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Gez Medinger & Professor Danny Altmann
THE LONG COVID HANDBOOK

Contents
Introduction
Chapter 1: What Is Long Covid?
Chapter 2: Who Gets Long Covid and Why?
Chapter 3: Can Children Get Long Covid?
Chapter 4: What Causes Long Covid?
Chapter 5: The Pathology of Long Covid
Chapter 6: Gender Bias and How to Tackle It
Chapter 7: The Impact of Long Covid on Mental Health
Chapter 8: How to Help Others Help You
Chapter 9: Tips for Managing Symptoms
Chapter 10: What about Treatment?
Chapter 11: What Does Recovery Look Like?
Chapter 12: The Emotional Journey
Chapter 13: What’s Next?
Conclusion
Acknowledgements
Notes
Resources

About the Authors
Gez Medinger is an investigative science journalist and patient advocate for
Long Covid. He was a film-maker and marathon runner when he became ill
with Covid in the early days of the pandemic. When he didn’t recover, Gez
put his efforts into researching the novel condition of Long Covid,
interviewing some of the world’s leading clinicians and turning his YouTube
channel into a huge resource for patients, conducting over a dozen patient-led
studies – which have been quoted in the global press, including the New York
Times, New Scientist and Men’s Health. In the process he has built a
worldwide community and his films currently have over 5 million views.
Professor Danny Altmann is a Professor of Immunology at Imperial
College London. His key research interests are the immunology of infectious
disease including severe bacterial infections, Zika virus, chikungunya virus
and SARS-CoV-2. He has also worked on autoimmune diseases including
multiple sclerosis and rheumatoid arthritis. During the Covid-19 pandemic he
has acted in several advisory roles, including on the House of Commons and
House of Lords Science Committees and the Immunology Task Force to the
Scientific Advisory Group for Emergencies (SAGE). He spent some years
working as the lead on strategy in Infection, Immunity and Population Health
at the Wellcome Trust, and has served more than twenty years as editor on
medical journals, including Immunology.

Introduction
In early March 2020, I was in the hills above Los Angeles – getting a suntan,
trying to get my second feature film off the ground and training for my fourth
marathon. The weather was delightful, my legs were strong, and I was
confident of hitting my two hours fifty minutes target in the London
Marathon the following month. The only problem was that somewhere in
central China a pangolin had partied too hard with a bat, and now a pandemic
was brewing.fn1 The world – and my life – was about to change
immeasurably.
I flew back to London on 6 March, and less than a week later had my first
symptom – a peculiar nausea. The following day, chills and stomach upset.
All the colleagues I’d shared a meeting room with a few days prior were ill
too. There were no tests, so no one could be sure, but Covid was exploding
across London.
My initial illness wasn’t too severe. I was able to work a few hours a day
and felt foolishly and quietly smug that my immune system was obviously
better than my colleagues’, who were feverish, coughing and having a
general shocker. The London Marathon now looked like it was going to be
cancelled, but I was so keen not to lose my hard-won fitness that in the
second week of the illness I tried going for short jogs.
By this point my colleagues were recovering. I was confident that in a few
days I’d be right as rain too. After all, the government was saying that if you
didn’t end up in hospital, then your isolation could end after a week, by
which point you’d be fit to go back to work.
Only I didn’t get better. I kept running – going slowly, telling myself that it
was only a matter of time – but the weeks went past and still I felt awful. And
then, five weeks in, I felt it: a very specific ‘grizzly’ feeling in my throat and
chest that I’d not experienced for twenty-two years. That feeling was the
signature symptom of post-viral fatigue syndrome (PVFS), which I

experienced for a year after being ill with glandular fever. Oh God no, I
thought, I can’t be doing that for another whole year. Not now.
So, I decided to make a film for my nascent YouTube channel to examine
the potential links between the novel coronavirus and PVFS. Could it be
possible that swathes of people would be struck down with a complex, poorly
understood and often completely debilitating condition, even after a mild
initial Covid infection? I wasn’t sure if anyone would find their way to the
film (especially given my paltry subscriber base at the time), but it gained an
audience in the tens of thousands immediately – people all around the world,
who were crying out for someone to recognise what was happening to them.
I thought I’d make only one film on the subject. But then I made another.
And why not one more? It’ll be a trilogy, I thought. And now here I am, more
than two years and eighty films later. Still not back to where I was at in Los
Angeles, running 20km at race pace every day, but able to live a busy life
without relapsing every week as I did in the beginning.
The vast improvement in my quality of life has been due in large part to
making myself Guinea Pig No. 1, incorporating every piece of expert advice
and research accumulated on my journey into my own life to aid my
recovery. Having made a lot of progress, my goal now is to share the lessons
that I, and other recovered long haulers, have learnt – often the hard way.
I couldn’t be more pleased to be collaborating on this project with
Professor Danny Altmann, one of the UK’s most respected immunologists
and an expert on post-viral conditions to boot. Since early in the pandemic,
he has been prepared to put his head above the parapet and speak on behalf of
patients struggling to get recognition from the medical establishment. Danny
is also running a large research project at Imperial College London that is
investigating the role of immune system abnormalities and autoimmunity
(which describes when our immune system attacks our own cells) in Long
Covid, and so is at the very forefront of biomedical understanding of the
illness.
Between us, we hope to present a spectrum of the knowledge that exists at
the time of writing – from the anecdotal experiences that I have observed in
the Long Covid community through to my own patient-led studies and the
hard science that’s accumulating as more research, trials and publications
reach the light of day.
Perhaps you’re a Long Covid sufferer yourself, or a family member or
partner of someone who is. Or perhaps you’re a clinician seeing patients and

