health recommendations are made in terms of
low/moderate intake. Although there is no universal definition of the term “moderate intake”, the 2005 Dietary Guidelines for Americans define moderate intake as no more than one drink per day for women and no more than two drinks per day for men (4). A standard drink in the United States includes 13.7 grams (0.6 ounces) of pure alcohol. This translates to either 12 ounces of beer, 5 ounces of wine, 8 ounces of malt liquor or 1.5 ounces of 80-proof distilled spirits such as gin, vodka, rum or whiskey (Table 1) (5). Consequently, it is imperative that when evaluating the relevance of research studies we accurately quantify the amount of alcohol consumed. The sections below briefly discuss the role of alcohol in carcinogenesis, and some specific mechanisms of action by which alcohol may increase the risk of breast cancer.
Alcohol Metabolism and cancer risk
The liver is the primary site of alcohol metabolism, which involves three key pathways (6). The primary pathway used for ethanol metabolism involves alcohol dehydrogenase (ADH). Two additional pathways include the microsomal ethanol oxidizing system catalyzed by cytochrome P4502E1 (CYP2E1), and the nonoxidative pathway catalyzed by fatty acid ethyl ester synthase (6). None of these pathways act in isolation, and therefore metabolic consequences are dependent on the primary pathway used for ethanol metabolism. More specifically, while the majority of ethanol metabolism is regulated by the ADH pathway, chronic exposure to
Alcohol Consumption and Breast Cancer Risk
Mridul Datta, MS, RD, LDN
Introduction
Breast cancer is the most common cancer diagnosis and the second
most frequent cause of cancer mortality among women. Over 192,000
women are expected to be diagnosed with breast cancer in 2009,
accounting for about 27% of female cancers. Modifiable risk factors
include overweight and obesity (especially after menopause), physical
inactivity, use of hormone therapy, and daily consumption of one or
more alcoholic beverages (1). While moderate alcohol consumption,
defined as no more than one drink per day for women and two drinks
per day for men, has been linked with decreased risk of ischemic heart
disease (2), increased alcohol consumption has been linked with a
greater risk of developing female breast cancer in addition to cancers
of the oral cavity, pharynx, larynx, esophagus, liver, and colon (1). This
paper will explore some of the mechanisms by which alcohol increases
the risk of breast cancer, and provide some recommendations for
clinicians and practitioners working with women at risk for or
concerned about breast cancer.
(Continued on next page)
Table 1.
Alcohol content, source of sugars used to produce alcohol, and the recommended portion of common
alcoholic beverages
Beverage Percent alcohol by volume (3) Produced from (3) Portion (3)
Beer Generally 3-7%, but some specialty Barley primarily, but other 12 ounces brands are higher or lower in alcohol grains may be used
Wine Generally 9-15% but fortified wines Grapes primarily, but may be made 5 ounces may contain between 16-20% alcohol from rice (sake) and other fruits
Spirits/Liquor 35-50% Grains and other plant foods (such 8 ounces malt liquor; 1.5 ounces as fruits, potatoes, agave, and or a “shot” of 80-proof distilled cactus plant) spirits or liquor (such as gin, rum,
alcohol induces the CYP2E1 pathway (6,7). Increased expression of CYP2E1 has been linked to greater tolerance of larger quantities of alcohol, production of toxic metabolites in the liver, and production of reactive oxygen species (ROS), leading to ethanol induced liver injury. Acetaldehyde, the highly toxic ethanol metabolite, is generated by each of the three pathways (8).
Because a greater consumption of alcoholic beverages is associated with an increased cancer risk, ethanol has been indicted as the culpable factor (7). Ethanol is considered a co-carcinogen (9), and acetaldehyde, the primary ethanol metabolite, may damage DNA after heavy alcohol consumption in humans (10). Acetaldehyde is generated during alcohol metabolism and can also be produced by oral and fecal bacteria (7). Large amounts of acetaldehyde are also present in some alcoholic beverages (e.g., Calvados apple brandy) and in cigarette smoke (11). Possible mechanisms by which alcohol consumption may increase cancer risk include the following: generation of actaldehyde; acting as a solvent to enhance tissue absorption of other carcinogens; inhibiting detoxification of carcinogens; increasing estrogen levels; suppressing the immune system; and increasing tissue exposure to oxidants (7). Presence of
preservatives, pesticide residue, N-nitroso compounds, mycotoxins and natural products such as ketones, aldehydes and phenols in some beers and wine can also contribute to carcinogenesis (12,13).
Alcohol intake and Breast cancer
Among women, breast cancer accounts for about 60% of alcohol-related cancers (2). Tables 2 and 3 summarize select research studies investigating the relationship between alcohol intake and pre- and post-menopausal breast cancers. Some of the mechanisms by which alcohol may increase the risk of breast cancer include oxidative damage, mutagenic changes caused by acetaldehyde, disruption of estrogen metabolism, and a decrease in folate intake and utilization (14–20). Figure 1 provides a schematic representation of some of the mechanisms by which alcohol may induce breast cancer.
Changes in Hormone Metabolism
Is there a difference in the effects of alcohol consumption between pre- and post-menopausal women? Researchers have found that higher concentrations of endogenous estradiol significantly increased the risk of developing postmenopausal breast cancer (15,16). Women who developed breast cancer had a 15% higher serum estradiol concentration comparedwith women who were cancer free (16). In a review by Purohit et al (1998), researchers suggested that alcohol may decrease estradiol clearance and consequently increase serum estradiol levels (15).
Researchers have demonstrated a significant increase in serum concentration of estrone sulfate and dehydroepiandrosterone sulfate (DHEAS) in postmenopausal women with the consumption of 1-2 drinks (15 or 30 gm of alcohol) per day (17). At least one review suggested that consuming an average of one drink (12-18 gm alcohol) per day over their lifetime increased their risk of developing breast cancer by as much as 40% (21). This review also suggested that women who consumed over three drinks per day (providing more than 33 gm/day of alcohol) demonstrated a two-fold increase (Relative Risk (RR) = 2.00; 95% confidence interval (CI) = 1.48-2.71) in the risk of developing breast cancer as compared to women who never drank. While not statistically significant, post-menopausal women had a stronger alcohol-breast cancer relationship than pre-menopausal women (21).
