Preventive Neurology

Wesley Tingey, Unsplash As I get older and hopefully wiser I am beginning to realise that it is the simple pleasures of life that may be the most beneficial for healthy ageing. Exercise being numero uno. In this, Women’s Health Initiative, study below light-intensity physical activity improves mobility among older women. It is really a no-brainer. As we unpack the biology of exercise and ageing there are sound biological mechanisms that underpin exercise as a treatment for ageing. Exercise increases levels of important growth factors such as brain-derived neurotrophic factor (BDNF) and other growth hormones. Exercise enhances neurotransmission and activates signalling pathways in brain cells. Exercise downregulates several inhibitory pathways for CNS regeneration. Exercise increases levels of the so-called nuclear factor erythroid 2–related factor 2 (NRF2) transcription factor and downstream anti-oxidant pathways. NRF2 is likely to be the main antiageing pathway that is common to multi

Picture from AllGo - Unsplash Good and bad news. It is clear that the pharmaceuticalization of obesity means its treatment will need to be long-term. Should the emergence of so-called glucagon-like peptide-1 receptor agonists as a treatment for obesity be celebrated? Yes, if you have vested interests in the pharmaceutical industry and you think the long-term risks of these treatments are less than the comorbidities associated with obesity. No, if you think obesity can be managed successfully with lifestyle and behavioural modifications. The study below of once-weekly subcutaneous semaglutide shows that if you stop the drug after 20 weeks the treatment effect of continued weight loss is reversed and the inevitable weight gain The class of glucagon-like peptide-1 receptor agonists increase the production of insulin. Insulin lowers the blood sugar level, enhances the growth of β cells in the pancreas, which is the site of insulin production. The downside of increased insulin production is

I am often criticised for politicising medicine. Some people believe that medicine and politics shouldn’t mix. However, as soon as you realise that social determinants are the best predictor of clinical outcomes in most diseases you realise medicine and its practice has to be politicised. How do we as individual healthcare practitioners change the social determinants of health outcomes without the help of politicians? Obesity may be a lifestyle disease, but it is clear that most people who are obese can’t help it. In other words, they are obese because of their circumstances. “But people’s ability to take personal responsibility is shaped by their circumstances. People cannot take responsibility if they cannot control what happens to them.” Michael G. Marmot,  The Health Gap: The Challenge of an Unequal World Obesity is a risk factor for many diseases including all-cause dementia and multiple sclerosis. This is why it is so important for us to think about ways to reduce obesity. I am

I have almost completed a paper with a colleague and friend Viqar Chamoun. He was a contemporary of mine when I did my PhD. Chamoun and I worked in the same laboratory and we spent many hours chewing the cud together. Chamoun is a very deep thinker and got me interested in medical philosophy and the application of logic to defining a disease. Chamoun worked on neurosarcoidosis and developed a set of logical steps to show that contemporary diagnostic criteria for neurosarcoidosis were based on tautology. Despite his logical approach we never got his seminal paper published. The plan is to publish it now and in parallel with a paper defining MS as a biological disease and setting-out the principles of how we should incorporate biomarkers into the diagnostic criteria to improve both the sensitivity and specificity of the current criteria. Viqar Chamoun - thinker extraordinaire   Surprise, surprise one of the biomarkers we want to explore is EBV seropositivity. However, to validate a new s

"What is it that one wants to achieve?" 'Traditionally preventive medicine is a combination of medical practices that are designed to avoid disease and illness. It is a proactive approach to patient care with the aim of using evidence-based preventative measures to ensure that any sickness is minimised and detected early so that a patient has the best chance of recovery to optimum health.' This definition is based on a medicalised worldview of preventive medicine. Why can't we use social or political practices to avoid disease and illness? Surely the aim is better population health and is not necessarily about the individual? A healthier population will have a better quality of life, less need for healthcare and in theory should be happier and more content than an unhealthy population.  I have been criticised for jumping onto the social determinants of health bandwagon now that it is a hot topic. I counter this by stating that it is only a hot topic because COVID-

