S1. Lifestyle Modifications and Policy Implications For Primary and Secondary Cancer Prevention - Diet, Exercise, Sun Safety, and Alcohol Reduction
S1. Lifestyle Modifications and Policy Implications For Primary and Secondary Cancer Prevention - Diet, Exercise, Sun Safety, and Alcohol Reduction
S1. Lifestyle Modifications and Policy Implications For Primary and Secondary Cancer Prevention - Diet, Exercise, Sun Safety, and Alcohol Reduction
OVERVIEW
Improved cancer treatments and cancer detec on methods are not likely to completely eradicate the burden of cancer.
Primary preven on of cancer is a logical strategy to use to control cancer while also seeking novel treatments and earlier
detec on. Lifestyle modifica on strategies to improve primary preven on and risk reduc on for the development of can-
cer include choosing a healthy diet with an emphasis on plant sources, maintaining a healthy weight throughout life, being
physically ac ve, regularly using sunscreen and wearing protec ve clothing, limi ng sun exposure during the hours of
10 AM to 2 PM, avoiding indoor tanning, and reducing or elimina ng alcohol use. In addi on to con nued use of ongoing
educa on of the public, health care providers, and cancer support communi es, other policy and public health efforts
should be pursued as well. Examples of supported and successful policy approaches are included in this ar cle, including
efforts to limit indoor tanning and improve community-wide interven ons to reduce ultraviolet radia on exposure as well
as to formally support various alcohol policy strategies including increasing alcohol taxes, reducing alcohol outlet density,
improving clinical screening for alcohol use disorders, and limi ng youth exposure to alcohol marke ng and adver sing.
These preven on strategies are expected to have the largest impact on the development of melanoma as well as breast,
colorectal, head and neck, liver, and esophageal cancers. The impact of these strategies as secondary preven on is less
well understood. Areas of addi onal needed research and implementa on are also highlighted. Future areas of needed
research are the effects of these modifica ons a er the diagnosis of cancer (as secondary preven on).
From the Carbone Cancer Center and University of Wisconsin School of Medicine and Public Health, Madison, WI; Department of Surgical Oncology, Melanoma and Skin Center,
The University of Texas MD Anderson Cancer Center, Houston, TX; Department of Health Promo on Sciences, Mel and Enid Zuckerman College of Public Health, University of Ar-
izona Cancer Center, Tucson, AZ; Biobehavioral Health Sciences Division, College of Nursing, University of Arizona Cancer Center, Tucson, AZ; Department of Medicine, University
of Wisconsin School of Medicine and Public Health, Madison, WI; Be Well Communi es, Cancer Preven on and Control Pla orm, The University of Texas MD Anderson Cancer
Center, Houston, TX.
Disclosures of poten al conflicts of interest provided by the authors are available with the online ar cle at asco.org/edbook.
Corresponding author: Noelle K. LoConte, MD, Carbone Cancer Center and University of Wisconsin School of Medicine and Public Health, 600 Highland Ave., CSC K4/538
(MC 5666), Madison, WI 53792; email: ns3@medicine.wisc.edu.
SIDEBAR 1. American Cancer Society and American Ins tute for Cancer Research/World Cancer Research Fund
Guidelines for Cancer Preven on
Adapted from the American Cancer Society8 and the American Ins tute for Cancer Research/World Cancer Research Fund.9
as well as mely cancer screening. The guidelines are sum- Public, private, and community organiza ons should work
marized in Sidebar 1.8,9 collabora vely at na onal, state, and local levels to imple-
ACS expanded its recommenda ons in 2012 to include the ment policy and environmental changes that:
following call for community ac on to improve the diet and (1) Increase access to affordable, healthy foods in com-
exercise of communi es: muni es, worksites, and schools and decrease access
to marke ng of foods and beverages of low nutri onal
value, par cularly to youth, and
PRACTICAL APPLICATIONS (2) Provide safe, enjoyable, and accessible environments
for physical ac vity in schools and worksites and for
• Lifestyle behaviors play a substan al role in reducing transporta on and recrea on in communi es.
cancer incidence, comorbidity, and survival.
• As such, clinicians should rou nely evaluate lifestyle The American Ins tute for Cancer Research/World Cancer
behaviors and promote healthy lifestyles to reduce the
Research Fund guidelines are con nuously reviewed and the
cancer burden.