There are no conclusive data linking alcohol intake and hormone receptor profiles (e.g. estrogen receptor (ER) or progesterone receptor (PR)). Current-users and ever-users
Table 2.
Select research studies investigating the relationship between alcohol intake and premenopausal
breast cancer
Alcohol Intake
Authors Country Study type Participants Assessment Conclusion
Kropp et al Germany Case-control 706 cases and 0 to ≥ 10 g/day Reduced (30%) breast cancer
2001 (35) 1,381 controls risk with low to moderate ETOH
(wine) intake (up to 18 g/day) and significantly higher risk with > 31 g/day in premenopausal women. Petri et al Denmark Cohort 13,074 women No. of drinks Increased risk of breast cancer 2004 (36) (20-91 years) (<1 to > 27) per week in premenopausal women with total
ETOH intake of >27 drinks/week and in postmenopausal women with > 6 drinks/week (hard liquor) Berstad et al US Case-control 1,728 cases and No. of drinks Intake of ≥ 2 drinks/day 2008 (37) 435 controls (0 to 7+ per week increased breast cancer risk
(Continued on next page)
who consumed ≥ 30 grams of alcohol a day had a significantly higher overall risk of developing breast cancer and of developing infiltrating lobular carcinoma (IBC) and hormone receptor positive (ER+, PR+ and ER+/PR+) tumors (22). Other researchers have also reported a positive association with moderate alcohol consumption and increased risk of hormone receptor positive breast cancer (23–25). These studies contribute to the existing literature (select summaries provided in Tables 2 and 3) in supporting the hypothesis that alcohol intake causes changes in the metabolism of sex hormones that can increase the risk of breast cancer in postmenopausal women.
Folate intake, alcohol intake, and
cancer risk
Folate has an established role in DNA synthesis and methylation, and even a mild folate deficiency has been linked to an increased risk of carcinogenesis. Case-controlled studies have provided some evidence of a link between dietary folate
intake and the risk of breast cancer (26). In the Nurses’ Health Study, no association was found between total folate intake and the overall risk of breast cancer. However, the risk of breast cancer was highest (RR = 1.32; 95% CI = 1.15-1.50) among women who consumed at least 15 grams of alcohol per day and had low (< 300µg/day) folate intake (27). Sellers et al (2001) reported that with increasing alcohol intake, postmenopausal women with very low (≤ 172 µg) dietary intake of folate have a higher risk of developing breast cancer (28). For women with very low dietary intake of folic acid, the RR of developing breast cancer with alcohol intake of more than four grams per day was 1.59; 95% CI = 1.05-2.41) (28). A follow-up analysis by Sellers and colleagues (19) demonstrated that women consuming very low dietary folate and consuming more than four grams of alcohol a day had a significantly higher RR for ER-breast tumors. Women who consumed ≤ 251 µg total folate a day and drank more than four grams of alcohol a day had a significantly
higher RR (RR= 2.14; 95% CI = 1.18 – 3.85) for ER-breast tumors (19). While some researchers have confirmed this inverse association between low folate intake and ER-breast cancer risk in women consuming more than 15 grams of alcohol a day[29], other researchers found no association between folate intake, daily alcohol consumption, and the increased risk of developing breast cancer (30). In addition, the exact mechanism by which folate and alcohol synergistically influence risk of breast cancer is not yet known. However, the role of folate in DNA methylation (29) and the direct carcinogenic effect of acetaldehyde are potential mechanisms that could explain the role of folate supplementation in attenuating the risk of alcohol-related breast cancer (19,28). Researchers have proposed that folate requirements could potentially be higher in women who routinely consume alcohol (29). To date, recommendations regarding daily folic acid intake (400 µg/day for non-pregnant females over the age of 14 years) do not include increased amounts for those who routinely consume alcohol.
Ethanol Metabolism
Ethanol is converted to acetaldehyde by the enzyme alcohol dehydrogenase (ADH). Acetaldehyde is catalyzed to acetate by aldehyde dehydrogenase (ALDH) (10) and by xanthine oxioreductase (XOR) and aldehyde oxidase (AOX) (14). Breast tissue contains ADH, ALDH (31) and XOR, but only XOR and AOX can generate ROS,
(superoxide anion, hydroxyl radicals and hydrogen peroxide). In the female breast, only the hydroxyl radical has been reported to induce DNA adducts, strand breaks and base deletions, which increase the risk of cancer (14).
Any variation in the ADH and ALDH genes will impact a person’s ability to metabolize ethanol. To evaluate metabolic differences in ADH and ALDH activity in breast tissue of healthy women and women with stage I-IV breast cancer, Jelski et al. analyzed biopsy specimens. Significantly lower levels (p<0.001) of class I ADH, which is the
Figure 1.
Schematic representation of some of the mechanisms by which
alcohol may induce breast cancer Additives /contaminants may include
preservatives, pesticide residue, mycotoxins, and natural products such as
ketones, aldehydes and phenols.
primary isoenzyme for ethanol-metabolism within breast tissue, have been reported in breast cancer cells (0.133±0.019 nmol/min/mg of protein) when compared to healthy breast tissue (0.248±0.038 nmol/min/mg of protein). Conversely, other ADH isoenzymes
(class II-IV) demonstrated higher activity in cancer cells. A progressive decline in total ADH and specifically class 1 ADH activity has also been correlated with disease progression. While the levels of ADH I were significantly lower in all stages of breast
cancer, there was no correlation with the stage of the tumor. This led the researchers to speculate that these changes were perhaps occurring prior to the tissue becoming neoplastic. The ratio of ADH to ALDH activity was determined to be 15:1 in
Table 3.
Select research studies investigating the relationship between alcohol intake and postmenopausal
breast cancer
Authors/ Study
Country Type Subjects Alcohol Intake Conclusions
Longnecker Case-Control 6,662 cases and 0 to ≥ 33gm/day Alcohol consumption increased breast cancer risk (over et al 1995[19] 9,163 controls 1 drink=12-18 gm two-fold increase in risk with consumption of > 3 drinks/day), U.S. of alcohol with a stronger (but not statistically significant)
relationship in post-menopausal women
Kinney et al Case-Control 890 cases and < 13 to ≥182 gm/day No association of breast cancer with recent or lifetime 2000[35] 841 controls 1 drink=12.8 gm alcohol consumption, age at which drinking began, U.S. of alcohol duration of drinking, or binge drinking in either
African-American or Caucasian women.
