Overcoming Multiple Sclerosis E-Book

George Jelinek MD

• Herausgeber: Allen & Unwin
• Kategorie: Ratgeber
• Sprache: Englisch

Seitenzahl: 848

Veröffentlichungsjahr: 2017

Beschreibung

Overcoming Multiple Sclerosis is an established and successful program of treatment. Once a diagnosis of MS meant inevitable decline and disability. Now thousands of people around the world are living healthy, active lives on the Overcoming Multiple Sclerosis recovery program. Overcoming Multiple Sclerosis explains the nature of MS and outlines an evidence-based 7 step program for recovery. Professor George Jelinek devised the program from an exhaustive analysis of medical research when he was first diagnosed with MS in 1999. It has been refined through major ongoing international clinical studies under Professor Jelinek's leadership, examining the lifestyles of several thousand people with MS world-wide and their health outcomes. Overcoming Multiple Sclerosis is invaluable for anyone recently diagnosed with MS, living with MS for years, or with a family member with MS. It makes an ideal resource for doctors treating people with MS.

Leseprobe

First published in 2016

Copyright © George Jelinek 2016

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without prior permission in writing from the publisher.

Allen & Unwin

c/o Atlantic Books

Ormond House

26–27 Boswell Street

London WC1N 3JZ

Phone: [phone]

Email: [email protected]

Web: www.allenandunwin.com/uk

A CIP catalogue record for this book is available from the British Library.

ISBN 9781760293192

eISBN 9781952535543

Internal design by Midland Typesetters

Internal illustrations by Tor Ercleve

Index by Puddingburn

Set by Midland Typesetters, Australia

Cover design: Squirt Creative

Cover photograph: Kucher Serhii/Shutterstock

For Eva Jelinek

1923–1981

CONTENTS

List of tables and figures

Acronyms and abbreviations

Preface

Acknowledgements

PART I: BACKGROUND

Chapter 1About MS

What is MS?

Symptoms of MS

How common is MS?

Genetics of MS

Types of MS

Immunity and auto-immune disease

Degenerative disease

Causes of MS

Diagnosis

Course of MS

Overview

Chapter 2Preventive medicine and chronic Western disease

Preventive medicine and MS

Developing the OMS Recovery Program

Validating the OMS Recovery Program

Chapter 3Validating the OMS Program: The STOP-MS study and the HOLISM study

Introduction

The STOP-MS study

The HOLISM study

PART II: THE OMS RECOVERY PROGRAM

Step 1Eat well

Introduction

Why

How

Overview

Step 2Get enough sun and vitamin D

Introduction

Why

How

Overview

Step 3Exercise regularly

Introduction

Why

How

Overview

Step 4Meditate and use the mind–body connection

Introduction

Why

How

Overview

Step 5Take medication if needed

Introduction

Why

How

Overview

Step 6Prevent family members from getting MS

Introduction

Why

How

Overview

Step 7Change your life, for life

Introduction

Why

How

Overview

Notes

Index

LIST OF TABLES AND FIGURES

TABLES

1 Summary of validated tools used

2 Fat consumption 1979–81 by country, in order of highest to lowest MS mortality

3 Results for participants in Swank’s saturated fat study

4 Foods to eat and foods to avoid

5 Healthy substitutes for unhealthy foods

6 MS mortality rates (per million people) for men and women aged 45–74 by latitude, 1983–89

FIGURES

1 Breakdown of participants in the HOLISM study

2 Pathways in the body for omega-3 and omega-6 fatty acids

3 Relapse rate (number per year) before and after going on a low-fat diet

4 The effects of fat consumption on early, mildly disabled (0, 1, 2; solid line), and late seriously disabled (3, 4, 5; broken line) patients in the Swank study

5 Physical health quality of life by dietary factors

6 Mental health quality of life by dietary factors

7 Quality of life outcomes by frequency of fish consumption

8 Quality of life outcomes by level of alcohol use

9 UVB from the sun acting on skin to make vitamin D

10Exercise is good for the brain

11Quality of life by level of physical activity

12Triggering the fight or flight response

13Meditation slows brain waves

14Quality of life, comparing individual DMDs with all other DMDs and no DMD use

15The roller-coaster to stability

16Smoking—both active and passive—is an important risk factor in MS

17Quality of life by smoking status

18Quality of life at one and five years after an OMS retreat

19The old shower habit

ACRONYMS AND ABBREVIATIONS

ACNEM

Australasian College of Nutritional and Environmental Medicine

ALA

alpha-linolenic acid

ARMS

Action for Research into Multiple Sclerosis

BBB

blood–brain barrier

BDNF

brain-derived neurotrophic factor

BMI

body-mass index

CAMS

Cannabinoids in MS (study)

CIS

Clinically Isolated Syndrome

CNS

central nervous system

CoQ10

Coenzyme Q10

CSEP

Canadian Society for Exercise Physiology

CSF

cerebrospinal fluid

CT

computerised tomography

CV

curriculum vitae

DHA

docosahexanoic acid

DHQ

Diet Habits Questionnaire

DMD

disease-modifying drug

DRI

dietary reference intake

EAE

experimental auto-immune encephalomyelitis

EBV

Epstein-Barr Virus

ECTRIMS

European Committee for Treatment Research in Multiple

Sclerosis

ED

emergency department

EDSS

Expanded Disability Status Scale

EPA

eicosapentanoic acid

GDP

gross domestic product

HHV-6

human herpes virus 6

HOLISM

Health Outcomes and Lifestyle Interventions in a Sample

of people with Multiple Sclerosis (Study)

HSCT

Haematopoietic stem cell transplantation

IFN

interferon

Igs

immunoglobulins

IL

interleukin

IOM

Institute of Medicine (US)

IPAQ

International Physical Activity Questionnaire

IRIS

immune reconstitution inflammatory syndrome

IV

intravenous

IVIgs

Intravenous immunoglobulins

JCV

John Cunningham Virus (or JC Virus)

M-G

mitoxantrone followed by glatiramer

MBP

myelin base protein

MBSR

mindfulness-based stress reduction

MitoQ

Mitoquinone

MP

methylprednisolone

MRI

magnetic resonance imaging

MS

multiple sclerosis

MSQOL-54

MS Quality of Life-54 (questionnaire)

