Cancer is a severe life-threatening condition that occurs due to a deterioration of the body’s genetic and immune machinery to fight against a variety of infections. There are a plethora of mechanisms predisposing individuals to this health assault. Cancer is strongly involved in causing mortalities irrespective of age and sex. Various therapeutic interventions have been in progress to circumvent the metastatic lesions at their initial stages. But to date, no satisfactory drug medication was believed to provide a complete remedy to the malignant disorders. However, nutrition was considered reliable in contrast to all the available therapies. There is a need to explore the role of nutrition and therefore the present description deals with highlighting its impact on oral, breast cancers, and colon cancers.
Previously, it was reported that approximately 35% of cancer deaths in the United States were reported to be managed by the modification of diet (Willet 1995). This is because of issues relating the consumption of red meat to the development of colon cancers. Here, physical activity was also reported to strengthen the pivotal role of nutrition (Willet 1995).
Although, there is a controversy regarding the connection between certain foods like a fat-enriched diet and breast cancer, the intake of fruits and vegetables was shown to confer resistance to wide a range of cancer-causing agents (Willet 1995). Hence, data indicating the lessening effects of diet modification on the incidence of cancer deaths provides better supporting research where the methodology involved retrieving the prevalence indices accumulated so far (Willet 1995). However, there seems to be narrow information on the effects of fat on the metabolism that may play role in the episode of cancer.
Later studies were feeble in supporting the compelling evidence obtained from animal and ecological concepts regarding the nutritional aspects of breast cancer (Hunter and Willett, 1996). Although the risk was attributed to the intake of fat in low amounts or early life, it was hypothesized that fat enriched food, childhood and adolescence growth rate could serve as risk factors (Hunter & Willett, 1996). Olive oil may have some benefits where a low intake of vegetables and increased alcohol consumption were considered risky (Hunter and Willett, 1996). This study has better addressed the issues of food intake and the risk of breast cancer with special emphasis on early age in contrast to the previous evidence on mid-life involvement (Hunter & Willett, 1996).
Next, the trends in dietary style might influence cancer incidence. In Spain, breast cancer mortality (BCM) rates have increased dramatically from the lowest rates over the past 30 years (Fátima Prieto-Ramos et al. 1996). This was revealed when a study was conducted at the ecological level to determine the past and current dietary patterns associated with breast cancer mortality (Fátima Prieto-Ramos et al. 1996). The methodology was significant as it involved a reasonable sample size in various provinces with a good time. The findings have shed light on the increased proportion of breast cancer rates in vulnerable people with an age range of 35–64 years group (Fátima Prieto-Ramos et al. 1996).
The reasons could be attributed to an accelerated switch in food consumption patterns from the traditional diet accompanied by a history of beef and total meat consumption (Fátima Prieto-Ramos et al. 1996). This may indicate that the non-vegetarian risky diet in the involvement of breast cancer may require management through proper hygienic changes.
Therefore, the role of nutrition could be better strengthened with vegetables and fruits that might serve as valuable dietary tools when supplemented.
The link between nutrition and oral cancer has been reported from the data obtained from the ecologic and case-control studies (Marshall & Peter, 1996). Geographical variation has a pivotal role in influencing the impact of nutrition variation. Fruits and vegetables were described to confer protection against oral cancer with few contradictions (Marshall & Peter, 1996). Similarly, certain foods do not serve a protective role in all cases when compared with those of smoking and alcohol consumption (Marshall & Peter, 1996). The reason behind this controversy was not properly addressed in the article. Here, tobacco use and alcohol consumption were considered as two main risk factors than nutrition as far as the nutritional epidemiology of oral cancer is concerned (Marshall & Peter, 1996). As such, oral hygiene was reported to be largely influenced by the above-mentioned risk factors that could also deserve the role of confounders (Marshall & Peter, 1996).
Therefore, tobacco use and alcohol consumption have become the major sources of oral cancer. But geographical variation could play role in influencing cancer incidence (Marshall & Peter, 1996). Hence, there is a need to explore the frequency of tobacco and alcohol consumption across various nations. This report has provided some valuable insights on oral cancer and could be strengthened with much more data from further studies.
This might greatly modulate and stabilize nutrition intervention programs in both developed and developing countries. However, there is a need for information regarding the cancer survivors’ beliefs about the causes of prostate, colorectal, or breast cancers (Wold et al. 2005).
