Background: Obesity and cancer are recognized worldwide health threats. While there is no reported causal relationship, the increasing frequency of both conditions results in a higher incidence of obese patients who are being treated for cancer. Physiological data indicate that there is a relationship between obesity and susceptibility to pain; however, currently, there are no specific pharmacological interventions. Objective: To evaluate the self-reported intensity of postoperative pain in obese and nonobese lung cancer who receive either thoracotomy or video-assisted thoracic surgery (VATS) surgical therapy. Material and Methods: In 50 obese [mean body mass index (BMI) of 34.1 ± 3.2 kg/m 2 ] and 62 nonobese (mean BMI of 24.9 ± 3 kg/m 2 ) lung cancer patients, the intensity of pain was estimated every 4 h using a visual analog scale (VAS, 0 indicating no pain and 10 indicating “worst imaginable pain”) beginning shortly after surgery (Day O) and continuing until the day of discharge (Day D). Results: The self-reported pain was more severe in obese than in nonobese patients, both at the time of the operation [Day O (4.5 ± 1.2 vs 3.4 ± 1.1; p < 0.0001)] and at the day of discharge [Day D (3.9 ± 1.4 vs 2.6 ± 0.9, p < 0.0001)]. This finding was consistent both in the patients after thoracotomy and after video-assisted thoracic surgery (VATS, p < 0.0001). The patients with severe pain shortly after surgery (VAS score >4) had significantly higher BMI (31.8 ± 5.6 kg/m 2 vs 28.8 ± 5.2 kg/m 2 , p < 0.01) and were hospitalized longer than the remaining patients (13.0 ± 13.6 days vs 9.5 ± 3.6 days, p < 0.05). Conclusion: The reported perception of pain in obese lung cancer patients is greater than in nonobese patients undergoing the same thoracic surgery. In obese patients, severe pain persisted longer. Pain management is an important consideration in the postoperative care of lung cancer patients, even more so with obese patients.

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: There is increasing number of the patients worldwide with sleep disturbances and diabetes. Various sleep disorders, including long or short sleep duration and poor sleep quality of numerous causes, may increase the risk of diabetes. Some symptoms of diabetes, such as painful peripheral neuropathy and nocturia, or associated other sleep disorders, such as sleep breathing disorders or sleep movement disorders, may influence the sleep quality and quantity. Both sleep disorders and diabetes may lead to cognitive impairment. The risk of development of cognitive impairment in the diabetic patients may be related to vascular and non-vascular and other factors, such as hypoglycemia, hyperglycemia, central insulin resistance, amyloid and tau deposits and other causes. Numerous sleep disorders, e.g., sleep apnea, restless legs syndrome, insomnia and poor sleep quality most likely also associated with cognitive impairment. Adequate functioning of the system of clearance of the brain from toxic substances, such as amyloid β, i.e. glymphatic system, is related to undisturbed sleep and prevents cognitive impairment. In case of coexistence, sleep disturbances and diabetes either independently lead to and/or mutually aggravate cognitive impairment.

Obesity and sarcopenia, i.e., decreased skeletal muscle mass and function, are global health challenges. Moreover, people with obesity and sedentary lifestyles often have sleep disorders. Despite the potential associations, metabolic disturbances linking obesity, sarcopenia, and sleep disorders with cancer are neither well-defined nor understood fully. Abnormal levels of adipokines and adipomyokines originating from both adipose tissue and skeletal muscles are observed in some patients with obesity, sarcopenia and sleep disorders, as well as in cancer patients. This warrants investigation with respect to carcinogenesis. Adipokines and adipomyokines may exert either pro-carcinogenic or anti-carcinogenic effects. These factors, acting independently or together, may significantly modulate the incidence and progression of cancer. This review indicates that one of the possible pathways influencing the development of cancer may be the mutual relationship between obesity and/or sarcopenia, sleep quantity and quality, and adipokines/adipomyokines excretion. Taking into account the high proportion of persons with obesity and sedentary lifestyles, as well as the associations of these conditions with sleep disturbances, more attention should be paid to the individual and combined effects on cancer pathophysiology.