Background Neck pain is one of the most common musculoskeletal disorders, having an age-standardised prevalence rate of 27.0 per 1000 population in 2019. This literature review describes the global epidemiology and trends associated with neck pain, before exploring the psychological and biological risk factors associated with the initiation and progression of neck pain. Methods The PubMed database and Google Scholar search engine were searched up to May 21, 2021. Studies were included that used human subjects and evaluated the effects of biological or psychological factors on the occurrence or progression of neck pain, or reported its epidemiology. Results Psychological risk factors, such as long-term stress, lack of social support, anxiety, and depression are important risk factors for neck pain. In terms of the biological risks, neck pain might occur as a consequence of certain diseases, such as neuromusculoskeletal disorders or autoimmune diseases. There is also evidence that demographic characteristics, such as age and sex, can influence the prevalence and development of neck pain, although further research is needed. Conclusions The findings of the present study provide a comprehensive and informative overview that should be useful for the prevention, diagnosis, and management of neck pain.

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Migraine affects more than one billion individuals each year across the world, and is one of the most common neurologic disorders, with a high prevalence and morbidity, especially among young adults and females. Migraine is associated with a wide range of comorbidities, which range from stress and sleep disturbances to suicide. The complex and largely unclear mechanisms of migraine development have resulted in the proposal of various social and biological risk factors, such as hormonal imbalances, genetic and epigenetic influences, as well as cardiovascular, neurological, and autoimmune diseases. This review presents a comprehensive review of the most up-to-date literature on the epidemiology, and risk factors, as well as highlighting the gaps in our knowledge.

Our results showed that the Pro12Ala polymorphism in the PPARgamma2 gene is associated with obesity in Iranian subjects and the presence of the Ala allele could predict higher BMI.

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Methylenetetrahydrofolate reductase (MTHFR) polymorphism may play an important role in the pathophysiology of obesity and diabetes accompanied by obesity due to its influence on plasma homocysteine levels. There are significant and sometimes very strong relationship between levels of homocysteine and several multi-system diseases including CHD and CVA. To examine the association between MTHFR gene C677T polymorphism in diabetes and obesity with serum homocysteine levels. A total of 682 subjects were recruited in four groups (Normal, obese, diabetic and obese and diabetics). MTHFR gene C677T polymorphism was detected using PCR-RFLP technique. Serum homocysteine levels were measured using HPLC. There was a significant increase in the mean serum homocysteine levels in subjects carrying TT genotype (34.6 +/- 26.5) compared to subjects carrying CC (15.1 +/- 8) or CT genotype (16.4 +/- 7.8) (P < 0.000). We found no significant differences for MTHFR allele and genotype frequencies between different groups. Our data have confirmed the association between serum homocysteine levels and MTHFR C677T genotype reported in other populations.

Abstract.Objective: Both adaptive and innate immune systems are involved in coronary artery disease (CAD). The aim of this study was to evaluate TH17 cytokines expression profiles in un-stimulated peripheral blood lymphocytes (PBMCs) of patients with coronary artery disease. Methods: Expression profiles of IL-17, IL-23, and TGF-β1 were determined in individuals with and without CAD using Real-time PCR.Results: A significant decrease in IL-23 gene expression in un-stimulated PBMCs of patients with CAD compared to those without CAD was found (p = 0.003, OR = 0.045, 95% CI: 0.006-0.355). Conclusion: Our data reinforce the potential role of the IL-23 as a critical regulatory molecule that bridges the innate and adaptive arms of the immune system in the complex mechanisms associated with the development of atherosclerosis.