ஊட்டச்சத்து அறிவியல் ஆராய்ச்சி இதழ்

சுருக்கம்

Childhood obesity 2020: Analyzing the role of high pro-inflammatory diets and childhood obesity in the risk of adult carcinogenesis in South Carolinian children- Ashley E Knowell- South Carolina State University

Ashley E Knowell and Shanora Brown

Childhood obesity has been a growing epidemic in the United States with about one in five of U.S. children considered overweight or obese. The increased number of overweight and obese children can be linked to several factors including nutrition and social economic status. Obesity in children can lead to numerous health complications such as diabetes, high blood pressure, chronic inflammation and carcinogenesis. Therefore, the goal of this study is to eliminate or reduce preventable risk factors such as unhealthy nutrition and childhood obesity, which in turn may reduce clinical manifestations of adult cancer outcomes. Areas of South Carolina have an extended history of being under-developed which contribute to numerous problems like obesity, poverty and sub-par health care. We have enrolled SC children from varying degrees of rurality to work out if obesity and/or high-fat pro-inflammatory diets contribute to increased levels of pro-inflammatory markers and obesity related genes to include: Adiponectin, leptin, SAA1/2, Interleukin 1 and 6. Subjects were be randomized into obese and non-obese groups based on BMI guidelines. The transcriptional levels of pro-inflammatory genes were measured by quantitative Real-time polymerase chain reaction. The results suggest increased expression of these pro-inflammatory markers are directly correlated to diet irrespective of weight class (normal, overweight, obese). Reducing childhood obesity and pro-inflammatory diets, while providing access to healthy foods are beneficial in the reduction of cancer risk and will serve as preventive measures for early-stage onset of adult cancers. The role that obesity plays in carcinogenesis has been delivered to the fore by data like the rapid rise of oesophagus adenocarcinoma over the past 20 years. In fact, whether oesophageal reflux is associated with adenocarcinoma, or whether it is favoured by obesity, the change in oesophageal cancer morphology from squamous to adenocarcinoma has followed the worldwide rise in obesity. A further example is provided by weight accumulation with age which is also linked to an increase in postmenopausal breast cancer risk in women who do not follow a menopausal hormone therapy regime, while cohort studies have shown that breast cancer risk was lowered by 50% in women who intentionally underwent weight loss higher than 10 kg after menopause. In addition, the Swedish Obese Subjects (SOS) study, an outsized prospective study which established that bariatric surgery achieves a mean of 20 kg weight reduction in obese patients with BMI higher than 40 kg/m2 and that matched the surgery group with untreated morbidly obese women, reported a significant reduction in cancer incidence in association with substantial weight loss on a follow-up longer than 10 years. Concerning the role of childhood obesity in adult cancer, a study performed during a cohort of two ,347 subjects retrospectively evaluated cancer risk associated with age and sex-specific BMI standard deviation scores (SDS) of subjects aged 2–14. Among these subjects, the danger of cancer in adult life was increased by 9% per SD increase in childhood BMI. Also, an excess of weight in teenagers was linked to doubling the mortality risk of colon cancer in adulthood. Because of the delay in cancer development within the presence of adiposity, the standard follow-up is longer than 10 years in cohorts assessing cancer risk, and it is thought that this is often an “average” lag period for obesity-related cancer development. However, the lag period could also be shorter when hyperoestrogenemia may be a predominant mechanism, because it occurs in postmenopausal breast and endometrial carcinoma .The American Cancer Society has furnished data which suggest that overweight and obesity are correlated to liver and pancreatic cancers death rates, as are both myeloma and non-Hodgkin’s lymphoma .Data published over the last 25 years emphasize that obesity may be a explanation for about 20% of deaths from cancer in women while the speed is around 14% in men. These rates are second only to smoking for the number of avoidable cancers. However, these data are possibly underestimated, since average weight has continued to rise in the worldwide population over the same time. Recently, Jaggers et al. found a positive multivariable-adjusted association between cancer mortality and abdominal obesity that increases the danger of cancer mortality up to 24%. Epidemiological studies have also shown that obesity is a contributing factor in both increased incidence and mortality from cancers of the colon, the endometrium, the kidneys, and the breast (in postmenopausal women). In the European Union , it's been calculated that not becoming overweight could reduce the annual incidence of carcinoma by up to 21,000 cases and carcinoma by up to 13,000 cases. The higher cancer death rate within the obese also accounts for a decreased survival rate, which will flow from to the enhancing effects of obesity on cancer potency and progression. A study on invasive ductal breast cancer in 1,177 women found that those in the highest quartile of BMI developed tumours with a higher histological grade, mitotic cell count, and larger tumour size compared to women in the lower quartiles. Furthermore, by considering solely large tumours up to 2 cm of diameter, those in the group of the highest BMI quartile largely expressed markers of high proliferation, supporting their fast growth, as compared to those with similar-size tumours in nonobese women. However, it has been reported that chemotherapy dosages are often not adequate in women of excess weight receiving breast cancer treatments in comparison to dosages in lean women, thus implying that an overall full weight-based adjusted dose would allow better outcomes. Obesity is liable for approximately 20% of all malignancies, although its influence is gender and site specific. The association between obesity and a better cancer risk is especially thanks to anthropometric parameters and lifestyle factors which activate different biological mechanisms. Anthropometric parameters are BMI, weight increase, and the amount of body fat, particularly visceral fat. Lifestyle factors include sedentary habits and diet parameters, like a hypercaloric and/or low-quality diet.We do not yet have a clear scientific demonstration that avoiding increasing or reducing body weight significantly reduces the risk of cancer; however, the data from the surgical treatment of obese patients with a BMI higher than 40.0 are leading in this direction.