Background: Obesity has become a major global health concern and has been frequently associated with numerous pathological conditions, one of which is kidney stones, also known as nephrolithiasis. Both these conditions present a significant burden on healthcare systems, and their coexistence amplifies the challenges for both the patients as well as the healthcare systems. To develop effective management strategies, it is crucial to understand the pathophysiological mechanisms connecting these two conditions. Aim: This study aims to explore the pathophysiological mechanisms linking obesity and kidney stone formation, along with presenting cost-effective strategies, including dietary and lifestyle modifications, which can help decrease the incidence of obesity-related kidney stone formation. Methodology: This study is performed by reviewing reporting items, including systematic reviews and meta-analyses, using electronic databases such as PubMed and Google Scholar. The search term for this purpose was “Obesity AND Kidney Stones,” and articles were reviewed from 2002 to 2024. Result: The study displays that obesity increases the risk of kidney stone formation through multiple pathways. Increased uric acid excretion, increased calcium levels, insulin resistance, and a sedentary way of living contribute to the pathophysiology of kidney stones. The study also analyzes the economic burden of these diseases and explores cost-effective strategies for their management. Conclusion: The risk of kidney stones in obese people can be reduced by using individualized strategies. Improving daily physical activity levels and healthy diet intake has proved to be increasingly important in the prevention of obesity-related kidney stones.

Methylmercury is a neurotoxin present in fish tissues that permeates the blood-brain barrier after consumption. Previous research has shown that methylmercury is harmful to neurons, causing pH alterations, oxidative stress, excitotoxicity, and parenchymal damage. Methylmercury is a known factor of neurological disorders including Alzheimer's and Parkinson's. The method by which methylmercury passes through the blood-brain barrier is largely unknown. According to preliminary studies, one way methylmercury crosses the blood-brain barrier is by creating a complex with L-Cysteine, which facilitates its passage by the LATs system through mimicking another amino acid existing in the body. The human blood-brain barrier was studied using C. elegans as a model organism. It was hypothesized that if methylmercury passes through the blood-brain barrier of C. elegans faster with L-Cysteine present than without L-Cysteine present, the methylmercury's adverse effects (death and locomotive difficulty) will occur sooner. Each of the four experimental groups contained one C. elegans: the control, the L-Cysteine group, the methylmercury group, and the methylmercury and L-Cysteine combination group. The effects of L-Cysteine and methylmercury on C. elegans were studied using three metrics: viability, locomotive disability, and time for locomotive effects to occur. The group that received both methylmercury and L-Cysteine had reduced viability rates and a decreased time for locomotive difficulty to develop, supporting the hypothesis. These findings suggest that L-Cysteine aids methylmercury permeation through the blood-brain barrier. Because the experiment indicates how methylmercury penetrates the blood-brain barrier, these results aid in finding a therapeutic solution to reverse methylmercury neurotoxicity in the brain. Additionally, this study further opens channels into potential therapeutic and preventative measures for dementia, improving morbidity and mortality in neurodegenerative diseases.