• Health promo on for cancer risk reduc on should include
epidemiologic evidence evalua ng the role of diet, physical
healthy food choices, regular physical ac vity, reduc on ac vity, and cancer is updated based on new evidence. The
or avoidance of alcohol, and sun-protec ve behaviors. ACS guidelines are updated by experts in the field every 5 to
• Policy strategies are an effec ve approach to limi ng 7 years; a 2018 update is currently underway. Among the ex-
ultraviolet radia on exposure and reducing high-risk pected advances will be a greater emphasis on the combined
alcohol consump on, thereby reducing the incidence of impact of cancer-preven ve health behaviors in reducing can-
cancer. cer risk and cancer mortality as well as the need to promote
• Whether lifestyle behavior changes can influence cancer healthy ea ng pa erns,10 including the Mediterranean diet.11
recurrence or secondary cancer development is an area
In the area of obesity, beyond adult weight gain and
of needed future research.
high body mass index, guidelines are expected to include
FIGURE 1. Biologic Mechanisms by Which Diet, Physical Ac vity, and Obesity Modulate Cancer Risk
greater emphasis on metabolic health. Recent evidence no reduction in prostate cancer risk with selenium and
suggests that even those with a normal body mass index vitamin E supplementation,16 similar to null or even ad-
may demonstrate metabolic dysregula on, which promotes verse findings from other supplement trials with com-
cancer.12 In addition, work from the Caan laboratory at pounds such as beta-carotene (CARET study)17 or B vitamins
Kaiser Permanente suggests that beyond adiposity, there is (VITAL study).18 There are currently essen ally no random-
a vital role for lean mass in rela on to cancer survival, as ized controlled trials evalua ng the effect of physical ac vity
evidenced for colorectal cancer.13 on cancer risk.
In the area of cancer survivorship, randomized controlled
MECHANISMS: DIET AND PHYSICAL ACTIVITY trials have largely focused on modula on of intermediate
MODULATION OF CANCER RISK biomarkers of cancer risk, including many of the mechanis-
In addi on to the substan al epidemiologic evidence demon- c biomarkers defined in Figure 1. In general, the trials con-
stra ng rela onships between diet, physical ac vity, and ducted have been focused on the more common cancers—
cancer, there are relevant biologic mechanisms that support predominantly breast cancer, as well as prostate, colorectal,
a modifying effect of these lifestyle exposures on cancer risk and endometrial cancers. The impact of interven ons on
and recurrence, as illustrated in Figure 1. cancer-related outcomes is summarized with select studies
Diet, physical activity, and weight control each have in Table 1.19-27
independent and potentially additive effects on these In summary, the role of diet, physical ac vity, and weight
cancer-modula ng biologic mechanisms. Healthy lifestyle management in cancer preven on and survivorship is
choices promote a cancer-suppressing environment at the well established in terms of the epidemiologic evidence
host/systemic, organ/ ssue, and DNA/gene c levels, thus and biologic plausibility. Randomized controlled trials re-
amplifying the poten al together to reduce cancer risk. main sparse and are largely focused on recurrent disease
among cancer survivors. The effect of interven ons has
EVIDENCE FROM RANDOMIZED CONTROLLED been demonstrated but not consistently, par cularly when
TRIALS recruitment includes rela vely “healthy” volunteers. Rec-
The evidence suppor ng a role for diet and physical ac vity ommenda ons for obesity clinical trials in cancer survivor-
in cancer risk reduc on is largely limited to epidemiology. ship have been published, including a 2015 report from
A few randomized controlled trials have been conducted. ASCO.28 Guidelines suggest that trials be conducted by mul-
The largest trial was the Women’s Health Ini a ve, which disciplinary teams, focus on more common obesity-related
included an evalua on of a low-fat diet for the preven on cancers with higher mortality or recurrence risk, and be
of breast and colorectal cancer as well as the role of vitamin sta s cally powered to evaluate cancer outcomes and eco-
D plus calcium supplementa on. These trials showed no sig- nomic endpoints as well as current approaches focused
nificant (p = .07 for ref 14, p = .51 for ref 15) overall reduc- largely on intermediate biomarkers. Priority should be given
on in cancer risk a er an es mated 8 years of follow-up.14,15 to transla ng the evidence for diet, ac vity, and weight
There was a 9% lower risk for breast cancer among women management into clinical and community prac ce as rec-
randomly assigned to the low-fat diet who entered the ommended by the Na onal Comprehensive Cancer Net-
trial with higher dietary fat intake.14 The SELECT trial showed work and others.29-32
Trial Name Reference Popula on Par cipants Diet Ac vity Weight Loss Interven on Outcome
FRESH START Demark-Wah- Breast and prostate 543 X X X RCT with assignment to nontailored Both groups improved; however, the
nefried et al cancer survivors print vs. tailored print materials for tailored print group experienced
(2007)26 improving healthy lifestyle behaviors greater gains in minutes of exercise
per week (+59 vs. +39 minutes), fruit
and vegetable intake (+1.1 vs. +0.6
servings per day), and BMI (−0.3 vs.
