obesity

Barts-MS rose-tinted-odometer: ★★★ (a dark blue Saturday; a chastised weekend warrior #00008b )

I was accused this week by some commentators on social media for blaming, and by implication shaming, people with MS about lifestyle factors that may impact the long term outcome of their MS. One person said, “stop pushing ‘lifestyle changes’ code for lose weight on people as a fix. It’s insulting and belittling”. In fact, this is incorrect. My dietary recommendations (caloric restriction, intermittent fasting and ketogenic diets) are directed at biohacking and using ketosis as a neuroprotective and pro-remyelinating strategy rather than weight loss. Similarly, exercise (aerobic and HIIT) is about inducing changes within the CNS to promote recovery of function and anti-inflammatory effects in the periphery. The fact that these dietary interventions and exercise can lead to, but not necessarily, weight loss is really not that relevant. Saying this obesity is an issue for pwMS in that that there is a lot of evidence that obesity itself impacts MS outcomes and affects the quality of life of pwMS. In addition, obesity is associated with and causes many comorbidities, which in turn impact MS outcomes (see figure below).

So is obesity a disease or a lifestyle choice? Although this would be a good debate for medical philosophers I am firmly in the camp that at a population level obesity is a metabolic disease that needs to be treated. However, it is up to individuals to choose whether or not they want their obesity treated, in the same way, they have the right to have their MS treated or not.

Some people with MS may not agree with me and hence choose not to have their obesity treated. In these people, obesity is a lifestyle choice and they are presumably well-informed and comfortable with the consequences of being obese. In this situation, who am I to interfere? However, I still feel I have a responsibility to ask the question about the problem?

Because of the sensitive issue of fat-shaming, it is important to open the discussion about weight in a respectful and non-judgmental way. You will be more open to talk about it and seek help if you feel respected. Before asking patients if they wish to discuss their weight, I mention the impact being overweight can have on MS and general health. I usually bundle the weight issue with a discussion about general health and wellbeing. I use the term weight or BMI, which people prefer to the terms such as obesity, obese, fat, excess fat and being overweight. I also cognizant about cultural differences, for example, in certain cultures being overweight is still viewed as a sign of being healthy and/or affluent.

So as a neurologist who manages people with MS should I ignore lifestyle issues such as smoking, alcohol misuse, poor diet, obesity, sedentary behaviour? Maybe this should be left to the GP or family doctor? What does your neurologist do? Another commentator made the point that as I don’t have MS, i.e. have a lived experience of what it is really like to have MS, I shouldn’t expect pwMS to self-manage aspects of their disease such as lifestyle factors. Do you agree?

Please note weight also swings both ways. I have numerous patients who are too thin. Some have eating disorders, others caloric restrict too much to treat their MS, others don’t eat to avoid food coma and others may have a systemic disease associated with loss of weight that needs to be diagnosed and managed. Being too thin is also associated with poor health outcomes. So asking about weight is very relevant to the holistic management of MS.

Please note that over the last 20 years the dogma that obesity is due to ‘too many calories in (overeating) and too few calories out (too little exercise)’ has been debunked. Not all calories are made equal, i.e. not all calorific foods are obesogenic. Obesity is a metabolic or endocrine disorder and there are well-established ways to treat obesity. The corollary is also true, there are well-established ways to become obese. So if you have concerns about your weight, be it that you are underweight or overweight please discuss it with your HCP.

Mendizabal et al. Comorbid disease drives short-term hospitalization outcomes in patients with multiple sclerosis. Neurol Clin Pract . 2020 Jun;10(3):255-264.

Objective: Readmission is used as a quality indicator and is the primary target outcome for disease-modifying therapy (DMT) for multiple sclerosis (MS). However, data on readmissions for patients with MS are limited.

Methods: Using the US Nationwide Readmissions Database, we performed a retrospective cohort study of adults hospitalized for MS in 2014. Primary study outcomes were within 30- and 90-day readmissions. Descriptive analyses compared patient, clinical, and hospital variables readmission status. Multivariable logistic regression models estimated the associations between these variables and readmission.

