Bronchial asthma, a chronic disease affecting 330 million people worldwide, is characterized by airway inflammation and hyperresponsiveness (1, 2), with asthma patients having abnormally elevated levels of multiple inflammatory factors such as interleukin-1 (IL-1), IL-6, IL-17, and tumor necrosis factor-α (TNF-α) (3). These inflammatory factors can cause skeletal muscle loss through a variety of pathways [such as nuclear factor κb (NF-κB)], leading to sarcopenia (4). Sarcopenia is an emerging global health problem characterized by the gradual decline of skeletal muscle mass and can lead to adverse complications (5). About 3% of the world’s population suffers from sarcopenia (6), and individuals with asthma have a higher prevalence of this condition. According to research, the prevalence of sarcopenia in individuals with asthma can be as high as 17.6%, and approximately 5.5% of asthmatic are affected by severe sarcopenia (7). Furthermore, individuals with both asthma and sarcopenia were also at higher risk of osteoporosis, decreased lung function, and depression (7), and asthma patients with sarcopenia experience more severe shortness of breath and airway obstruction (8). Therefore, it is necessary to prevent sarcopenia among patients with asthma.

Inflammation is one of the causes of sarcopenia in asthmatic patients, which make anti-inflammatory intervention promising as an effective measure to prevent sarcopenia among individuals with asthma. Regulating inflammation can be achieved through dietary. Many components of the diet have been linked to inflammation. For instance, consuming higher amounts of cholesterol and carbohydrates has been found to contribute to increased levels of inflammation markers in the body (9–11). Increasing intake of dietary fiber, folic acid, and garlic has a positive effect on reducing levels of markers of inflammation (12–14). Nonetheless, due to the diversity of daily diets and the complex nature of individual food components, it remains a challenge to gage a person’s comprehensive dietary inflammation level. Therefore, previous studies developed a dietary inflammation index (DII) that takes into account the anti-inflammatory and pro-inflammatory properties of different food components. This enables a more comprehensive evaluation of the overall extent of dietary inflammation in individuals (15). Previous study has shown that asthmatic patients with elevated DII levels had a higher risk of experiencing all-cause mortality (16). However, to our knowledge, few studies have investigated whether there is an association between DII and sarcopenia in asthmatic patients.

The objective of this investigation was to examine the correlation between DII and the sarcopenia among individuals with asthma, and to provide some valuable insights for the prevention of sarcopenia in patients with asthma.

A total of 3,389 asthmatic patients were enrolled in this study. Our findings indicate a noteworthy positive correlation between the DII and sarcopenia among asthmatic patients. After stratification by age, sex, BMI, smoking, COPD, hypertension, DM and antiasthmatic drugs, no substantial alteration in the correlation between DII and sarcopenia was observed.

According to a meta-analysis, an elevated DII level was found to be significantly linked to the occurrence and progression of chronic illnesses, including CVD, cancer, and respiratory disease (19). In a study conducted on individuals with asthma, Han et al. (20) demonstrated that a higher DII level was connected to an elevated risk of wheezing. Additionally, Yuan et al. (16) observed that asthmatic patients with elevated DII levels had a higher risk of experiencing all-cause mortality. Nevertheless, the relationship between DII and sarcopenia in asthmatic individuals remains poorly investigated.

Several studies have demonstrated that increased levels of DII are a risk factor for the onset of sarcopenia in older adults (21–23). Similarly, heightened DII have also been linked to an elevated risk of sarcopenia in patients with DM, hypertension, Crohn’s disease, and CKD (24–26). It is well-established that aging is associated with a chronic state of low-grade inflammation in older adults (27). Many studies observed elevated levels of proinflammatory factors in the blood of people with hypertension and diabetes (28, 29). Additionally, both Crohn’s disease and CKD are characterized by persistent inflammation (30, 31). Like these population, asthma is also a chronic inflammatory disease (32), and studies have shown that people with asthma were more susceptible to the pro-inflammatory effects of dietary factors when compared to those without asthma (20). Furthermore, it should be noted that numerous asthma drugs have been found to contribute to the development of sarcopenia (33, 34). Sarcopenia in patients may exacerbate their asthma symptoms, thereby necessitating more anti-asthma medication, leading to a vicious cycle. Therefore, as with the elderly, DM, hypertension, Crohn’s disease, and CKD patients, the prevention of sarcopenia in asthma patients is also worthy of attention. Our study fills a gap in this area by using DII to assess the risk of sarcopenia among patients with asthma. Our findings suggest that DII was significantly correlated with the risk of sarcopenia in patients with asthma. Following the adjustment for potential confounders, the relationship between the two did not change significantly. In addition, stratified results by age, sex, BMI, smoking, hypertension, diabetes, and anti-asthma medications did not change significantly, and no interaction was observed between DII and these variables.

