Overweight and obesity can alter both innate and adaptive immune responses. Adipose tissue is metabolically active and releases inflammatory mediators, including cytokines and adipokines. Persistent low-grade systemic inflammation may disrupt normal immune regulation and impair the body’s response to infectious agents.
Obesity has been associated with:
It is therefore more accurate to describe obesity as causing immune dysregulation rather than simply “weakening” the immune system. Obesity may simultaneously promote chronic inflammation while reducing the effectiveness of specific protective immune responses. (PubMed)
The relationship between obesity and respiratory infection is influenced by additional factors such as diabetes, cardiovascular disease, reduced mobility, impaired respiratory mechanics and obstructive sleep apnoea. These comorbidities may increase the severity of infection even when the risk of initially acquiring the infection is not substantially increased.
Frequent or severe lower respiratory tract infections can contribute to chronic respiratory morbidity. Infections occurring early in life may interfere with normal lung development and have been associated with a greater risk of chronic lung disease later in life. In adults, recurrent infections may also identify individuals with pre-existing structural lung disease, impaired airway clearance, smoking-related damage or immune dysfunction.
However, recurrent respiratory infections should not be described as a direct or sufficient cause of COPD. The principal established risk factors for COPD include:
A history of recurrent lower respiratory tract infections is clinically relevant when evaluating a patient for COPD, but the diagnosis requires persistent post-bronchodilator airflow obstruction on spirometry. (goldcopd.org)
Excess body weight is associated with an increased risk of developing asthma. A major meta-analysis found that overweight and obesity combined were associated with approximately 1.5 times the odds of incident asthma compared with normal weight. The relationship was dose-dependent, with a greater risk among individuals with obesity than among those who were merely overweight. (PubMed)
The magnitude of risk varies between studies and population groups. Sex, age, abdominal fat distribution, metabolic health, physical activity and the definition of asthma may all influence the observed association. It is therefore preferable not to present a single relative-risk figure as universally applicable.
Potential mechanisms linking obesity and asthma include:
Obesity-associated asthma may be more difficult to control and may be accompanied by more frequent symptoms, poorer quality of life and a reduced response to some standard asthma treatments.
Adipose tissue around the abdomen and thorax restricts the movement of the diaphragm and chest wall. Increased abdominal pressure displaces the diaphragm upwards, especially when the patient is lying supine. At the same time, fat accumulation around the rib cage reduces chest-wall compliance.
These mechanical changes produce several physiological consequences:
The functional residual capacity, or FRC, is the volume of air remaining in the lungs at the end of a normal passive expiration. It acts as an oxygen reservoir and helps keep peripheral airways open between breaths.
FRC decreases progressively as body mass index and central adiposity increase. The reduction may be substantial in severe obesity, but a fixed value such as 33% should not be applied to every individual. Published measurements vary according to body position, sex, fat distribution, severity of obesity and the method used to measure lung volumes.
A reduction in FRC decreases the volume available for normal tidal breathing. Many individuals with obesity compensate by breathing at a lower lung volume and increasing their respiratory rate.
The resulting breathing pattern is often characterised by:
Although this compensatory response may maintain adequate gas exchange while the patient is awake, it can become insufficient during sleep, respiratory infection, sedation or severe illness. Individuals with severe obesity are therefore more vulnerable to hypoxaemia, atelectasis and ventilatory failure under these conditions.
When FRC falls, the airways operate at a lower lung volume. Reduced radial traction from the surrounding lung tissue allows the airways—particularly the small peripheral airways—to narrow more readily.
This may lead to:
The effect is usually greatest in the small airways, which may close when the closing capacity approaches or exceeds FRC. This process is particularly relevant when the patient is supine or under general anaesthesia.
Obesity does not necessarily cause fixed bronchial obstruction. Standard spirometry may remain normal because small-airway dysfunction can develop before clear abnormalities appear in forced expiratory volume or the FEV₁/FVC ratio.
More sensitive methods, such as oscillometry, nitrogen washout or detailed lung-volume measurement, may demonstrate peripheral-airway dysfunction when conventional spirometry is inconclusive.
In healthy individuals, a deep inspiration normally stretches airway smooth muscle and temporarily widens the airways. This physiological bronchodilatory effect may be reduced in obesity because the lungs operate at lower volumes and the respiratory system is mechanically constrained.
As a result:
This phenomenon does not mean that bronchodilator medication is generally ineffective in patients with obesity. Rather, the normal mechanical bronchodilatory action of a deep breath may be impaired. Pharmacological bronchodilator responsiveness must be assessed separately using spirometry before and after bronchodilator administration. (PubMed)
Obesity is one of the strongest modifiable risk factors for obstructive sleep apnoea. Fat deposition around the tongue, pharynx and neck reduces upper-airway calibre and increases airway collapsibility during sleep. Reduced lung volume also decreases the stabilising traction exerted on the upper airway.
The Sleep AHEAD study, an ancillary study of the Look AHEAD trial, evaluated obese adults with type 2 diabetes. At baseline, approximately 86% of the 306 participants had obstructive sleep apnoea when an apnoea–hypopnoea index of at least five events per hour was used. Around one third had moderate OSA, and approximately one fifth had severe OSA. (PubMed)
This high prevalence should be interpreted within the study population. The participants were adults with both obesity and type 2 diabetes who were enrolled in a weight-loss trial. The result should not be generalised to all people with obesity or all patients with diabetes.
Clinically important symptoms and signs of OSA include:
Questionnaires such as STOP-Bang can identify patients at increased risk, but they cannot establish the diagnosis. Confirmation requires polysomnography or an appropriate home sleep-apnoea test in selected patients.
Weight loss can improve several obesity-related respiratory abnormalities. Potential benefits include:
In the Sleep AHEAD trial, an intensive lifestyle intervention reduced body weight and improved OSA severity. Long-term follow-up showed that OSA remission was more common among participants assigned to the lifestyle intervention, although residual OSA remained common and weight loss did not eliminate the need for sleep-specific assessment or treatment. (PMC)
Weight reduction should therefore be viewed as an important component of respiratory management rather than as a substitute for established treatments such as inhaled asthma medication or positive airway pressure therapy.
Respiratory symptoms in an individual with obesity should not automatically be attributed to excess body weight. Evaluation should consider:
Depending on the clinical presentation, investigations may include:
Awake hypercapnia should raise concern for obesity hypoventilation syndrome and requires further evaluation.
Management should address both respiratory disease and underlying metabolic risk. Important measures include:
Routine use of unproven “immune-boosting” supplements is not recommended. Nutritional supplementation should be based on a confirmed deficiency or another recognised clinical indication.
Obesity is associated with chronic inflammation and dysregulated immune defence, but it should not be described simply as global immunosuppression.
The association between obesity and respiratory infection varies according to the pathogen, population and accompanying medical conditions. Obesity is more consistently associated with severe outcomes from certain infections than with a uniformly increased risk of acquiring every respiratory infection.
Overweight and obesity increase the risk of incident asthma, although the magnitude of risk varies between populations.
Obesity reduces FRC and expiratory reserve volume. This promotes peripheral-airway narrowing, premature airway closure and increased respiratory effort.
Obesity may impair the normal bronchodilatory effect of deep inspiration, but this is not equivalent to resistance to bronchodilator medication.
The Sleep AHEAD study found OSA in approximately 86% of its selected population of obese adults with type 2 diabetes. This figure should not be applied to the general population.
Recurrent respiratory infections may be relevant to COPD assessment, but COPD requires persistent airflow obstruction and is most strongly associated with inhalational exposures and abnormal lung development.