Results: Of 16,629 individuals meeting the study criteria, most were women (73.7%), aged 35-54 years (48.0%), and Medicare program participants (36.8%). In total, 49.7% of inpatients with MS had 1-2 comorbid medical conditions and 23.7% had 3 or more. Having 3 or more comorbidity conditions associated with increased adjusted odds of the 30-day readmission (adjusted odds ratio [AOR] 1.92, 1.34-2.74). Anemia (AOR 1.62, 1.22-2.14), rheumatoid arthritis/collagen vascular diseases (AOR 2.20, 1.45-3.33), congestive heart failure (AOR 2.43, 1.39-4.24), chronic pulmonary disease (AOR 1.35, 1.02-1.78), diabetes with complications (AOR 2.27, 1.45-3.56), hypertension (AOR 1.25, 1.03-1.53), obesity (AOR 1.35, 1.05-1.73), and renal failure (AOR 1.68, 1.06-2.67) were associated with the 30-day readmission. Medicare insurance and nonroutine discharge were also associated with readmission, whereas patient characteristics (sex, age, and socioeconomic status) were not. The most frequent (26.7%) reason for readmission was multiple sclerosis. Ninety-day analyses produced similar findings.

Conclusions: Comorbid diseases were associated with the readmission for persons with multiple sclerosis. Evaluations of the real-world effectiveness for DMTs in reducing hospitalizations in patients with MS may need to consider comorbid disease burden and management.

Stenberg et al. Bariatric and metabolic surgery in patients with morbid obesity and multiple sclerosis – a nationwide, matched cohort study. Surg Obes Relat Dis. 2021 Jun;17(6):1108-1114.

Background: Despite an association between obesity and multiple sclerosis (MS), very little is known regarding the safety and efficacy outcomes for patients with MS and severe obesity undergoing metabolic surgery.

Objectives: The aim of the present study was to evaluate early complications and efficacy outcomes of metabolic surgery in patients with severe obesity and MS.

Setting: Nationwide, Sweden.

Methods: In this, matched cohort study, 196 patients with an MS diagnosis in the Swedish MS register who were undergoing metabolic surgery (gastric bypass or sleeve gastrectomy) with a registration in the Scandinavian Obesity Surgery Registry (SOReg) were matched 1:10 with a control group without MS diagnosis from the SOReg. A 2-stage matching procedure was used (exact match by surgical method, followed by propensity Score matching, including age, sex, preoperative BMI, surgical center, surgical access, year of surgery, hypertension, diabetes, sleep apnea, and dyslipidemia).

Results: Weight loss at 2 years after surgery was similar for patients with MS and controls (total weight loss 31.6 ± 9.1 versus 31.8 ± 9.2, P = .735). No significant differences were seen in either the overall postoperative complication rate (7.9% versus 7.2%, P = .778), or serious postoperative complications (3.7% versus 2.8%, P = .430). All aspects of health-related quality of life (HRQoL) improved in both groups but less so for the physical aspects of HRQoL in patients with MS.

Conclusion: Metabolic surgery is a safe and efficient treatment for severe obesity in patients with MS, and it leads to subsequent improvements in HRQoL. Further studies addressing the effects of metabolic surgery on MS-related symptoms are needed.

Conflicts of Interest

Preventive Neurology

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General Disclaimer: Please note that the opinions expressed here are those of Professor Giovannoni and do not necessarily reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust and are not meant to be interpreted as personal clinical advice.

#MSCOVID19 Boris Johnson is obese

Obesity has taken centre stage after Boris Johnson admitted that his recent coronavirus scare may have been related to his obesity. He is now pledging to do something about it. His sudden interest in the UK’s obesity problem is getting a lot of ink space in both the tabloids & broadsheets and airtime on radio & TV. Andrew Marr even covered it this morning on his BBC talk show. Will anything become of it?

A few weeks ago when I was on the medical wards there was a social media shit storm when Krispy Kreme doughnuts pledged to give NHS staff free doughnuts and dropped off a free delivery to the Royal Free staff. The issue, raised by many critics, is that Krispy Kreme (big business) and doughnuts (ultra-processed foods) represent the problem with our food environment.

Yes, we have a massive problem in the UK. Well over 50% of calories consumed in the UK are from ultra-processed foods (see study below), which are produced by the large food companies. These foods increase dramatically the amount of free sugar we consume and hence drive up insulin levels and over time it causes the cascade that leads to obesity, impaired glucose tolerance, insulin resistance and the metabolic syndrome.