+0.1 kg/m2)
CanChange Hawkes et al Colorectal cancer 410 X X X RCT with assignment to either usual Par cipants in the interven on
(2013)27 survivors care or a telephone-based health increased moderate to vigorous
coaching interven on for 6 months physical ac vity by 28.5 minutes per
week and 0.4 servings of fruits and
vegetables per day compared with
the control and decreased calories
from fat by 7% and BMI by 0.9 kg/m2
Abbrevia ons: BMI, body mass index; hsCRP, high-sensi vity C-reac ve protein; RCT, randomized controlled trial.
FIGURE 2. 2017 Tanning Bed Restric on: Under Age 18 Legisla on Across the United States (as of July
2017)
Reprinted from the Centers for Disease Control and Preven on.68
facilities take additional measures to improve the over- and mul disciplinary research ini a ve known as the Moon
all safety of these devices66; this is currently on hold.67 In Shots Program,72 The University of Texas MD Anderson Can-
2012, the first two states enacted legisla on to restrict minors cer Center (MD Anderson) served as the primary scien fic
younger than age 18 from indoor tanning facili es. As of and clinical resource for the Texas Legislature in 2013 on
January 2018, 17 states and the District of Columbia have adop on of a law prohibi ng tanning beds for minors younger
prohibited indoor tanning among minors younger than age than age 18. MD Anderson partners with the ACS–Cancer
18 (Fig. 2).68 Ac on Network to share lessons learned and disseminate
Importantly, there are evolving data to support that these the policy to other states.73 Aligning these approaches with
legisla ve and regulatory ini a ves are having an impact. In a education about the harms of indoor tanning and UVR
study in Texas, 81% of tanning facili es contacted in a mystery overexposure, beginning with our youth, holds tremendous
shopping–style study were compliant.69 Furthermore, results promise toward reducing the burden of melanoma.
from the 2015 Youth Risk Behavior Survey70 and the Na onal
Health Interview Survey71 showed a significant decline in in- Youth Educa on Approaches
door tanning among both students and adults (Figs. 2 and 3).68 In the United States, approximately 55 million students
Efforts con nue to empower policymakers to make in- will a end public and private elementary and secondary
formed decisions regarding the dangers of indoor tanning, schools.74 Because UVR overexposure increases the risk of
such as those led by the ACS–Cancer Ac on Network, a melanoma,75 it is important to implement skin cancer pre-
nonprofit advocacy affiliate of the ACS. As part of its coor- ven on ini a ves early, making schools an ideal se ng for
dinated commitment to melanoma preven on, a collabora ve such efforts. Recognizing the need to reach children early,
FIGURE 3. Percentage of U.S. High School Students Who Used an Indoor Tanning Device in the Past
Year, by Sex, 2009 to 2015
Reprinted from the Centers for Disease Control and Preven on.68
MD Anderson developed Ray and the Sunbeatables, a sun child care center–based interventions, (2) primary and
safety program for preschoolers, kindergarteners, and first- middle school–based interventions, (3) interventions in
grade students as part of the melanoma preven on ini a- outdoor occupa onal se ngs, (4) interven ons in outdoor
ve of the Moon Shots Program.76 This evidence-based cur- recrea onal and tourism se ngs, and (5) mul component
riculum educates children, parents, and teachers about sun community-wide interven ons.81
protec on and promotes sun safety behaviors.76 In the later Mul component community-wide interven ons to pre-
grades, programs such as SunWise and SunSmart have been vent skin cancer combine individual-directed strategies
instrumental in increasing sun safe messages throughout (e.g., items 1–4 above), mass media campaigns, and en-
the United States and Australia to effect lifestyle change.77,78 vironmental and policy changes across mul ple se ngs
According to the 2014 School Health Policies and Prac ces within a defined geographic region in an integrated effort to
Study, 66% of U.S. elementary, middle, and high schools imple- influence ultraviolet-protec ve behaviors. These interven-
mented sun safety or skin cancer preven on instruc on.68,79 ons have been shown to prevent skin cancer by increas-
Despite this progress, fewer than one-half of schools rec- ing ultraviolet-protec ve behaviors by increasing sunscreen
ommend and almost no schools require policies and prac- use.81 An example of this type of programming is being
ces related to sun safety, such as allowing or encouraging implemented by MD Anderson’s Be Well Communi es, a
students to apply sunscreen while at school, encouraging community-driven, place-based approach to cancer preven-
students to wear sun-protec ve clothing, or scheduling on and control.82
outdoor ac vi es when the sun is not at peak intensity.79 Another important feature of the community-wide ap-