There has been a significant difference between the beliefs of cancer survivors and experts on the causative factors of cancers (Wold et al. 2005). The reasons were attributed to unawareness about the risk contributing agents which might help the survivors to overcome the adverse effects. The data obtained from a survey on 416 patients with breast cancer, 165 with prostate cancer, and 89 with colorectal cancer revealed that cancer survivors furnished information on hereditary factors, smoking, pollutants or occupation, and stress as the causative factors of their cancer types(Wold et al. 2005). Further, the role of behavioral factors such as obesity and physical inactivity were not mentioned by the participants (Wold et al. 2005). This could be a flaw in the description. Hence, it can be inferred that obese individuals with minimum physical activity may be at an increased risk of developing cancer in addition to other known etiologies. As such, they may also need to be consulted with proper questionnaire format along with the survivors of prostate, colorectal, or breast cancers.
Henning et al (2007) described the association between Nutrition and lifestyle as an important modulator of chronic diseases. In countries like the US, unhygienic diet habits such as high intake of processed foods rich in fat and low intake of fruits and vegetables, secondary lifestyle has become major health-compromising factors (Henning et al. 2007).
As such, assessing the toxicity of environmental pollutants with diet being the major source, has received much research attention. There are foods with fat-soluble pollutants containing higher levels of persistent organics than vegetable contents (Henning et al. 2007).
Since, nutrition has the potential to guide lipid milieu, oxidative stress, and antioxidant status within cells, an effective modulation in the diet may induce good benefits on biological processes (Henning et al., 2007). Therefore, nutritional interventions could become reliable tools in preventing diseases associated with environmental toxic insults (Henning et al. 2007).
This description has provided valuable insights on the methodology focused on the negative impact of toxins such as polychlorinated biphenyls (PCBs) and the beneficial effect of fruits and vegetables, rich in antioxidants and anti-inflammatory nutrients or bioactive compounds (Henning et al. 2007). Although this is a worth deserving report, it seems narrow as it failed to address certain issues of various environmental toxins that may cause a plethora of complications.
Apart from environmental agents, malnutrition and quality of life were reported to be associated with malignant disorders like squamous cell carcinoma (SCC) of the oral, oropharyngeal, and hypopharyngeal cavity (Vandenberg Manon et al. 2008). A study conducted on 47 patients with SCC revealed that patients on radiotherapy and treatment modality of radiotherapy with surgery or chemotherapy were prone to malnutrition without any significant changes in body weight or quality of life (QoL) (Vandenberg Manon et al., 2008).
To overcome the adverse effects of malnutrition, nutrition support may need to be provided for a rapid diagnosis (Vandenberg Manon et al. 2008). But the mechanism of how malnutrition contributes to adverse effects needs to be explored as there is little sanctity in the information provided despite reasonable and convincing data. It is reasonable to assume that malnutrition could also play role in the episode of colon, prostate, and breast cancers. As such, the effects of malnutrition could be better understood and may be applied in an evidence-based manner. So, the parameters that are likely to contribute to the cancer risk are the human diet, pesticides, food additives, and packaging materials (Ojeswi et al. 2008).
This information could help to devise a proper nutritional paradigm for alleviating the mortality rates associated with cancer incidence.
The reasons could be the fact that the certain ingredients of food such as calories, fat, sodium chloride, fruits and vegetables, and products of food processing, synthetic dietary carcinogens, unintentional and intentional food additives were reported to be significantly correlated with cancer at a higher rate (Ojeswi et al. 2008).
As pesticides run the risk of toxicity, they may be better regarded as environmental toxins. Lethal doses might enter the food chain and cause potentially life-threatening complications. Hence, this part of the description provides a reasonable connection with the previous report of Henning and his co associates on the role of environmental toxins in influencing cancer incidence. The controversy surrounding diet and cancer has led the United States Food and Drug Administration (FDA) to receive a health claim petition for calcium supplements and for lessening the risk of colorectal, breast, and prostate cancers (Kavanaugh et al. 2008). These were focused on emphasize the relationship between food or food components and diseases like cancer or cardiovascular disease or health-related condition such as hypertension (Kavanaugh et al. 2008). Labeling of conventional foods and dietary supplements is a mandatory prerequisite strongly required by FDA (Kavanaugh et al. 2008). Hence, this initiative could be of valuable help to cancer-fighting individuals.
But some of the flaws were that the agency did not find reasonable evidence to assist the health claims for calcium and a reduced risk of breast and prostate cancers in contrast to a limited evidence for the relationship between calcium intake and colorectal cancer risk. (Kavanaugh et al. 2008). The reason behind this imbalance was not well addressed in the report. Further, investigations may be required.