What needs to be considered is that the consumption of ultra-processed foods and the associated obesity epidemic are a core component of the social determinants of health (SDoH). For Boris Johnson to address obesity from a political perspective he is going to have tackled a much wider set of social issues. Is he up to it? I doubt it. However, I am hopeful that the COVID-19 epidemic, his near-death experience and resulting social consequences of the lock-down will give him the necessary motivation to support a ‘nanny state’ that he as always so despised in the past.

Historians have been pointing out that it often takes an international crisis to bring people together for the common good and to make them realise that we are all in it together. A good example is the NHS; it was created in response to the sense of togetherness induced by the national response to the second world war. I suspect the same thing will happen post-COVID-19. It is predicted that all politicians will move left and more money and resources will be lavished on social spending. Let’s hope this reduces inequality, improves education and the lived environment and tackles our reliance on cheap processed and ultra-processed food. The consequences could be slimming down of the national waistlines and a healthier nation.

How is this relevant to MS? Getting ready for having COVID-19, which may be just around the corner for many of us, is maximising our chances of not getting the severe form of the disease. To do this you may have to improve your lifestyle and get all your comorbidities treated and under control. For some of us this may be shedding a few pounds. I am aware that this is easier said than done, which is why I would recommend you consider trying intermittent fasting or a low carbohydrate diet. The good thing about these two diet options is that they may have additional benefits for your MS.

Fernanda Rauber et al. Ultra-Processed Food Consumption and Chronic Non-Communicable Diseases-Related Dietary Nutrient Profile in the UK (2008⁻2014). Nutrients. 2018 May 9;10(5):587.

We described the contribution of ultra-processed foods in the U.K. diet and its association with the overall dietary content of nutrients known to affect the risk of chronic non-communicable diseases (NCDs). Cross-sectional data from the U.K. National Diet and Nutrition Survey (2008⁻2014) were analysed. Food items collected using a four-day food diary were classified according to the NOVA system. The average energy intake was 1764 kcal/day, with 30.1% of calories coming from unprocessed or minimally processed foods, 4.2% from culinary ingredients, 8.8% from processed foods, and 56.8% from ultra-processed foods. As the ultra-processed food consumption increased, the dietary content of carbohydrates, free sugars, total fats, saturated fats, and sodium increased significantly while the content of protein, fibre, and potassium decreased. Increased ultra-processed food consumption had a remarkable effect on average content of free sugars, which increased from 9.9% to 15.4% of total energy from the first to the last quintile. The prevalence of people exceeding the upper limits recommended for free sugars and sodium increased by 85% and 55%, respectively, from the lowest to the highest ultra-processed food quintile. Decreasing the dietary share of ultra-processed foods may substantially improve the nutritional quality of diets and contribute to the prevention of diet-related NCDs.

CoI: multiple

Not COVID-19: obesity and MS

Are you sick and tired of hearing about COVID-19 and MS? How about something completely different; the destigmatization of obesity?

Finally, the medical community or at least a part of it are making amends for the half-century or more of treating obesity as a disorder of self-control. The joint internal consensus statement for ending the stigma of obesity is long overdue (see article and box below).

Even when I have done factual posts about childhood and adolescent obesity as a risk factor for developing MS I have been criticised by commentators for fat-shaming. I am not. All I am doing is quoting the evidence that childhood/adolescent obesity is associated with an increased risk of developing MS and may in fact be in the causal pathway that leads to developing MS.

What the consensus statement below is finally acknowledging is the irrefutable evidence that obesity is a disorder of metabolism; an endocrine disorder that leads to patients increasing the amount of energy they store as fat. Finally, the dogma that obesity is due to the excess consumption of calories and/or the reduced expenditure of calories is finally being put to rest as not being the root cause of obesity.

A simplified way of explaining the mechanisms that lead to obesity is that your metabolism gets hijacked by a hormonal imbalance that results in energy be hoarded away in your adipose tissue and it not being released for consumption by the remainder of the body. This triggers the brain to think that you are starving and sets off a behavioural response to seek more food or calories. In other words, the metabolic state associated with obesity causes hunger and the food-seeking behaviour associated with it and not the other way around.

