Perspective - (2021) Volume 11, Issue 9
Received: 09-Sep-2021 Published: 30-Sep-2021, DOI: 10.35248/2161-0509.21.11.154
Dietary factors are known to have a substantial impact on cancer risk, with various dietary ingredients both increasing and decreasing risk. Physical inactivity appears to be linked to a 7% risk of cancer development, while diet and obesity may be linked to up to 30-35 percent of cancer deaths. According to a study published in 2011, total caloric intake has an impact on cancer incidence and development. While many dietary advice have been made to minimise cancer risk, only a few have substantial scientific data to back them up. Obesity and alcohol consumption have been linked to the occurrence and progression of certain malignancies. Reduced use of sugar-sweetened beverages is advocated as a way to combat obesity. A diet strong in red meat and low in fruits and vegetables has been suggested but not proven, and the effect may be minor in well-nourished persons who maintain a healthy weight. Some foods have been related to certain malignancies. Breast cancer, colon cancer, prostate cancer, and pancreatic cancer have all been related to eating red or processed meat, which could be explained in part by the presence of carcinogens in meals cooked at high temperatures. Aflatoxin B1, a common food contaminant, raises the risk of liver cancer, whereas coffee consumption lowers the risk. Chewing betel nuts causes oral cancer. Because of its high salt diet, stomach cancer is more common in Japan. Immigrant communities are more likely to develop the risks of their new nation within one generation, implying a significant relationship between diet and cancer. Weight management and eating "primarily vegetables, fruit, whole grains, and fish, with a reduced intake of red meat, animal fat, and refined sugar" are against cancer. The Breuss diet, Gerson therapy, the Budwig common cancer-prevention dietary suggestions. A variety of diets and diet-based regimens have been claimed to be effective in the fight regimen, and the macrobiotic diet are all popular "anti-cancer" diets. None of these diets have been proven to work, and several have even been proven to be dangerous. Multivariate statistics, such as principle components analysis and factor analysis, are used by nutritional epidemiologists to determine how patterns of dietary behaviour influence the risk of acquiring cancer. (The Mediterranean diet is the most researched dietary pattern.) Epidemiologists divide people into quantiles based on their dietary pattern score. They measure the relationship between quantiles and the distribution of cancer prevalence (in case-control studies) and cancer incidence to estimate the impact of dietary behaviour on cancer risk (in longitudinal studies). Other factors are generally included in their statistical model to account for other differences between cancer patients and non-cancer patients (confounders). In the case of breast cancer, there is a consistent tendency that women who eat a more "prudent or healthy" diet, i.e. a diet rich in fruits and vegetables, have a decreased risk of developing the disease. A "drinker dietary pattern" is also linked to an increased risk of breast cancer, although there is no link between a more westernized diet and an increased risk of breast.
Pickled foods have been connected to the development of cancer.
A lot of malignancies are linked to drinking alcohol. Alcohol consumption is responsible for 3.6 percent of all cancer cases and 3.5 percent of all cancer deaths worldwide. Women's alcohol use has been connected to breast cancer. Alcohol also raises the chance of oral, esophageal, pharyngeal, and laryngeal cancers, as well as colorectal, liver, stomach, and ovarian cancers. The data on the effect of dietary fibre on colon cancer risk is inconsistent, with some types of research indicating a benefit and others indicating a lack of benefit. While eating fruits and vegetables offers health benefits, it has a lower impact on cancer prevention than previously thought. Phytoestrogens are abundant in soy. Phytoestrogens are naturally occurring substances with modest estrogenic activity. High fibre consumption was linked to a lower risk of premenopausal and postmenopausal breast cancers, as well as a longer survival rate in breast cancer patients, according to two meta-analyses published in 2020. Despite the fact that multiple cellular systems are involved in food intake, many studies have pointed to abnormalities in the methionine metabolic pathway as a cause of carcinogenesis in recent decades. In rodents, for example, a lack of the main dietary sources of methyl donors, methionine and choline, leads to the development of liver cancer. Methionine is an essential amino acid that must be obtained from proteins or methyl donors in the diet (choline and betaine found in beef, eggs and some vegetables). S-adenosyl methionine (SAM), a critical metabolite for polyamine synthesis, such as spermidine, and cysteine production, is generated from assimilated methionine (see the figure on the right). Homocysteine remethylation and methylthioadenosine (MTA) conversion both recycle methionine breakdown products back into methionine (see the figure on the right). The cofactors B6, B12, folic acid, and choline are required for these reactions. SAM is the substrate for DNA, RNA, and protein methyltransferases to catalyse methylation processes. Methylated DNA, RNA, or proteins, as well as S-adenosylhomocysteine, are the end products of these processes (SAH). As a methyltransferase inhibitor, SAH has a negative feedback on its own synthesis. As a result, the SAM:SAH ratio regulates cellular methylation directly, whereas vitamin B6, B12, folic acid, and choline levels influence methylation indirectly via the methionine metabolism cycle. Maladaption of the methionine metabolic pathway in response to genetic or environmental factors, leading in SAM depletion and/ or SAM-dependent methylation, is a nearly universal characteristic of cancer. Whether it's a lack of enzymes like methylthioadenosine phosphorylase, cancer cells' dependence on methionine, high levels of polyamine synthesis in cancer, or induction of cancer through a diet devoid of extrinsic methyl donors or high in methylation inhibitors, tumour formation in mice, rats, and humans is strongly linked to a decrease in SAM levels. According to a 2012 assessment, "there is still inadequate research to give appropriate nutritional recommendations" because the effect of methionine restriction on cancer has yet to be investigated directly in humans.
Citation: Matthew S (2021) A Quick Overview of Diet and Cancer. J Nutr Disorders Ther vol 11: 154.
Copyright: © 2021 Matthew S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.