Moreover, many states have rules or policies that may proach is that it can simultaneously target mul ple aspects
make using sunscreen or being protected from the sun of cancer preven on; successful implementa on can have
more difficult, such as restric ons on wearing hats during a beneficial mul plica ve effect by favorably impac ng life-
the school day. Furthermore, the FDA considers sunscreen styles that support cancer preven on ini a ves. For exam-
as an over-the-counter drug product; as a result, in some ple, one way to address obesity, which is itself a risk factor for
schools, students are prohibited from bring sunscreen cancer (as described above), is to increase physical ac vity.83
without a note from a physician.68 To address the issue If individuals are encouraged to be physically ac ve out-
of limited sunscreen availability, an increasing number of doors in a way that also addresses prolonged periods of sun
states have adopted legisla on to allow children to pos- exposure, mul ple beneficial endpoints may be achieved.
sess and use sunscreen on public school property and at For example, increased ac ve use of parks has been linked
school events.68,80 to the availability of shade and/or shade-providing devices
among parents and/or caregivers.84-86
Community-Wide Interven ons Focused on In summary, abundant epidemiologic and gene c data
Modifying Healthy Behaviors Including Decreasing support the role of UVR exposure in increasing melanoma
UVR Exposure risk. Development and successful implementa on of pri-
The Community Preven ve Services Task Force, an inde- mary prevention strategies that support The Surgeon
pendent, nonfederal panel of public health and preven on General’s Call to Ac on have the capacity to reduce mel-
experts that provides evidence-based recommenda ons anoma risk. Lifestyle changes—informed and promulgated
about community preven ve interven ons, conducted a by broad- and evidence-based educational programs,
comprehensive systema c review of interven ons for skin legisla ve efforts, and mul component community-wide
cancer. They iden fied five areas for implementa on: (1) initiatives—represent important elements of an overall
effort to significantly reduce the public health burden of The IARC undertook a review of the role of alcohol in car-
melanoma in the future. cinogenesis. In its 2012 monograph on the evalua on of car-
cinogenic risks in humans,94 the IARC synthesized evidence
ADDRESSSING ALCOHOL AS AN APPROACH from a number of sources suppor ng alcohol as a carcino-
TO CONTROL CANCER gen. Mice and rat data on the oral consump on of ethanol/
ASCO has recently joined a number of other interna onal can- acetaldehyde show an increase in the incidence of a number
cer care and public health organiza ons in suppor ng mea- of tumor types compared with controls.94 Coadministra on
sures to reduce high-risk alcohol consump on. In its recently of alcohol with known carcinogens in the drinking water of
published statement on alcohol and cancer,87 which represents rats and mice further enhanced tumor growth.94
its first formal statement on the topic, the ASCO Cancer Pre- The IARC monograph goes on to discuss the oxida ve
ven on Commi ee outlines a number of specific goals. Namely, pathway by which alcohol is metabolized and concludes
in publishing the aforemen oned statement, the commi ee that those persons with impaired ability to oxidize acetal-
seeks to educate the public regarding the causal link between dehyde (e.g., those with one inac ve allele coding for the
alcohol abuse and cancer, support policy changes to curtail ex- aldehyde dehydrogenase-2 [ALDH2] enzyme) to acetate are
cessive alcohol use, educate oncology providers regarding the at increased risk to develop alcohol-related cancers.94 East
role of alcohol in carcinogenesis, and iden fy research needs Asian popula ons have the highest prevalence of a high-risk
to further explore the role of alcohol in cancer risk. gene c variant [(rs671)*2] of ALDH2. This variant encodes
an inac ve form of the ALDH2 enzyme. Studies involving
Epidemiology of Alcohol-Related Cancers these East Asian popula ons correlate the presence of the
The cancer burden a ributable to alcohol is significant. In high-risk genotype with increased risk of cancers of the up-
2012, an es mated 5.6% of worldwide cancer deaths were at- per aerodiges ve tract.95
tributable to alcohol.88 In the United States, alcohol accounted The IARC authors outline a number of addi onal carcino-
for roughly 3.5% of cancer deaths for 2009. Upper airway and genic mechanisms. These mechanisms include oxida ve stress,
esophageal cancers accounted for the majority of alcohol- increased androgen/estrogen produc on, enhanced liver
a ributable deaths among men. Breast cancer accounted fibrogenesis, and decreased folate concentra ons.96 More-