The sad thing is that we the medical profession have known about this insight for centuries, but we decided to forget or ignore the metabolic research underpinning obesity being a metabolic disease in the 70’s and 80’s when we were hoodwinked by dodgy science and fake news. Yes, the high saturated-fat heart hypothesis of cardiovascular disease is to blame. The conspiracy underpinning the change in the dietary guidelines that have caused the global obesity pandemic has been well highlighted by investigative journalists in several extremely well-crafted exposes. The tragedy is as the population replaced saturated fat in our diets with polyunsaturated fats and carbohydrates, in particular, processed and ultra-processed carbohydrates, we created a metabolic storm that has resulted in an epidemic of obesity, diabetes, hypertension, fatty liver and the other ills associated the metabolic syndrome.

Shifting the focus sway from obesity as a result of an individual’s lack of self-discipline to it being a metabolic disease driven primarily by diet will allow us to tackle the epidemic, i.e. to flatten the curve and hopefully chop off its tail to steal a COVID-19 analogy.

The metabolic cause of obesity is rather quite simple; it is driven predominantly by raised insulin levels or hyperinsulinaemia. High blood sugar or glucose levels stimulate the pancreas to produce insulin. The insulin works to reduce blood glucose levels by signalling to the liver and muscles to make glycogen (short-term glucose storage) and to the liver and adipose tissues to make fat. Whilst insulin levels are high the adipose tissue is unable to release fat as an energy source and so the adipose tissue continues to take-up glucose to convert into fat. As glucose levels drop it triggers a counter-regulatory hormonal response that causes you to become hungry and you then seek out sugary foods. This then starts a vicious cycle that results in insulin levels being raised most of the day, instead of only being raised for a few hours after a meal. This hyperinsulinaemia eventually causes the liver and muscles to become resistant to insulin’s action, but less so in adipocytes particularly the adipocytes around the abdomen and internal organs. The latter causes the so-called centripetal and visceral obesity that is typical of insulin resistance.

The only way to break this vicious metabolic cycle is to try and lower your insulin levels as much as possible. This is why low carbohydrate or ketogenic diets work so well at correcting the metabolic syndrome (hyperinsulinaemia) and result in loss of weight. The good thing about keeping insulin levels low is that the body gets used to a new normal or steady-state glucose level that is driven by another metabolic process called gluconeogenesis (glucose from protein), which does not trigger the counter-regulatory hormonal response that makes you feel hungry. In addition, the ketones your body produce, particularly β-hydroxybutyrate, is known to suppress appetite and explains why people on ketogenic diets don’t feel the same levels of hunger as people on high carbohydrate diets.

If you have MS having high levels of circulating β-hydroxybutyrate maybe be good for your MS. β-hydroxybutyrate activates the hydroxycarboxylic acid receptor 2 (HCA2), which is also known as niacin receptor 1 (NIACR1) and GPR109A. This is the same receptor that fumaric acid works on. I suspect that ketosis works at a cellular level in the same way that dimethyl fumarate (DMF) and diroximel fumarate work, which are both licensed MS disease-modifying therapies (DMTs). By binding to the HCA2 receptor β-hydroxybutyrate stimulates a transcription factor called NRF2 and downregulates NFKappa-B the master regulator of inflammation. The NRF2 mechanism of ketosis almost certainly overlaps with what has been described in animals with intermittent fasting and the drug metformin to promote the rejuvenation of oligodendrocyte precursors, remyelination and recovery of function.

Despite criticism from dietary zealots the evidence that low-carbohydrate/ketogenic diets are bad for you is very weak. In fact, I would argue that from an evolutionary perspective man was first a low-carbohydrate species and only acquired the sophisticated carbohydrate metabolic response to fatten up for winter when fruits and grains are plentiful at the end of summer. We were never meant to metabolise carbohydrates 24/7 365 days a year. Feast and famine was the norm, which is how our primate cousins live in the wild.

Although we need controlled evidence before promoting low-carbohydrate/ketogenic diets as a treatment for MS and for MS prevention there is no reason why pwMS can’t try these dites improve their metabolic health. If I had MS I would not hesitate to hack my metabolism with either a low-carbohydrate/ketogenic diet or intermittent fasting, but not caloric restriction. The scientific case for using these former diets as an adjunct to other MS therapies is simply too compelling to ignore.

