severe COVID-19 – Prof G's MS Blog Archive

#MSCOVID19: get vaccinated

Barts-MS rose-tinted-odometer: ★ (Blue Thursday #000080)

Where are all the new MS patients gone? We have national data showing that there has been a 30% fall in the number of new patients with MS starting on disease-modifying therapies (DMTs) during the COVID-19 pandemic. Where are these patients? I suspect due to the reconfiguration of the NHS because of COVID-19 many of these patients have yet to find their way through the diagnostic pathway.

Many patients may have had neurological symptoms suggestive of a demyelinating syndrome and decided against seeking medical attention during the crisis. As these symptoms may have remitted they have now gotten on with their lives. Others are waiting for MRI scans, lumbar punctures and evoked potentials.

We were hoping our Barts-MS service would get back to some form of new normal, but this is unlikely to happen for some time. A big concern is a recent increase in COVID-19 cases as a result of the Delta or Indian variant of SARS-CoV-2. More worrying is the low rate of vaccine uptake in our local area due to vaccine hesitancy.

UK Government Data – accessed 17-June-2021

As you can see from the latest Government figures infections rates in Whitechapel are surging well above the national average and the vaccine data figures are very worrying; the majority of adults in Whitechapel have not been vaccinated and more importantly, less than a quarter (24.3%) have not had two doses compared to close to 60% nationally. At the Royal London Hospital, we are therefore bracing ourselves for a third/fourth wave of admissions. This will have knock-on effects and affect routine hospital services such as our Barts-MS service. The best thing you can do as an individual is to #GetVaccinatedASAP to prevent hospital admissions and deaths and to allow the NHS to get routine services back to normal.

I have little doubt based on the principle that ‘time is brain’ that many people yet to be diagnosed with MS will do worse because of the inevitable delays in the management of their MS.

Conflicts of Interest

Preventive Neurology

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Medium

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: pulse oximetry

If you are single I suggest going to extraordinary lengths to protect yourself if you have to self-isolate with COVID-19.

You may have heard about the tragic death of a young surgical trainee who died alone at home from COVID-19 in Belfast last week. He probably died from pulmonary complications of COVID-19 that had gradually crept up on him and by the time he needed hospitalisation and ventilatory support he was probably too unwell to do anything about it. A big issue is that as you become hypoxic (lack of oxygen) your thought processes become clouded and your ability to make a judgement about your own health become erratic.

I know of two close colleagues who self-isolated with COVID-19 and both of them developed severe exertional shortness of breath at the height of their infection. My one colleague said he could barely make it from his bed to the toilet due to shortness of breath. Fortunately, both have made a recovery now and are doing well.

A third colleague who has recently recovered from COVID-19 was bed-bound for two weeks and was on the verge of calling an ambulance, but decided against it. Fortunately, his wife is a GP and was monitoring him at home with a pulse oximeter, a device to measure how much oxygen is in your blood, that she uses for home visits. This colleague tells me that he did try and call 111 and after waiting 90 minutes hung-up. Waiting ninety minutes or longer for advice and to then be told to call an ambulance could be the difference between life and death.

When we do our ward rounds on patients with COVID-19 we don’t have to examine them, we mainly assess how well their lungs are functioning based on their oxygen saturation in their blood relative to how much oxygen they are getting, be it from room air (21% oxygen) or via a nasal cannula or face mask. When we use nasal cannula or a face mark we deliver oxygen at different flow rates and this is also taken into account.

In general, most people have an oxygen saturation rate above 94%. It does vary with age and altitude. It is relatively easy to measure yourself, but you need to have a pulse oximeter. In early COVID-19 pneumonia, exertional oxygen saturation levels fall first, i.e. if you attempt to walk or exercise and your blood saturation levels fall, for example, below 90% despite being normal at rest. This would indicate that your lungs are in trouble and that you probably need to go to hospital. People with COVID-19 can deteriorate very rapidly, i.e. within hours, so having an early warning system should help.

I wonder if the young surgeon above had been monitoring himself with a pulse oximeter and had notice that his exertional blood oxygen saturation levels dropped with exertion (walking in his home) he would have gotten himself to hospital and survived?

