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Patients with ankylosing spondylitis have been breast fed less often than healthy controls: a case-control
Insights
Breastfeeding may protect against ankylosing spondylitis (AS), a chronic inflammatory spine disease. This study found that patients with AS were breastfed less often than their healthy siblings and unrelated controls, suggesting a protective effect.
Area of Science:
- Rheumatology
- Immunology
- Microbiome Research
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory disease impacting young adults, particularly the spine and pelvis.
- The development of AS is linked to the HLA-B27 gene and influenced by the gut microbiota.
- Breastfeeding is known to shape the infant gut microbiota.
Purpose of the Study:
- To investigate the potential protective role of breastfeeding against the development of ankylosing spondylitis.
- To explore the relationship between breastfeeding and AS occurrence in HLA-B27-positive individuals.
Main Methods:
- Recruited 203 HLA-B27-positive AS patients and 293 healthy siblings from a rheumatology department.
- Included 280 healthy unrelated controls and 100 rheumatoid arthritis patients with their siblings.
- Collected data on feeding type (breast or bottle), duration, age, gender, and family history.
Main Results:
- Patients with AS reported lower rates of breastfeeding compared to healthy controls (OR 0.6).
- Within families, AS patients were breastfed less frequently than their healthy siblings (57% vs 72%, OR 0.53).
- Breastfeeding was associated with a reduced familial prevalence of AS.
Conclusions:
- The study suggests a protective effect of breastfeeding against the occurrence of ankylosing spondylitis.
- This is the first study to examine breastfeeding history in relation to AS.
- Breastfeeding may influence AS development through its impact on the gut microbiota.
Objective:
Ankylosing spondylitis (AS) is a chronic inflammatory disease affecting the spine and pelvis of young adults. On the HLA-B27 genetic background, the occurrence of AS is influenced by the intestinal microbiota. The goal of our study was to test whether breast feeding, which influences microbiota, can prevent the development of AS.
Methods:
First, 203 patients with HLA-B27-positive AS fulfilling the modified New York criteria were recruited in the Department of Rheumatology, Ste Marguerite hospital in Marseilles. A total of 293 healthy siblings were also recruited to make up a control group within the same families. Second, 280 healthy controls, and 100 patients with rheumatoid arthritis and their siblings were recruited. The data collected were age, gender, number of brothers and sisters, age at disease onset, type and duration of feeding (breast or bottle).
Results:
Patients with AS had been breast fed less often than healthy controls. In families where children were breast fed, the patients with AS were less often breast fed than their healthy siblings (57% vs 72%), giving an OR for AS onset of 0.53 (95% CI (0.36 to 0.77), p value=0.0009). Breast feeding reduced familial prevalence of AS. The frequency of breast feeding was similar in the AS siblings and in the 280 unrelated controls. However, patients with AS were less often breast fed compared with the 280 unrelated controls (OR 0.6, 95% CI (0.42 to 0.89), p<0.01).
Conclusions:
Our study suggests a breastfeeding-induced protective effect on the occurrence of AS. To our knowledge, this is the first study of breastfeeding history in patients with AS.
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