Rubino et al. Nat Med 2020 Apr;26(4):485-497.

Rubino et al. Joint International Consensus Statement for Ending Stigma of Obesity. Nat Med 2020 Apr;26(4):485-497.

People with obesity commonly face a pervasive, resilient form of social stigma. They are often subject to discrimination in the workplace as well as in educational and healthcare settings. Research indicates that weight stigma can cause physical and psychological harm, and that affected individuals are less likely to receive adequate care. For these reasons, weight stigma damages health, undermines human and social rights, and is unacceptable in modern societies. To inform healthcare professionals, policymakers, and the public about this issue, a multidisciplinary group of international experts, including representatives of scientific organizations, reviewed available evidence on the causes and harms of weight stigma and, using a modified Delphi process, developed a joint consensus statement with recommendations to eliminate weight bias. Academic institutions, professional organizations, media, public-health authorities, and governments should encourage education about weight stigma to facilitate a new public narrative about obesity, coherent with modern scientific knowledge.

CoI: multiple

#MSCOVID19: Fighting diet dogma

I did a video consultation yesterday with a patient with MS who in the event of getting COVID-19 is at very high risk of severe COVID-19. This patient has type 2 diabetes with poor glucose control, is hypertensive and is also obese (BMI of 32). I asked what their GP had done to help them lose weight. The GP had recommended exercise and believe it or not hadn’t discussed diet with them.

The idea that exercise is a primary treatment for obesity is a myth. Obesity and metabolic syndrome is an endocrine disorder due to hyperinsulinaemia (high insulin levels). The idea that can you treat obesity with exercise, and not address the hyperinsulinaemia, is a dogma that has been disproven years ago. I actually take the contrary view that you first have to start losing weight to exercise properly. If you have a BMI of 32 and you start doing unsupervised exercise you are likely to get an injury and then become less active.

The other dogma is that obesity is too many calories in and too few out; i.e. obesity is a simple imbalance of what you eat with what you expend. This dogma has also been disproven. Not all calories are made equal. Carbohydrates, in particular, processed carbohydrates with a high glycemic index are much more obesogenic compared to fats, proteins and complex carbohydrates (low glycaemic index).

I briefly explained this to this patient and referred her to Dr David Unwin’s or ‘the diet doctor’s’ website. David Unwin is one of the NHS’ heroes and deserves to be knighted to his contribution to the health of the nation. David Unwin has been treating metabolic syndrome with a low carbohydrate diet and getting over 50% of his patients with type 2 diabetics off medication; he is putting their diabetes into remission. The science behind low carbohydrate diets as a treatment for obesity, hypertension and type 2 diabetes is well-grounded; in my opinion, it’s irrefutable.

The other positive spin-off of a low carbohydrate diet, beyond weight loss, is that it is also ketogenic. Ketosis may have other health benefits for pwMS. There is very compelling data from animal models that ketosis is neuroprotective and may promote remyelination (please see my blog post ‘COULD DIET BE THE NEW ADD-ON DMT?’ from 21-Feb-2020).

So if you consider yourself of being at-risk of severe COVID-19 and you are obese and/or diabetic and/or hypertensive maybe it is the right time to try a low carbohydrate diet.

I am not saying in this post that you shouldn’t exercise. However, exercise is a powerful appetite stimulant and what happens is that if you exercise without addressing your diet you will simply end up eating more calories than you expend. You need to get your diet right first. A correct diet allows you to maximise the benefits of exercise.

If you are interested in reading more about my thoughts on diet, I would recommend reading my Medium posts ‘Diet as a Philosophy’ and ‘Evolutionary Medicine: why low-fat diets are bad for you’.

Dare I suggest that you owe it to yourself, your family and friends and the NHS to de-risk yourself from getting severe COVID-19?

CoI: multiple

The war on sugar (more posts below today)

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.

This graph shows you the strong association between per capita sugar consumption and obesity. It is extraordinary that politicians are not doing more to tackle global sugar consumption.

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

How much do you weigh?

Barts-MS rose-tinted-odometer ★

When last have you weighed yourself and calculated your BMI (body mass index)?

BMI = body mass (kg) / the square of the body height (m) [kg/m²]; to save you time and effort you can simply use the NHS BMI calculator, which takes imperial measurements as well.