I personally think the Government’s and NICE’s guidance on when to be admitted to a hospital is potentially dangerous. The NICE guidance suggests using the following symptoms and signs to help identify who has more severe COVID-19 and may need admission to hospital:

severe shortness of breath at rest or difficulty breathing
coughing up blood
blue lips or face
feeling cold and clammy with pale or mottled skin
collapse or fainting (syncope)
new confusion
becoming difficult to rouse
little or no urine output

Can you imagine trying to pick these symptoms and signs up if you live alone and are self-isolated? I am sure self-monitoring of your peripheral blood oxygen saturation levels, in particular documenting their deterioration, will save lives during the COVID-19 pandemic.

So after reading about the tragic case of the young surgeon dying alone at home, I purchased my own pulse oximeter online. It is an insurance policy for my family and any of my neighbours or friends who may get COVID-19 and have to self-isolate and self-monitor. I think the NHS or local communities should arrange for pulse oximeters to be dropped off for single people with COVID-19 who are self-isolating and given guidance on how to use them and at what point to call 999. I am sure home pulse oximetry will take some pressure off the 111 services and save lives. The sceptics will say that as home self-monitoring of oxygen saturations is an untested technology we would need to study this intervention first before recommending it at a population level. I would say bollocks. My sister has a progressive interstitial lung disease and is on 24-hour home oxygen therapy. She and her cohort of fellow patients all manage their home oxygen therapy using pulse oximeters. If she can use a pulse oximeter so can most people in the general population. In fact, technology companies should think about building pulse oximetry into the next versions of their smartwatches and make the technology ubiquitous.

I am not saying that everyone should purchase a pulse oximeter, but if you are single and live alone without someone to monitor your status when you get COVID-19 it would be advisable to have one. I am convinced that my two colleagues who struggled through self-isolation at home would have been better off if they had known their own peripheral blood oxygen saturation levels, both on exertion and at rest. I suspect if they had they may. or at least one of them may, have been admitted to hospital for observation.

Do you agree with me that we should add access to home pulse oximetry, particularly if you are single, to my list of things to do to prepare for getting COVID-19?

CoI: none

#MSCOVID19: vitamin D & zinc

I have already made the case for pwMS to prehabilitate, i.e. to prepare themselves for getting COVID-19. You can read my proposed prehabilitation programme on MS-Selfie. One of the topics I cover is diet and I mention that you should ensure that you are vitamin D (vD) replete. There are three ways to do this. (1) The first is to get a healthy daily exposure to sunshine (~20mins of upper body exposure around midday in summer), which can be difficult if you are disabled and stuck indoors and it is winter where you live.

(2) Another source of vD is eating foods that are high in vD, for example, fatty fish. However, even the latter is often insufficient to raise your blood levels above 75 or 80 nmol/L, which are the two most common lower levels of normal used by UK laboratories. If you apply evolutionary medicine principles, i.e. what are the vD levels in hunter-gatherers or people who work outdoors, a level of above 100 nmol/L is probably normal. (3) The easiest way to get above 100nmol/L is with dietary supplements. I have always recommended the Vitamin D Council’s advice which is to take 5,000 U of vD3 per day. I note that the Vitamin D Council’s website has gone offline and I don’t know why. Does anybody know the reason?

The following small study below from Indonesia shows that low vD levels were associated with a higher chance of dying from COVID-19. As with all studies of this nature, it could be reverse causation, i.e. COVID-19 patients with the greatest level of inflammation in their lungs consumed more vD as part of the inflammatory process. In other words, inflammation caused the low vD levels not the other way round. I am prepared to go as far as saying that in inflammatory or infectious diseases the lower the vD levels the worse the prognosis; this is called the consumptive vD hypothesis of inflammation.

What is needed is a clinical trial to see if vD supplements prevent you from getting severe COVID-19. This type of trial is very difficult as a large number of the population are already taking vD3 supplements and a lot of vD experts will say we don’t have equipoise in that they think people should be vD replete for general health reasons regardless of COVID-19.

As low dose vD3 supplementation is safe and most of the UK population is vD deficient I would advise taking vD supplements rather than not taking them. Do you agree?

I am also asked what other supplements should you take? If you have a healthy balanced real food diet you don’t need to take any other supplements. However, if you eat an unbalanced diet for humans, for example, a purely plant-based diet, I would advise you to review your micronutrient intake. While not all vegans have low blood levels of zinc, a recent review showed that vegetarians — and especially vegans — have lower zinc intakes and slightly lower blood levels of zinc than omnivores. I focus on zinc because zinc deficiency is associated with an increased risk of infections and complications of infections. There is also a hypothesis that zinc may act against SARS-CoV-2 at several different points in its replicative cycle (see the article from below) and zinc is also important for anti-bacterial activity. A large number of COVID-19 deaths are due to secondary bacterial pneumonia.