looking for a resource that brings everything we know about Long Covid
together. This is that resource. Danny and I have tried to make the
knowledge, lessons and science herein as accessible as possible, because if
anyone knows how difficult it is to absorb information with brain fog, it’s
someone with Long Covid.
We will break down the key topics into short chapters. Rather than present
you with a solid wall of text, I will be your narrator, while Danny will break
down the knotty and established science relevant to each topic in separate
‘boxout’ sections, like that below. At the end of most chapters, there is a
quick Q&A with Danny and other key contributors, picking up some of the
outstanding questions.
Like Gez, my introduction to the world of Covid also came in March
2020, when my research team opted to pivot from our ‘day jobs’
investigating infection and immunity to efforts at decoding immunity to
severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the
virus that causes Covid. More than two years in, we have all become so
expert in the topic that it’s hard to think back to that time of a virtually
blank canvas. Although I’ve spent my life researching the molecular
immunology of pathways (i.e. how the body’s immune system responds
to infection) in a wide variety of bacterial, viral, fungal and autoimmune
diseases, here was a new disease about which we knew nothing. Since
that period, we’ve worked on Covid immunity pretty much seven days a
week, publishing our findings in journals such as The Lancet, Science and
Nature. Within a few months, one of my oldest friends who’d been
infected early in that first wave gave me a detailed and accurate
description of what was to become known as Long Covid. Previously an
extremely busy, active person, she felt she’d had the wind knocked out of
her, could barely walk around the block and felt constantly fatigued. This
was vaguely familiar and alarming.
One of the flagship ‘day-job’ projects we’d had to suspend was a
collaboration across clinical sites in Brazil, which aimed to establish why
so many patients infected with the mosquito-borne chikungunya virus go
on to develop a chronic, disabling illness that can drag on for years. One
of our next papers, published in the British Medical Journal, was a kind
of manifesto for the route forward to understand Long Covid. I’d always
been quite motivated about the need to communicate about research with

the public, press and policymakers. This communication began to seem
really critical in a time of uncertainty and panic. No one wants to come
across as a smart alec or mansplainer, but here was a situation in which
you couldn’t turn on the TV or radio without a politician expounding on
‘antibodies’ or ‘herd immunity’, topics that I’d lived and breathed from
the first day of my PhD studies at the age of twenty-one. My diary began
to fill up with daily sessions with journalists, TV crews, politicians and
patient groups. During one of these sessions, I met Gez making one of his
films. We’ve kept in close touch ever since, often exchanging news of the
latest research findings. The Long Covid story is remarkable in the sense
that the medical agenda has been driven entirely by patients themselves
and their communication across social media platforms. I’ve met terrific,
medically articulate people through those groups and acquired from them
a crash course in living with this disease that now informs all our
research. With that in mind, my aspiration here is to do right by people
with Long Covid in trying to offer an honest and accessible distillate of
all I’ve learnt and anything that could be helpful. The price I pay for this
is that, while Gez’s narrative will often come across as dramatic and
exciting, I’m cast in the role of ‘Professor Boring’, as the voice of the
medical establishment. It’s a role I’m content to take if it offers useful
illumination.
It will be self-evident from this book that Long Covid research is in its
embryonic stage, sitting at an interface between the patient advocates and
the medical research professionals. In that context it’s hopefully useful
that this book has two distinct voices from those different perspectives.
The two views can inevitably become polarised at times. Gez has his role
in drawing together the lived experience of the sufferers including their
search for therapeutic answers. It is this clamour for answers that will in
time wend its way into formal research studies. My career has drummed
into me the paramount need to ignore anecdotes in favour of a laser-focus
on the statistically-powered, controlled trial. That is, when hearing about
‘evidence’ in Long Covid, I set the bar in exactly the same place as if I
were asked to peer review it for Nature or The Lancet. This means that
sometimes Gez and I will not agree. I don’t endorse every statement he
makes, and vice versa. Long Covid has yet to achieve consensus so we
see this breadth as a plus. It also means that my formality may sometimes
annoy you – you may find that the hypothesis or treatment that seems

most central to your view has received short shrift from me because it
hasn’t yet crossed that bar. Who knows, with time (and data) you may
have the last laugh.
So, without further ado, let’s begin.