NARCOMS

North American Research Committee on Multiple

Sclerosis

NGF

nerve growth factor

NHMRC

National Health and Medical Research Council (Australian)

NICE

National Institute for Health and Care Excellence (UK)

OCT

optical coherence tomography

OMS

Overcoming Multiple Sclerosis

PML

progressive multifocal leukoencephalopathy

PMR

progressive muscle relaxation

PPMS

primary progressive MS

PRT

progressive resistance training

PSA

prostate-specific antigen

PwMS

people with MS

RA

rheumatoid arthritis

RDA

recommended daily (or dietary) allowance

REP

Rest–Exercise Program

RIS

radiologically isolated syndrome

REM

rapid eye movement

SLE

systemic lupus erythematosus

SPMS

secondary progressive multiple sclerosis

STOP-MS

S

Tudying

O

utcomes of

P

eople attending

MS

retreats

T1D

type 1 diabetes

T2D

type 2 diabetes

TNF

tumour necrosis factor

TRIGR

Trial to Reduce IDDM in the Genetically at Risk

UL

upper level (or upper intake level)

VZV

varicella-zoster virus

PREFACE

I leant over and kissed her on the cheek. She was already cold. Strangely, I couldn’t feel sad—only overwhelming relief. Relief that the suffering had finally stopped. Relief that Mum wouldn’t have to fight any more.

So this is how it ends, I thought. The insidious tentacles of multiple sclerosis (MS) had taken sixteen years to pull her down, but they couldn’t beat her in the end. Mum had chosen to take her own life rather than get any worse, rather than be completely degraded.

She looked so peaceful. I had kissed her goodnight the previous night, not knowing it would be the last time I would see her alive. What must she have been going through? To have been so brave right to the end, to have not let on as she said goodnight to the most precious parts of her life for the last time. I felt my eyes misting, but no tears would come. We had all known this was coming for a long time. Most of us had already grieved while she was alive. But now it was real. The image of me sitting there alone on her bed will stay with me forever.

How could I know that, eighteen years later, I would be sitting in a neurologist’s office some 7 kilometres away, listening but not listening as he was trying to tell me I had MS? I would not let myself hear what he was saying. When it did hit me, all the memories of Mum came flooding back. I relived the gradual deterioration, the descent into paralysis, the indignity of urinary catheters and bedpans, the loneliness and frustration. And it was going to happen again. To me.

I don’t know when I resolved that it wouldn’t. Things just seemed to lead me down a path where answers kept turning up—real answers. Now, approaching two decades of good health, relapse-free, I am confident about my future, and also about the possibilities for others diagnosed with this illness.

How old was Mum when she got MS? I don’t know. Perhaps 42 or 43. One night Mum was on her way to a night shift when she had a car crash that landed her in the Intensive Care Unit at Royal Perth Hospital. That’s when it started. A few months later, Mum started dropping things. Soon there were doctors’ appointments and tests, but the real significance of what was happening still didn’t sink in. Until she began to deteriorate.

At first it was just the occasional stumble. I can’t remember when she went into a wheelchair. Modifications started appearing around the house: shower rails, showering chair, ramp up the front stairs. The car was modified too. More and more, as time went on, when I’d come home for the night I would catch Mum looking at me from her wheelchair with a tear in her eye. You knew, when she had that look, that the big things in life were going through her mind: loss, separation, death, the burden she felt she was. This was her recurring theme: she was adamant she wouldn’t be a burden to anyone. It was also one of my first thoughts when I was told I had MS.

I could see the neurologist’s lips moving, but I couldn’t hear anything. It was a beautiful late Sunday afternoon in Perth. The light was coming through the leaves from a low angle, firing them up with late autumn colour. In an instant, my whole world had changed. I was not to know it, but I would never feel the same way about life again, and my orderly, seemingly successful life would soon fall apart.

‘It’s not the worst thing I could be telling you right now,’ I heard as if in some sort of dream. It certainly felt like the worst. We were suddenly talking about me having a magnetic resonance imaging (MRI) scan that night at the hospital. He was ringing the radiologist. All I could think of was my family. My daughter was only seven. All the plans I had, all the aspirations. Suddenly a big hand had reached into my life and taken away my future. And inexorably altered that of my family.

On the outside, I was calm and grateful that he had taken up so much of his valuable Sunday afternoon to see me and make the diagnosis. Inside, I was numb. Why hadn’t I realised that I had MS? I now know that it is many times more common in family members, but somehow I had just assumed that lightning wouldn’t strike twice. Not me!

One morning at work, I noticed that the shoelace on my left shoe kept falling down into my shoe. But every time I looked for it, it was no longer there. As the day wore on, the feeling of something being there became more and more marked. By the next day, it was a feeling of numbness—like having been to the dentist—over all the toes of my foot. By now I was starting to remark on how odd it was. By the next day, it had spread up the outside of my lower leg. I was getting nervous. Being an emergency physician, I am not prone to panicking. I started thinking about all the possibilities. A slipped disk? I had had back problems for years, but swimming regularly had fixed that. Some unusual peripheral neuropathy? I let it go for another day, but by the Thursday I knew I was in trouble. The numbness was progressing pretty rapidly all the way up the leg, and around my backside. I hardly slept that night. The next morning I had a colleague from the emergency department (ED) look at me. I spent an anxious hour or two waiting in x-ray while another friend tried to squeeze me into the burgeoning Friday queue for the MRI.

To my surprise, there was nothing there. But what you find depends on where you look, and they looked for a slipped disk and missed the MS lesion two levels higher. I found this really puzzling. On the Sunday, I asked a neurologist with whom I worked to look me over. The MRI gave me the answers I did not want.

