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Alcohol Intake and Breast Cancer Prevention in Women Ages 45 or Older
 
 
 
 
 
Abstract
Moderate alcohol intake is associated with around 30-50% high risks in breast cancers. Cohort and case-control studies provided data to support modest increases. Recent epidemiologic and molecular cancer biology studies have crucial evidence that supports the association between alcohol intake and breast cancer risk is real and not endorsed by correlation of the studies’ exposures, factors, and outcomes. The reviews of women who carried BRCA1 and 2 gene mutations are not at increased risk of breast cancer. Heart disease incidence is more significant than breast cancer. Modest alcohol intake could reduce the risk of heart diseases; the latest evidence to evaluate if alcohol intake reduction and prevention should focus on women at increased risk of breast cancer. Most evidence has shown the effects of alcohol intake on breast tumor recurrence and survival rates for patients diagnosed with breast cancer.

Introduction  
Breast cancers are diseases in breast cells that grow uncontrollably and are many subtypes of breast cancer, based on specific cells in the breasts develop into cancers. The breasts have three main parts: ducts, lobules, and connective tissue (U.S. Department of Health and Human Services 2020). Breast cancers may form in different parts of the breast. Moreover, breast cancers have occurred in women 45 years old or older and grow in the ducts or lobules. The two primary common types of breast cancers are invasive ductal carcinoma and invasive lobular carcinoma. Invasive ductal carcinoma cells can extend outside the ducts into other parts of the breast tissues and metastasize to other organs’ parts of the body.
Invasive lobular carcinoma cells grow from the lobules to the breast tissues locally and spread to other body organs. Each year in the U.S., approximately 250,000 breast cancer cases are newly diagnosed in women, and about 42,000 die each year from breast cancers. African American women have higher rates of death than White women from breast cancers. Studies have shown that women’s risks for breast cancers are factors, including getting older, being a woman, and alcohol intake (U.S. Department of Health and Human Services 2020).
Alcohol intake is associated with breast cancer risks with a 7-10 percent increase in risk for each 10g (~1 drink) daily alcohol intake by women over 45. Breast cancer risk significantly increases by 4-15 percent for a small number of alcohol intakes (≤1 drink per day or ≤12.5g per day) that do not increase cancer risks in other organs in women (McDonald et al. 2004).
Alcohol intake raises both public health and medical concerns because almost half of the women of childbearing age drink alcoholic beverages and 15 percent of female drinkers at these ages have at least four or more drinks at a time.  Around 4-10 percent of female breast cancers in the U.S. are attributable to alcohol intake, accounting for 9000-23,000 newly diagnosed invasive breast cancers every year. Having risk factors does not reply; an individual will have a disease, and all risk factors do not have the same effects (Morch et al. 2007).
Therefore, a better understanding of how alcohol intake may increase breast cancer risk is needed to prevent breast cancers in these groups.
Alcohol Intake Related to Genes and Breast Cancers
Ethanol can metabolize by alcohol dehydrogenase (ADH) to Acetaldehyde (AA) and can remove by aldehyde dehydrogenase (ALDH) to acetate. The genes, which encode for ALDH and ADH are polymorphic. The enzymes they encode to determine a rate of ethanol metabolisms and concentrations of intermediate metabolites, including a carcinogenic AA (Scoccianti et al. 2014).
Suppose associations between alcohol intake and breast cancer are attributable to an unmeasured confounder. In that case, we could not expect the strength of alcohol intake and breast cancer association to change based on the genotype of enzymes that regulate ethanol metabolisms unless a confounder is also mapped to a genotype. Modifications of alcohol intake and breast cancer association by enzymes’ activities could support evidence that associations are causal (Chen et al. 2011).
Moreover, AA could play a crucial role in alcohol-related carcinogenesis. Activities of gene encoding ADH determine levels. Some studies evaluated the effect modification of the association of breast cancer risk and alcohol intake by genes encoding ADH isozymes (Suzuki et al. 2005).
There are many classes of ADH genes in humans. It is a class I ADH isozymes that are involved in ethanol oxidations. Several genes, which encode these certain enzymes are ADH1A, ADH1B, and ADH1C. ADH1B polymorphism is found mostly in Asians, and the genetic variants ADH1B have nearly 40 times more enzymatic activities than a wild-type ADH1B.
Therefore, having ADH1B causes prolonged exposure to AA and is thought to increases breast cancer risks. Some studies have reported that a type of ADH1B allele present modifies the association between alcohol intake and breast cancer (Coronado et al. 2011).
However, AA is responsible for side effects related to alcohol intake. Therefore, the homozygous recessive carrier of ADH1B has severe side effects from alcohol intake. They are alcohol abstainers, making this genotype less studied due to small numbers of alcohol intake. (Tjonneland et al. 2004). In addition to ADH1B, ADH1C also affects enzymatic activities, but to a lesser extent: ADH1C alleles have nearly 2.5 times more enzymatic activity than ADH1C. Polymorphisms in the ADH1C genes are mostly found in Whites than polymorphisms in ADH1B; they have been more studied in the US population.
In a population-based study, Terry et al. (2006) stated that there were 1,047 breast cancer patients and 1,101 controls; the authors found that ADH1C carriers who had moderate alcohol intake (15-30 grams per day) were at nearly two times risk of having breast cancer that to nondrinkers (OR 1.97, 95% CI 1.10-3.54). These findings show the interaction of the ADH1C genotype with the alcohol-breast cancer association support that this association is causal.
Alcohol Intake and Breast Density
In addition to their metabolites’ carcinogenesis roles, alcohol may alter estrogen levels, causing to change in breast density, resulting in breast cancer risks. The breast cancer risks related to breast cancer hormone are mammographic density, connective and epithelial tissues in the breast. Greater density means a 4-6-fold increase in breast cancer risks. Additionally, alcohol intake has been linked to modifying the mammographic density in dose-response ways.
The correlations between alcohol intake and breast density provide more evidence that alcohol is linked to breast cancer.
Epidemiologic studies have applied different parameters to assess mammographic densities with previous research using qualitative measures, such as the Wolfe parenchymal patterns (Conroy et al. 2012).
Some frequently used qualitative measures in recent studies are BI-RADS (breast imaging reporting and data system) or applying the computer-based threshold measure program ranging from 0-100%. We can categorize breast density using Wolfe patterns into four types:

• N1 (predominately fat)
• P1 (ductal prominence in <25 percent of the breast)
• P2 (ductal prominence in >25 percent of the breast)
• DY (extensive dysplasia)

Previous studies have assessed breast densities using Wolfe patterns; one study by Jeon et al. (2011) stated a 30 percent prevalence rate related to high density and high alcohol intake. Another study by Yaghjyan et al. (2012) showed that the prevalence rate was 21percent (Table 1). The Wolfe patterns reflect significantly much more significant changes in density than other quantitative measures.
Table 1
Table1 shows study findings of an association between alcohol intake and mammographic density.

Authors and Year	Recruited Year	Study Population	Age	N	Prevalence	Results	Adjustment
Jeon et al. 2011	2008	Mammography Screening (Korea)	40-80 mean 50.6	516	30% of current/past users	Outcomes: BI-RADS (III/IV versus I/II) Versus nonusers: Current/past users OR 1.36, 95% CI 0.87- 2.14	BMI, age, Menopausal status, Family history, Ages at menarche, parity, OC use, and Educational background
Yaghjyan et al. al. 2012	1990-2008	Fernald Community Cohort (USA)	mean 51.3	1125	21% users	Outcomes: BI-RADS (IV versus I) Versus nonusers: users OR 2.0, 95% CI 1.4-2.8	BMI, Age at mammogram, menopausal status, age at menarche, age at first birth, family history, and smoking history

