How chubby were you as a child?
Childhood and adolescent obesity increases your risk of getting multiple sclerosis. What should you do with this information?
We know that childhood and adolescent obesity increases your risk of getting multiple sclerosis (MS). The latest Swedish study below confirms this. This study adds to the data by showing a dose-response relationship based on the degree. Those with class 2 obesity (BMI 35-39.9) had a much greater risk of developing MS than those with class 1 obesity (BMI 30.0-34.9). In a past paper, we estimated that about 15% of the attributable MS risk could be explained by obesity. In other words, if we eliminate childhood and adolescent obesity, we will reduce the incidence of MS by about 15%.
The biggest question from this data is how does childhood and adolescent obesity increase one’s risk of getting MS? Several Mendelian randomisation studies suggest that the genetic variants leading to obesity are associated with MS risk. Hence, obesity is in the causal pathway.
Others posit that obesity leads to a state of chronic inflammation and acts as a non-specific pro-inflammatory signal that reduces your threshold of developing MS and other autoimmune diseases. Obesity is associated with changes in the gut microbiome, which can also lead to inflammation. Obesity is also related to hormonal changes and reduced vitamin D levels. Low vitamin D is a risk factor for developing MS. Finally, obesity changes immune functions. These changes may tip the balance in favour of autoimmunity.
I have investigated diet and autoimmunity. It was clear that since humans made sugar a commodity and our sugar intake increased, so did obesity and autoimmunity. This is why anyone thinking about MS prevention should engage in public health policies to reduce childhood and adolescent obesity. Sugar taxes and other initiatives to reduce processed carbohydrate consumption are part of MS prevention.
Please be aware that obesity still requires EBV. If you remove EBV from the equation, obesity is not a risk for developing MS. EBV is necessary but insufficient for someone to develop MS, which is why I am so focused on EBV as a target for MS prevention.
How many of you were chubby as children or were overweight or obese as adolescents? Please be aware that the majority of people who develop MS will not have been obese as children or adolescents. All the data shows is that obesity increases your risk.
What should you do with this information? If you have MS and have children or adolescents who are overweight, you should try and get them to lose weight to lower their risk of developing MS.
Paper 1
Background: Emerging evidence implies a link between high pediatric body mass index (BMI) and an increased risk of multiple sclerosis (MS). However, previous research suggests this association is only present for adolescent obesity and not childhood obesity. The present study aimed to assess the association between pediatric obesity and risk of developing MS, and to investigate if degree of obesity and age at obesity treatment initiation affects the risk. In a subgroup, response to obesity treatment on MS risk was assessed.
Methods: In this cohort study, patients aged 2-19 years from the Swedish Childhood Obesity Treatment Register (BORIS), and matched individuals from the general population were followed prospectively. MS was identified through the National Patient Register. Hazard ratios (HR) adjusted for parental MS were calculated.
Results: The study included 21,652 individuals with pediatric obesity and 102,187 general population comparators. The median age at follow-up was 21 (Q1, Q3 18, 25) years. The adjusted HR (95% CI) for developing MS in the pediatric obesity cohort was 2.28 (1.45-3.58). In stratified analyses, obesity class I was not associated with MS, HR = 1.34 (0.64-2.81), while the association between obesity class II and MS was strengthened, HR = 3.42 (1.89-6.19). MS was associated with both childhood obesity, HR = 3.16 (1.12-8.87), and adolescent obesity, HR = 2.12 (1.28-3.51). A decrease in BMI SDS was not associated with lower likelihood of MS, HR = 1.09 (0.92-1.29) per 0.25 BMI SDS unit decrease.
Conclusions: Both childhood and adolescent obesity are associated with an increased risk of MS. Moreover, a dose-response relationship between the degree of obesity and the risk of future MS was indicated, while response to pediatric obesity treatment did not affect the association, highlighting the importance of preventing high degree of obesity early in life.
Paper 2
Background: Smoking and childhood and adolescent high body-mass index (BMI) are leading lifestyle-related risk factors of global premature morbidity and mortality, and have been associated with an increased risk of developing multiple sclerosis (MS). This study aims to estimate and project the proportion of MS incidence that could be prevented with elimination of these risk factors.
Methods: Prevalence estimates of high BMI during childhood/adolescence and smoking in early adulthood, and relative risks of MS, were obtained from published literature. A time-lag of 10 years was assumed between smoking in early adulthood and MS incidence, and a time-lag of 20 years was assumed between childhood/adolescent high BMI and MS incidence. The MS population attributable fractions (PAFs) of smoking and high BMI were estimated as individual and combined risk factors, by age, country and sex in 2015, 2025 and 2035 where feasible.
Results: The combined estimated PAFs for smoking and high BMI in 2015 were 14, 11, 12 and 12% for the UK, USA, Russia and Australia in a conservative estimate, and 21, 20, 19 and 16% in an independent estimate, respectively. Estimates for smoking are declining over time, whereas estimates for high early life BMI are rising. The PAF for high early life BMI is highest in the USA and is estimated to increase to 14% by 2035.
Conclusions: Assuming causality, there is the potential to substantially reduce MS incidence with the elimination of lifestyle-related modifiable risk factors, which are the target of global public health prevention strategies.
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Please note that the opinions expressed here are those of Professor Giovannoni and do not necessarily reflect the positions of Queen Mary University of London or Barts Health NHS Trust. The advice is intended as general and should not be interpreted as personal clinical advice. If you have problems, please tell your healthcare professional, who will be able to help you.
Your comments prove the point I make that the majority of people who develop MS were not obese in childhood and adolescence. I think the science behind how obesity increases the risk of developing MS is more important than the observation itself. And I don't believe we have the science pinned down. All the current explanations are rather woolly.
A super sporty kid who became a PE teacher….. and still got ms…. and was also outside all the time in the UV light teaching…. and playing sport 🤷♀️