Obesity is a chronic disease caused by an excess of adipose tissue that may impair health by altering the functionality of various organs, including the lungs. Excessive deposition of fat in the abdominal area can lead to abnormal positioning of the diaphragm and consequent reduction in lung volume, leading to a heightened demand for ventilation and increased exposure to respiratory diseases, such as chronic obstructive pulmonary disease, asthma, and obstructive sleep apnoea. In addition to mechanical ventilatory constraints, excess fat and ectopic deposition in visceral depots can lead to adipose tissue dysfunction, which promotes metabolic disorders. An altered adipokine-secretion profile from dysfunctional adipose tissue in morbid obesity fosters systemic, low-grade inflammation, impairing pulmonary immune response and promoting airway hyperresponsiveness. A potential target of these adipokines could be the NLRP3 inflammasome, a critical component of the innate immune system, the harmful pro-inflammatory effect of which affects both adipose and lung tissue in obesity. In this review, we will investigate the crosstalk between adipose tissue and the lung in obesity, highlighting the main inflammatory mediators and novel therapeutic targets in preventing pulmonary dysfunction.

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Adipose Tissue Inflammation and Pulmonary Dysfunction in Obesity

A case of narcolepsy

This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) provides clinicians an overview of sleep-disordered breathing, (e.g., sleep-related hypopnea, apnea), and other obesity-related sleep disorders. The scientific support for this CPS is based upon published citations, clinical perspectives of OMA authors, and peer review by the Obesity Medicine Association leadership. Obesity contributes to sleep-disordered breathing, with the most prevalent manifestation being obstructive sleep apnea. Obesity is also associated with other sleep disorders such as insomnia, primary snoring, and restless legs syndrome. This CPS outlines the evaluation, diagnosis, and treatment of sleep apnea and other sleep disorders, as well as the clinical implications of altered circadian system. This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) on “Sleep-Disordered Breathing, Sleep Apnea, and Other Obesity-Related Sleep Disorders” is one of a series of OMA CPSs designed to assist clinicians in the care of patients with the disease of obesity. 

Sleep-disordered breathing, sleep apnea, and other obesity-related sleep disorders: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022

Sleep-disordered breathing (SDB) is a group of sleep-related breathing disorders which includes obstructive sleep apnea (OSA), central sleep apnea (CSA), and obesity hypoventilation syndrome (OHS). OHS is characterized by a combination of obesity, daytime hypercapnia and hypoxemia, and sleep-disordered breathing without other known hypoventilation causes, such as severe obstructive or restrictive parenchymal lung disease, kyphoscoliosis, severe hypothyroidism, neuromuscular disease, or congenital central hypoventilation syndrome. Four hundred ninety potentially eligible references were identified; of these, 462 abstracts or full texts were excluded because they did not fulfil inclusion criteria. We reviewed the full text of the remaining 38 papers which fulfilled the inclusion criteria. The role of gender in SDB and particularly in OHS is not well known. In general, the diseases are under-recognized in women and only a few studies have reported the impact of gender on clinical presentation and treatment outcome. On the other hand, there is often a delay in diagnosing these diseases in women as compared to men; therefore, they are often more advanced when diagnosed in women. Better understanding and clinical awareness of the higher OHS prevalence in postmenopausal women may lead to earlier diagnosis and a more timely and appropriate treatment. Further studies are needed to assess the prevalence of OHS in women, the effect of menopause on OHS, and the increased risk of OHS, which will hopefully lead to optimizing OHS patient care. 

Gender differences in obesity hypoventilation syndrome

Obesity is a significant and increasingly common cause of respiratory compromise. It causes a decrease in static and dynamic pulmonary volumes. The expiratory reserve volume is one of the first to be affected. Obesity is associated with reduced airflow, increased airway hyperresponsiveness, and an increased risk of developing pulmonary hypertension, pulmonary embolism, respiratory tract infections, obstructive sleep apnoea and obesity hypoventilation syndrome. The physiological changes caused by obesity will eventually lead to hypoxic or hypercapnic respiratory failure. The pathophysiology of these changes includes a physical load of adipose tissue on the respiratory system and a systemic inflammatory state. Weight loss has clear, well-defined benefits in improving respiratory and airway physiology in obese individuals. Obesity has significant and wide-ranging effects on respiratory function, and is an important contributor to morbidity and mortality https://bit.ly/3k8bGmX

/pdf/respiratory-complications-of-obesity-from-early-changes-to-24skyl5v.pdf

Respiratory complications of obesity: from early changes to respiratory failure

With increasing prevalence of obesity, the substantial contribution of obesity hypoventilation syndrome (OHS) to morbidity and mortality is likely to increase. It is therefore crucial that the condition has a clear definition to allow timely identification of patients. OHS was first described as “Pickwickian syndrome” in the 1950s; in subsequent decades, case reports did not clearly delineate between patients suffering from OHS and those suffering from obstructive sleep apnoea. In 1999, the American Academy of Sleep Medicine published a guideline that delineated the cause of daytime hypercapnia as either predominantly upper airway or predominantly hypoventilation. This was the first formal definition of OHS as the presence of daytime alveolar hypoventilation (arterial carbon dioxide tension >45 mmHg) in patients with body mass index >30 kg·m−2 in the absence of other causes of hypoventilation. This definition is reflected in the most recent guidelines published on OHS. Recent developments in defining OHS include proposed classification systems of severity and demonstrating the value of using serum bicarbonate to exclude OHS in patients with a low index of suspicion. Educational aims To provide an overview of the historical basis of the definition of obesity hypoventilation syndrome. To explain the rationale for the current definition of obesity hypoventilation syndrome. To demonstrate areas that need further investigation in defining obesity hypoventilation syndrome.

https://breathe.ersjournals.com/content/breathe/17/3/210089.full.pdf

Sonia Shrimanker

Papers

Defining obesity hypoventilation syndrome