for the majority among women.89 Addi onal cancers causally over, the role of direct contact of acetaldehyde with cell sur-
linked to alcohol include hepatocellular carcinoma and col- faces should be noted, par cularly given the distribu on of
orectal cancer.90 Cancer risk correlates with increasing alcohol cancers clearly associated with alcohol consump on. Acet-
consump on for cancers in which alcohol is implicated.91,92 aldehyde forma on begins in the oral cavity, primarily me-
In its 2010 monograph on the evalua on of carcinogenic diated by oral bacteria. The highest levels of acetaldehyde
risk to humans, the IARC outlines alcohol as a cause of the are indeed within the saliva of the oral cavity immediately
aforemen oned cancer types (oral cavity, pharynx, larynx, a er alcohol consump on, corresponding with the sites of
squamous cell carcinoma of the esophagus, colorectum, liver, cancers most strongly linked to alcohol consump on.95
and female breast) a er thorough assessment of the evi-
dence.93 In this same report, the ques on of type of alcoholic Dose-Response Rela onship
beverage is addressed. The conclusion is that the cancer risk Understanding the dose-response rela onship between
appears to be linked to ethanol irrespec ve of the specific cancer risk and alcohol consump on is important for a
alcoholic beverage (e.g., beer, wine, or hard liquor).93 number of reasons. Understanding the cancer risk increase
Alcohol has been implicated in a number of other cancers rela ve to increase in alcohol consump on is important for
as well, and the full breadth of causal rela onships remains educa ng pa ents. Moreover, apprecia ng when cancer
to be determined defini vely. For example, suspicion that risk begins to increase as it relates to alcohol consump on
alcohol causes gastric and lung cancers is high based on furthers our understanding as oncology prac oners, be er
several studies. However, strong correla ons with other risk allowing us to counsel pa ents.
factors (i.e., Helicobacter pylori infec on in gastric cancer Table 2 summarizes the results of a large meta-analysis92
and smoking in lung cancer) has led to an inability to estab- addressing the rela ve risks of cancers linked to alcohol rel-
lish alcohol as an independent risk factor.93 a ve to the amount of alcohol being consumed. Light drink-
ing, moderate drinking, and heavy drinking correspond to
Carcinogenic Mechanisms of Alcohol consuming 12.5 g or less, 50 g or less, and more than 50 g
It is clear that alcohol plays an important role in carcinogene- of alcohol per day, respec vely. As a point of reference, a
sis, and evidence points to the fact that the specific alcoholic standard drink was considered to contain 12.5 g of alcohol.92
beverage does not meaningfully propagate or mi gate risk.6 Table 2 demonstrates mul ple valuable points. First, note
Recall that ethanol is eliminated from the body by oxida on that the magnitude of risk differs for different cancer types,
to acetaldehyde—mediated by alcohol dehydrogenase— with the greatest risk noted for cancers of the oral cavity
and eventually to acetate. Although the exact mechanism and pharynx. For heavy drinkers, the rela ve risk of oral cav-
by which alcohol leads to carcinogenesis remains unclear, ity and pharyngeal cancers was more than five mes that of
animal models suggest that it is acetaldehyde rather than nondrinkers. Not surprisingly, the greatest risks were seen
ethanol itself that is carcinogenic and mutagenic.94 in cancers where alcohol and its metabolites come in direct
TABLE 2. Summary of the Rela ve Risks From a Meta-Analysis for the Associa on Between Amount of Alcohol
Drinking and Risk of Cancer
Light Drinker
(< 1 Drink Moderate Drinker (2–4 Heavy Drinker (> 4 Drinks
Type of Cancer Nondrinker per Day) Drinks per Day) per Day)
Oral cavity and pharynx 1.0 (referent) 1.13 (1.0–1.26) 1.83 (1.62–2.07) 5.13 (4.31–6.10)
Esophageal squamous cell 1.0 (referent) 1.26 (1.06–1.50) 2.23 (1.87–2.65) 4.95 (3.86–6.34)
Larynx 1.0 (referent) 0.87 (0.68–1.11) 1.44 (1.25–1.66) 2.65 (2.19–3.19)
Liver 1.0 (referent) 1.00 (0.85–1.18) 1.08 (0.97–1.20) 2.07 (1.66–2.58)
Female breast 1.0 (referent) 1.04 (1.01–1.07) 1.23 (1.19–1.28) 1.61 (1.33–1.94)
Colorectal 1.0 (referent) 0.99 (0.95–1.04) 1.17 (1.11–1.24) 1.44 (1.25–1.65)
contact with the target ssues. Although rela ve risks are Areas of Needed Research and the Role of the
clearly highest with moderate and heavy drinking, risk per- Oncologist
sists even among light drinkers.92 Looking to the future, research ques ons in need of inves-
In a meta-analysis looking specifically at cancer risks with ga on are numerous. Although the causal link between
alcohol consump on of one drink per day or less, elevated alcohol and some cancers is clear, increased knowledge re-
risk persisted for some cancers.97 Specifically, the summary garding the mechanisms underpinning cancer risk is needed.
