User:Aspillutla/Week 4 Aamani Pillutla

Epigenetics and Yoga

Yoga, which includes physical movements and mindfulness and meditation exercises, has been shown to have an effect on the long-term health of the human body. It can improve the redox state of the body and aid in coping with stress conditions. It has also been found that yoga can reduce cellular aging and maintain neuroplasticity in the brain, thereby helping counteract neurodegeneration.

Yoga has been shown through longitudinal observation to cause an increased rate of gene expression changes in peripheral blood mononuclear cells in the immune system. A study using an eight-hour yoga meditation session revealed a swift change in the global modification of histones, as well as the reduced expression of histone acetylase and some pro-inflammatory genes. In addition, a study done on humans involving those experienced in meditation and those inexperienced being put in the same environment, it was found that histone deacetylases which modulate certain inflammatory pathways may be impacted by mindfulness-based therapies such as yoga. In relation to more specific epigenetic processes, in a pilot study involving an 8-week long program using women who reported psychological distress, yoga was found to reduce DNA methylation of the tumor necrosis factor region, though the other immune function genes tested, IL-6 and CRP, remained unaffected. DNA methylation normally occurs at certain CpG sites. These CpG sites are found at promoter regions that undergo age-related changes. There is also evidence of an effect of yoga on molecular processes involved in male infertility.

Data also supports that yoga as a form of mind-body intervention can help reverse epigenetic aging processes, lower cortisol, and reduce inflammation. As such, findings support that meditation, which is encompassed by yoga, can stimulate anti-inflammatory cytokines and endorphins. The suppression of inflammatory cytokines is linked to the lowering of expression of nuclear factor kappa B, which is involved in sympathetic nervous responses, which has been shown to lessen as a result of mind-body intervention. This can be applied to the mitigation of type 2 diabetes. The above understandings indicate yoga can be used as a therapeutic method for inflammation-related and other diseases, though more study is required for a clearer understanding of the mechanisms involved. In conclusion, it is clear that yoga-based activities interact with and alter epigenetic phenomena and can cause long-term effects in a person.

Some figures that could be employed in this Wikipedia article are those showing the mouse models in relevant studies as well as pictorial representations showing the results relating to the tumor necrosis factor region and CpG sites. Visual representations can also be made for the results for NF kappa B and inflammatory cytokines, showing how meditation and mindfulness in yoga lead to reduced inflammation and reduced stress.

Free to a good home (completely new proposal draft)

Obesity is defined by the World Health Organization as “abnormal and excessive fat accumulation that presents a risk to health.” Rates of obesity and overweightness have increased, with obesity in children and adolescents ages 5 to 19 going from 4 percent in 1975 to 18 percent in 2016 worldwide (World Health Organization). Genetic and epigenetic processes have been found to be implicated in human obesity. Obesity occurs as a result of interaction between genetic and environmental factors. Searches for genetic variants contributing to high susceptibility to obesity have been found. Certain epigenetic marks known as imprinting have been found to be involved in obesity. More specifically, failure in imprinting has been found to cause extreme forms of obesity, such as those caused by genetic ailments such as Prader-Willi syndrome. As obesity is linked to an increased risk of type 2 diabetes, cardiovascular disease, mortality, and other life-impeding issues, it is important to understand the epigenetic mechanisms behind obesity in humans (Herrera et al).

Genomic imprinting is an epigenetic process that creates a balance between the parental alleles expressing influence on growth (Butler et al.). Imprinted genes are also implicated in development and metabolic function, among other processes (Smith F.M. et al.). When imprinting fails, the expression of growth and cellular differentiation factors can lead to obesity. This can be because of translocation, inversion, duplication, paternal disomy, and hyper- or hypo-methylation, among other genetic events. Prader-Willi syndrome is an example of such a phenomenon, wherein early onset obesity due to paternal deletion of uniparental disomy at a certain gene can be life-threatening (Shapira et al.). Genomic imprinting is mediated by DNA methylation at several loci and is also impacted by histone modification. Such epigenetic effects, when introduced in a prenatal child’s early development, has been associated with increased risk of obesity. One example is the finding that obese mothers have a higher statistical likelihood of having obese children (Dabelea et al.). It has also been shown that clinical intervention for the purposes of maternal weight loss may reduce the risk of offspring obesity (Smith J. et al.). This is possibly due to disturbances in methylation during fetal development, as well as interactions between epigenetics and the environment (Herrera et al.). Though study about the linkage between epigenetics and obesity is still ongoing, epigenetic processes have been found to be involved in obesity of various kinds and causes, along with interaction with the environment. This therefore warrants a Wikipedia article detailing the findings of the epigenetics of obesity.

Some figures that could be used are those describing DNA methylation and histone modification, which are available. Furthermore, figures that pictorially describe the effect of methylation practically in terms of obese children and obese mothers can be helpful to understand the consequences of epigenetic processes in obesity.

Bibliography (for free to a good home, in which Herrera et al. is the main review)

Butler M. G. (2009). Genomic imprinting disorders in humans: a mini-review. Journal of assisted reproduction and genetics, 26(9-10), 477–486. https://doi.org/10.1007/s10815-009-9353-3

Dabelea, D., Mayer-Davis, E. J., Lamichhane, A. P., D'Agostino, R. B., Jr, Liese, A. D., Vehik, K. S., Narayan, K. M., Zeitler, P., & Hamman, R. F. (2008). Association of intrauterine exposure to maternal diabetes and obesity with type 2 diabetes in youth: the SEARCH Case-Control Study. Diabetes care, 31(7), 1422–1426. https://doi.org/10.2337/dc07-2417

Herrera, B. M., Keildson, S., & Lindgren, C. M. (2011). Genetics and epigenetics of obesity. Maturitas, 69(1), 41–49. https://doi.org/10.1016/j.maturitas.2011.02.018

Shapira, N. A., Lessig, M. C., He, A. G., James, G. A., Driscoll, D. J., & Liu, Y. (2005). Satiety dysfunction in Prader-Willi syndrome demonstrated by fMRI. Journal of neurology, neurosurgery, and psychiatry, 76(2), 260–262. https://doi.org/10.1136/jnnp.2004.039024

Smith, J., Cianflone, K., Biron, S., Hould, F. S., Lebel, S., Marceau, S., Lescelleur, O., Biertho, L., Simard, S., Kral, J. G., & Marceau, P. (2009). Effects of maternal surgical weight loss in mothers on intergenerational transmission of obesity. The Journal of clinical endocrinology and metabolism, 94(11), 4275–4283. https://doi.org/10.1210/jc.2009-0709

Smith, F. M., Garfield, A. S., & Ward, A. (2006). Regulation of growth and metabolism by imprinted genes. Cytogenetic and genome research, 113(1-4), 279–291. https://doi.org/10.1159/000090843

World Health Organization. (n.d.). Obesity. World Health Organization. Retrieved February 27, 2022, from https://www.who.int/health-topics/obesity#tab=tab_1