The first few days were awful. Should the kids be told? Should I tell anybody? What about the financial implications of not being able to work? The boys had only just started at an expensive private school. There were just no answers. But I realised I had to face this. My initial reaction of not telling anyone just wouldn’t work. How could I deal with this illness without acknowledging to the world that I had it? Keeping it a secret was impossible. I realised I had to start somewhere. Over the course of the day, I resolved to tell my brother and sisters. First, though, I had an appointment at the hospital to get my first dose of high-dose intravenous steroids. I wasn’t prepared for how difficult that would be: there was just no way to avoid the diagnosis. I could feel the pity in the eyes of the staff. I had nothing to hang on to. I felt like a man sentenced to a merciless, gradual destruction from which there was no escape.

That evening, it was hard to organise telling my brother and sisters all together, but I did the best I could, and we cried together all night. Driving home from my sister’s place, I was feeling really empty but surprisingly calm. I now realise how important this immediate expression of grief was, and how it so quickly led me to start finding answers in myself and to gain some feeling of control over the disease. Feeling so calm allowed me to start thinking logically and without fear. I began thinking and wondering, as I was driving down the freeway, why this illness had happened to me just when it did. Why did I have MS? What emotional needs was it serving for me to get ill just then? Was my subconscious knocking on the door of my seemingly well-ordered life, trying to tell me something was wrong? I was beginning to tackle MS.

So I arranged a meeting with my old mentor from intern days, Dr Ian Hislop. In his calm and measured way, he led me through the feelings I was experiencing. Every time I mentioned Mum, I found it almost impossible to speak without becoming tearful. It was clear that I was seeing my own illness and future through the filter of Mum’s disease and history. Until I could separate myself from those feelings a little, I would not get anywhere.

Ian listened quietly, occasionally interjecting with something to prompt me. Finally he gave me some assessment of what he thought I could do. First and foremost, he said, put yourself first. He suggested I take a long time off work in order to start doing some work on myself. This was great advice, but really difficult for me. Just the day before, I had told my colleagues I would be back in two weeks. For such a great challenge to one’s life, two weeks simply doesn’t do it justice. Ian was suggesting that perhaps I may not want to go back to work at all—that I should consider all possibilities. I knew he was right. I was at a crossroads, and anything was possible.

I wasn’t to know it, but the simple process of trying to put myself first was to start a chain reaction of events that led my outwardly appearing ‘perfect’ life to simply fall apart, to head in directions I had never anticipated, to cause seismic shocks in the lives of my immediate family and many of my friends. Continuing to trust in this process of having faith in myself and my feelings, and going where they led me, has been extremely difficult at times—both for me, and for many of those I love and have loved. But my life has now finally reached a point of stability.

Finally, Ian asked a question that was to start me on a greater journey than confronting MS. He wanted to know whether I had ever thought much about my spirit. I searched for an answer. I soon realised that this was an extremely important part of me, one of which I was aware but that I had put to one side because of the demands of the rest of my life. It was a simple question, yet I didn’t even have the vocabulary to answer it. Within the question lay the beginnings of a whole new journey for me.

Saturday morning arrived and I had finished my steroids. Now I was doing what the neurologist had termed ‘doing nothing’, and waiting. He had said that if I was still okay in six months we should repeat the MRI to see whether there were any new ‘silent’ lesions. I wasn’t sure I liked this idea. If there were new lesions, surely finding out about them would just knock my optimism and confidence. The steroids had done their job. I still had numbness and pins and needles but in a smaller area, and I still had a bit of trouble telling where my leg was in space unless I was looking at it.

I was following Ian’s advice and had let everyone at work know that I would not be back and that my leave was indefinite. I refused to say how long. I needed to marshal every resource I had to start this process. On Ian Hislop’s advice, I had bought a copy of Carolyn Myss’s wonderful book Anatomy of the Spirit and was starting to explore my own spirit.

The thing that started my search was a small, insignificant email from my brother, about Tuesday. I haven’t kept it, because I didn’t realise its significance at the time. It said something like, ‘A friend’s wife reckons you ought to try gamma-linolenic acid. She’s taken it for ten years and hasn’t had a relapse. There was something in the medical journals about it a few years ago.’ A message like that tends to wake you up when you feel there’s no hope.

I fired up MEDLINE and plugged in the key words ‘gamma-linolenic acid’, then cross-referenced it with multiple sclerosis. A few abstracts of papers came up from the 1980s. I was a bit surprised to see that, yes, there did seem to be a small benefit for patients with MS who took gamma-linolenic acid. In one of the papers, there was a bit about linoleic acid deficiency in MS, and it referred to another paper on patients getting better with linoleic acid supplements.

My search had begun in earnest. What I discovered in the literature shocked me. It rapidly became clear that with a preventive medicine approach, there was a real possibility that people with MS (PwMS) could slow or stop the otherwise relentless progression of MS into disability. Paper after paper reinforced this view, until I simply had to make the information public—and, of course, I immediately adopted it myself. Within months, I had collated all the evidence that went into the first book I wrote, Taking Control of Multiple Sclerosis, which later became Overcoming Multiple Sclerosis as I continued to build the evidence base.

From there, I began running live-in retreats for PwMS in early 2002, started a website with a community forum in 2008 and became a frequent user of social media so as to better disseminate my important message. As the number of PwMS who were doing well following this approach grew, I found I had more and more willing volunteers to help spread the news. Overcoming Multiple Sclerosis, or OMS, the community-based charity and support for PwMS grew from this process in 2012, through the passion and enthusiasm of Linda Bloom, a participant who had been to one of my early retreats and had recovered.

But spreading the message about the research findings of all the scientists in the world who had looked into this illness in detail was one thing. It was quite another to find credibility among my medical peers by undertaking my own research in the area. So began not only my research into the outcomes of people who had attended our retreats, but also a novel project recruiting PwMS from social media sites, where I had garnered quite a following, to try to find more evidence of the potential effect of lifestyle factors on the progression of and outcomes from MS.

This book represents a distillation of the evidence I have accumulated over nearly two decades since my diagnosis, as well as the experience I have gained of overcoming MS and watching countless others recover. I hope it helps on the journeys of many people diagnosed with this illness as they do the same.