Feigelson et al Cohort 24,2010 No. of drinks Higher breast cancer risk and mortality in postmenopausal 2001[36] US (< 1 to 3+) per day women who drank alcohol (beer, wine or liquor)
Chen et al Cohort 44,187 post- 0.1 to ≥ 20 gm/day Increased risk of breast cancer (30%) with ≥ 20gm 2002[37] U.S. menopausal (1.5-2 drinks/day) of alcohol consumption daily. Women
women using HRT (≥ 5 years) and consuming > 1 drink/day had twice the relative risk of developing breast cancer. Lenz et al Case-Control 556 cases and No. of drinks/week Wine (possibly hard liquor) increases risk of postmenopausal 2002[38] 557 controls (≤1 to >9) breast cancer with 2.5 times increased risk with routine
Canada wine consumption on or before age 40.
Tjonneland Cohort 23,778 0-60 gm/day Increasing risk of breast cancer in postmenopausal women et al 2003[39] with increasing alcohol intake (beer, wine or liquor) Denmark
Petri et al Cohort 13,074 women No. of drinks/week Increased risk of breast cancer in premenopausal women 2004[33] aged 20-91 years (<1; 1-6; 7-13; with total alcohol intake of > 27 drinks/week and in post-Denmark 14-27; >27) menopausal women with > 6 drinks/week (hard liquor) Zhang et al Cohort 38,454 0 to ≥ 30gm/day Postmenopausal women with high alcohol intake had an 2007[23] 1 drink=10-12.8 gm increase in breast cancer risk. Women consuming > 10gm U.S. of alcohol of alcohol (> 1 drink) daily, had higher RR for total breast
cancer, invasive breast cancer and ER+PR+ tumors. Total breast cancer risk also higher in women consuming > 10gm of alcohol and on HRT
Li et al Cohort 70,033 No. of drinks (<1 to Increasing risk of breast cancer in women consuming 2009[22] ≥ 3) per day and per ≥1 drink per day. Alcohol associated with ER+
U.S. month (<1 to > 1) breast cancer only
Allen et al Cohort 128,0296 No. of drinks/week Increased breast cancer risk with increasing alcohol 2009[40] (≤2; 3-6; 7-14; ≥15) consumption. In women up to age 75, for every additional UK 1 drink=10 gm drink consumed daily, incidence of breast cancer increased
of alcohol by 11 per 1000 women
cancerous tissue and 13:1 in healthy tissue, suggesting that the cancerous tissue remains capable of oxidizing exogenous ethanol but not removal of acetaldehyde, which has been implicated in promoting carcinogenesis. The researchers concluded that a decrease in class I ADH isoenzymes may be indicative of significant changes in the metabolism of compounds essential to repair the precancerous transformations in the healthy breast tissue (31).
In addition, several ADH gene polymorphisms have been identified among people of different ethnic backgrounds. The mutant ALDH2*2 allele (which causes the unpleasant alcohol-flush reaction) present in some Asians, is protective against excessive alcohol consumption (32). Increased alcohol metabolism has been reported with the presence of the high risk ADH31allele (33). Women with the fast metabolizing allele (ADH31-1) had a two-fold increase in risk of developing breast cancer with lifetime alcohol consumption of 15-30 gm (1-2 drinks) alcohol per day, compared to slow (ADH32-2) and intermediate (ADH
31-2) metabolizing groups. This effect was significantly pronounced in the
premenopausal fast metabolizers (20,33).
Conclusions
The above overview highlights potential causes and relationships between greater alcohol intake and increased risk of developing breast cancer. Several other factors such as breast density, nulliparity, gene polymorphisms (genes associated with estrogen synthesis and metabolism such as CYP17, CYP19, CYP1B1, and COMT), p53 mutations, and oxidative stress also play a role in the development of alcohol related breast cancer (14). A discussion of these risk factors and their interaction in promoting breast cancer are beyond the scope of this review. However, as continuing research provides additional answers, we will better understand the mechanistic pathways linking alcohol intake with female breast cancer.
(Continued on next page)
While the exact mechanistic pathways remain uncertain, a review of the literature makes it exceedingly difficult to ignore the correlation between alcohol consumption and the risk of developing breast cancer. The 2007 joint report by the World Cancer Research Fund and the American Institute for Cancer Research concluded that there is convincing evidence that alcoholic beverages influence risk of breast cancer in both pre- and post-menopausal women and that there is no “safe limit” of intake (3). While acknowledging the cardioprotective effects of alcohol, the report recommends limiting alcohol intake, and that if alcohol is consumed, women should limit
consumption to one drink (10-15 grams ethanol) per day (3). Postmenopausal women with cardiac disease should be encouraged to discuss the risks and benefits of alcohol consumption with their health care provider (e.g., physicians, RD). In addition to limiting intake of alcoholic beverages, women should be counseled about adequate folate intake and modifying other risk factors such as dietary intake (fat, total calories), body weight, and activity level to further decrease their risk of developing breast cancer.
Key Recommendations
• Women should decrease or eliminate their intake of alcohol, especially women with a family history of breast cancer. If alcohol is consumed, then intake should be limited to no more than one serving of alcohol per day. • Women should be counseled to modify
other existing risk factors such as diet and activity level.
• Adequate intake of folate should be encouraged not just during reproductive years, but during menopause as well. Women may need to be counseled to include more folate-rich foods in their diets.
Mridul Datta, MS, RD, LDN, is a PhD candidate in Nutrition at the University of North Carolina - Greensboro.
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28. Sellers TA, Kushi LH, Cerhan JR, Vierkant RA, Gapstur SM, Vachon CM, Olson JE, Therneau TMa, and Folsom AR. Dietary folate intake, alcohol, and risk of breast cancer in a prospective study of postmenopausal women. Epidemiology.
2001;12(4):420–428.