CHAPTER 1
What Is Long Covid?
One of the hardest parts of trying to describe Long Covid is that it may be
very different for you from how it is for me. But for almost all of us who
experience it – long haulers, as we are sometimes known – the illness impairs
almost every aspect of day-to-day life. Most long haulers are unable to
socialise or work as they could before, they are most certainly unable to
exercise as they could before and often they are even unable to eat and drink
as they could before.
Other than some bags under the eyes, you might look pretty normal. Those
around you – unless they’ve experienced chronic illness themselves – may
struggle to understand what you’re going through. Although perhaps that’s
not surprising: Long Covid comes with a bewildering array of symptoms –
203 of them, according to a patient-led study published by The Lancet
Group.1 Of course, no one experiences all 203 of these symptoms. The
Covid lottery is something of an (un) lucky dip. Long Covid can encompass a
single symptom such as anosmia, through to the more common cluster of
multiple (usually around 5–20) symptoms. The term is also applicable to
someone with a known complication after Covid-19, such as a stroke or
severe lung damage. This book won’t take a dogmatic stance on the duration
of persistent symptoms that count as a Long Covid case – both 4 weeks or 12
weeks from start of infection have been applied. Since many do improve
significantly from 4–12 weeks, the latter cut-off is useful for demarcating
those set on more of a ‘long-hauler’ trajectory.
What is Long Covid in a single sentence?

Long Covid is a long-term consequence of SARS-CoV-2 infection,
lasting beyond the initial ‘acute’ phase of infection, affecting multiple
bodily organs and systems, causing a huge variety of symptoms and of
varying severity and duration, potentially relapsing and remitting over
time.
Crucially, long haulers’ symptoms are not likely to be consistent. They vary
from week to week, day to day, even minute to minute. Day-to-day tasks and
planning even as far ahead as tomorrow are difficult when you have no idea
how you’ll be feeling at any point in the future.
Long Covid is debilitating by nature. People who haven’t experienced
fatigue, the most common symptom of Long Covid, often imagine it to be
close to the feeling of tiredness after heavy exercise or an extremely long day.
Before the pandemic hit, if you’d asked me, I would have said I knew what
spending every last drop of energy felt like too, as someone who’d run
several marathons and ran my own business, frequently putting in
consecutive all-nighters.
But the systemic exhaustion that Long Covid deals up is on an entirely
different level – perhaps only familiar to those with severe chronic illnesses,
such as myalgic encephalomyelitis, also known as chronic fatigue syndrome
(ME/CFS). This exhaustion really needs a new word to describe it, because
‘fatigue’ doesn’t do it justice. In my patient-led research, this ‘fatigue’ is
repeatedly cited as the most crippling symptom for long haulers across the
board. Fatigue is exhaustion down to your very bones. Even simple activities
like reading or watching TV are too much, let alone the absurd idea of being
able to hold a conversation.
One American study compared 1,295 Covid long haulers with 2,395
patients with cancer, and in the process found that the long haulers were
roughly twice as likely to self-report poor physical health or pain as those
with cancer.2 Of course, while fatigue might be the most frequently reported,
there’s over 200 other symptoms which, on any given day, might knock you
for six.
The symptoms

Without making an exhaustive list of all 203 symptoms, here are some of the
most common:
fatigue
brain fog (aka cognitive dysfunction)
chest pain or tightness
insomnia
heart palpitations
dizziness
joint pain
depression and anxiety
tinnitus and earaches
nausea, diarrhoea and stomach aches
headaches
skin problems (peeling, rashes, itching)
continued loss of taste and smell.
But there’s no end of unusual stuff being reported by long haulers, from the
profoundly disabling to the merely ‘upsetting’, such as:
hair loss
tingling and numbness
nerve pain
menstrual changes
erectile dysfunction
urinary incontinence
blurred vision
hallucinations.
If you’ve got more than one of these symptoms (for the first time) and have
recently had Covid, then it’s possible you’re suffering from Long Covid. As
you may have gathered, there’s very little correlation between the symptoms
you might have experienced in your acute infection and those you could
experience in Long Covid, which can present in almost any system of the
body.
And, in the UK at least, where so many people did not have access to
Covid tests early in the pandemic, clinicians can now diagnose the condition
without needing evidence of infection – or, for that matter, a diagnostic test.

Because, at the time of writing, a reliable, easily accessible test that proves
you have Long Covid does not exist.
Historically this absence of ‘testability’ has contributed to poor
understanding of post-viral conditions. It’s simply too easy to write off the
symptoms as stress, anxiety or burnout, which has happened to innumerable
people with ME/CFS and Lyme disease for decades.
Long-term effects of Covid-193

From a clinical and academic perspective, what’s different or
interesting about Long Covid?
Modern medicine is meant to be about preventing painful and debilitating
disease. We’re grappling with a new virus which, depending on which
estimates you use, has caused at least 5 million deaths so far. The World
Health Organization recently upped the estimated global death toll to 15
million in May 2022.
Yet in medicine, we don’t just count deaths, we count symptoms and
quality of life. So, there’s actually a much larger number of people who
are affected in the long term by a chronic disease that impairs their life on
a day-to-day basis – whether it’s their ability to function normally, work
normally or even get out of bed in the morning.
You can’t easily quantify it, and it is often assigned less importance
than death, but the point I’ve often made is: let’s just suppose that in an
ideal world our vaccines work so well that we cease to worry about
intensive care units (ICUs) being overrun and a daily death toll. We
might still be talking about this pandemic in terms of the Long Covid
impact for years to come, long after we’re worrying about trying to deal
with the acute disease.
What’s particularly challenging is that, as we learn more and more, it’s
impossible for any one doctor or clinician to understand absolutely
everything about modern medicine. It takes a lifetime just to get your head
round everything we know about the immune system, for example.
So, we get increasing degrees of specialisation, and knowledge gets siloed.
You have specialists for each organ system or different parts of physiology.
But the problem with Long Covid is that it doesn’t, in most cases, neatly fall
into one or two of those silos. It seems to involve all of them, and thus is
outside the remit of any one conventional specialist.
More to the point, Long Covid defies easy testing. Recent research has
suggested that low cortisol levels (a hormone responsible for regulating stress
response and suppressing inflammation) may be implicated in Long Covid
and could at some stage form part of a diagnostic test, but there is yet to be
widespread agreement on markers that indicate severity or what might be
going on. It’s even possible that a single diagnostic test might not ever be
developed for such a heterogeneous disorder.4 Solving the question of what
Long Covid actually is seems to me to need a helicopter view at the same

