Introduction
Obesity, defined by the World Health Organization as a body mass index (BMI) exceeding 30 kg/m2, is a growing global health concern. In Taiwan, a BMI of 27 kg/m2 or higher is considered the threshold for obesity, while a BMI exceeding 40 kg/m2 is classified as morbid obesity. Once rare, the global prevalence of obesity has surged from less than 1% in 1975 to 6%-8% in 2016. In the United States, between 2017 and 2018, over 42% of adults were obese, with nearly 10% experiencing severe obesity. Central obesity, characterized by excess abdominal fat, affects a significant portion of the global population, with the highest prevalence in Southern and Central America. Obesity is a risk factor for chronic diseases, and strategies for weight management should be incorporated into health promotion programs to prevent chronic diseases.
Herpes zoster (HZ), commonly known as shingles, is caused by the reactivation of the varicella-zoster virus (VZV), presenting as painful vesicles with a dermatomal distribution. The incidence of HZ varies worldwide, with women generally experiencing a higher incidence than men. Immunocompromised patients face a significantly elevated risk of HZ. Stress has also been identified as a trigger for VZV reactivation. Musculoskeletal chronic pain and endocrine disorders like polycystic ovary syndrome (PCOS) have been associated with HZ development.
Obesity and Herpes Zoster: An Emerging Link
The relationship between obesity and herpes zoster (HZ) occurrence is an area of growing interest. While previous research has established connections between obesity and various chronic diseases, including diabetes mellitus (DM), chronic kidney disease (CKD), musculoskeletal conditions, and endocrine disorders like PCOS, the direct impact of obesity on HZ reactivation has remained unclear. This study investigated the association between obesity and HZ occurrence.
Study Methodology
This cohort study utilized data from the National Health Insurance Research Database (NHIRD), which contains health insurance claims data for 99% of Taiwanese residents. The study population included patients aged 20-100 years with obesity from 2000 to 2017 (tracked to 2018). Obesity was indicated by the presence of two or more outpatient diagnoses or at least one admission record (ICD-9-CM: 278.0; ICD-10-CM: E66). To assess the impact of obesity severity, obesity was categorized into two groups: non-morbid obesity (ICD-9-CM: 278.00; ICD-10-CM: E66.09, E66.1, E66.8, E66.9) and morbid obesity (ICD-9-CM: 278.01; ICD-10-CM: E66.01, E66.2). The index date was defined as the date when obesity was diagnosed, and patients with HZ (ICD-9-CM: 053; ICD-10-CM: B02) before the index date were excluded. The obesity and control cohorts underwent 1:1 propensity score matching based on age, sex, comorbidities, and index year. The covariates were comorbidities, such as diabetes mellitus (DM) (ICD-9-CM: 250; ICD-10-CM: E08-E13), chronic kidney disease (CKD) (ICD-9-CM: 585; ICD-10-CM: N18.4-N18.9), coronary artery disease (CAD) (ICD-9-CM: 410-414; ICD-10-CM: I20-I25) and cancer (ICD-9-CM: 140-208; ICD-10-CM: C).
Statistical analysis involved comparing frequencies and percentages of variables using chi-square tests and t-tests. Multivariable Cox proportional hazards models were used to determine the incidence rate (IR) and hazard ratios (HR) of HZ, adjusted for age, sex, and comorbidities. The Kaplan-Meier method was used to derive the cumulative incidence curve of obesity. A two-sided p-value less than 0.05 was considered significant.
Read also: Weight Loss Guide Andalusia, AL
Study Results
The study found that the obesity cohort had a significantly higher risk of HZ than the control cohort. Further analysis revealed that the morbid obesity group had a significantly higher risk of HZ than the non-morbid obesity group. The risk of HZ in patients with comorbidities was significantly higher than in those without comorbidities. The cumulative incidence of HZ in the obesity cohort was higher than that in the control cohort.
