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IMPORTANT NOTE REGARDING WORD LIMIT REQUIREMENTS:

Please note that each and every assignment has its own word limit.

Obesity is the major risk factor for nonalcoholic fatty liver disease (NAFLD), whereas an excessive intake of alcohol is the main driver of alcoholic fatty liver disease (AFLD). However, not all obese individuals have NAFLD, and not all individuals who consume large amounts of alcohol develop AFLD. Also, far from all individuals with simple steatosis (the first stage of both NAFLD and AFLD) go on to develop steatohepatitis, cirrhosis, or end-stage liver disease. A large part of this inter-individual variation is due to genetic factors. Some individuals carry susceptibility-increasing genetic variants that make them more vulnerable to developing NAFLD, and to the progression of the disorder. Conversely, some lucky individuals carry genetic variants that protect their livers from the deleterious effects of obesity or alcohol intake. Twin studies indicate that 50% of the risk of fatty liver disease is genetically determined. This heritability estimate is comparable to those of other complex traits such as obesity, type 2 diabetes, or ischemic heart disease. Additional evidence in support of a strong genetic component to NAFLD is the fact that the disorder varies greatly in prevalence among different ethnic groups. Three common (minor allele frequency > 0.05) steatogenic genetic variants with robust and replicable effects have been identified so far: PNPLA3 I148M, TM6SF2 E167K, and GCKR P446L. Together these variants explain less than 10% of the variation in hepatic fat content or approximately 20% of the total heritable component of hepatic steatosis. Thus, the major fraction of genetic variation that contributes to the development of fatty liver disease remains unknown. With only three genome-wide association studies GWAS published so far (two of these based on the same cohort), the field of fatty liver GWAS is still in its infancy. Nonalcoholic fatty liver disease is a complex disease in which genetic variations and environmental factors interact to determine disease phenotype and progression. Progress in the understanding of the genetic risk of NAFLD might offer the unique opportunity to translate this information into clinical practice. However, only a minor fraction of the genetic risk for fatty liver disease has been discovered. Furthermore, the relative importance of genetic and environmental factors will vary between populations depending on background modifier genes, lifestyle choices/challenges, and other factors such as the intestinal microbiome (Stender, Grarup, Hansen, 2019)

Although any of the standard epidemiologic study designs can be used for testing interactions, cohort studies have the great advantage of allowing the collection of time-dependent exposure information before disease develops, overcoming the problem of “reverse causation” (the disease or its treatment affecting exposure or its measurement). Since cohort studies of rare diseases would require enormous sample sizes or long follow-up (especially for diseases with long latent periods), case-control studies are the design of choice for studying rare diseases with common exposures. Reverse causation is a non-issue for genetic effects and generally not as big a concern for G×E interactions as for pure environmental effects. Nested case-control and case-cohort designs exploit the advantages of the basic designs, combining the avoidance of bias of cohort designs with the cost-efficiency of case-control designs. In general, the relative efficiency of the various designs for G×E interactions is similar to that of main effects(Thomas, 2010).

Reference

Stender S., Grarup N., Hansen T. (2019) Genetic Aspects of Non-alcoholic Fatty Liver Disease (NAFLD). In: Krag A., Hansen T. (eds) The Human Gut-Liver-Axis in Health and Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-98890-0_12

Thomas D. (2010). Methods for investigating gene-environment interactions in the candidate pathway and genome-wide association studies. Annual review of public health, 31, 21–36. https://doi.org/10.1146/annurev.publhealth.012809….

Respond to the bold paragraph ABOVE by using one of the option below… in APA format with At least two references and a minimum of 200 words….. .(The List of References should not be older than 2016 and should not be included in the word count.)

  • Ask a probing question.
  • Share an insight from having read your colleague’s posting.
  • Offer and support an opinion.

  • Validate an idea with your own experience.
  • Make a suggestion.
  • Expand on your colleague’s posting.


Be sure to support your postings and responses with specific references to the Learning Resources.

It is important that you cover all the topics identified in the assignment. Covering the topic does not mean mentioning the topic BUT presenting an explanation from the context of ethics and the readings for this class

To get maximum points you need to follow the requirements listed for this assignments 1) look at the word/page limits 2) review and follow APA rules 3) create subheadings to identify the key sections you are presenting and 4) Free from typographical and sentence construction errors.

REMEMBER IN APA FORMAT JOURNAL TITLES AND VOLUME NUMBERS ARE ITALICIZED.