time as a deep dive. How in the current system do you do both
simultaneously?
What’s the solution to this need for both a deep and broad
understanding of Long Covid, given the constraints of the current
medical system?
It’s unbelievably challenging. One of the things that happens is that, in
any professional specialty, we always think that we’re better, more
knowledgeable and better trained than the previous generation, and also
that ‘the youngsters don’t know what they’re talking about’.
The perennial whinge of the older generation is that the young doctors
of today have been so shoddily trained that they barely understand their
own specialty and are terrified of seeing anybody outside it. But, to
understand complex diseases, you do need to understand the whole
person and you need an excellent command of general internal medicine.
I often compare Long Covid to lupus. Let’s say you’re a doctor sitting
in your clinic and the medical textbook chapter on lupus had never been
written. A patient walks in – let’s say it’s a young woman who doesn’t
know what to do because she’s got a skin rash. Maybe if you were clever
or empathetic you’d refer her to a dermatologist and you’d think, Wow,
that was a bit tedious.
Then she comes back three months later for a repeat appointment. Her
rash has cleared up, but she has incredible respiratory problems and tells
you that she can’t walk up hills any more. You think, Last time she said it
was her skin, this time she says it’s her lungs. Is she attention-seeking?
What’s going on with her? So perhaps you refer her to a respiratory team.
Three months later she turns up again and says she’s having trouble
walking because her joints are really playing up. Now you’re perhaps
wondering if this could be psychosomatic, but you refer her to a
rheumatologist.
Perhaps you can see where I’m heading with this. You might assume
that the woman was an attention-seeker unless you understood lupus and
the fact that there’s a common mechanism underlying all the symptoms
she had. And, of course, this person wasn’t making it up. She had a bona-
fide autoimmune disease called systemic lupus erythematosus, which
merits a multi-system, multi-organ, multi-specialty treatment approach.

So, at the end of my laboured metaphor, I think that’s where we are
with Long Covid. People have diverse symptoms that are remitting and
relapsing, coming and going. Some people are being empathetic, whereas
others are thinking, Are they making it up? because we haven’t yet
written the textbook chapter on Long Covid. While there’s still a long
way to go, I’d like to think we’re making progress and that perhaps this
book can help fill some of the knowledge gaps.
Scientists and clinicians are using fancy, high-tech tool kits to figure
out how Long Covid works at a functional, cellular level. In the end, the
devil is in the detail, and we’re quite good at measuring detail. I’m
optimistic that it won’t take too long until we understand Long Covid as
well as – or maybe even better than – we understand lupus.
No matter how tired, exhausted and sick you may feel right now, or how hard
it is to get through paragraph after paragraph, Danny’s optimism is merited,
despite what people with other post-viral conditions have experienced for the
past twenty or thirty years. More on the reasons for that optimism a little
later. But right now, let’s stay on topic. That was symptoms. Now let’s
address phenotypes.
The phenotypes
Some questions to get us going. If you look at everyone with Long Covid, is
there a pattern around the grouping of symptoms? For example, why might
you have joint pain and shortness of breath, while I have headaches and
palpitations?
Are there lots of people who have these same combinations of symptoms,
and if so, what could that tell us about how the disease works? Is it possible
that understanding these groupings and what causes them could help people
avoid Long Covid altogether? It is these groupings of symptoms that we call
phenotypes – literally, how the disease process looks.
These are huge, important questions that medicine hasn’t quite answered
yet. But research is ongoing that might shine some light on the answers.
How easily can we demonstrate phenotypes of symptoms for Long
Covid?