A supplemental dose of 5mg or 10mg per day of zinc should be sufficient with other dietary sources to ensure you are zinc replete.

In the absence of a SARS-CoV-2 vaccine and an effective antiviral are you ready yet to get COVID-19? If not you need to start today. Prehabilitation is an attempt to lower your chances of getting severe COVID-19 and dying from the complications of COVID-19. If you haven’t please act now!

Vitamin D – the sunshine vitamin

Raharusun et al. Patterns of Covid-19 Mortality and Vitamin D: An Indonesian Study. SSRN April 26, 2020.

This is a retrospective cohort study which included two cohorts (active and expired) of 780 cases with laboratory-confirmed infection of SARS-CoV-2 in Indonesia. Age, sex, co-morbidity, Vitamin D status, and disease outcome (mortality) were extracted from electronic medical records. The aim was to determine patterns of mortality and associated factors, with a special focus on Vitamin D status. Results revealed that majority of the death cases were male and older and had pre-existing condition and below normal Vitamin D serum level. Univariate analysis revealed that older and male cases with pre-existing condition and below normal Vitamin D levels were associated with increasing odds of death. When controlling for age, sex, and comorbidity, Vitamin D status is strongly associated with COVID-19 mortality outcome of cases.

Zinc – an essential micronutrient

Skalny et al. Zinc and Respiratory Tract Infections: Perspectives for COVID‑19. Int J Mol Med. 2020 Apr 14. doi: 10.3892/ijmm.2020.4575.

In view of the emerging COVID‑19 pandemic caused by SARS‑CoV‑2 virus, the search for potential protective and therapeutic antiviral strategies is of particular and urgent interest. Zinc is known to modulate antiviral and antibacterial immunity and regulate inflammatory response. Despite the lack of clinical data, certain indications suggest that modulation of zinc status may be beneficial in COVID‑19. In vitro experiments demonstrate that Zn2+ possesses antiviral activity through inhibition of SARS‑CoV RNA polymerase. This effect may underlie therapeutic efficiency of chloroquine known to act as zinc ionophore. Indirect evidence also indicates that Zn2+ may decrease the activity of angiotensin‑converting enzyme 2 (ACE2), known to be the receptor for SARS‑CoV‑2. Improved antiviral immunity by zinc may also occur through up‑regulation of interferon α production and increasing its antiviral activity. Zinc possesses anti‑inflammatory activity by inhibiting NF‑κB signaling and modulation of regulatory T‑cell functions that may limit the cytokine storm in COVID‑19. Improved Zn status may also reduce the risk of bacterial co‑infection by improving mucociliary clearance and barrier function of the respiratory epithelium, as well as direct antibacterial effects against S. pneumoniae. Zinc status is also tightly associated with risk factors for severe COVID‑19 including ageing, immune deficiency, obesity, diabetes, and atherosclerosis, since these are known risk groups for zinc deficiency. Therefore, Zn may possess protective effect as preventive and adjuvant therapy of COVID‑19 through reducing inflammation, improvement of mucociliary clearance, prevention of ventilator‑induced lung injury, modulation of antiviral and antibacterial immunity. However, further clinical and experimental studies are required.

CoI: multiple

#MSCOVID19: wow!

I am on call at the Royal London Hospital and sitting in my office digesting some of my daily COVID-19 reading. However, something has just hit me between the eyes and I have to say wow aloud!

WOW!!

The paper and editorial below show you just how infective SARS-CoV-2 really is and why we are not going to win this battle for our vulnerable people without an effective anti-viral and/or vaccine. It also tells me that if we don’t get a vaccine things will not normalise for a very long time.

Who said the R0 (R-zero) for this virus was less than 3 and therefore we would get herd immunity at about a 60% seroprevalence rate? Not me!

R-zero or the basic reproduction number for SARS-CoV-2 is the expected number of cases infected by one case in a population where all individuals are susceptible to infection. The original calculations were based on symptomatic index cases and symptomatic contacts with positive swabs. The fact that a large number of people (possibly up to 50%) have now been shown to get asymptomatic infections and that the test for the virus is not 100% specific. This means that approximately 25% of cases with COVID-19 defined by clinical definition have negative nasopharyngeal (nose & throat) swabs; i.e. 25% of infected people who may be shedding are not detected with the swab test. Based on these assumptions I have estimated that in normal life (no social distancing) that the R-zero is likely to be somewhere between 6 and 7. This means that to get herd immunity, a point when natural transmission in the population stops, you need somewhere between 80% and 86% of the population to have immunity.

