Introduction:
Obesity is linked to higher prevalence and incidence rates of asthma, as well as higher asthma morbidity. It has been established that fat increases the likelihood of acquiring asthma. Obese asthmatics experience worse asthma control while receiving typical asthma therapy, lower quality of life specifically related to their condition, and greater rates of healthcare use. The many difficulties and complexities in comprehending this association are highlighted by the fact that not all obese asthmatics are similarly affected by weight increase. The relationships between obesity and other phenotypic traits, such as age at asthma onset, gender, and race, may determine vulnerability rather than obesity alone.
What Is Obesity?
When excess body fat has built up to the point where it may have a harmful impact on health, it is called obesity, a medical condition that is occasionally referred to as a disease. Body mass index (BMI), calculated by dividing a person's weight by the square of height, is used to describe obesity. A body mass index of 25 to 30 kilograms/meter square is considered overweight. Obesity is a significant contributor to disability and is linked to a number of illnesses and ailments, including osteoarthritis, type 2 diabetes, obstructive sleep apnea, several types of cancer, and asthma.
Individual, socioeconomic, and environmental factors all contribute to obesity. Diet, physical activity, mechanization, urbanization, genetic predisposition, drugs, mental illnesses, economic policies, endocrine problems, and exposure to endocrine-disrupting substances are a few examples of recognized causes. The primary method of treating obesity is weight loss through dietary and activity regimens.
What Is Asthma?
Inflammation of the lungs' airways over a lengthy period of time is asthma. It is distinguished by sporadic and recurrent symptoms, reversible airflow restriction, and easily induced bronchospasms. Episodes of wheezing, coughing, chest tightness, and shortness of breath are symptoms. It is hypothesized that a mix of hereditary and environmental factors contribute to asthma. Exposure to allergens and air pollution are examples of environmental influences. Beta-blockers and Aspirin are two other possible triggers. Symptom patterns, therapy response over time, and spirometry lung function testing are typically used to make a diagnosis. The frequency of symptoms forced expiratory volume in one second (FEV1), and peak expiratory flow rate are used to classify asthma.
Although asthma cannot be cured, it can be managed. By avoiding triggers like allergens and respiratory irritants, symptoms can be avoided and reduced with the help of inhaled corticosteroids. If asthma symptoms are still not under control, long-acting beta-agonists (LABA) or anti-leukotriene medications may be administered in addition to inhaled corticosteroids. An oral corticosteroid plus an inhaled short-acting beta-2 agonist, such as Salbutamol, are typically used to treat rapidly worsening symptoms. Magnesium sulfate, intravenous corticosteroids, and hospitalization may be necessary in severe cases.
What Effect Does Obesity Have On Managing Asthma?
Obesity has several implications on pulmonary physiology and mechanics, which may aggravate asthma in a variety of ways. Increased adiposity around the chest wall and abdomen can lead to the development of limitations, which can significantly impact pulmonary physiology. This can lead to decreased total lung capacity and, most significantly, low expiratory reserve volume from upward diaphragmatic displacement brought on by an increase in abdominal fat. As a result, the dependent lung zones' airways close at or above functional residual capacity, which can cause serious ventilation or perfusion mismatching.
Leptin levels rise, and adiponectin levels fall directly proportional to increased body fat. Both of these alterations have been connected to the development of obesity-related asthma. Asthmatics have greater leptin levels, which rise in correlation with plasma leptin levels and body mass index. Leptin is easily detectable in the airways. Leptin receptors, which are decreased with greater asthma severity and are linked to changes in the remodeling of the airways, are expressed by human airway epithelial cells. According to peripheral research linking bronchial hyperresponsiveness to the degree of leptin receptor expression in visceral fat, obesity-asthma may be a condition affecting peripheral adipose tissues. It has been demonstrated that leptin causes alveolar macrophages from obese and overweight asthmatics to respond more oxidatively and inflammatory.
What Is the Role of Diet in Obese Asthma?
The relationship between obesity and asthma may be influenced by particular micronutrients. Low levels of vitamin D in the blood are linked to obesity. Prenatal vitamin D insufficiency has been linked to obesity in the offspring, and prenatal vitamin D treatment resulted in a little reduction in the incidence of wheezing sickness at age three. These findings suggest that vitamin D deficiency may be a risk factor for the development of both obesity and asthma. Since there is growing evidence linking vitamin D deficiency to an increased risk of respiratory infections, asthma exacerbations, and corticosteroid resistance, vitamin D deficiency may predispose individuals to develop obesity, which in turn may lead to a phenotype of increased asthma severity and corticosteroid resistance.
How Is Obese Asthma Treated?
Although there are no medications specially designed to treat obese asthmatics, weight loss therapies, including surgical and nutritional ones, have been studied and found to differ in their ability to help these patients' respiratory health. It has been demonstrated that the average asthma control questionnaire and asthma control test scores considerably increase after a year of basic metabolic index reduction following bariatric surgery. Moreover, in one study, bronchial hyperresponsiveness only improved in patients with low or normal immunoglobulin E levels, indicating that different phenotypes may benefit differently from weight loss.
Low vitamin D levels, which are known to be inversely related to the body mass index and linked to higher asthma morbidity, may possibly be a secondary cause of obesity-mediated steroid resistance. Early research in asthmatic children and adults revealed that a vitamin D deficiency is linked to worsened airway hyperresponsiveness, more severe asthma, and a reduced response to corticosteroid therapy. Vitamin D supplementation in asthma was not found to be any more efficacious in obese asthmatics in the recent National Institutes of Health (NIH) asthma net clinical trial of vitamin D.
Conclusion:
The relationship between obesity and asthma has traditionally been seen as unidirectional; those with severe asthma become less active and deconditioned, gain weight, and the cycle of weight gain is further aggravated by the greater use of oral corticosteroids (OCS). In a fraction of the population, obesity may exacerbate the severity of asthma and contribute to its poor control. It seems unclear that there is a single distinct phenotype of obese asthma. The combination of other clinical and demographic factors, such as gender, race, age at which asthma first appeared, and atopy, may affect a patient's vulnerability to obesity-mediated effects on asthma. The only specific treatment for the consequences of obesity on asthma is weight loss. The degree of weight loss and other phenotypic characteristics may affect this intervention's effectiveness.