I think the jury is still out, simply because you can look at it in so many
different ways.
In medicine we tend break it down into the ‘lumpers’, who are
attempting to understand the whole of this disease, and the ‘splitters’,
who slice the disease into an infinite number of thin little slices.
Until you’ve got a clear picture of the disease mechanism (i.e. how
exactly the disease produces symptoms on a physiological level), trying
to delineate phenotypes is always a bit like putting the cart before the
horse. You say to yourself, ‘I’ve got to simplify my question, so I’m
going to look only at patients who report mainly respiratory symptoms –
the people who can’t have any kind of exertion and permanently feel
breathless.’
And it then might be useful to say, ‘Let’s look at the respiratory folk
who are predominantly experiencing breathlessness compared to the
neuro folk who are predominantly troubled by brain fog and word-finding
problems.’ I have a feeling that if I tried to do that, I might be bombed
out of the water by people saying, ‘Well, I’m both’ or ‘I’m respiratory but
the respiratory symptoms only came after my joint and skin problems.’
It might turn out that my categories are a load of nonsense, because
you can’t get the answer until you’ve got the answer.
Some of the large research projects to date5 , 6 have clustered Covid long
haulers into the following groups based on the severity of the initial infection:
mild disease, not hospitalised
hospitalised
admitted to ICU.
But when it comes to understanding the disease, these groupings can only
take us so far. For one, the vast majority of long haulers out there fall into the
first category. Furthermore, those in the third category – people who were
admitted to the ICU – are more likely to be experiencing the effects of organ
damage than the potentially more diverse drivers of Long Covid in others. So
ultimately we will need a finer level of categorisation by symptom clusters to
determine mechanism and then develop effective, ideally individualised
treatments.
This finer categorisation is coming, with recent research (using huge
volumes of data from the ZOE app) suggesting certain symptom clusters.7

However, based on what I’ve observed in more than two years embedded in
the community and from surveying thousands of long haulers in my own
patient-led research, I would like to propose some phenotypes which might
help us when it comes to treating and managing symptoms. If we break down
the first category of ‘mild disease, not hospitalised’ in terms of symptoms, I
would argue three main groupings have emerged:
increased intolerance to foods, allergies, headaches, skin issues,
breathing problems and gut issues
brain fog, fatigue, post-exertional malaise (i.e. a worsening of symptoms
after physical, mental or emotional activity, commonly known as PEM)
and cognitive exhaustion
increased heart rate (palpitations), nausea, dizziness (especially on
standing), insomnia, anxiety, chest pain, vision problems and irregular
temperature regulation.
Now, you might have symptoms from all three groups! That isn’t uncommon
at all. But what seems to be the case is that long haulers’ conditions are
predominantly led by one group of symptoms, which respond particularly to
one set of triggers – or indeed treatment. The symptoms in the first grouping,
for example, might be related to mast cell activation.
What is mast cell activation syndrome?
Mast cells are a type of immune cell found all over the body. Some
investigators suggest that some Long Covid symptoms might be related
to what is known as mast cell activation syndrome (MCAS). The limits of
symptoms that could have an MCAS-like origin is a source of
controversy among allergy/immunology/dermatology experts. For
example, many lung problems following Covid-19 have other known or
likely mechanisms other than MCAS. In MCAS, mast cells are
hyperactivated, which leads to excessive release of histamine. In Long
Covid, this histamine potentially operates via the same immune pathways
that are up-regulated in people with conditions such as asthma, eczema
and food and dust allergies to cause some of the symptoms discussed
above.
If you’ve ever experienced allergies (such as hay fever) before, or have had
eczema or asthma, then the chances of your Long Covid experience being

influenced by something related to MCAS may be high.8 The symptoms
mentioned are by no means exclusive – MCAS can present in many different
ways, from disrupted gut function to aching joints, skin problems and
shortness of breath.
The second group of symptoms might be related to metabolic dysfunction.
In simple terms this means that the chemistry that produces energy in your
body’s cells has been affected. One of the most interesting theories proposed
so far suggests that this metabolic dysfunction might be due to a deficiency of
nicotinamide adenine dinucleotide (NAD+).9 , 10 NAD+ is a co-enzyme
that’s critical in the creation of adenosine triphosphate (ATP), which powers
just about all our cellular function, and neural, muscle or other tissue.
A deficiency of NAD+ leads our body to use alternative metabolic
pathways that are less efficient, leading to the symptoms mentioned in the
second grouping (again, this list is most definitely not exclusive!).
The third group is perhaps the most common symptom cluster in Long
Covid: symptoms potentially related to dysautonomia and postural orthostatic
tachycardia syndrome (PoTS). Dysautonomia can be thought of as
malfunctioning of the autonomic nervous system, which is normally
responsible for the regulation of bodily functions such as heart rate, digestion,
breathing, balance, temperature, blood pressure and more.
PoTS is defined as an increase in your heart rate by thirty beats per minute
or more when you sit or stand up. It is related to dysautonomia and very
common in long haulers.11 It might not sound like much on paper, but it can
be incredibly disabling, leaving people bedbound and able to move only short
distances. Climbing a flight of stairs can feel like attempting to summit
Everest for some people with PoTS.
Many long haulers report a combination that resembles mast cell
activation, metabolic dysfunction and autonomic dysfunction in greater or
lesser proportions. Each of the conditions has different treatment and
management strategies, and how well you respond to those treatments could
suggest what your personal balance of them might be.
We will discuss why you might have your particular blend of symptoms in
the next chapter. If you’re desperate to jump ahead to those treatment or
management strategies, then you’ll be wanting chapters 9 and 10. I wouldn’t
blame you!
How can people ‘prove’ that they have Long Covid?