Garavello, Giordano and Bosetti (2008) described that diet diversity could play a beneficial role in seeking a hygienic diet and preventable cancer. This was revealed in a large case-control study carried out between 1991 and 2005 in Italy. The methodology has especially focused on variety in food intake calculated as the total number of foods consumed at least once per week in 805 patients with cancers of the oral cavity and pharynx, and 2,081 patients admitted for acute, non-neoplastic diseases, unrelated to tobacco or alcohol consumption (Garavello et al. 2008).
It was revealed that a greatly diversified or diet varied in vegetables and fruit could serve as a reliable indicator of oral and pharyngeal cancer risk in contrast to that served by alcohol and tobacco consumption alone as cancer causing factors (Garavello et al. 2008). This report seems to be narrow as it is more concerned with oral and pharyngeal cancer. But it is reasonable to mention that the information could be retrieved in an evidence-based manner to address issues arising from colon and breast cancers.
Therefore, it could be inferred that the variation in dietary patterns may tremendously influence cancer incidence. In the earlier part of this description, the content has emphasized the role of fruits and vegetables with trends in dietary styles.
This was recently supported by a study that determined the role of dietary patterns in the recurrence of cancer and mortality of early-stage breast cancer survivors. It involved the participation of nearly 1,901 patients whose diet habits were assessed with a food frequency questionnaire (Marilyn et al. 2009). Here, high intakes of fruits, vegetables, whole grains, poultry, and high intakes of red and processed meats and refined grains were identified as prudent and western patterns of diet, respectively (Marilyn et al. 2009).
The study group has identified 128 cases of breast cancer out of 268 recurrences and 226 all-cause deaths. A significant decrease in the risk of overall death and death from non–breast cancer causes were the result of a prudent dietary pattern (Marilyn et al. 2009).
This has contradicted the western dietary pattern that has contributed to a comparatively increased risk of overall death and death from non–breast cancer causes (Marilyn et al. 2009). It was described that hygienic dietary patterns could enhance survival if adopted for women diagnosed with early-stage breast cancer (Marilyn et al. 2009). The data is enough to provide convincing evidence.
Although, no association was reported between these dietary patterns and risk of recurrence or deaths from breast cancer, a much detailed investigation on various cancer markers like BRCA1 and association with nutrition parameters could provide useful information. Hence, this report seems to be inadequate in furnishing this information. Daniel et al. (2009) mentioned that dietary intake of omega-6 and omega-3 fatty acids could lessen the risk of colorectal cancer. This study involved a large cohort of data obtained from 43,108 men and 55,972 women.
The hypothesis was that the intake of omega -6 and omega -3 fatty acids may or may not be associated with the incidence of colorectal cancer in men and women (Daniel et al. 2009). Here, linolenic acid was reported to be the primary contributor of total -3 intake presenting the increased risk in women whereas total -6 and marine -3 intake were reported to present with higher and lower risk, respectively (Daniel et al. 2009). This data could indicate a somewhat controversial regarding the validation of the hypothesis and the reasons were attributed to sex differences and sudden findings (Daniel et al. 2009).
Hence, it can be inferred that the role of a diet rich in omega 6 and omega 3 fatty acids could be better understood with a more clear elucidation of unexpected findings as mentioned in the report. Further, there is no clear description regarding the assessment of linoleic acid in addition to fat or meat. This could be because a significant portion of women was reported to acquire breast cancer from the imbalanced fat intake as revealed from the previous description (Willet 1995). It is not completely known whether these women are imprudent regarding the diet constituents that might serve a pivotal role in influencing the cancer rates.
Similarly, in men, the diet habits could be altered more frequently with alcohol consumption or cigarette smoking when compared to women who exhibit a moderate intake of these components (Hunter & Willett, 1996). These differences could have largely interfered with the data as unexpected or sudden findings. The data obtained is enough to provide reasonable evidence on the safety that may be associated with the intake of omega fatty acids. There is a need for additional information on the involvement of other fatty acids that fall under the category of omega group.
To this end, researchers have described that walnut consumption could provide the essential components that contain omega 3 fatty acids in addition to phytosterols, polyphenols, carotenoids, and melatonin (Hardman & Ion, 2008). The findings from the data revealed that walnut consumption has led to decreased tumor cell proliferation but has not influenced apoptosis which is a key component in most cancers (Hardman & Ion, 2008). This is a flaw in the description and needs to be explored further. In addition to these findings, racial differences could also predispose individuals to develop cancer.
In a case–control study, dietary patterns were assessed in African Americans and Whites with colon cancer risk (Satia et al. 2009). Although the methodology involved a food frequency questionnaires and intake patterns, there is inadequate information regarding alcohol consumption and smoking. This may not totally strengthen racial differences in colon cancer incidence.