The mechanism by which a pro-inflammatory diet induces sarcopenia in asthmatic patients is unclear, but previous studies have provided some theoretical evidence. The study suggests that trans fatty acids have been shown to increase airway inflammation and circulating CRP levels in asthma patients (35, 36). In addition, inflammatory factors such as platelet-derived growth factor (PDGF), interferon-γ (IFN-γ), IL-1, and TNF-α were significantly increased in mice with high cholesterol intake (37). Excessive intake of refined carbohydrates increases circulating TNF-α levels via the NF-κB pathway (38). In contrast, ingestion of PUFAs produces anti-inflammatory mediators and inhibits the production of pro-inflammatory factors (39). A randomized controlled trial confirmed that increasing MUFAs intake helped lower CRP and IL-6 (40). TNF-α can induce sarcopenia through pyrodeath mediated by Gasdermins (41). IL-6 can be indicated by glycoprotein 130 (gp130)/Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT)/Suppressor of Cytokine Signaling (SOCS) pathways increase protein degradation and decrease protein synthesis to mediate skeletal muscle atrophy (42). Britta Walling-Larsson et al. (43) indicated that CRP can lead to downregulation of serine/threonine kinase Akt promoting muscle atrophy. PDGF can cause muscle fibrosis and hinder muscle repair by activating RHO-associated kinases (44). IFN-γ interferes with the differentiation of muscle satellite cells, leading to the accumulation of muscle satellite cells and the loss of skeletal muscle mass (4). Therefore, the loss of muscle mass caused by a pro-inflammatory diet may result from a number of pathways.

It should be emphasized that the correlation between protein and inflammation is not solely linked to consumption but also to the origin of protein. Animal-derived proteins lead to increased levels of pro-inflammatory factors, while plant-derived proteins help reduce inflammation throughout the body (36). A recent study showed that intake of animal protein increases the risk of developing frailty (a phenotypic manifestation of sarcopenia) (45–47), while increasing plant protein intake was linked with a lower possibility of developing frailty (48, 49). Therefore, when consuming protein, choosing to consume more plant protein may help prevent sarcopenia.

As mentioned above, the major pro-inflammatory parameters in DII, such as carbohydrates, cholesterol, trans fatty acids and animal protein, were strongly associated with the onset and development of sarcopenia. Thus, reducing the consumption of these pro-inflammatory components may yield beneficial effects in preventing sarcopenia. Increasing the intake of anti-inflammatory food components such as PUFAs, MUFAs, and plant proteins in DII can reduce the level of inflammation throughout the body and is one of the potential interventions to prevent sarcopenia. Therefore, we recommend that people with asthma reduce their intake of pro-inflammatory food components in the DII dietary pattern and increase their intake of anti-inflammatory food components. Although a causal relationship between DII and sarcopenia in asthmatic patients need to be further confirmed in randomized clinical trials. However, prior research has established that patients with asthma experienced a decrease in wheezing attacks and all-cause mortality by maintaining low levels of DII. Therefore, despite being a cross-sectional study, we still recommend that patients with asthma adopt a healthy low-DII dietary pattern.

There was a significant positive correlation between DII and the risk of sarcopenia. However, additional randomized controlled trials are necessary to establish a definitive causal connection between the DII and the onset of sarcopenia.

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

The studies involving humans were approved by National Center for Health Statistics. The studies were conducted in accordance with the local legislation and institutional requirements. The human samples used in this study were acquired from this study utilized data from the National Health and Nutrition Examination Survey (NHANES), which is sponsored by the National Center for Health Statistics (NCHS). Written informed consent for participation was not required from the participants or the participants’ legal guardians/next of kin in accordance with the national legislation and institutional requirements.

ZC designed the research and is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. SL conducted the analysis and wrote the first draft of the paper. SL, XS, LC, and ZC revised the manuscript. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.