Sadly, we’re now in a phase when improved clarity on the definition of
Long Covid is becoming ever more critical. The premise throughout
much of this book has been that no unequivocal diagnostic criteria exist,
and that in many regards they are superfluous, as long haulers are in little
doubt about their changed health status following SARS-CoV-2 infection.
Medical professionals with an interest in Long Covid are well aware of
the urgency and continue to work hard to define and refine a consensus
working definition.12
However, we are hurtling into a brave new world in which
interpretation of Long Covid diagnostic criteria will become the stuff of
daily disputes at employment tribunals and disability benefit assessments,
as well as being questioned by pension providers and health insurers.
This is in addition to the more basic requirement to clearly define cases
for healthcare referrals into treatment pathways and for healthcare
budgeting purposes. Clear diagnostic definitions will also be crucial for
defining entry and stratification in clinical trials.
For my taste, notwithstanding many plausible academic articles and
their press releases that have passed across my laptop claiming to fill this
need for a diagnostic test, we are simply not there yet. It is possible to
have full-blown, bona-fide Long Covid either with or without PCR proof
of infection, or evidence of detectable antiviral antibodies. According to
WHO criteria, the requirement is a clinical picture compatible with
having had Covid-19. Only a small minority of people infected with
SARS-CoV-2 have undergone any type of imaging or scans. However,
enough data has already been gathered to be sure that it is possible to
have persistent Long Covid symptoms without having any visible end-
organ damage seen on routine imaging. Conversely, it’s possible to have
organ changes visible in scans but to have no persistent symptoms.13 , 14
As researchers race to identify reliable biomarkers to be the basis for a
consensus laboratory test for Long Covid, we need an interim,
internationally agreed working definition. Until we can do better, a
working definition can be accrued from comparison with health status
before infection, evidence in support of having had Covid, and then
evidence of newly persistent symptoms from the Long Covid list. At the
other end of the process, we also need much more clarity on reporting of
symptom changes to facilitate analysis of clinical trial outcomes.

GEZ: How similar is Long Covid to other long viral conditions, such as long
chikungunya or PVFS (post-viral fatigue syndrome) after glandular fever or
other viruses?
DANNY: It’s another unwritten medical textbook chapter. I can’t think of any
book I’ve ever seen written on post-viral syndromes, or any medical school
lectures that have ever been given on the topic because it hasn’t been a thing.
I might try to pull it all together and write something about it soon, because
I’m someone who really likes infectious disease and also really likes
autoimmunity. I’ve previously looked at chikungunya virus and
autoimmunity, Ebola virus and autoimmunity, herpesviruses and
autoimmunity – and now at Covid and autoimmunity.
It’s really hard to pull together any common denominators, but the
simplest place to start is to ask: ‘What is autoimmunity?’ Autoimmunity is
the breakdown of immunological tolerance so that the immune system does
something that it’s not meant to do, which is to start recognising and
responding to your own tissues, your own proteins.
There is a whole branch of medicine dedicated to post-infectious
autoimmunity, so most doctors would recognise the existence of reactive
arthritis, for example: this is the idea that you could have salmonella food
poisoning and then come down with joint disease.
So, at least we’ve got a starting point of being able to link an infection to
an autoimmune consequence. But when it comes to commonalities between
long viral conditions after Ebola, chikungunya, glandular fever and Covid,
we just don’t know enough yet.
GEZ: The closest other viral infection we’ve got to compare Covid with is
severe acute respiratory syndrome (SARS), which was caused by a similar
coronavirus. Are there any academic papers out there on the long-term
consequences of that?
DANNY: Yes, a few, and we need to dig them up. But unfortunately, with the
benefit of hindsight, it’s clear that for both SARS and Middle East respiratory
syndrome (MERS) we should have done the homework and the follow-up so
much better.
With SARS and MERS, the acute emergency came and went and was dealt
with. So many of the questions that should have been addressed afterwards

haven’t been. But there’s a small number of quite decent papers on the long-
term consequences of SARS that look very much like what we’re talking
about here.15 So, that’s a big deal: an almost identical virus and almost
identical consequences.
GEZ: How easy is it to track down the patients who were reviewed in those
initial follow-up studies one to three years after having SARS?16 Seeing how
they did subsequently would almost be like seeing into the future for those
with Long Covid now.
DANNY: There absolutely was a persistent, long-Covid-like syndrome after
SARS and MERS. There was no funding and no pressure to look at it. It’s
only with hindsight that people are looking at it now. The best hope is
probably the cohort in Singapore, who have undergone quite a lot of
immunological testing, as well as the healthcare workers who were infected
in Toronto. To some extent, those people are indeed our crystal ball into the
future for Long Covid. I recently managed to make contact with one of the
consultants who treated the Toronto patients during the 2002–04 outbreak
there and followed them up for many years. The outlook he described was
rather discouraging. There’s quite a large caveat, which is that this isn’t really
a like-for-like comparison with the global Long Covid caseload. All the
consultant’s patients were hospitalised with their initial infections and so their
chronic symptoms developed from a baseline with an element of post-
traumatic stress disorder.
Summary
Long Covid is a very long way from some people’s perception of it as ‘being
a bit out of sorts’. The condition can’t be easily categorised and can be
extremely severe, impacting on people’s quality of life in multiple, highly
debilitating ways. Long Covid can vary from hour to hour, day to day and
week to week, and new symptoms can appear months into the experience.
For most people, it will be an illness unlike any other they’ve ever had, which
raises the question you’ve been thinking about for months: why me?