 
Some previous studies examined alcohol intake, and breast density has found a positive association. The Minnesota breast cancer family study stated that a positive association between alcohol and high-density (Jeon et al. 2011).
In their study, Yaghjyan et al. (2012), the longitudinal Fernald Community cohort (N=1,125) study, using BIRADS to measure breast density, (N=11125). They found that breast density was linked to BMI at mammogram (P for trend<0.001), and parity (P for trend=0.02) and related to alcohol intake (users vs. nonusers: odds ratio 2.0, 95 percent confidence interval was 1.4-2.8). Alcohol intake was associated with breast density positively. The association was more significant in women with a family history of breast cancers (P<0.001) and women with previous HRT (hormone replacement therapy) (P<0.001). Parity was associated with breast density in most subsets, except premenopausal women and women with non-family history. The parity associations with breast density were greater in women with HRT history (P<0.001). Consideration on Alcohol Intake for Breast Cancer Prevention
According to the Healthy People 2020 initiative goals, one is to decrease an average alcohol intake annually by 10% over ten years. To meet a goal, public health and medical workers will need to develop an effective strategy to adjust alcohol drinking behaviors in women who drink over one drink per day. The national epidemiologic survey on alcohol intake and associated conditions (NESARC) reported that over three years, female drinkers were at baseline, 11 percent reported abstaining from alcohol intake in three years of study. In current woman drinkers who did not exceed drinking limits at baseline, 20 percent stated exceeding drinking limits in the past year. These results reflect that though alcohol intake trends may appear stable, women may change drinking habits. Epidemiologic evidence, complemented further by genetic factor studies and intermediate markers, suggests that alcohol intake may increase breast cancer risk. High alcohol intake has been linked to other health conditions, including liver diseases such as alcoholic hepatitis and cirrhosis, high blood pressure and cardiomyopathy, and various types of cancers, such as pharynx, mouth, esophagus, larynx, and colon (Li et al. 2010)
Alcohol abuse could lead to crimes, accidents, and mental health issues. However, modest alcohol intake has lined to a low risk of CHD (coronary heart disease). In a meta-analysis, woman drinkers had a 29 percent reduced risk of CHD incidence and a 21 percent reduced risk of CHD mortality rate than non-drinkers.
According to the 2009-2010 NHANES study, over fifty percent of U.S. women were drinkers who had more than 12 drinks in the past year. Forty-one percent were moderate drinkers (≤7 drinks per week), and ten percent were heavy drinkers (>7 drinks per week). The prevalence rate of heavy drinking was greater in non-Hispanic white women (12%) compared to Non-Hispanic Black (7%) or Hispanic women (4%). In non-Hispanic Black and Hispanic groups, young adult women (20-39 years) tended to consume alcohol more than older women (≥60 years). Moreover, the prevention challenges in those women at great risk of breast cancer are that cardioprotective benefits of alcohol among women could be fewer consequences; however, the evidence has not supported that increased risk women of breast cancer who drink alcohol are at higher risk because of their alcohol intake (Li et al. 2010).
Furthermore, BRCA1 and 2 are the most well-known studies of genes affected by hereditary breast and ovarian cancers. BRCA1 and 2 genes may protect the individual from having a particular type of cancers; however, mutations in BRCA1 and 2 genes cause them not to work correctly; consequently, if a person inherits one of these gene mutations, you are more likely to have breast, ovarian cancers.
More studies have focused on women with BRCA1 or BRCA2 gene mutations. In a large case-control study conducted in postmenopausal BRCA1 or BRCA2 gene carriers (N=1,925), alcohol intake was not related to BRCA-associated with breast cancer (McCarty et al. 2012).
The BRCA gene studies have been retrospective, depending on their samplings, which could be affected by survivor bias. The low prevalence of BRCA gene carriers could limit the ability to detect alcohol and carrier status associations. Although the empirical evidence does not suggest that high-risk women have an increased risk of breast cancer from alcohol intake, prospective confirmation of study findings across women at a higher continuum of risk, including BRCA1 & 2 gene carriers, is needed.
Conclusion
Alcohol intake is associated with an increase in breast cancer risk. The association has been studied in cohort studies and case-control, reducing the likelihood of explaining selection biases. Effect modifications of this relationship by the ADH1C genotype, and the associations between alcohol intake and high breast density, provide more evidence to support the causal effect. Although all recent studies do not support increased breast cancer risks with heavy alcohol intake in women at high risk of breast cancer, prospective studies are needed to rule out biases. The well-known evidence suggests that increased risk women are not at increased risk from moderate alcohol intake. With the prevalence of alcoholic drinking in U.S. women, many could benefit from staying within the drinking guidelines of ≤1 drink per day for overall health to reduce breast cancer risk in 45 or older women.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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