ACKNOWLEDGEMENTS

There are many, many people to thank. First, I thank my wife, Sandra. Our lives have been inextricably linked since early in this millennium. Whenever I am confronted with doubt or fear, I instinctively reach for her and she is always there. Thank you, sweetheart, for never wavering. I thank my children, Sean, Michael, Pia, Ruby and John, for the love, support and humour they bring to my life, and for just being who they are. I am also grateful for the unfailing support of my siblings and extended family. Special thanks to a wonderful neurologist and good friend, Dr Peter Silbert, for his constant support and the very constructive suggestions made to the manuscript. I cherish the close connections I share with the OMS team, an international group of wonderful people that continues to grow, and particularly thank Emily Hadgkiss for her help with the figures, Dr Keryn Taylor for all that she does for people with MS, Dr Claudia Marck for the drive she brings to our research, and Linda Bloom and Gary McMahon for the enormous passion they have for the important work of OMS. Thanks also to my emergency physician colleague and friend, Dr Tor Ercleve, whose drawings have added significantly to the book. And to the colleagues, friends, and MS community with whom I have shared my life, I offer my continuing gratitude for your support and wisdom.

PART I

BACKGROUND

CHAPTER 1

ABOUT MS

Multiple sclerosis (MS) is a highly variable, unpredictable disease and one of the most life-altering diagnoses a person can receive.

Nancy Holland and Michele Madonna

WHAT IS MS?

Multiple sclerosis is a disease of the brain and spinal cord, usually resulting in progressive disability. It is the most common disabling neurological disorder in young adults, and has a very uneven distribution geographically, being common in so-called Western industrialised countries but also progressively more common further away from the equator. MS is a disease of affluence,1 as are other auto-immune diseases;2 research clearly shows that it is generally more common in countries with greater gross domestic product (GDP)—that is, with greater spending power.

MS is usually a progressively disabling disorder more common in affluent countries further from the equator.

MS is described as an inflammatory demyelinating condition. This means that parts of the brain and spinal cord (together called the central nervous system, or CNS) become inflamed, resulting in loss of the fatty coating—called the myelin sheath—around the connections between nerves. At a microscopic level, the immune system sends its first line of defence—white blood cells—to the area. These cells secrete messenger chemicals that cause the inflammation, and destroy part of the myelin around some nerves.

The brain and spinal cord are mainly made of fat; the type of fat depends on what we eat. The membranes of cells—their outer envelopes—are made of a double layer of fat. After changing to a diet consisting of different types of fats, there are quite marked changes in the make-up of these cell membranes.3 This is because our bodies are not static, unchanging structures; we are literally what we eat. Deepak Chopra says, ‘Just one year ago, 98 per cent of the atoms in our bodies were not there. It’s as if we live inside buildings whose bricks are being systematically taken out and replaced.’4

Importantly, because of the different melting points of the various different types of fats we eat, the cell membranes of people who consume mainly unsaturated fats are more fluid and pliable than those of people who consume saturated fats. For people who eat mainly saturated fats, cell membranes are more rigid and inflexible, and more prone to degenerative changes.3

Typically, inflammation of a portion of the myelin sheath of a nerve in the brain or spinal cord is followed by loss of some of the myelin. This forms the so-called lesions of MS. In these inflammatory lesions, white cells of the immune system gain access to the myelin sheath, which they usually can’t do because of what is called the ‘blood–brain barrier’ (BBB), a tight junction between the blood vessels around the brain and the brain itself. Further white cells are probably attracted by some of the chemical messengers released by these initial white cells. The demyelination strips the insulating coating on the connections or axons between nerves; this is followed by some repair and scarring, as with any episode of inflammation. The result is that nerve impulses don’t travel along the nerve as well as they did before.

SYMPTOMS OF MS

The symptoms of MS depend entirely on which particular parts of the brain or spinal cord are affected, which is why symptoms vary so much from person to person. If a nerve axon in the spinal cord bringing sensory messages up from the legs to the brain is affected, then the person might notice tingling or numbness. If it is carrying motor messages down from the brain to the leg muscles, there may be some weakness. If they are nerves inside the brain responsible for, say, the sense of balance, the person may become very unsteady. Because inflammation causes swelling, there is some pressure on surrounding axons, causing them to work less well. As this swelling subsides, these surrounding nerve cells start to work again. So there is some recovery for this reason alone, but there is also some repair of the damaged nerve cells (a process called remyelination)—particularly early in the disease—so the symptoms settle further. This remyelination is a process whereby certain cells in the nervous system start to wrap themselves around the axons again. It occurs throughout the disease, and is more prominent than previously thought.5

Symptoms of MS vary markedly from person to person.

Thus the area of numbness or tingling may become smaller, or the weakness may improve gradually, as the lesion heals and scars. Recovery is often incomplete, though, and people are left with persistent symptoms—although less severe than when the attack was at its peak—in the same part of the body. These residual symptoms typically wax and wane depending on numerous factors. Heat makes nerves conduct less well, and so makes these residual symptoms worse for most people. But it doesn’t actually damage the nerves. So exercising that heats the body up is fine, even if it makes the symptoms temporarily worse. Some people find the reverse is true: that cold makes their symptoms worse.

As the disease progresses, these lesions grown in number, and more and more pathways are knocked out. Hence the person notices a gradual decline in function. Some of these lesions occur in ‘silent’ parts of the brain and are not noticed. Those we really notice occur in the spinal cord or in the nerves leading to the eye. Virtually all of these nerve fibres in the spinal cord are essential for things like sensation, power, balance and vision. Even a small lesion here is therefore usually noticed.

The nervous system has an amazing capacity to regenerate, so that impulses can now ‘detour’ around the damaged lesion.6 The brain changes as well, recruiting new nerve cells and pathways to compensate for what is missing, in a process of ‘re-wiring’ called neuroplasticity. This is well described in Norman Doidge’s book The Brain that Changes Itself.7 When there are only a few lesions, the brain is really good at this regeneration and compensation process, even if there isn’t much remyelination. If the damage continues, these processes become overwhelmed and progressive disability occurs. That is why it is so important to stabilise the illness and prevent further damage as quickly as possible.