CHAPTER 2
Who Gets Long Covid and Why?
If you’ve been dealing with Long Covid, whether for months or years, at
some point you’ve probably thought, why me? We’ve all looked at the people
who got Covid at the same time and wondered why they bounced back to full
health in a week or two, when we didn’t. What’s different about us?
This is actually a very profound question, and a comprehensive answer
would likely reveal the full pathology underpinning the condition.
Unfortunately, we’re not quite able to fully answer it yet, but we’re starting to
see studies published in high-profile journals like Nature Communications
and Cell that identify certain risk factors for developing Long Covid.1 , 2
Who is more likely to get Long Covid?
Several studies have looked at large cohorts of thousands or hundreds of
thousands of acute cases of Covid (the initial week or two of infection,
from which most people recover) to see which individuals went on to
develop Long Covid.3 –5 The following characteristics emerged as being
statistically associated with an increased risk of Long Covid:
hospitalisation during acute infection (and particularly admission to
the ICU)
high number of symptoms during acute infection
female sex
higher-than-average body-mass index (BMI)
asthma
poorer baseline health (indicated by a high number of other pre-
existing conditions).

These associations were based on statistical analysis of a large number of
cases. Thus, there are clearly many people with Long Covid who do not
have any of these risk factors, and may indeed have excellent baseline
health.
One of the challenges with large data samples like these is that there are
frequently distortions due to the nature of data collection in the early days of
the pandemic, when for the most part only people who were hospitalised got
a PCR test (and thus were included in these samples). Many of the ‘mild’
cases in the community in early 2020 (including me) went on to develop
Long Covid without ever having had a positive test. (The quotation marks
around ‘mild’ are necessary – for many of us the experience didn’t feel mild
at all!) Thus, there is a huge community subset (who arguably account for the
majority of people with Long Covid) who do not appear in these statistics.
What we’re looking at then in these figures is perhaps an indication of the
damage done by the virus, as opposed to the disease engine (my term for
describing the ‘things going wrong in the body’ that cause symptoms) of
Long Covid. It seems like these might be two different things. Those who
were hospitalised have organ damage commensurate with the severity of their
acute infection, whereas ‘mild’ acute cases may go on to develop severe
Long Covid without necessarily having any visible organ damage under
magnetic resonance imaging (MRI) investigation. So, the cause of symptoms
in these two groups (i.e. the ‘disease engine’) might be different, yet both
groups might currently be considered to have Long Covid. This is a necessary
distinction that is rarely made in the scientific literature or by the media.
Early published papers on Long Covid tend to focus on the first group (those
who were hospitalised during the initial infection), whereas my patient-led
research tends to reflect the second (‘mild’ acute cases that did not require
hospitalisation).
Why are these risk factors associated with Long Covid?
Looking at the words most frequently mentioned in the abstracts
(summaries) of the research papers published to date,6 –10 the most
common is probably ‘female’. Then you’ll see terms like ‘middle-aged’,
‘asthma’, ‘post-menopause’, ‘EBV reactivation’ and ‘high BMI’. Age
and high BMI are associated with an increased probability of being
hospitalised in the acute phase of Covid infection.

I think we have to be careful about how we group these risk factors,
lest we create more rather than less confusion. High BMI being a risk
factor likely relates to the fact that people with high BMI are more likely
to have been hospitalised with severe Covid. In terms of Long Covid
history and symptoms, we may come to think of the group hospitalised
with severe Covid as quite distinct from the person with Long Covid who
is more likely to be younger, female and to not necessarily have a raised
BMI, or to have been hospitalised. The object of this distinction is not to
infer any judgement about the different groups, but rather to acknowledge
that we may have a way to go in sorting out stratification of Long Covid
‘phenotypes’ (clinical causality and appearance) in a way that will really
be useful for treatment pathways and clinical trials.
However, some elements of these findings make sense in terms of what
we know about the condition at the moment. Long Covid certainly looks
like other conditions characterised by autoimmunity and
immunopathogenesis (diseases that result from some part of an immune
response). Women have a much higher propensity for developing
autoimmune disease – this is true of relatively common autoimmune
diseases like rheumatoid arthritis or lupus, for example. One of the
reasons for this is that the immune system interacts strongly with the
endocrine system (which governs your hormones). The key difference
between sexes are the endocrine cascades. All those hormonal differences
you learn about in biology class don’t just affect secondary sexual
characteristics (armpit hair and breasts in women, beards and deep voices
in men, for example), they also feed into many of the nuances of immune
programming. It is fair to say that this seems to lead to differences in
immune regulation between sexes, and women tend to have more
‘activatable’ immune systems.
Asthma seems to be a genuine risk factor for Long Covid. Let’s go
back a step to explain why. Much work over recent years has been
devoted to defining the genetics and immune programming that
predisposes someone to asthma. People who have asthma walk around for
their whole lives with what could be called skewed immune
programming at one end of the allergic (sometimes called ‘atopic’)
spectrum – such that their immune system overreacts to certain triggers.
By describing people at one end of this ‘allergic spectrum’, we simply
mean the ones who may be generally more prone to the type of immunity

