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A new study found smoking affects serum leptin levels for patients with obstructive sleep apnea on positive airway pressure therapy. Serum leptin levels increased in 40% of active smokers with obstructive sleep apnea but did not increase in any of the non-smokers.
After continuous positive airway pressure therapy—used to treat obstructive sleep apnea (OSA)—smokers had increased leptin levels and non-smokers had stable or decreased leptin levels, according to a new study.1
OSA, a condition which briefly stops breathing during sleep multiple times in the night, interferes with oxygen flow and increases the risk of heart disease, heart attack, stroke, high blood pressure, obesity, and diabetes.2 Smoking increases the risk of OSA, as well as intensifying the sleep breathing condition by causing chronic inflammation and neuromuscular dysfunction in the upper airways.
To help OSA, individuals can go through continuous positive airway pressure therapy.1 The therapy also has other advantages, other than improving sleep apnea, such as decreasing total cholesterol, low-density lipoprotein cholesterol, and glycosylated hemoglobin (HbA1c) levels in patents with OSA. Yet, smoking affects the treatment’s benefits.
The study, led by Merve Aktan Suzgun, MD, of the neurology department at Istanbul University-Cerrahpasa, examined the effects of smoking on the parameters of metabolic syndrome in OSA patients treated with positive airway pressure therapy. The investigators divided the participants as active smokers (defined as inhaling mainstream smoke, including occasional use in social events) and non-smokers (never smoked in their life). The team excluded electronic cigarette users due to the uncertainty of the effects and dosages. The investigators noted down participant’s age, gender, body mass index, and the circumstances of the neck, waist, and hip.
The team collected fasting blood samples from all participants, studying the parameters: plasma glucose, glycated hemoglobin (HbA1c), serum insulin, oral glucose tolerance test, plasma triglycerides and low-density lipoprotein (LDL), serum leptin, and homeostasis model assessment-estimated insulin resistance (HOMA-IR) index.
All participants had positive airway pressure therapy in the sleep laboratory, as well as having a follow-up examination 3 months later. Effective positive airway pressure therapy lasted for ≥ 5 nights a week and for ≥ 4 hours per night. Participants who did not do the therapy for the correct amount of time were excluded from the study.
After exclusion, the study included 115 patients (62.6% males n = 72) with a mean age of 53.4±14.3 years. A little over half (53.3%) were active smokers, and active smokers were significantly younger than non-smokers (P = .034).
The mean apnea-hypopnea index was lower in active smokers than non-smokers, but the difference was not significant ((32.8±20.1/hour vs. 47.2±25.6/hour, P =.169). Also, severe OSA was significantly higher in non-smokers than active smokers (P = .049).
After the follow up, changes in plasma triglycerides and LDL levels, fasting plasma glucose, oral glucose tolerance test at hour 1 and 2, HOMA-IR index, blood HbA1c level, and serum insulin and leptin levels did not show significance difference in active smoker and non-smoker obstructive sleep apnea patients.
Yet, in an analysis of stable, decreased, or increased parameters, the investigators noticed the serum leptin level was decreased in 78.6% of non-smoker OSA patients after 3 months of treatment but decreased only 46.7% in active smoker patients (P = .029). Adjusting for confounding factors, such as gender, age, and weight, confirmed the significant difference (P = .034).
Also, leptin levels were increased in 40% of active smokers but did not increase in any of the non-smokers. A Spearman correlation analysis revealed raised leptin levels in active smokers positively correlated with triglycerides and HOMA-IR before and after the treatment—but they were not significantly different.
Moreover, a subgroup analysis showed leptin levels in obese active smoker OSA patients positively correlated with HOMA-IR at follow-up but with no significant difference (P = .062).
“Leptin plays an important role in energy balance and lipid storage, and increased levels are associated with obesity and insulin resistance,” the investigators wrote. “In the present study, HOMA-IR was increased as leptin level increased; although this positive correlation was not significant, it was more pronounced in obese patients.”
The investigators pointed out raised serum leptin levels played an important role in several hormonal, metabolic, thrombotic, and inflammatory processes, which can cause systemic complications. The bidirectional relationship between OSA and leptin levels showcases the importance of effective obstructive sleep apnea treatment with positive airway pressure therapy, as well as improving lifestyle choices like losing weight and quitting smoking.
“Because high serum leptin level is closely associated with leptin resistance characterized by increased central leptin expression and decreased leptin receptors, smoking may play a predisposing role in leptin resistance in patients with [obstructive sleep apnea] despite [positive airway pressure] therapy,” the investigators concluded. “To better understand leptin resistance in smoker and non-smoker subjects with OSA, further biomarker studies are needed on the metabolic consequences of leptin resistance in active smoker and non-smoker patients with OSA."