I am not sure if you are aware that childhood and adolescent obesity is an important risk factor for developing MS. We estimate that smoking and obesity could account for 1 in 5 new cases of MS. Obesity is a complex disorder that tends to run in families. The familial link is not only due to the effect of genes but cultural and social factors. If you are obese, or very obese, you need to do something at a personal level that may inform what the next generation does about it; good habits are infectious.

I have little doubt that obesity impacts on MS outcomes. Obesity affects mobility and is associated with deconditioning and poorer outcomes. I recall a patient of mine with primary progressive MS losing over 30 kg in weight, with his BMI dropping from over 30 to less than 24, and in parallel, his EDSS improved from 6.5 to 5.5. The latter improvement was from him getting fit from his 5-day per week exercise programme and making the effort.

As you are aware obesity is associated with a metabolic shitstorm that impacts on many disease processes. Obesity causes metabolic syndrome (hypertension, insulin resistance, glucose intolerance, diabetes and dyslipidaemia) and a systemic inflammatory syndrome that may worsen MS. Therefore, there is a good reason why, if you are obese you should consider doing something about it. This is easier said than done. To start I would recommend you read “Why we get fat and what to do about it”, by Gary Taubes or you can watch his lecture on YouTube. Understanding the metabolic issues that underlie obesity will allow you to understand what to do about it. The latest science behind obesity is not rocket science.

Why this post just before Christmas? Christmas is a time of excess and maybe this post will make you mindful of what and how you eat. I was horrified when I read the forecast in this week’s New England Journal of Medicine that by 2030 1 in 2 US adults will be obese. The conclusion of the paper says it all.

“We project that given current trends, nearly 1 in 2 U.S. adults will have obesity (BMI>30) by 2030, and the prevalence will be higher than 50% in 29 states and not below 35% in any state — a level currently considered high. Furthermore, our projections show that severe obesity (BMI>35) will affect nearly 1 in 4 adults by 2030 and become the most common BMI category among women, black non-Hispanic adults, and low-income adults.”

**Estimated Prevalence of Overall Obesity and Severe Obesity in Each US State, from 1990 through 2030.** Image from the NEJM.

I suspect the UK is not far behind the US. What we need to realise that underlying this epidemic in obesity is an MS epidemic. Don’t you think we should do something about it?

Ward et al. Projected U.S. State-Level Prevalence of Adult Obesity and Severe Obesity. N Engl J Med, 381 (25), 2440-2450 2019 Dec 19.

Background: Although the national obesity epidemic has been well documented, less is known about obesity at the U.S. state level. Current estimates are based on body measures reported by persons themselves that underestimate the prevalence of obesity, especially severe obesity.

Methods: We developed methods to correct for self-reporting bias and to estimate state-specific and demographic subgroup-specific trends and projections of the prevalence of categories of body-mass index (BMI). BMI data reported by 6,264,226 adults (18 years of age or older) who participated in the Behavioral Risk Factor Surveillance System Survey (1993-1994 and 1999-2016) were obtained and corrected for quantile-specific self-reporting bias with the use of measured data from 57,131 adults who participated in the National Health and Nutrition Examination Survey. We fitted multinomial regressions for each state and subgroup to estimate the prevalence of four BMI categories from 1990 through 2030: underweight or normal weight (BMI [the weight in kilograms divided by the square of the height in meters], <25), overweight (25 to <30), moderate obesity (30 to <35), and severe obesity (≥35). We evaluated the accuracy of our approach using data from 1990 through 2010 to predict 2016 outcomes.

Results: The findings from our approach suggest with high predictive accuracy that by 2030 nearly 1 in 2 adults will have obesity (48.9%; 95% confidence interval [CI], 47.7 to 50.1), and the prevalence will be higher than 50% in 29 states and not below 35% in any state. Nearly 1 in 4 adults is projected to have severe obesity by 2030 (24.2%; 95% CI, 22.9 to 25.5), and the prevalence will be higher than 25% in 25 states. We predict that, nationally, severe obesity is likely to become the most common BMI category among women (27.6%; 95% CI, 26.1 to 29.2), non-Hispanic black adults (31.7%; 95% CI, 29.9 to 33.4), and low-income adults (31.7%; 95% CI, 30.2 to 33.2).