However, the study below just published in the New England Journal of Medicine makes me think this may even be an underestimate. In a well done ‘classic’ epidemiology study in a nursing home in Seatle, 23 days after the first positive test result in a resident, 64% tested positive for SARS-CoV-2; more than half (56%) of the residents were asymptomatic at the time of testing. Only half of these residents then went on to develop symptoms a few days later. A quarter of shedders never became symptomatic and most of these ‘asymptomatic shedders’ were shown to shedding viable virus. Tragically of the 57 residents who were shown to be infected with SARS-CoV-2 infection 15 died; a mortality rate of 26%.

Why is this so important? In short, a high or very high R-zero means that the government policy of relying on herd immunity to protect the vulnerable is not going to work.

Let me explain. Whilst we are socially distancing we reduce the R-zero of SARS-CoV-2 to less than 1 and hence the number of new cases falls and we flatten the curve. This is what is happening in the UK and many other countries at present. However, as soon as we stop the lockdown and allow social interaction the R-zero will rise above one and we will get more cases. But because this virus is so infectious we may need herd immunity to be well above 80% (possibly 90%) for the epidemic to peter out. At which time point the government is hoping to let vulnerable people remerge from self-isolation and feel confident that they will not be susceptible to being infected and dying from severe COVID-19.

The bad news is that 15.2% of the UK population is over 70 years of age (data from Age Concern) the government definition of the vulnerable population based on age. This is not taking into account all the other vulnerable groups who are less than 70 years of age, i.e. those who are obese and/or have diabetes, cardiovascular, respiratory diseases. This means that by the time we get herd immunity many more people will die from COVID-19. This is why the scientific community needs to push for anti-virals and an effective vaccine. But herein lies a problem.

To develop and test an effective vaccine we really need an epidemic to be in full swing, i.e. on the upside of the curve and not on the tail. A vaccine trial is like a drug trial; subjects are randomised to an active or SARS-CoV-2 vaccine arm or a comparator arm (placebo or another vaccine) and then you see whether or not there are fewer cases of COVID-19 on the active arm compared to the comparator arm. However, if there are too few cases developing COVID-19 because of social distancing, using face masks, hygiene measures, etc. it will take too long to get enough events or trial subjects getting COVID-19, to show the vaccine is working. This is why we the rich-world may need to go to parts of the world where social distancing etc. is not feasible and the R-zero remains high, i.e. the squatter camps, shantytowns, favelas or slums of the low and middle-income countries of the world.

We, the rich world, may have no choice but to take this low/middle-income route for the sake of the world. But if ‘we’ do take this route to develop an effective vaccine we have to make it ethical. We will have to offer these countries priority access to the vaccine. If we don’t it will be a travesty. I can imagine the headlines in the press if we don’t. ‘Vaccine Imperialism: How the Rich World Exploited The Poor!’

What are the implications for you if you have multiple sclerosis. If you are vulnerable you need to be prepared to self-isolate/shield for a very long time. If you are not vulnerable then you really need to prepare yourself for becoming infected with SARS-CoV-2 and getting COVID-19. I have a section on MS-Selfie that addresses this issue. I will be updating this section over the weekend as there are additional things you can do as an individual and as a family to help derisk your chances further.

I am sorry for bringing you bad news at the beginning of the weekend, but as always I feel it is important, to be honest, and frank.

The information in this post is quite complex so if you have any questions please feel free to ask.

Gandhi et al. Asymptomatic Transmission, the Achilles’ Heel of Current Strategies to Control Covid-19. NEJM April 24, 2020 DOI: 10.1056/NEJMe2009758

Arons et al. Presymptomatic SARS-CoV-2 Infections and Transmission in a Skilled Nursing Facility. NEJM April 24, 2020 DOI: 10.1056/NEJMoa2008457

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can spread rapidly within skilled nursing facilities. After identification of a case of Covid-19 in a skilled nursing facility, we assessed transmission and evaluated the adequacy of symptom-based screening to identify infections in residents.