29. Zhang SM, Hankinson SE, Hunter DJ, Giovannucci EL, Colditz GA, and Willett WC. Folate intake and risk of breast cancer characterized by hormone receptor status. Cancer Epidemiol Biomarkers Prev.2005;14(8):2004–2008. 30. Feigelson HS, Jonas CR, Robertson AS,
McCullough ML, Thun MJ, and Calle EE. Alcohol, folate, methionine, and risk of incident breast cancer in the American cancer society cancer prevention study II nutrition cohort. Cancer Epidemiol Biomarkers Prev. 2003;12(2):161–164. 31. Jelski W, Chrostek L, Szmitkowski M, and
Markiewicz W. The activity of class I, II, III and IV alcohol dehydrogenase isoenzymes and aldehyde dehydrogenase in breast cancer. Clin Exp Med. 2006;6(2):89–93. 32. Thomasson H, Crabb D, Edenberg H,
and Li T-K. Alcohol and aldehyde dehydrogenase polymorphisms and alcoholism. Behav Genet. 1993;23(2): 131–136.
33. Terry MB, Gammon MD, Zhang FF, Knight JA, Wang Q, Britton JA, Teitelbaum SL, Neugut AI, and Santella RM. ADH3 genotype, alcohol intake and breast cancer risk. Carcinogenesis.2006; 27(4):840–847.
34. Newcomb PA, Nichols HB, Beasley JM, Egan K, Titus-Ernstoff L, Hampton JM, and Trentham-Dietz A. No difference between red wine or white wine consumption and breast cancer risk.
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As stated by the authors “the Revised SOP and SOPP for RDs in Oncology Nutrition Care are innovative and dynamic documents” (1). They are also “complementary documents and key resources for RDs at all knowledge and performance levels” (1). RDs may use these standards in daily practice to demonstrate their competency and value to oncology patients and the medical team.
Thanks to Kim, Lori, Laura, Nicole, Rhone, and Sarah, volunteer leaders in ON DPG and respected oncology nutrition professionals, who contributed their expertise and time to revise the SOP and SOPP for oncology nutrition RDs.
1. Robien K, Bechard L, Elliott L, Fox N, Levin R, Washburn S. American Dietetic Association: Revised Standards of Practice and Standards of Professional Performance for Registered Dietitians (Generalist, Specialty, and Advanced) in Oncology Nutrition Care.
Journal of the American Dietetic Association
2010;10(2):310–317.
The Revised Standards of Practice (SOP) and Standards of Professional Performance (SOPP) for Registered Dietitians (Generalist, Specialist, and Advanced) in Oncology Nutrition Care have been published in the February 2010 issue of the Journal of the American Dietetic Association (JADA).
Written by ON DPG members Kim Robien, PhD, RD, CSO, LD, FADA; Lori Bechard, MEd, RD, LDN; Laura Elliott, MPH, RD, CSO, LD; Nicole Fox, RD, LMN; Rhone Levin, MEd, RD, CSO, LDN; and Sarah Washburn, MS, RD, CSO, this document replaces the 2006 standards. It builds on ADA’s Code of Ethics and ADA’s 2008 revised SOP for RDs in Nutrition Care and SOPP for RDs, which guide the practice and performance of RDs in all settings. The revised standards reflect recent advances in the field of oncology nutrition, including the Oncology Evidence-Based Nutrition Practice Guidelines, which were published in 2007. They also provide evidence based statements to support practitioner decisions about appropriate oncology nutrition interventions during cancer
treatment. Authors also utilized current resources in the field of oncology nutrition such as cancer program standards of the Commission on Cancer (COC), several National Cancer Institute (NCI) documents, and resources used to develop the board certification credential in oncology, the Certified Specialist in Oncology Nutrition (CSO). Approved by the Commission on Dietetic Registration (CDR) in 2008, CSOs meet minimum practice experience requirements and have successfully completed the Board Certification as a Specialist in Oncology Nutrition examination.
The new document, which members can find in the February 2010 issue of JADA,
defines three levels of practice in oncology nutrition care: generalist, specialty, and advanced. It also provides recommendations on using the revised standards in the
Professional Development Portfolio (PDP)
process and in different practice roles such as practitioners, managers, and researchers.
Professional Update
Revised Standards of Practice (SOP) and Standards of Professional
Performance (SOPP) for Registered Dietitians (Generalist, Specialist,
and Advanced) in Oncology Nutrition
The polls for ADA elections and our own DPG are open NOW!!
VOTE for your national leaders and for the 2010-2011 Executive Committee of the
Oncology Nutrition Dietetic Practice Group!
February 1st - March 3rd, 2010.
Please go to www.eatright.org/elections, log on, and exercise your right to vote! We have fabulous people running in the DPG election and the national election. Check out Barbara Grant, MS, RD, CSO under the ADA elections!! The elections only take 5 minutes out of your day today, so go ahead and vote!
You can go to our website — www.oncologynutrition.org and check out our candidates and their thoughts for ON-DPG’s future under News and Articles on the homepage!!
The ON DPG’s slate of candidates for leadership positions for the 2010-2011 year:
Chair-elect
Denise Snyder, MS, RD, CSO, LDN
Secretary (vote for one)
Alison Ryan, MS, RD, CNSC Aimee Shea, MPH, RD, CSO, LDN
Nominating Committee Chair (vote for one)
What is GE cancer, how is it staged,
and how common is it?
AC was diagnosed with Stage III adenocarcinoma of the GE junction, the lower part of the esophagus that connects to the stomach. Squamous cells naturally line the esophagus, and squamous cell carcinoma can form from these cells.
Prolonged gastric reflux can damage squamous cells, causing them to be replaced by glandular cells. Adenocarcinomas form from glandular cells (1). In most patients, it is believed that adenocarcinomas of the GE junction resemble esophageal cancer (2). At Stage III, GE cancer has spread to tissues or lymph nodes near the esophagus, but may not have spread to other parts of the body (3).
Although the incidence of squamous cell cancer has decreased over the past decade, the incidence of adenocarcinoma, specifically at the GE junction, has significantly increased.
In 2005, there were 497,700 new cases and 416, 500 deaths from esophageal cancer. The prevalence is expected to increase approximately 140% by 2025 (2). This increase in adenocarcinoma is thought to be associated with increased prevalence of obesity, gastroesophageal reflux disease (GERD), and Barrett’s esophagus (4).