As MS is likely to be a preventable disease we should be doing everything we can to reduce our exposure to modifiable risk factors. Smoking, passive smoking, solvent exposure and air pollution have all been linked to an increased incidence of MS. It has always been argued that air pollution may work by acting as a filter for ultraviolet light and hence increases one's risk of getting MS by reducing UVB exposure, which is important for vitamin D synthesis in the skin. However, I am not sure this is the case as common to all these exposures, including air pollution, is inflammation in the lungs. The current hypothesis is that inflammation in the lungs changes or alters proteins via a process called post-translational modification, which converts normal proteins in highly immunogenic autoantigens that trigger autoimmune disease. There is good support for the latter hypothesis in rheumatoid arthritis, but to the best of my knowledge outside of animal models, the evidence in MS remains

How soon is early enough? The study below supports the need for lifestyle behaviours to improve Brain Health having to start early even before you are middle-aged. In this study of 40- to 54-year-old employees of the Banco Santander in Madrid, Spain who didn’t have any apparent cardiovascular disease were assessed using the 30-year Framingham cardiovascular risk score (FCRS) and other investigations to detect atherosclerosis. A proportion of the 946 of the subjects who had early atherosclerosis underwent metabolic PET imaging of their brain to assess brain metabolism. Higher 30-year FCRS was associated with global and regional brain hypometabolism, particularly in the parietotemporal region. The carotid artery atherosclerosis burden was associated with this brain hypometabolism, which is an early biomarker of neurodegeneration. These people have poor brain health a reduced brain reserve and are at greater risk of dementia in the future. Importantly, it was hypertension that was the ma

Obesity is a hot potato topic. People who are overweight don’t want to be fat-shamed. However, it is now evident that given our current environment, which favours a sedentary lifestyle and has a different food landscape to the one our species evolved in, that obesity is a disease. Yes, a metabolic disease that is associated with systemic inflammation, which puts obese people at risk of a large number of diseases including multiple sclerosis and dementia . We estimate that about 10-15% of incident cases of MS could be prevented if we could prevent childhood and adolescent obesity. This is easier said than done. Obesity is now one of the major social determinants of health (SDoH). Obesity is strongly linked to deprivation and lower socioeconomic class. Why? Because cheap food is to blame. I have little doubt that most obesity is attributable to the imbalance in our macronutrient content and the relative excessive consumption of processed and ultra-processed carbohydrates.  Changing our

"Professor Giovannoni, you tell me that my daughter has a 1 in 40 chance of developing multiple sclerosis and that MS has reached epidemic proportions in parts of the world? Is there anything I can do to reduce her chances of getting MS? Is there anything we can do to stop other people from getting MS?" Although multiple sclerosis (MS) is a complex disease due to the interaction of genetic and environmental factors data on the occurrence of MS at the population level (epidemiology) supports the Epstein Barr Virus (EBV) as being necessary, but not sufficient, for someone to develop MS. In other words, EBV is probably the cause of MS. Of all the putative causative agents that have been proposed to be associated with MS, EBV is the only one where the risk of getting MS if you are EBV negative is close to zero or zero if you limit the analyses to those studies which use a technique called immunofluorescence microscopy as the gold-standard assay to detect anti-EBV antibodies. EBV

I have been complaining about my low productivity levels since I have gotten back to work after my accident. However, last night with a single one hour webinar we have managed to set-up a new international collaboration to study and address the social determinants of health (SDoH) and their impact on MS. Our focus is going to be on which SDoH can we modify and hence improve the outcome for people with MS (pwMS)? Smoking is one such modifiable factor and needs to be addressed at a (1) population level with policy and legislation, (2) at a local or community level, (3) with the family and (4) at an individual level target the people with MS (pwMS). We know that pwMS who smoke have a worse outcome than people who don’t smoke. The effect of smoking is equivalent to negating the treatment effect of being on an injectable therapy such as interferon beta. Put simply smokers with MS start using a walking stick (EDSS = 6.0) about 6 years earlier than pwMS who don’t smoke. Getting pwMS to stop s