METHODS: We conducted two serial point-prevalence surveys, 1 week apart, in which assenting residents of the facility underwent nasopharyngeal and oropharyngeal testing for SARS-CoV-2, including real-time reverse-transcriptase polymerase chain reaction (rRT-PCR), viral culture, and sequencing. Symptoms that had been present during the preceding 14 days were recorded. Asymptomatic residents who tested positive were reassessed 7 days later. Residents with SARS-CoV-2 infection were categorized as symptomatic with typical symptoms (fever, cough, or shortness of breath), symptomatic with only atypical symptoms, presymptomatic, or asymptomatic.

RESULTS: Twenty-three days after the first positive test result in a resident at this skilled nursing facility, 57 of 89 residents (64%) tested positive for SARS-CoV-2. Among 76 residents who participated in point-prevalence surveys, 48 (63%) tested positive. Of these 48 residents, 27 (56%) were asymptomatic at the time of testing; 24 subsequently developed symptoms (median time to onset, 4 days). Samples from these 24 presymptomatic residents had a median rRT-PCR cycle threshold value of 23.1, and viable virus was recovered from 17 residents. As of April 3, of the 57 residents with SARS-CoV-2 infection, 11 had been hospitalized (3 in the intensive care unit) and 15 had died (mortality, 26%). Of the 34 residents whose specimens were sequenced, 27 (79%) had sequences that fit into two clusters with a difference of one nucleotide.

CONCLUSIONS: Rapid and widespread transmission of SARS-CoV-2 was demonstrated in this skilled nursing facility. More than half of residents with positive test results were asymptomatic at the time of testing and most likely contributed to transmission. Infection-control strategies focused solely on symptomatic residents were not sufficient to prevent transmission after SARS-CoV-2 introduction into this facility.

CoI: none for this post

#MSCOVID19: good news for anti-CD20ers

I am being asked why I have moved ocrelizumab and other anti-CD20 therapies into the low-risk categories of DMTs in my latest version of my DMT table.

The reasons I use to justify the change are several-fold.

Anti-CD20 therapies deplete B-cells and only have a small impact on T-cell counts and innate immune cell function. This is important because anti-viral responses don’t seem to be affected to a great extent on ocrelizumab and other anti-CD20 therapies. In the phase three ocrelizumab trial programme apart from seeing a small herpes zoster signal there was no clear viral infection signal. When viral infections occurred they tended to be mild or moderate. The severe infections were bacterial (pneumonia, UTIs and cellulitis).

We are seeing an increasing number of patients who have been treated with anti-CD20 therapies who have had COVID-19 doing well. We have just published a case report in MSARDs of a man with PPMS treated with ocrelizumab who did well (see below). This has to be good news for patients on anti-CD20 therapies.

Ocrelizumab also blunts antibody responses, which may be important in severe COVID-19. This may delay or prevent damage to the COVID-19 lung as some of the damage seems to be mediated by complement activation and microthrombi. The latter is indicative of damage consistent with IgG3 anti-viral responses and IgG antibody-dependent cellular cytotoxicity by macrophages and in some instance neutrophils. Antibody production against the SARS-CoV-2 spike protein may promote cytokine production that activates macrophage to become more destructive. Blunting these antibody responses with an anti-CD20 therapy may actually be beneficial, which is why we are predicting that anti-CD20 treated patients will have a lower risk of getting severe COVID-19.

What about hypogammaglobulinaemia then?

Yes, this does occur with anti-CD20 therapies but occurs at a relatively low level. As SARS-CoV-2 is a new human pathogen and hence we don’t have immunological memory against the virus this makes little difference to the risk of becoming infected with SARS-CoV-2. Hypogammaglobulinaemia may, however, put you at risk of getting secondary bacterial infections. Fortunately, these can be treated with antibiotics.

What about vaccine responses?

Yes, anti-CD20 and other immunosuppressive therapies can blunt antibody responses to some vaccines. And yes, contrary to the dogma patients on anti-CD20 therapies do make antibodies to viruses and vaccines. I assume this happens because we still have B-cells in secondary lymphoid organs and/or there may be CD20 negative B-cells that can takeover antibody production. Please note that the latter is a hypothesis.

Antibody responses to glycoproteins (sugar antigens) are particularly affected by anti-CD20 therapies and this may be important in the context of coronavirus immunity as the spike protein is heavily modified with sugar molecules. However, all these arguments are theoretical; until a vaccine emerges I would focus on getting MS treated. We can cross the vaccine bridge if and when it gets built. I am still of the opinion that the government’s strategy is herd immunity and hence the majority of us will at some point become infected with SARS-CoV-2. Waiting for a vaccine that never arises is going to be difficult for individuals; how long can you realistically self-isolate and/or shield?