Finally, cancer mortality rates have been described to be significantly reduced by dietary zinc in contrast to iron that enhances the risk of developing oral, breast, and colon cancer in addition to other cancers (Grant 2008). Here, the roles of zinc and iron need to be clearer despite the data obtained on a large ecological study was sufficient for reliable dietary indices of zinc and iron.
Because of the above description, nutrition has potential benefits to lessen the incidence of cancer. Fruits and vegetables have a beneficial role in contrast to fatty acids especially omega 3 and 6. This particular aspect has tremendously influenced breast cancer incidence rates where controversy remains to be addressed. The issues of oral and colon cancers have been well addressed but may require further confirmation regarding the methodology as seen with gender and racial differences. Dietary patterns could also influence cancer to a maximum extent. However, studies dissecting the relationship between the mechanisms and the pathogenesis have to be evaluated. Walnut consumption has better cancer-curing strategies as it has several components in addition to omega fatty acids. There seem to be inverse relationships of zinc and iron on their protective factors. This needs to be investigated for concrete evidence.
A nutshell diet enriched with protective components could serve as a reliable tool to reduce cancer incidence.
References
Daniel, C.R., McCullough, M.L., Patel, R.C. 2009.Dietary Intake of omega-6 and omega-3 Fatty Acids and Risk of Colorectal Cancer in a Prospective Cohort of US Men and Women. Cancer Epidemiology Biomarkers & Prevention, 18,516-525.
Fátima Prieto-Ramos, Lluís Serra-Majem, Carlo La Vecchia, José M. Ramon, Ricard Tresserras, Lluís Salleras.1996. Mortality Trends and Past and Current Dietary Factors of Breast Cancer in Spain. European Journal of Epidemiology, 12(2);141-148.
Grant WB. 2008 An ecological study of cancer mortality rates including indices for dietary iron and zinc. Anticancer Res 28(3B):1955-63
Hardman, WE, Ion, G. 2008. Suppression of implanted MDA-MB 231 human breast cancer growth in nude mice by dietary walnut. Nutr Cancer 60(5):666-74.
Hennig, Bernhard., Adrenne S. Ettinger et al. (2007).Using Nutrition for Intervention and Prevention against Environmental Chemical Toxicity and Associated Diseases. Environmental Health Perspectives, 115 (4); 493-495.
Hunter, DJ & Willett, WC. 1996. Nutrition and breast cancer. Cancer Causes & Control 7(1); 56-68
Kavanaugh, Claudine J, Trumbo, Paula R, Ellwood Kathleen, C. 2008. Qualified Health Claims for Calcium and Colorectal, Breast, and Prostate Cancers: The US Food and Drug Administration’s Evidence-Based Review. Nutrition and Cancer-An International Journal 61,157-164.
Marilyn L Kwan, Erin Weltzien, Lawrence H Kushi, Adrienne Castillo, Martha L Slattery, Bette J Caan. (2009). Dietary Patterns and Breast Cancer Recurrence and Survival among Women with Early-Stage Breast Cancer. Journal of Clinical Oncology, 27,919-926
Marshall James R & Peter Boyle 1996. Nutrition and Oral Cancer. Cancer Causes & Control 7(1); 101-111.
Ojeswi B K, Khoobchandani Menka, Hazra DK., Srivastava, M M.2008. Nutrition and Dietary Carcinogens: Risk and Aggressiveness. National Academy Science Letters-India, 31, 311-318.
Satia JA, Tseng M, Galanko JA, Martin C, Sandler RS. 2009 Dietary patterns and colon cancer risk in Whites and African Americans in the North Carolina Colon Cancer Study. Nutr Cancer 61(2):179-93
Van Den Berg Manon, GA, Rasmussen-Conrad Ellen L, Van Nispen Lillian, Van Binsbergen Jaap J, Merkx Matthias AW. 2008. A Prospective Study on Malnutrition and Quality of Life in Patients with Head and Neck Cancer. Oral Oncology 44(9); 830-387.
Werner Garavello, Laura Giordano, Cristina Bosetti , Renato Talamini, Eva Negri, Alessandra Tavani, Patrick Maisonneuve, Silvia Franceschi and Carlo La Vecchia. Diet Diversity and the Risk of Oral and Pharyngeal Cancer. European Journal of Nutrition, 47, 280-284.
Willet, Walter C.1995 Diet, nutrition, and avoidable cancer. Diet, Nutrition, and Avoidable Cancer. Environmental Health Perspectives 103 (8): 165-170.
Wold, K.S., Byers, T., Crane, L.A, Ahnen, D. (2005). What do cancer survivors believe causes cancer? (United States). Cancer Causes Control, 16,115-23.