Cancer Related to Obesity and Diabetes

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The journal article that I chose to do a journal review on is written by Guido Eibl, Zobeida Cruz-Monserrate, Murray Korc, Maxim S. Petrov, Mark O. Goodarzi, William E. Fisher, Aida Habtezion, Aurelia Lugea, Stephen J. Pandol, Phil A. Hart, Dana K. Andersen, published in 2017. The title of the article is called “Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer”, sourced from Journal of Academy of Nutrition and Dietetics.

The main objective of this journal article is to gain insights on how factors identified by large epidemiologic and cohort studies such as obesity and type 2 diabetes mellitus affect risk factors for the expected to become the seconding leading cancer-related cause of death by 2030, pancreatic ductal adenocarcinoma (PDAC) development. Preventing PDAC is a better solution as currently the cure for PDAC is not efficient and thus, efforts have been put in by researchers to understand how risk factors such as obesity and type 2 diabetes mellitus lead to development of PDAC. With greater understanding, researchers can attempt to come up with preventive strategies which is of utmost importance.

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The research was done through archival study, by using various reports and studies conducted. Hyperinsulinemia and high levels of insulin-like growth factor-1(IGF-1) which is commonly found in most obese people and people who are suffering from type 2 diabetes mellitus can act as a detrimental growth-promoting factor of PDAC. PDAC may be influenced by dietary intake such as carbohydrate and fat intake, meat, fruits and vegetables. A prospective cohort study shows that it is statistically significant that saturated fat from animal source was associated with higher PDAC risk strongest among the other types of fat. Recent studies showed that metformin and n-3 polyunsaturated fatty acids can decrease or inhibit cancer cell growth and lower risk of PDAC. However, the article argues that PDAC molecular mechanisms and interaction are still not explored extensively even though the risk factors that encourage PDAC development have been known for decades. For example, the exact molecular and signalling pathways and their intricate interaction are still not sufficiently explored. Precise contribution and molecular signals of different adipose tissue depots and possible gender differences on development of PDAC are still unknown.

The literature review was able to reveal gaps in the knowledge clearly and allow readers to gain insights on the mechanism and interaction of PDAC prevention in relation to dietary factors. The author was able to clearly define and state their research topic and objectives. Diagrams were used to show how type 2 diabetes mellitus promotes PDAC and how adipose tissue dysfunction during obesity which helps readers to understand better. Figures were used to show geographical indications of prevalence of diabetes mellitus, obesity and pancreatic cancer. The author indicated that investigators of the study of chronic pancreatitis, diabetes and pancreatic cancer are applying lessons learnt from this article to gain insights in the mechanism of how diabetes and inflammation promotes PDAC.

The full form of abbreviations was given and examples of were provided for some phrases. For example, in the article, examples of histologic features of adipose tissue inflammation was given. Alternative of specialized terminology were also stated. For example, in the article, the alternative stated in bracket for desmoplastic reaction is stated as dense fibroblastic reaction. The details of the studies conducted were stated such as the sample sizes and methods of each study. For example, in the article, under ‘Fruits and Vegetables’ section, they have stated the sample size of 81,922 individuals in Sweden using multivariate analysis. However, the sample size varies from different studies. Some studies have smaller sample size whereas some have greater sample size.

The authors of this article did summarize the pre-existing knowledge that are related to possible causes of PDAC. They have stated in the conclusion that there is no definite factor discovered yet that promotes or prevent PDAC. For example, it was stated that obesity caused by high carbohydrate intake or calorie intake increases the prevalence of PDAC.

The authors recommended that more efforts should be taken to further understand the relation between obesity, diabetes and PDAC. They have also suggested that available pre-clinical animal models can be used to aid in further understanding of this study. The references used were from reliable sources and were properly referenced.

The limitations of the study discussed were that the results and factors were uncertain due to lack of studies and research on PDAC prevention. For example, the effect of signals of different adipose tissue depots on development of PDAC is still currently unknown. The gender and age range of sample were not stated in some of the studies that were used to support research. Gender and age may also be a factor of PDAC prevention or promotes PDAC and thus, leading to inaccuracy. The methods and instrument used for measuring results were not clearly stated and explained in detail. Under the dietary factor section of the article, only one prospective cohort study is used to support how various dietary related influences affect risk for PDAC which is insufficient. A greater number of studies are required in order to support its findings.

In conclusion, this article highlights the current knowledge of the linkage between obesity and type 2 diabetes with PDAC development, aiming to outline knowledge gaps and gain insights on PDAC prevention as the authors believed that the current cure for PDAC is inefficient due to insufficient studies and research on PDAC which expected to become the second leading cause of cancer-related death. Multivariate analysis in prospective cohort studies was used to research on dietary factor of PDAC. I agree with the author that more research efforts need to be put into PDAC development to efficiently prevent PDAC as signalling pathway and mechanism are still unknown. Overall, in my opinion, the article did well on presenting current knowledge of diet related factors that can affect development of PDAC and was able to achieve their main objective.

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Cancer Related to Obesity and Diabetes. (2022, Jun 29). Edubirdie. Retrieved July 15, 2024, from https://edubirdie.com/examples/cancer-related-to-obesity-and-diabetes/
“Cancer Related to Obesity and Diabetes.” Edubirdie, 29 Jun. 2022, edubirdie.com/examples/cancer-related-to-obesity-and-diabetes/
Cancer Related to Obesity and Diabetes. [online]. Available at: <https://edubirdie.com/examples/cancer-related-to-obesity-and-diabetes/> [Accessed 15 Jul. 2024].
Cancer Related to Obesity and Diabetes [Internet]. Edubirdie. 2022 Jun 29 [cited 2024 Jul 15]. Available from: https://edubirdie.com/examples/cancer-related-to-obesity-and-diabetes/
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