BackgroundSchizophrenia is one of the most common devastating psychiatric disorders that negatively affects the quality of life and psychosocial functions. Its etiology involves the interplay of complex polygenic influences and environmental risk factors. Inflammatory markers are well-known etiological factors for psychiatric disorders, including schizophrenia.ObjectiveThe aim of this study was to investigate the association of proinflammatory cytokine genes, tumor necrosis factor (TNF)-α (−308G/A) and TNF-β (+252A/G) polymorphisms with schizophrenia susceptibility.Subjects and methodsTNF-α and TNF-β genes were amplified using amplification refractory mutation system primers in 180 schizophrenia patients and 200 healthy matched controls recruited from the Psychiatry Clinic of Prince Sultan Military Medical City, Riyadh. The frequencies of alleles and genotypes of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms in patients were compared with those in controls.ResultsThe frequencies of TNF-α (−308) allele A and genotype GA were significantly higher, while those of allele G and genotype GG were lower in schizophrenia patients as compared to controls, indicating that genotype GA and allele A of TNF-α (−308G/A) may increase susceptibility to schizophrenia, while genotype GG and allele G may reduce it. On the other hand, the distribution of alleles and genotypes of TNF-β (+252A/G) polymorphism does not differ significantly in patients from controls; however, the frequency of genotype GG of TNF-β (+252A/G) was significantly higher in male patients than in female patients. The distribution of TNF-α (−308G/A) and TNF-β (+252A/G) polymorphisms was almost similar in schizophrenia patients with negative or positive symptoms.ConclusionTNF-α (−308G/A) and TNF-β (+252G/A) polymorphisms may increase the susceptibility to schizophrenia in Saudi patients and could be a potential risk factor for its etiopathogenesis. However, further studies are warranted involving a larger sample size to strengthen our findings.

ObjectivesPersistent oxidative stress is one of the several risk factors that may be associated with the etiology of obesity. The present study is aimed to investigate association between GSTM1 and GSTT1 polymorphisms with obesity and their relationship with plasma lipoproteins, body mass index (BMI) and hypertension.DesignThe GSTM1 and GSTT1 deletion polymorphisms were analyzed by multiplex polymerase chain reaction. The lipoproteins were measured in plasma using commercially available kit and the weight, height, systolic (SBP) and diastolic (DBP) blood pressures by standard procedure of measurements.SettingPrince Sultan Military Medical City, Riyadh Saudi Arabia.ParticipantsA total of 420 overweight/obese cases and 234 normal weight controls belong to young age Saudis.Main outcomes measuresGSTM1/GSTT1 polymorphisms may be associated with obesity.ResultsWeight, BMI, low-density lipoprotein (LDL) and SBP were significantly higher while high-density lipoprotein (HDL) was significantly lower in cases in comparison to controls. Frequency of GSTM1+/GSTT1− (OR = 2.70, 95% CI = 1.52–4.81, p = <0.001) and GSTM1−/GSTT1− (OR = 2.43, 95% CI = 1.15–5.15, p = 0.018) was significantly higher in cases as compared to controls. BMI and weight were significantly higher in GSTM1+/GSTT1− and GSTM1−/GSTT1− genotypes, and LDL, DBP and SBP significantly higher in GSTM1−/GSTT1− null genotype while HDL was significantly lower in GSTM1−/GSTT1+ and GSTM1−/GSTT1− genotypes in comparison to GSTM1+/GSTT1+ genotype.ConclusionsThe GSTM1+/GSTT1− and GSTM1−/GSTT1− null genotypes were significantly associated with obesity and have shown relationship with obesity risk factors in cases. Hence, these genes may be associative genetic risk factor for obesity among young age Saudis.