What is the prognosis of GE cancer?
The 5-year survival rate of GE cancer is 10%, but survival rate is influenced by tumor stage. In a review of 469 patients with stage III esophageal cancer who underwent transhiatal esophagectomy, 31.7% (27.4–36.2) survived three years and 11.1% (8.2–14.5) survived five years (4).What is the usual treatment for
GE cancer?
Surgical resection is the preferred treatment for GE cancer. Neoadjuvant chemotherapy, sometimes combined with radiation
treatment, frequently precedes surgical treatment and is given to shrink a tumor prior to surgery (1). However, it is still considered investigational (5). A phase III trial conducted by the British Medical Research Council evaluated the effect of the ECF (epirubicin, cisplatin and 5-fluorouracil) MAGIC regimen given before and after surgery in resectable gastroesophageal cancer. Five-year survival rates were 36% among those who received perioperative chemotherapy versus 23% in the surgery group (6).
Is malnutrition(as defined by
underweight BMI status, severe
weight loss, and loss of lean body
mass) common in GE cancer?
The incidence of malnutrition at the time of any cancer diagnosis is approximately 15% to 20%, and 80% to 90% of patients with advanced cancer (of any type) are malnourished. Prevalence of malnutrition does differ among types of cancer, with incidence in esophageal cancer ranging from 60% to 80% (7–9).Should Nutrition Risk Screening be
limited to the hospital setting, and
was AC at nutrition risk when he
began chemoradiation therapy?
As stated in chapter 6 of The Clinical Guide to Oncology Nutrition (2nd edition), “In the oncology setting, health care professionals consider nutrition screening to be the identification of cancer-related malnutrition and cachexia and/or associated nutrition impact symptoms.”This resource also stated that nutrition issues be addressed “at diagnosis and throughout the course of cancer care” (10). The American Dietetic Association recognizes that nutritional risk exists in a variety of settings, including the emergency room, ambulatory clinics, and home care, and thus “screening for nutritional risk in outpatient settings is important” (11).Nausea, vomiting, and anorexia are common side effects of chemotherapy. Acute effects of radiation to the thoracic area (including the esophagus) include dysphagia, heartburn, fatigue, and anorexia.
Case Study: Gastroesophageal Cancer
Daniel Kahn, Dietetic Intern
Introduction
This case study reviews the nutritional status and care of AC, a
55-year-old Caucasian male who was diagnosed with gastroesophageal
(GE) cancer in April 2009, and admitted to the hospital in September
2009 with malnutrition. Prior to his diagnosis, AC was generally healthy
and without significant medical history. He was married with three
children, and was employed as a mechanical engineer. In April 2009, AC
was diagnosed with GE cancer, and began chemotherapy and radiation
treatment in an outpatient cancer treatment center that did not
employ a registered dietitian (RD). During an office visit in September
2009, after completing chemoradiation therapy, AC’s physician
became concerned about ongoing involuntary weight loss,
abdominal pain, vomiting, and dysphagia. AC was admitted to the
hospital for evaluation of these problems, where the RD assessment
revealed weight loss of over 60 pounds since April 2009. Ten pounds
were lost during the week prior to admission. The medical doctor
(MD) recognized that AC’s depleted nutrition status made him a poor
candidate for surgery, and the goal of admission was to replete his
nutritional status and “fine tune” his medical status prior to surgery
to resect his gastroesophageal tumor.
Radiation therapy has the potential to compound eating difficulties expected from chemotherapy. The high risk of these potential side effects should have triggered a positive nutrition screening and a referral for nutrition assessment by a registered dietitian (RD).
What does the Evidence Analysis
Library (EAL) of the American Dietetic
Association (ADA) state about cancer
and medical nutrition therapy (MNT)?
In their Evidence Analysis Library (EAL), ADA has published the following statement about chemoradiation and medical nutrition therapy for esophageal cancer: “The Dietitian should provide MNT consisting of a pre-treatment evaluation(Continued on next page)
and weekly visits for six weeks during chemoradiation treatment for esophageal cancer to improve outcomes. MNT may reduce the amount of weight loss, unplanned hospitalizations, and length of stay (LOS) if hospitalized, and may improve tolerance to treatment and increase the likelihood of receiving the radiation dose prescribed.” (12).
Case:
AC experienced poor appetite and abdominal discomfort during neoadjuvant treatment, which led to progressive weight loss. Upon admission to the hospital in September 2009, AC weighed approximately 118 pounds (53.6 kg) and stood 70 inches tall (177.8 cm). AC’s usual body weight (UBW) was 180 pounds (81.8 kg) and usual body mass index (BMI) was 25.9. His ideal body weight (IBW) was estimated at 166 pounds (75.5 kg).
How is malnutrition diagnosed in cancer patients?
Malnutrition has many negative consequences in cancer patients, including reduced quality of life, decreased response to treatment, increased prevalence of chemotherapy toxicity, and reduced survival (13). As a result, clinicians have developed many tools to assess nutritional status so that patients at highest risk of malnutrition can be identified and referred for appropriate MNT. Subjective Global Assessment (SGA) is a process developed in the 1980s that uses subjective and objective data and physical examination to rate nutritional status (14). A rating of “A” suggests the patient is well-nourished, while a rating of “B” suggests moderate malnutrition and “C” suggests severe malnutrition. Based on SGA criteria, AC’s nutrition parameters, including weight loss, intake deficit, nutrition impact symptoms, and loss of subcutaneous tissue (as evidenced by his cachectic appearance), correlate with a severely malnourished state.
What is the nutritional significance of AC’s current BMI, percent weight loss over three months, percent Usual Body Weight (UBW),
and percent Ideal Body Weight (IBW)?
AC’s weight changes and BMI suggest a compromised nutritional status (11).
Table 1.
Weight Assessment Criteria (11)
Criteria AC’s Values Classification
BMI 16.9 Underweight
Potential for moderate to severe malnutrition is c/w BMI < 18.5.
