Barts-MS rose-tinted-odometer ★★★
Just back from the NMSS ‘Pathways to Cures’ meeting in Washington DC during which we pledged to STOP, RESTORE and END multiple sclerosis.
The END refers to prevention. We discussed at the meeting modifiable risk factors that could be tackled to reduce the incidence (new cases) of MS and one risk factor childhood and adolescent obesity. One theory has been that obesity affects MS risk by interacting with vitamin D (vD); either by lowering levels due to the breakdown of vD in fat or secondary to systemic inflammation associated with obesity.
In this genomics study below it is clear that obesity itself increases your risk of MS and is independent of vD levels.
So how do we tackle obesity and the obesity epidemic? It is clear that obesity is caused by sugar and the change in the dietary guidelines that occurred in the 1970s and 1980s when governments launched a war on fats and started to promote a low-fat diet as being ‘heart-healthy’. We now know that the low-fat diet was wrong and that what was driving heart and vascular disease was processed carbohydrates, in particular, sugar consumption, and not saturated fats. Fortunately, the world is now beginning to acknowledge that saturated fats are healthy and that processed and ultra-processed foods, which are largely made up of carbohydrates and polyunsaturated fats are unhealthy culprits and are what is causing the obesity epidemic.
Another factor driving obesity is our sedentary lifestyle and reduced exercise.
To tackle obesity we need governments to declare ware on sugar and the food industry and to put in place national policies to tackle our sedentary lifestyle. This is easier said than done. Politicians are not as powerful as they used to be; most of them rely on lobby money to get elected and once elected they represent the vested interest groups that got them elected. Sadly this often includes sugar money.
The sugar industry is heavily subsidised, which keeps the price of sugar artificially low. Sugar subsidies interfere with the global market and have resulted in a sugar glut. This is one of the reasons why junk food is so cheap and real-food is so expensive.
Obesity is not only a risk factor for causing MS it also affects people with established MS. Obesogenic diets cause a metabolic shitstorm that impacts on MS indirectly. Obesity causes metabolic syndrome (hypertension, insulin resistance, glucose intolerance, diabetes and dyslipidaemia) and a systemic inflammatory syndrome that worsens MS. Therefore, there is a good reason why, if you are obese you should consider doing something about it.
I recommend you read “Why we get fat and what to do about it”, by Gary Taubes or you can watch one of his lectures on YouTube. Understanding the metabolic issues that underlie obesity will allow you to understand what to do about it.
Then there is the responsibility you have to your siblings, children and relatives. If you have MS your direct family are at increased risk of getting MS and you should get them to modify their risk factors, i.e. make sure they stay slim, or if they are obese they need to lose weight, get them to exercise and to start taking vD supplements. Tell them about the link between smoking and MS; they should either stop smoking or get them to pledge not to start smoking in the future.
MS prevention is about education, education, education and education begins in the home. We estimate that ~15-20% of new cases of MS could be prevented by preventing childhood obesity and smoking. This is why we need to declare war on sugar and smoking as part of our END MS campaign. Do you agree?
Jacobs et al. BMI and Low Vitamin D Are Causal Factors for Multiple Sclerosis: A Mendelian Randomization Study. Neurol Neuroimmunol Neuroinflamm, 7 (2) 2020 Jan 14.
Objective: To update the causal estimates for the effects of adult body mass index (BMI), childhood BMI, and vitamin D status on multiple sclerosis (MS) risk.
Methods: We used 2-sample Mendelian randomization to determine causal estimates. Summary statistics for SNP associations with traits of interest were obtained from the relevant consortia. Primary analyses consisted of random-effects inverse-variance-weighted meta-analysis, followed by secondary sensitivity analyses.
Results: Genetically determined increased childhood BMI (ORMS 1.24, 95% CI 1.05-1.45, p = 0.011) and adult BMI (ORMS 1.14, 95% CI 1.01-1.30, p = 0.042) were associated with increased MS risk. The effect of genetically determined adult BMI on MS risk lessened after exclusion of 16 variants associated with childhood BMI (ORMS 1.11, 95% CI 0.97-1.28, p = 0.121). Correcting for effects of serum vitamin D in a multivariate analysis did not alter the direction or significance of these estimates. Each genetically determined unit increase in the natural-log-transformed vitamin D level was associated with a 43% decrease in the odds of MS (OR 0.57, 95% CI 0.41-0.81, p = 0.001).
Conclusions: We provide novel evidence that BMI before the age of 10 is an independent causal risk factor for MS and strengthen evidence for the causal role of vitamin D in the pathogenesis of MS.
CoI: this work was done by our Preventive Neurology Unit