In the obesity cohort, the risk of HZ in women, those aged 30-39 years, and without comorbidities was significantly higher than that of the control cohort. Within the morbid obesity group, the risk of HZ across different genders was significantly higher than in the control group. Among the age groups 40-49 and ≥ 50, the risk of HZ in the morbid obesity cohort was also significantly higher compared to the non-morbid obesity cohort. Additionally, the analysis of comorbidities revealed that the morbid obesity cohort consistently displayed a higher risk of developing HZ compared to the non-morbid obesity cohort, irrespective of the presence of comorbid conditions.
Discussion: Unpacking the Link Between Obesity and Herpes Zoster
The study findings suggest a significant association between obesity, particularly morbid obesity, and an increased risk of HZ. This connection may be mediated by several factors.
Obesity and Related Chronic Diseases
Extensive research has revealed a strong correlation between obesity and various chronic diseases, such as DM and CKD. Additionally, obesity has been found to be associated with musculoskeletal conditions like sciatica and endocrine-related disorders such as PCOS. It is noteworthy that these diseases have also been linked to the reactivation of HZ. This connection underscores the intricate interplay between obesity, its related health conditions, and their potential impact on the reactivation of HZ.
- Diabetes Mellitus (DM): Abdominal obesity is strongly associated with DM. Patients with DM have a higher risk of HZ than those without DM.
- Chronic Kidney Disease (CKD): Obesity increases the risk of CKD development. Patients with predialysis CKD had a 1.4-fold increased risk of developing HZ compared with patients without CKD.
- Sciatica: BMI was significantly associated with an increased risk of sciatica. Patients with sciatica were more likely to develop HZ compared with those without sciatica.
- Polycystic Ovary Syndrome (PCOS): Women with PCOS had a higher rate of overweight and obesity.
Immunocompromised State
Treatment for inflammatory bowel disease (IBD) often involves immunosuppressants. Suppressing the immune system can increase the risk of developing opportunistic infections. Immunosuppressive treatment for IBD can lead to some people becoming immunocompromised. This status may then contribute to the reactivation of the virus, potentially resulting in more severe symptoms and complications like herpes simplex virus colitis.
Read also: Beef jerky: A high-protein option for shedding pounds?
Inflammatory Response
Reduced appetite and body weight loss are typical symptoms of inflammatory diseases. A number of inflammatory stimuli are responsible for the imbalance in energy homeostasis, leading to metabolic disorders. The brain is an important target for proinflammatory cytokines that affect the neuronal circuits controlling food intake and energy homeostasis. Inflammation in the brain results in a profound state of negative energy balance that is an adaptive response to infection. Herpes virus entry mediator (HVEM) deficiency attenuates the inflammatory responses of adipose tissue and glucose intolerance in diet-induced obesity. The HVEM signaling in the brain contributes to acute inflammation-induced anorexia and weight loss.
Herpes Simplex Virus (HSV) and Obesity
Obesity may play a role in the susceptibility to HSV1 infection. Obese persons were 1.5 times more likely to be infected with HSV1 when compared to infected persons with normal weight. The association of obesity and HSV1 could possibly be explained by predisposition to the altered production of hormones involved in metabolism in obese people that could lead to a change in immune responses. Obesity may be linked to an increased level of herpes virus entry mediators (HVEM), which could potentially increase viral entry.
Managing Herpes Outbreaks: Diet and Lifestyle
There is no cure for herpes. Once you have the virus in your body, it remains there for the rest of your life, most of the time dormant (inactive). Food can trigger flareups. Studies show that arginine, an amino acid found in many foods, may contribute to the spread of herpes. Therefore, it is best to avoid eating foods like turkey breast, pork loin, chicken breast, nuts (especially peanuts), pumpkin seeds, chickpeas, soybeans and lentils that are high in arginine. Lysine is a naturally occurring amino acid produced within the body. Its consumption has been linked to inhibiting arginine activity.
Read also: Inspiring Health Transformation
tags: #herpes #and #weight #loss #connection