We are very keen to do an anti-SARS-CoV-2 seroprevalence study in pwMS to see how many have been exposed to the virus and have not developed COVID-19 and to also look at antibody responses to SARS-CoV-2 in patients on different DMTs. We hypothesise that patients on anti-CD20 therapies will have as good an antibody response to SARS-CoV-2 as patients not on anti-CD20 therapies. This hypothesis refers to qualitative antibody responses, i.e. neutralising or protective antibody responses.

For the reasons above I have not stopped offering patients with active MS anti-CD20 therapies during the pandemic. This refers to both starting and retreatment. Some patients have chosen to delay their treatments until the pandemic is over and others have taken my advice and gone ahead with their treatments; this is their choice. But as I have said before the pandemic won’t be over anytime soon; the tail is likely to extend for 18-24 months and possibly longer. Therefore all the guidelines that have recommended delaying or postponing treatment with depletion therapies, i.e. the anti-CD20s, cladribine, alemtuzumab, mitoxantrone, cyclophosphamide and HSCT will have to be reviewed. We can’t stop treating MS or offering patients less effective options for the next 18-24 months. If we do what will be the consequences?

How many swallows does it take to make a summer? I am aware that one case report is not much, but there are an increasing number of patients being reported on social media who have been treated with an anti-CD20 and have had gotten through COVID-19 without a problem.

I would urge all the national register studies to be please report your data on COVID-19 outcomes in pwMS as soon as possible. We need the data to formalise our treatment guidelines and to help allay the fears of our patients. Please use one of the archive repositories to get your data out to the MS community as soon as possible. Thank you.

Giovanni Novi et al. COVID-19 in a MS Patient Treated With Ocrelizumab: Does Immunosuppression Have a Protective Role? Mult Scler Relat Disord 2020 Apr 15;42:102120.

Background: Coronavirus disease 19 (COVID-19) is a novel disease entity that is spreading throughout the world. It has been speculated that patients with comorbidities and elderly patients could be at high risk for respiratory insufficiency and death. Immunosuppression could expose infected patients to even higher risks of disease complications due to dampened immune response. However, it has been speculated that overactive immune response could drive clinical deterioration and, based on this hypothesis, several immunosuppressants are currently being tested as potential treatment for COVID-19.

Methods: In this paper we report on a patient that has been treated with ocrelizumab (a B-cell depleting monoclonal antibody) for primary progressive multiple sclerosis who developed COVID-19.

Results: Despite complete B cell depletion, patient symptoms abated few days after hospitalization, and he was discharged to home-quarantine. Phone interview follow-up confirmed that, after 14 days, no new symptoms occurred.

Discussion: This report supports the putative role of immunosuppressive therapy in COVID-19 affected patients.

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

Does immunosuppression protect you from severe COVID-19?

The hypothesis that immunosuppression may protect you from severe COVID-19 is gaining traction. New data released on the 4th April 2020 from the UK’s Intensive Care National Audit & Research Centre suggests it may. When comparing 2249 patients admitted to ITU in the UK with severe COVID-19 the proportion of immunocompromised patients was 3.7x lower than the proportion of immunocompromised patients admitted to ITU with viral pneumonia (the comparator) between 2017 and 2019 (2.3% vs. 8.5%). This was a highly significant difference (p<0.00001).

This clearly justifies the current research strategy being tested across the planet to see if immunosuppressive therapies may improve disease outcome in patients with COVID-19.

Does this mean we can now assume that immunosuppression protects against severe COVID-19 and COVID-19-related ARDS (adult respiratory distress syndrome)? Not yet. The UK’s ITU cohort of severe COVID-19 is biased in that those patients who are deemed too frail and/or disabled may never get to ITU, which may include a disproportionate number of immunosuppressed patients. Whereas this specific bias is unlikely to apply to ITU admissions between 2017 and 2019 (viral pneumonia cohort) when there was no such pressure on resources.

Despite this caveat, this is an important tidbit of information that will allow pwMS on immunosuppression to sleep a bit easier. I sincerely hope the wider MS community will reconsider their advice about not giving MS DMTs that are if anything mildly immunosuppressive to patients with active MS. By not treating our patients we may unintentionally be increasing their chances of developing severe COVID-19. Could our guidelines be another example of the law of unintended consequences? Let’s hope the real-world data that is being collected at present will answer this question.

CoI: multiple