% Weight Loss 34% Severe Weight Loss
(c/w > 7.5% weight loss in 3 months or 10% in 6 months) % Usual Weight 66% Severe Malnutrition
(a weight < 66% of usual increases morbidity from depletion of body cell mass)
Given information provided so far, what nutrition diagnosis would be appropriate for AC?
Several nutrition diagnoses may be appropriate, including:Case:
AC’s laboratory values were assessed on admission and throughout his hospitalization.
Table 2.
Sample Lab Values for AC
(16)
Laboratory values can be measured in two units: Standardized International (SI) and Conventional (CU). Both units are included in table 2. Abnormal values are bolded
Normal Range Day 1 Day 5 Day 8
Glucose SI: 3.8-5.5 mmol.L 7.92 mmol/L – 5.65 mmol/L
CU mg/dL: 70-100 mg/dL) 142 mg/dL 101.8 mg/dL
*conversion factor 0.0555
Sodium SI: 136-145 mmol/L 132 mmol/L 133 mmol/L –
CU: 136-145 mEq/L 132 mEq/L 133 mEq/L
conversion factor 1.0
Potassium SI: 3.5-5.0 mmol/L 3.6 mmol/L 3.5 mmol/L 3.0 mmol/L
CU: 3.5-5.0 mEq/L 3.6 mEq/L 3.5 mEq/L 3.0 mEq/L
conversion factor 1.0
Magnesium SI: 0.65-1.05 mmol/L 0.68 mmol/L 0.65 mmol/L 0.61mmol/L
CU: 1.3-2.1 mEq/L or 1.47-3.38 mg/dL 1.36 mEq/L 1.3 mEq/L 1.22 mEq/L
conversion factor 0.5 for mEq and 1.54 mg/dL 1.47 mg/dL 1.38 mg/dL
0.441 for mg/dL
Phosphorus SI: 0.74-1.39 mmol/L 0.77 mmol/L 0.5 mmol/L 0.72 mmol/L
CU: 2.29-4.3 mg/dL 2.38 mg/dL 1.55 mg/dL 2.23 mg/dL conversion factor 0.323 Albumin SI: 35-50 g/L 22 g/L 20 g/L <12 g/L CU: 3.5-5.0 g/dL 2.2 g/dL 2.0 g/dL <1.2 g/dL conversion factor 10.0 Prealbumin 0.18-0.38 g/L 0.18 g/L 0.16 g/L 0.15 g/L
Aspartate Amino- SI: 10-37 U/L – 74 U/L 78 U/L
transferase (AST) (only one unit is used to measure AST)
Alanine Amino- 25-65 U/L – 83 U/L 90 U/L
transfersase (ALT) (only one unit is used to measure ALT)
Alkaline 30-120 U/L – 343 U/L 161 U/L
Phosphatase (only one unit is used to measure Alk Phos) (Alk Phos)
Hgb 140-180 g/L 103 g/L 98 g/L 107 g/L
14.0-18.0 g/dL 10.3 g/dL 9.8 g/dL 10.7g/dL
conversion factor: 10 to convert between g/dL and g/L and 0.6206 to convert between g/dL and mmol/L
Hct 0.42-0.52 0.308 0.318 0.34
%
*Conversion factors:
To convert from the conventional unit to the SI unit, multiply by the conversion factor. To convert from the SI unit to the conventional unit, divide by the conversion factor.
What is the nutritional significance
of AC’s abnormal lab levels?
Albumin and Prealbumin:
AC’s admitting albumin was 22 g/L, consistent with moderate depletion. Over at least the past decade albumin’s utility as an acute sensor of early nutritional depletion or of nutritional status in the setting of acute illness has been questioned. As a negative acute phase reactant, Albumin will decrease during periods of inflammation such as acute medical stress (6). However, AC presented with an appearance of cachexia, and decreases in lean body mass and protein synthesis, as well as protein mobilization associated with cachexia, would be expected to result in a fall in albumin. Albumin is synthesized in the liver, and liver dysfunction, which was suggested by elevated liver enzymes measured on day 5, may compromise albumin synthesis. Albumin was measured <12 g/L on day 8, consistent with severely depleted stores, though this level could have also been influenced by IV hydration provided during AC’s admission (11,17).
Prealbumin level was 0.18g/L when admitted, which is the low point of the normal range, and decreased to 0.15g/L on day 8 of hospitalization. Prealbumin is a better indicated of a malnourished status as its shorter half-life provides a more current estimate of dietary intake and protein stores (11,17).
Glucose, Liver Function Tests,
Hemoglobin, and Hematocrit:
Blood glucose levels were elevated, and were likely associated with malnutrition and hepatic dysfunction (8). On day 5 liver enzymes were measured and found to be elevated. AC’s alkaline phosphatase level was 343 U/L, and Aspartate Aminotransferase, and Alanine Aminotransferase were elevated at 74 U/L and 83 U/L, respectively. These levels suggest possible liver dysfunction, and liver metastasis was later diagnosed. Below normal hemoglobin and hematocrit suggested anemia, which could be associated with chronic disease statusand/or prolonged low iron intake (8). On Day 8 all of the lab values were outside the normal range. Decreased levels of magnesium, phosphorus, and potassium were possibly associated with refeeding syndrome (11,17).
Sodium:
AC’s labs revealed a decreased sodium level of 132 mmol/L on day 1 of his admission. Below normal sodium level can be associated with edema, but AC appeared cachectic and was without edema when admitted. He was admitted with intermittent vomiting, and sodium levels are known to decrease due to vomiting, which may explain this value (15). However, the admitting sodium level was not close to its critical value of 120 mmol/L, which can result in neurologic symptoms such as confusion, dizziness, and seizures. The admission value of sodium did not require nutrition intervention (17).
Case:
During the initial nutrition assessment, the RD determined that AC’s oral (PO) intake was primarily limited to liquids prior to admission, and that AC tolerated thin liquids better than thicker, energy dense liquids. The RD also determined that AC tolerated few solid foods.
What types of oral liquid nutrition
supplements might be most beneficial
for AC?