Conclusions: Our analysis indicates that the prevalence of adult obesity and severe obesity will continue to increase nationwide, with large disparities across states and demographic subgroups. (Funded by the JPB Foundation.).

CoI: multiple

How big is your need to exercise?

The evidence that exercise and I mean regular exercise is good for you is so overwhelming that it is hard to argue against the science. What I mean by this is that almost everyone accepts exercise as being good for the general population and for people with MS. The downside is that some MSers are so disabled and/or have so much fatigue that they find it difficult to exercise. I am prepared to accept the latter, but I am not prepared to accept this as a reason not to promote/prescribe exercise to the wider MS community. The question I have ‘Is how do we get MSers and healthcare professionals (HCPs) to exercise regularly?’.

Are you interested in hearing more about what you can do?

The review below argues for applying behaviour change theory in the design of exercise programs and promotion efforts. How about making it a challenge? Can you walk? Can you run?

In collaboration with the MS Trust, we are proposing starting a national exercise challenge/competition to get the MS community walking and running. We are proposing to use the Parkrun platform. Parkruns are 5km runs that are held each Saturday in a local park near you and allow you to complete 5km and log an official time. The challenge is to get every MS team in the UK, and possibly the world, to sign-up for the challenge and collect 5km runs. The team with the most Parkruns after a certain period of time, say a 6- or 12-month period, wins the challenge.

When I refer to teams I mean all MS stakeholders linked to a particular MS service or team. This would not only include people with MS, but their HCPs, friends and families, MS Society members, ShiftMSers and even Pharma reps. The only rule we would propose putting in place is that a member of a particular MS team can only sign-up for one team. Another idea is to combine Parkrun effort with a fundraising campaign for the MS Trust. However, the fundraising would be voluntary and not necessary for participating in the challenge.

I have suggested to the MS Trust that they create an annual Parkrun award for the team who wins the challenge and for the individual who completes the most Parkruns in the predefined period of time. Please note you can only really do one ParkRun a week and special one held on Christmas day and New Year’s day.

Do you think this is a good idea? If yes, what should we call the challenge? With my bias, I would say #ThinkRunning. Or what about ‘The Running and Proud MS Trust ParkRun Challenge’?

I know the naysayers will be saying, but I can’t run. I know there are some of you who can’t run but then there will be others who are simply deconditioned (the medical term for unfit). For you, I would suggest starting the ‘couch to 5K’ programme that is designed to get you off the couch and running 5km in just nine weeks. The plan involves three runs a week with a rest day in between and a different running schedule each week. The NHS is promoting this using an app developed by the BBC, the programme or app builds you up gradually with a mix of running and walking.

The good thing about making this initiative into a challenge is that it builds teams (people are competitive) and it will increase social participation. Theis will, in turn, enhance social capital, which should improve outcomes as well.

We have already had a discussion with one of Parkrun’s MS ambassadors and the MS Trust and they are very supportive of this initiative. Are you willing to give it a go? Please let us know even if it is helping with the naming of the challenge. Without your help, this won’t happen.

Let’s Do It!

Thank you.

Motl et al. Promotion of physical activity and exercise in multiple sclerosis: Importance of behavioral science and theory. Mult Scler J Exp Transl Clin. 2018 Jul 9;4(3):2055217318786745.

There is an obvious disconnect between evidence of benefits and rates of participation in exercise and physical activity among people living with multiple sclerosis (MS). We propose that the problem with exercise behavior in MS (i.e. lack of broad or increasing participation by people with MS despite evidence of meaningful benefits) might be ameliorated through the inclusion of behavior change theory in the design of exercise programs and promotion efforts, as has been undertaken in other populations such as breast cancer survivors. This paper reviews Social Cognitive Theory as an example approach for informing interventions for increasing exercise and physical activity behavior outside of MS and provides an overview of current knowledge regarding the application of this theory for physical activity in MS. We then outline future research necessary for informing trials that design, implement, and test theory-based interventions for physical activity promotion in MS. If theories of behavior change are adopted for informing exercise and physical activity research in MS, we can take a major step forward in addressing the problem of exercise and physical activity participation that has plagued the field for more than 25 years.

CoI: I am a runner, albeit one with a failing right hip