Optic neuritis

The first attack of MS quite often affects an eye. This is called optic neuritis, where the optic nerve—the major nerve carrying visual information from the retinas behind the eyes to the brain—becomes inflamed. Optic neuritis is a common cause of relatively sudden loss of vision in one eye in young people.8 People who develop optic neuritis have a 40–50 per cent chance of developing MS in the next fifteen years.9 The best predictor of the risk of going on to develop MS for someone who develops optic neuritis is whether they have other lesions in the brain on MRI at the time of the attack.10 About 25 per cent of people with no lesions at the time of the attack go on to get MS, but if there is one lesion or more, the risk is about 75 per cent. Women are also more likely than men to go on to develop MS after an attack. If there are spinal cord lesions at the time of the initial attack, that increases the risk of ultimately being disabled.11

Optic neuritis is the first sign of MS for about 15–20 per cent of people with MS (PwMS).12 Between one-third and one-half of all PwMS develop optic neuritis at some point in the illness. Even for those people, the long-term outlook for vision after an attack of optic neuritis is good, with 72 per cent having normal vision in at least one eye and two-thirds having normal vision in both at fifteen years.13

Many neurologists argue that people developing optic neuritis who have MRI changes that suggest a greater likelihood of developing MS should start on one of the disease-modifying medications immediately.14 Such therapy has been shown to delay or prevent the onset of MS considerably.15 This book makes the case that the OMS approach of an ultra-healthy diet, exercise, vitamin D and stress reduction should be started as early as possible after such an attack, whether or not one opts to take a medication. This should provide optimal protection against the development of MS.

The role of steroids in optic neuritis is not clear. Intravenous steroids are commonly prescribed to speed up recovery, but they don’t seem to affect the long-term outcome for vision.16

Cognitive function

Cognitive function describes higher level functions of the brain, such as reasoning, judgement, abstract thought, awareness, perception, the ability to learn and remember details, and so on. If nothing is done about stabilising MS, cognitive function is generally progressively impaired, often quite subtly. The impairment seems to relate quite closely to the loss of nerve cells that accompanies MS progression in people who are not proactive about the illness. MRI scans reveal a gradual shrinking or atrophy of the brain.

A decline in cognitive function is common in MS—even in those people with so-called benign MS.

Some doctors have been inclined to put complaints by PwMS about mild cognitive problems down to depression or other mental health issues, but studies have shown that such complaints are mostly due to genuine cognitive impairment and need to be taken seriously.17 Studies show that between half and three-quarters of PwMS have some degree of impairment of cognitive function, and many others probably have more subtle cognitive issues.18,19,20 Cognitive decline becomes progressively worse the longer people have had the disease, the worse the damage in the brain has become, and the more disabled people are—although more recent research shows that it occurs even very early in the disease and has an effect on quality of life.19,21 Even people with so-called benign MS, such as those who have only had one episode of optic neuritis and otherwise appear to be well, have been shown to have significant cognitive decline many years later.22

Researchers have suggested that PwMS be tested for any decline in cognitive function, as this is the most sensitive index of disease progression, and can even be used to measure whether disease-modifying therapies are working,23 although most neurologists would not be keen to pursue this strategy, as it is very confronting for the individual with MS. One important aspect of cognitive decline is that it can affect the ability to make decisions, and this can have a profound effect on daily life for PwMS, and also contribute to disability.24

HOW COMMON IS MS?

As a rule of thumb, MS occurs in about one in 1000 people. But that proportion varies a lot between and within countries. In the United Kingdom, it occurs in approximately one in 800 people, affecting around 90,000 people in total, and in Northern Europe it affects approximately one in 1000. In Australia, there are around 23,000 people with the illness, and there is a marked increase in how common it is with distance away from the equator. In Australia, for instance, the disease affects about twelve people per 100,000 in Far North Queensland, rising to about 36 per 100,000 in New South Wales and peaking at around 76 people per 100,000 in Tasmania. This effect of MS being more common the further one gets from the equator applies from country to country as well as within countries. In the United States, there are generally said to be between 250,000 and 350,000 PwMS, although a 2013 study put this much higher at around 570,000.25 There are said to be about 2.5 million PwMS worldwide, although this is almost certainly an under-estimate.

MS is becoming more common, probably because of less healthy lifestyle choices.

The disease is becoming more common. A 1922 review from the United States showed that the incidence had increased over the preceding twenty years.26 A 1952 report indicated that the incidence of MS doubled in Europe early in the twentieth century, and other data from Montreal show a 50 per cent increase from 1935 to 1958.27 A 2005 study from Sardinia, a high-risk area for MS, showed that the incidence of the disease on the island had increased more than five-fold over the 30 years to 1999.28 There are now data from several countries, including Japan, Canada and Ireland, showing that the incidence of MS is increasing.29,30,31 A US study showed that MS had become 50 per cent more prevalent there over the 25 years to 2007.32 Similar increases are being noticed everywhere.

Researchers in Tasmania have provided important data over many years on how common MS is. They have showed that the number of new cases per year per capita roughly doubled from the 1950s to the 2000s, and the number of people with the illness tripled from 1961 to 2009, going from about one in 3000 people to about one in 1000 people in Hobart.33 An editorial by Dr George Ebers from Oxford suggested that this was unlikely to be just due to detecting more cases because of MRI, because most of the change happened before MRI was available.34 More cases were being diagnosed in the elderly, and the increased longevity of the population may partly explain the increase, as more people now live long enough to get the disease, and the age of the study population had increased. However, the death rate from MS over the period had halved.

MS is a ‘modern’ disease. The first cases were described in the mid-1800s. By the turn of the twentieth century, the disease was commonly recognised. As environmental influences are the most important risk for developing MS, it is very likely that environmental factors have changed in a way that increases the risk of getting MS. These factors are the common environmental triggers for MS, such as sun avoidance, low levels of vitamin D, a diet high in saturated fat, omega-3 deficiency, lack of exercise and so on. There is little doubt that these risk factors are much more common today in developed countries than they were in the past, and are responsible for the explosion of chronic disease faced by our communities. Like heart disease, type 2 diabetes, high blood pressure and cancer, MS is becoming increasingly more common. It is interesting to note the interplay between these diseases, because having MS is no guarantee that we won’t get another of these diseases related to our lifestyles.

