Adhesive shoulder capsulitis is a condition characterised by stiffness or lack of mobility of the shoulder. This results in a negative impact on quality of life and increased health care costs. Inflammation is a key factor in the pathogenesis of these patients. In addition, poor sleep quality and/or sleep deprivation can increase the production of pro-inflammatory cytokines, which contributes to the development of chronic inflammatory and metabolic diseases. The most important function of sleep is recovery. Good sleep promotes healing, aids in the recovery of the immune, neurological, musculoskeletal systems and is necessary for pain sufferers to improve. The quantity and quality of sleep has an impact on the subject's inflammatory and metabolic markers. In relation to the quantity and quality of sleep, it has been shown that foods and/or beverages rich in methylxanthine such as coffee, tea and chocolate can alter these parameters. As is the case with exposure to blue light emitted by electronic devices. The population are faced with deep-rooted habits in their daily lives that do not help to control pain in these patients. HYPOTHESIS: Due to the above, the following hypothesis is established: Lack of consumption of food or beverages rich in methylxanthine and limiting the use of mobile devices two hours before going to sleep favours recovery from adhesive shoulder capsulitis.
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Pain and Disability Questionnaire (SPADI)
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Fasting glucose Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Insulin Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
HOMA Index Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Leptin Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Triglycerides Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Total Colesterol Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
HDL Colesterol Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
Uric Acid Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
High-sensitivity C-reactive Protein Metabolic Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
IL-1 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
IL-6 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
IL-17 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
IL-10 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
IL-33 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
HMGB1 Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
CRP Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.
TNF Inflammatory Profile
Timeframe: It was measured before starting treatment and at the end of treatment, an average of 6 months.