AC’s diet prior to admission was deficient in macro- and micronutrients, and he had difficulty tolerating solids. AC tested his ability to tolerate nutrient dense oral nutrition products such as Ensure Plus®
(18), which is produced by Abbott Nutrition and provides 350 calories, 13 grams protein, 51 grams carbohydrate, and 11 grams fat per 8 ounce serving. AC stated he could only accept thin liquid beverages and oral nutrition products such as Resource Breeze®(19), a clear-liquid beverage produced by Nestlé HealthCare Nutrition that provides 9 grams protein and 250 calories in an 8-ounce serving.
Based on AC’s nutrition assessment
criteria, is AC likely to replete his
nutritional status with thin liquids only?
Products such as Resource Breeze®(19) aremeant to supplement a diet. Diets limited to thin liquids, including oral (thin) liquid supplements, are usually inadequate in nutrients and should be used for limited amounts of time. AC initially refused a tube feeding, and demanded that he be given the opportunity to increase his oral intake via oral liquid nutrition supplements. The RD initiated a calorie count to assess his daily intake and implemented a care plan that included clear liquid oral nutrition beverages. Over a three day period AC’s intake provided approximately 33% of his estimated energy and protein needs.
Based on your clinical experience, is
AC a candidate for nutrition support,
and would you recommend enteral or
parenteral nutrition?
If the medical team concluded that AC is a candidate for further medical treatment, he is also a candidate for nutrition support. Nutrition support is indicated because he is
unable to meet his nutrition needs via clear liquid oral supplements, is unable to tolerate oral (PO) solids, meets standardized criteria for malnutrition, and has significant nutrition needs. Though AC experienced intermittent vomiting, he did not experience diarrhea, therefore enteral nutrition would be the preferred form of nutrition support.
The Evidence Analysis Library (EAL) of the American Dietetic Association (ADA) has published several recommendations regarding esophageal cancer treatment and nutrition support. The EAL states that: “Enteral nutrition (EN) may be used to increase calorie and protein intake in esophageal cancer in patients undergoing chemoradiation therapy. EN has been shown to maintain weight, however EN has not been shown to improve tolerance to therapy or survival (20).” Regarding parenteral nutrition (PN) for esophageal
cancer, the EAL states: “PN has not been shown to prevent weight loss or improve effectiveness of treatment” (21).
In 2009 the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) published clinical guidelines for the use of nutrition support therapy during adult anticancer treatment. These guidelines, meant to be used in conjunction with a practitioner’s clinical judgment, state that nutrition support therapy should not be used routinely as an adjunct to chemotherapy. They also state that nutrition support therapy should not be used routinely in patients undergoing major cancer
operations, but that perioperative nutrition support therapy may be beneficial in moderately or severely malnourished
patients if administered for 7-14 days preoperatively (22).
Do you believe that AC is at risk of
refeeding syndrome?
AC has several risk factors for refeeding syndrome, most significantly weight loss and anorexia. During prolonged starvation, the body utilizes fat stores, and to a lesser extent protein stores, for energy. Insulin secretion drops as carbohydrate intake decreases. In refeeding syndrome, the switch from a fat burning metabolism to a carbohydrate-burning metabolism, with its increased need for insulin, precipitates cellular uptake of phosphate (23).
Hypophosphatemia is considered a sentinel symptom of refeeding, but fluid and electrolyte disturbances also occur.
Physiologic effects of these symptoms can ultimately result in respiratory failure, hypotension, and sudden death (23).
Refeeding syndrome usually occurs within the first three or four days of initiating feeding, whether by oral, enteral, or parenteral route, but can be seen several weeks after refeeding begins. When a patient presents with risk factors for refeeding syndrome, it is essential to monitor for, and correct, hypophosphatemia, hypomagnesia, and hypokalemia when they occur. AC met common criteria for someone at high risk of refeeding, which include a BMI < 18.5, >10% involuntary weight loss over 3-6 months, and reduced PO intake. In addition, oncology patients are at risk of refeeding because of nutrition related side effects of oncology treatments.
Case:
The RD recommended enteral feedings, and cautioned the medical team about AC’s risk of refeeding syndrome.
How many calories should AC receive when nutrition support is initiated?
AC’s risk of refeeding syndrome influences his energy requirements. Clinicians should start with a low feeding volume and increase volume slowly and as tolerated. Energy recommendations for refeeding range from providing as few as 10 kcal/kg (20), to 15-20 kcal/kg (21), to a range of 25% to 50% of normal needs (24). Clinicians also frequently replace thiamine and B vitamins in patients at risk of refeeding, so that adequate levels of these nutrients are available for carbohydrate metabolism (25).
Table 3.
Energy Needs Per Various Standards for Refeeding Syndrome
Initial Daily Energy Recommendations Estimated Daily Energy Needs
for Refeeding Syndrome AC’s Weight for AC, Adjusted for Risk of Refeeding
10 kcal/kg (24) 53.2 kg 530 kcal
15-20- kcal/kg (25) 53.2 kg 780 to 1060 kcal
25-50% (26) 53.2 kg 300 to 700 kcal/day
Harris-Benedict Males (66 + (13.7 x kg) + 53.2 kg 66 + 729 + 889 - 374 = 1310 (5 x cm ) – (6.8 age) ) X stress factor for 0.85 x 1310 = 1110 kcal/day starvation (0.85 to 1.0) (11)
What enteral feeding route is most
appropriate for AC?
The RD recommended feeding AC via a percutaneous endoscopic jejunostomy (PEJ). Gastric feedings are considered physiologic because they support GI integrity and the mucosal barrier, but postpyloric infusion can reduce the incidence of aspiration associated with gastric feedings. Esophageal cancer is one of
several conditions that favor jejunal versus gastric feeding, as long as the naso-jejunal route is avoided. Jejunostomies may be inserted surgically, or more often via a PEJ.
PEJ feedings must be monitored for potential complications including
displacement of the jejunostomy, clogging, feeding-related diarrhea, abdominal cramping, and hyperglycemia. Isotonic
jejunal feedings are best tolerated; hyperosmotic feedings may result in diarrhea and abdominal cramping. Few studies have examined the optimal jejunal feeding, but it is safest to begin with a low rate of isotonic formula that is infused continuously (27).