MS and other diseases

While the research has been patchy in this area,35 it seems that, quite apart from MS, PwMS are sicker than other people in the population. They have more mental illness, with around half having depression at some stage during the illness and a third anxiety.36 But they also have considerably more physical illness, with high cholesterol and a poor fat profile in their blood (we will see later that this is no coincidence), high blood pressure, heart and blood vessel disease, and chronic lung disease. Having these additional diseases accelerates the progression of MS to disability, and results in worse quality of life.36–39 Heart disease is more common in PwMS than the rest of the population,40,41 and heart and blood vessel disease occurring at any time during the illness has the effect of making progression to disability more rapid.42 Canadian researchers looked at 8983 PwMS enrolled in the North American Research Committee on Multiple Sclerosis (NARCOMS) Registry, and analysed them according to whether they had vascular conditions such as heart disease, high blood pressure and diabetes.42 They found that having a vascular condition at the onset of MS, or developing one later, resulted in around a 50 per cent increased risk of having difficulty walking. The risk increased the more vascular conditions a person had. Whereas it took about nineteen years for a person with MS who did not have any vascular conditions to need assistance with walking, it took only thirteen years for someone with a vascular condition.

Sex and age distribution

MS mainly affects people in their twenties or thirties, but no age group is immune. It is the most common disabling neurological illness in young adults. MS has now been found in very young children and in the elderly; as many as 20,000 children in the United States may have the disease but are not yet diagnosed. Children have been diagnosed with MS at as young as eighteen months old. Women have always been affected more commonly than men, in a ratio of around 3:2, but the ratio is changing towards 3:1. This changing sex ratio shows that environmental factors play a major part in the risk of getting the disease, and therefore that many cases are preventable by changing these factors.

GENETICS OF MS

MS is more common in family members of PwMS. Many are unaware of this, and so are some doctors. If one has a first-degree relative with MS, like a brother or mother, the risk is 20–40 times greater that of the general population. Identical twins have 300 times the risk of other people of getting MS if the other twin has the disease. For 100 pairs of identical twins in which one of each pair gets MS, 24 of the other twins will get the disease—that is, a 24 per cent risk. For non-identical twins, the risk is 3 per cent.43

MS is a disease that runs in families.

The Canadian Collaborative Study Group has published a number of important papers on various aspects of the family risks of getting MS. Initial studies showed that the increased risk of MS in a family was due to genetic factors—that is, factors passed from parent to child—not factors in the shared family environment. The group has shown that adopted family members and step-siblings have no higher risk than the general population of getting MS; one has to be related to have the increased risk.44,45 The risk to a sibling of someone with MS is three to four times higher if a parent also has or had MS, if the disease occurred at an earlier age in the sibling (five times higher if the brother or sister got MS at age twenty years or less), and if the person in question is female. Thus, for sisters of someone with MS where a parent has had it as well, the risk is as high as 8 per cent, and even higher if that person got MS under the age of twenty.46 If environmental risk factors are present—for example, if the person smokes cigarettes—the risk is higher again: up to one in five.

There has been contradictory research on whether the majority of the risk comes from the mother or the father having MS; they probably confer equivalent risk.47,48,49 MS is not inherited as a result of a single gene, like cystic fibrosis or muscular dystrophy, but as a result of the interaction of several genes—probably over 100 of them, each with small effects.50,51,52 Hence predicting the occurrence of MS in one’s children is not possible at present, so genetic counselling is not particularly helpful. But it is important to remember that our children are at significantly increased risk, and that there are ways to reduce that risk by modifying the environmental influences on children.

Important research has shown that only around 2 per cent of the population has the genetic predisposition to MS.53 While men are slightly more likely to have this genetic background, women are much more likely to get the disease because they are more influenced by environmental factors. In this study, the environmental risk factors for getting MS were noted to be vitamin D level both prior to birth during the mother’s pregnancy and in childhood, and infection with the Epstein-Barr Virus (EBV), the glandular fever virus.

Genetics plays an important part in risk of developing MS. Interestingly, for someone in the 2 per cent of people with the genetic make-up to develop MS, one of the factors that reduces the risk is childhood exposure to a wide range of infectious diseases.54 It is felt that this exposure makes the immune system more tolerant of challenges to it later in life. This is often referred to as the hygiene hypothesis.

Environment

So around a quarter of the risk of getting MS is genetic, and only about one in 50 people has this genetic make-up. What, then, makes that risk of MS turn into an actual diagnosis of the disease? We now know that the majority of the risk of developing MS—the other three-quarters—is environmental. There are many risk factors in the environment that act in concert with the genetic risk to cause MS to develop. This book is really about going into those in great detail, because the majority of these factors are modifiable—that is, one can do something about them to reduce the risk, not only of developing the disease but also of it progressing. Later, we will see that while the environment is responsible for most (75 per cent) of the risk of actually getting MS, it is completely responsible for the risk of progression of the disease, although some of these environmental factors are not necessarily modifiable. The book will go into those risk factors that are able to be modified in great detail, from diet—especially the role of the balance between healthy and unhealthy fats—to sun exposure and vitamin D, smoking, and stress, in addition to certain viral infections—most of which we cannot currently control.

So environment is around three times more important than genetics in the risk of developing MS in the first place. But in terms of the disease progressing once someone is diagnosed, it is vital that everyone is aware of the ground-breaking research of the International Multiple Sclerosis Genetics Consortium, published in Nature, one of the world’s most important and influential journals. This group has mapped and compared the genome (all or most of the genes of a person) of 9772 PwMS of European descent with that of 17,376 other people without the disease.55 This massive study was done to assess how genetic variations are associated with the development and progression of MS. First, they confirmed that many genes interact to create the risk of getting MS, and the stronger that genetic background risk, the earlier in life one is likely to get the illness.

But—and here is the key reason secondary prevention is an essential part of MS management—they found that genes and genetic predisposition did not account at all for the clinical course or severity of disease. To quote directly from the paper, ‘We found no evidence for genetic associations with clinical course, severity of disease or month of birth …’ This means that environmental factors, rather than genes, influence the course of MS once a person has the disease; while some of these factors are out of our control—like previous viral infections—most of these environmental influences can be controlled. Many authorities are now recognising this role of the environment in determining outcome from MS; however, questions still remain about which particular factors are responsible and to what extent.