rela ve risk for squamous cell carcinoma of the esophagus The effects of concurrent use of alcohol while undergoing
was 1.30 (95% CI, 1.09–1.56). Similarly, the summary rela- treatment with surgery, radiation, chemotherapy, or any
ve risk for oropharyngeal cancer was 1.17 (95% CI, 1.06– combina on of therapies are largely unknown. The broader
1.29). Breast cancer risk was also elevated, with a summary ques on of how to best intervene in the general community
rela ve risk of 1.05 (95% CI, 1.02–1.08). No other cancer to reach those at risk for alcohol-related cancers remains
associa ons were evident.97 In the se ng of the above find- unanswered; in a similar vein, the cancer survivorship com-
ings, the American Ins tute for Cancer Research in conjunc- munity is in need of evidence-based interven ons to ad-
on with the World Cancer Research Fund recommended dress high-risk alcohol use in an effort to curb secondary
that “If alcoholic drinks are consumed, limit consump on to cancers related to alcohol.
two drinks a day for men and one drink a day for women.”79 The oncologist stands at the forefront of addressing the
Furthermore, they also recommended that “For cancer pre- issue of alcohol-related cancer risk. The oncologist plays a
ven on, it’s best not to drink alcohol.”80 cri cal role in trea ng cancers arising from alcohol use but
perhaps more importantly, he or she is a cri cal voice in the
Public Health Strategies to Control Alcohol Use preven on of such cancers—both prior to an ini al cancer
With the rela onship between alcohol and increased cancer diagnosis and in the capacity of preventing subsequent
risk well evidenced, the ASCO Cancer Preven on Commi ee malignancies. The aforemen oned research ques ons are
statement moves to promote meaningful change through le to the oncologist to answer. Taken as a whole, the oncol-
public health strategies. In so doing, ASCO joins a chorus of ogy community and the prac oners within it are charged
interna onal cancer care and public health organiza ons with addressing a culture, both in the United States and
already calling for such changes. Such policies are also evi- worldwide, that is very accep ng and o en promo ng of
dence based. ASCO specifically outlines strategies including, alcohol use. Perhaps the single greatest task before us is to
but not limited to, the following: promote an honest recogni on of the risks of alcohol, even
1. Develop clinical strategies to screen for at-risk alcohol in modera on.
use and provide treatments and/or referrals for those
in need of services.98 CONCLUSION
2. Reduce alcohol outlet density. Reduc on of sites Although cancer incidence and death rates are decreasing,
of legal alcohol sale has proven to be an effec ve the burden of cancer remains high in the United States
strategy in previous experiences.99-102 and globally. Preven ng cancer from developing, where
3. Increase taxa on and pricing of alcoholic beverages. possible, is a key method for reducing the burden of can-
These increases have been shown previously to cer. Primary preven on of cancers is possible via poten-
reduce excessive consump on.103-105 ally modifiable lifestyle changes, including maintaining a
4. Restrict youth exposure to adver sing of alcohol. healthy weight, obtaining regular physical activity, avoid-
Drinking at a young age leads to increased risk of ing high-risk sun exposures, and limi ng alcohol intake.
alcohol dependence.69 Guidelines have been published by various agencies with
recommenda ons for recommended lifestyle modifica- melanoma. The role of lifestyle modifica ons for second-
ons. This specifically has implica ons for breast, col- ary preven on is less well understood, and this is a cri cal
orectal, head and neck, esophageal, and liver cancers and area for future research.
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