Percutaneous endoscopic gastrostomy (PEG) has not been widely used for
esophageal cancers because of concerns about safety of dilatation and use of the stomach as an esophageal replacement. AC’s history of nausea and vomiting also suggest that gastric feeds may be a poor choice for him. However, in a retrospective review that evaluated the use of a PEG as a nutritional bridge during neoadjuvant chemoradiation treatment for esophageal cancer, researchers found that in 103 (of 119) patients in whom the PEG was
successfully placed (all of whom were experiencing dysphagia), the treatment was safe and useful. Seventy percent (70%) of these patients completed chemotherapy, as compared to 37.5% of patients who did not receive a PEG. In addition, the stomach was not compromised as an alimentary conduit. In 61 patients from this cohort who underwent surgery after neoadjuvant treatment, weight loss was 3.8% from the time of PEG placement (28).
What type of formula would you
recommend for AC?
The RD recommended an isotonic feed, starting at a low rate.
An isotonic feed initiated at a low rate (e.g., 20 to 30 mL/hour) is indicated. The rate should be increased gradually as tolerated. AC was unable to tolerate more than a 20 ml/hour infusion.
Case:
AC’s phosphorus decreased to 0.5 mmol/ml on day 5, 1 day after the tube feeding was initiated. On the same day his magnesium and potassium levels decreased, as compared to the first day of his admission, and were measured at the low end of the normal range. The MD managed AC’s electrolytes via IV fluid/electrolyte infusions.
Did AC experience refeeding?
Hypophosphatemia is a common sign of refeeding. Hypokalemia andhypomagenesiumia also frequently occur.
In AC’s case, these laboratory abnormalities occurred within 3 to 5 days of initiating feeding, the most common timing for refeeding syndrome. The medical team
agreed that AC probably experienced symptoms of refeeding syndrome (23–26).
Case:
From day 8 to day 12, the physician managed AC’s electrolytes via daily IV fluids, while AC continued to receive </= 20 mL/hour of tube feeding. AC was not able to tolerate a higher rate of tube feeding infusion. Unfortunately, on day 12 of his hospitalization, AC expired from complications related to his diagnosis.
Student Perspective:
As a dietetic intern, I found the cachectic condition of the patient (when admitted) as well as the lack of nutrition referral and the failure of the outpatient medical team to acknowledge or consider the patient’s deteriorating nutritional status difficult to understand. This case led me to question the state of health care for cancer patients. What is the role of the RD in oncology care? What can dietetic professionals do to prevent such cancer-nutrition related complications? First of all, involving RDs early in the care process has the potential to limit weight loss, which in turn has been shown to limit complications and allow patients to complete planned treatments. As treatment progresses, it is vitally important for patients to be referred to an RD when gastro-intestinal (GI) complications and involuntary weight loss continues. In addition to improving quality of life, this will provide the patient with the best opportunity for cure and/or life extension. In this case, when the patient was finally referred to an
RD and it was apparent that enteral nutrition was indicated, it is important to understand the reasons why patients may not want to be fed via a tube. What are their fears, concerns, and thoughts? We have to provide proper education regarding the significance and importance of having a feeding tube placed. In early intervention that utilizes discussions, handouts, or a video, RDs can convey the nutritional advantages and benefits of having this procedure done. At the same time, we need to be supportive and resourceful in helping patients cope with challenges. This case also presented with the challenge of refeeding syndrome, which initially requires providing smaller amounts of energy and protein than is usually recommended for nutritional repletion. Finally, we need to advocate staffing RDs in outpatient settings. This will ensure that patients utilizing outpatient services and treatments have the opportunity to meet with RDs, which can potentially prevent malnutrition as experienced by this patient.
Daniel J. Kahn is a Dietetic Intern with the 2009-2010 Dietetic Internship class at Virginia Polytechnic Institute and State University. In 2009 he received a BS degree in Nutritional Sciences from the University of New Hampshire.
References:
1. Detailed guide: Esophageal Cancer. American Cancer Society, Inc. 2009.
Internet:http://www.cancer.org/docroot/cri/ content/cri_2_4_1x_what_is_esophagus_ cancer_12. asp (accessed 13 October 2009). 2. DeMMeester, SR. Epidemiology and biology of esophageal cancer. Gastrointest Cancer Res.
2009; (suppl 1): S2–S5.
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Calling Oncology Nutrition Authors!
Oncology Nutrition Connectionprovides many opportunities to feature and develop your writing skills.
Feature Articlesprovide in-depth reviews of an oncology nutrition topic. They give you an opportunity to share oncology nutrition outcomes research and knowledge, and review a topic that you are passionate about.
Case Studiesgive you an opportunity to share ways your experience and expertise made a difference for a particular cancer patient and/or survivor.
Nutrition News Briefshighlight important aspects of current oncology nutrition topics in 500 words.
Member Spotlightsrecognize the work and dedication of ON DPG members, and alert dietetic students and new RDs to the roles and rewards of being an oncology dietitian. Nominate a friend or yourself for a spotlight!
Coming to
ONC!
Oncology Nutrition Matterswill provide ON DPG members with a format to ask clinical questions, editorialize about an oncology nutrition issue, pose questions to other members, and share professional challenges and successes. This feature will be open to all topics related to oncology nutrition.
Contribute Now!
If any of these opportunities interest you, contact the editor to begin the process of contributing to Oncology Nutrition Connection!
If you have writing experience, great. If you don’t, we will find a mentor for you. Contact Maureen Leser, MS, RD, LD, CNSD at [email protected]
Resveratrol is a non-flavanoid polyphenol that gained notoriety in the early 90’s, when an inverse relationship
between intake of red wine and cardiovascular disease incidence was reported (1). It is also recognized as a
plant antibiotic or phytoalexin because of its ability to inhibit fungal infections (2). In humans, absorption of
resveratrol occurs primarily in the duodenum, and while absorption of resveratrol is almost 70%, its
bioavailability is reported to be very poor because it is quickly metabolized and eliminated (3).
red wines (14). Wines produced in countries where the climate is warm and dry
(Australia, Spain, Italy, South Africa and South America) have the lowest resveratrol concentration (1) and a variation of up to 6.8 mg/L has been reported in red wine from different countries (15). However, even wines with the highest concentration of resverarol provide only small amounts, far less than would be able to exert positive health effects of this bioactive substance.
Supplements
The resveratrol supplement industry is booming. While rese