Genetics contributes about 25 per cent of the risk of developing MS, but has no role in progression of the disease.

TYPES OF MS

MS occurs in several forms, but it has still not been established whether the underlying disease process is different in these or whether there are more distinct types. Up to 20 per cent of PwMS are said to have benign MS, but most authorities put this figure at around 6 per cent. This means that they suffer one or two attacks, but either that is all or they have only very occasional further episodes and remain active. Often these are people whose first attack was of visual disturbance, or other sensory symptoms. Researchers have suggested, however, that we probably over-estimate the number of people who have benign disease because we don’t account for subtle problems like cognitive disturbance, fatigue, and social and psychological disturbances.56 It is becoming apparent that benign MS may in fact not be benign at all. Most definitions say that benign MS is where the patient remains fully functional fifteen years after the onset of the disease. However, recent findings show that although there may be no physical sign of classic MS symptoms, around 45 per cent of people diagnosed with so-called benign MS have problems with cognitive function.57,58 In some studies, the presence of cognitive dysfunction was also associated with higher handicap scale scores, suggestive of considerable disease-related psycho-social problems.

We now know that the brain is not fixed, but constantly changing, with the theory of neuroplasticity explaining how new neurons are born and new connections are formed, based on life experiences. This new understanding of how flexible the brain is goes some way towards explaining why people with benign MS retain function.

It has been suggested that people who do well on the OMS Recovery Program probably do so because they have benign MS, but this is very unlikely. The aim of the program is to reduce the risk factors responsible for disease progression, and therefore limit the amount of nervous system damage through a program based on immune modulation, coupled with the prevention of degeneration, so that people actually stay quite well and do not deteriorate, either physically or mentally. This is quite different from so-called benign MS. If people are told they have benign MS after being on this program for some years, it is because healthcare workers find it hard to believe that it is possible to stay well after a diagnosis of MS, and conveniently apply that label.

At the other end of the spectrum is primary progressive MS. This is said to occur in about 10 to 15 per cent of cases. In this form of MS, disability progresses steadily from the first attack, usually without obvious attacks or remissions.59 Around 65 per cent of PwMS begin with typical relapsing-remitting MS. This means that they have an attack, followed by some recovery—partial or sometimes total—then a period in which they have no further attacks. This period may be called a remission, because the symptoms remit. Remission is a bad term, though, because it implies that the disease is not active during this period. We know that it usually is, and can often see continuing nervous system damage on MRI scans. This period is then followed by another attack, or a relapse.

After some years of relapsing-remitting disease, most of these people end up progressing to secondary progressive MS. This is the typical later stage of relapsing-remitting MS, where disability again progresses steadily—presumably due to continued accumulation of lesion upon lesion. Evidence is coming to light now that, because damage continues to occur to the CNS even during periods of so-called remission, there may be progressive loss of brain tissue. This may become evident in subtle ways, such as the development of memory problems. The obvious attacks are only the tip of the iceberg, and this is one reason it is so important to get started with therapies to slow down or stop the disease as early as possible.

Relapsing-remitting MS is a poor term, as damage commonly still occurs during periods of remission.

More recently, doctors have begun to recognise a form of the disease that is progressive but still involves relapses. This is termed relapsing-progressive MS. It is important to remember that classifying MS in a particular individual is not an exact science. Essentially, the doctor looks at how the illness has gone over time, whether there are relapses and whether disability is progressing, and then chooses the most appropriate category. If things change—such as the person making major lifestyle changes and modifying risk factors—it is quite possible, and frequently happens, that the disease changes and a different label has to be applied. People on the OMS Program, for example, have been told they have benign MS after initial diagnosis of primary progressive MS, or relapsing-remitting MS after being called secondary progressive MS. This is a good sign that the course of the illness is changing as risk factors are modified, indicating that risk factor modification is actually influencing the underlying disease process.

IMMUNITY AND AUTO-IMMUNE DISEASE

The immune system is a set of structures and functions within the body without which we could not survive, as it protects us against a range of things that cause disease. When a bacterium or virus invades the body and starts to multiply, the immune system recognises the bug as foreign, and either sends cells to the site to try to eliminate it, or instructs particular cells to secrete antibodies to try to neutralise it. The cells performing these tasks are white blood cells called lymphocytes. Lymphocytes are classified as either T or B lymphocytes, both derived from bone marrow. To simplify very complex processes, T cells help to get rid of the invader or toxin essentially by recognising them as foreign, going to the area and destroying them, whereas B cells secrete antibodies, which are complex proteins specially and individually designed to recognise the foreign material, bind to it and neutralise it.

When the immune response is activated like this, it leads to inflammation. Inflammation can best be thought of by picturing how angry a wound gets when it becomes infected. It may help to recall a cut or abrasion that has become infected. Typically, the wound gets hot, red, swollen and painful, and the area experiences a loss of function. So the inflamed part stops working as well. These are the typical features of inflammation. At a microscopic level, the immune system sends white blood cells to the area. These cells secrete messenger chemicals that cause the inflammatory reaction, and they dispose of bacteria, debris and foreign substances in the wound.

Naturally, the immune system needs to have a balance between switching on this immune response that causes inflammation in the body as the lymphocytes secrete their inflammatory chemicals, and switching it off. It would make no sense to have a permanently activated immune response to each foreign chemical or organism with which we make contact. Our bodies would be in a constant state of inflammation. Life would be miserable, with hot, swollen, painful body parts that refused to work properly. So the immune system, like all other bodily systems, has an off switch. In simple terms, the on switch is called the Th1 response and the off switch the Th2 response. We need the ability to switch on the immune response and the associated inflammation to deal with external threats, but we also need the ability to switch it off. Without the Th1 response, we would not recover from the most trivial infections; without the Th2 response, inflammation would be present all the time, and we would never return to normal.

The immune system is in balance between switching on inflammation (Th1 response) and switching it off (Th2 response).

MS is well-known to be a Th1-predominant inflammatory condition. That is, PwMS have an exaggerated Th1 response, with a tendency towards inflammation. That needs to be balanced by a stronger Th2 response. Interestingly, a variety of environmental and other risk factors increase the Th1 response, including a predominantly high in saturated fat, Western diet, excess omega-6 fatty acids, obesity, stress, smoking, lack of exercise and depression; the Th2 response, in contrast, is increased by exercise, meditation, omega-3 fatty acids and vitamin D. This is one of the reasons these risk factors, discussed in much greater detail later, influence MS progression.

The immune system is a highly advanced, complex system that develops a detailed memory of every foreign agent or toxin it fights, so the next time it encounters the same agent, it can rapidly use that memory to begin a precise response tailored to that particular agent. This, of course, is the basis of vaccination. A non-toxic sample of whatever virus or bacterium one is vaccinating against is introduced to the body by injection or by mouth. The immune system develops this response and remembers the agent. If the agent is ever encountered again, the immune system remembers immediately, and cells and chemicals respond rapidly to neutralise the threat.

This is where the concept of molecular mimicry comes in. In the case of MS, it is widely thought that exposure to a particular protein in cow’s milk at a young age in certain people leads to the immune system recognising this as foreign. For this to happen, the individual has to have some disturbance of the lining of the intestine (‘leaky gut’) that allows whole pieces of the protein to get into the bloodstream. Normally, proteins from cow’s milk are broken down by enzymes in the intestine and absorbed into the blood as the individual amino acids that make up the protein. With leaky gut, fragments of the protein are absorbed whole without being broken down, and the immune system recognises them as foreign and mounts an immune response. Naturally, it would be counter-productive for the immune system to recognise amino acids—the building blocks of proteins—as foreign, as we have amino acids floating around in our bloodstream much of the time.

The issue in MS is that parts of cow’s milk protein are identical to the protein in myelin. This has been elegantly shown in experiments from the Max Planck Institute.60 In line with Poser’s theory of MS causation being a cascade of environmental impacts on a genetically susceptible individual61, people with leaky gut, exposed to cow’s milk from an early age, with a genetic susceptibility to MS, develop this immune system recognition of cow’s milk protein as foreign. Something disrupts the blood-brain barrier at some point (like EBV infection or trauma) and the lymphocytes that carry this memory get access to the brain, which they normally can’t access. When they encounter myelin protein, their memory of it as being foreign—because it looks just like cow’s milk protein—is triggered. This may result in some local immune response, with inflammation and formation of a lesion or two. Later—perhaps many years later—an environmental event like a death of a loved one or a trough in vitamin D levels, through their Th1 stimulating effect on the immune system, triggers full-blown MS.

DEGENERATIVE DISEASE

But MS is not just about the immune system.62 It is now well established that degeneration is also a key mechanism in MS right from the beginning of the illness,63 and particularly in the later, progressive phases. Degenerative disease is where the function or structure of tissues or organs progressively worsens over time, due to normal body wear and tear or lifestyle choices such as exercise or diet. So lifestyle choices can and do result in degeneration, and in Western countries, poor lifestyle choices are the commonest cause of degenerative diseases like heart disease, diabetes, high blood pressure, cancer, Alzheimer’s disease and osteoarthritis.

There is now solid MRI evidence that the process of degeneration of nerve cells begins very early in the course of MS.64,65 Even early on, when there may be only a few lesions on an MRI scan, damage to the CNS is very widespread in MS and is not just confined to these lesions. It is important to remember that the MRI is only a picture, a visual representation of what is going on in the brain and spinal cord. MRI can only ‘see’ abnormal tissue down to a certain size or resolution; smaller than that, and damage is essentially invisible to MRI, even though it is widespread. The concept of MS as a focal, demyelinating disease really does need to be re-examined: we should regard it as a diffuse disease of the brain and spinal cord with a major degenerative component.66,67 Increasing loss of nervous tissue over time seems to be what ultimately leads the disease to become progressive.

But while the disease has a degenerative component throughout its course, it appears to be largely immune-mediated early on (although perhaps not in primary progressive MS), and later mainly degenerative once secondary progressive disease has occurred—although some would argue that the distinction between immune and degenerative diseases of the nervous system is blurred, and that both processes probably contribute.68

The immune system drives the MS disease process early in the disease; later, degeneration is more important, but both processes are present throughout.

It is useful to keep in mind that both of these components—immunity and degeneration—contribute to the development and course of MS, as this helps when looking for lifestyle interventions that can affect the course of the disease. For instance, polyunsaturated fats have been shown to be useful in degenerative diseases of the nervous system, such as Huntington’s disease,69 Parkinson’s disease70 and the memory loss and deterioration in mental function that accompany ageing,71,72,73 as well as degenerative disease in general.74 One of the omega-3 fatty acids in fish oil, DHA, has been shown to be powerfully neuroprotective, and to prevent degeneration in a rat model of brain injury.75,76 Being overweight predisposes one to many degenerative diseases, including heart disease, diabetes and arthritis. Eating fewer calories—even every second day—can dramatically improve health and longevity.77,78 Fasting causes a shift to a Th2 cytokine pattern in animals with the animal model of MS (experimental auto-immune encephalomyelitis, or EAE) and delays the onset of the disease, with milder clinical symptoms observed.79

Many other lifestyle modifications affect the ageing process and associated degeneration. For example, daily walking prevents age-related dementia80 and a plant-based wholefood diet dramatically improves heart disease.81

CAUSES OF MS

Genetics

MS is often described by MS societies and fund-raising bodies as a mystery disease. This is rather surprising, because a great deal is known about what causes MS, and subsequently what influences the rate of progression. MS develops because of an interplay between genetic predisposition to the disease and environmental factors, many of them related to lifestyle. Without the particular genetic background towards developing MS carried by about 2 per cent per cent of the population, no matter how many adverse lifestyle and environmental factors there may be, one cannot develop the illness. Of course, other illnesses may develop—such as heart disease and diabetes—but not MS. That doesn’t mean that someone has to have a relative with MS to develop MS; our DNA comes