that can underpin anything from pollen or animal-fur allergies, to food
allergies and eczema. One theory to explain why people have such
immune programming is the so-called hygiene hypothesis, which argues
that our immune systems evolved over the millennia to deal with a
particular kind of pathogen and parasite load – particularly in the gut.
This type of immunity is generically called ‘Th2 immunity’. It’s a rather
aggressive form of immunity, useful if you need to be able to expel a
tapeworm from your gut.
Nowadays, though, most people in high-income countries don’t have
any parasite load at all. So, we’re walking around with a completely
inappropriate immune program that’s ready to be pushed over into
inappropriate Th2 responses. This is what causes what are known as
‘atopic’ diseases like asthma, eczema and hay fever, which affect around
20% of the population in Western countries. Several studies now suggest
that people with atopic conditions are more likely to get Long
Covid.11 –13
Finally let’s talk about Epstein-Barr virus (EBV), which, during acute
infection, is also known as infectious mononucleosis or glandular fever.
EBV is a herpesvirus that normally sits latent in the blood cells of people
who have been infected with it – think of it as hibernation. One of the key
findings in the Cell paper was that the presence of reactivated EBV in the
bloodstream during the acute Covid episode predicted an increased
likelihood of developing Long Covid. The finding that EBV reactivation
could play a role in Long Covid is exciting to me because scientists have
spent decades talking about latent EBV reactivation and what it means. It
has been hypothesised to be implicated in various autoimmune diseases,
and the publication of this paper in Cell coincided almost to the week
with the most impressive paper that’s ever been published on the subject
(in Science, another high-profile journal). The Science paper reported the
results of a huge study of EBV, which suggested that the virus plays a
role in causing multiple sclerosis (MS).14 This link has been debated for
several decades.
EBV is a very different kind of virus from SARS-CoV-2. Most of us
get it at an early age. As mentioned above, in most people it then sits
dormant inside a particular type of white blood cells called B
lymphocytes (the cells that make antibodies). Most people will be
positive for EBV and not know it, but you’ll also have heard the

stereotypical story of the teenager who goes off to university, discovers
snogging for the first time and then comes down with debilitating
glandular fever. In those cases, the patients’ immune systems are
disrupted, and they can’t function normally for up to a year or more –
finding it hard to study, let alone party, and becoming prone to every
passing bug and sniffle.
There are some real similarities with Long Covid. You can have a very
mild acute phase or a highly symptomatic one, but either way it can have
real long-term consequences. Trying to figure out why and when EBV
causes symptoms can feel a bit like watching arthouse cinema: you spend
a lot of time asking, ‘Why did that happen then!?’ It comes and goes
variably in different people with very different amounts of virus in their
system.
The discovery of the links between EBV and both MS (with an
extremely high probability) and Long Covid gives us a great starting
point to dive in deeper with future research.
One of the other findings of the Cell paper was that patients who had a high
viral load in the acute phase of their Covid infection were more likely to
develop Long Covid. While perhaps this isn’t surprising – it might even seem
logical – it could also explain the huge number of long haulers who were
‘created’ in the first wave in February–March 2020. In Western countries,
there were no mitigation measures for controlling the spread of disease at the
time – no social distancing, no face masks, no indoor ventilation and no
vaccines. Thus, the initial viral dose causing infection in many cases might
have been huge.
Further exploration of viral loads could perhaps offer some clues about the
various disease mechanisms implicated in Long Covid. Since SARS-CoV-2
is a virus that damages and kills infected cells in target organs such as the
lungs, heart and brain, leaving a trail of scarred tissue and inflammation in its
wake, a simple explanation would be that people with more virus in their
system for longer might be more likely to develop Long Covid. But in fact
this explanation points more towards the organ damage ‘disease engine’ that
we see in hospitalised cohorts, who often have a different presentation of
symptoms from those ‘mild’ cases in the community I mentioned earlier.
Long Covid clearly cannot be simply correlated just with how much virus

was around, as some of the most severe cases of Long Covid occur in people
who had mild or even asymptomatic acute episodes.
The Cell paper also suggested that the presence of certain autoantibodies
(antibodies that mistakenly attack the body’s own cells) was correlated with
the likelihood of developing Long Covid. But before we discuss this, it would
be helpful to take a closer look at what autoimmunity actually is.
What is autoimmunity?
What gets immunologists out of bed in the morning is the grand question:
‘What’s the immune system all about?’
The immune system recognises things that shouldn’t be inside your
body or that suggest that something dangerous is going on in your body.
When this happens, the immune system activates enormous – and
potentially damaging – inflammatory pathways via T cells and B cells
(types of white blood cell that fight pathogens), so that you can get rid of
the stuff that shouldn’t be there. These pathogens might be worms,
viruses, fungi, tumours or bacteria. As humanity evolved, our bodies
didn’t necessarily pre-emptively produce receptors that could specifically
recognise Ebola virus, for example. Rather, they produced millions of
receptors, with the hope that at least one of them would recognise the
virus. That’s how the immune system has always worked, in every
organism on the planet.
The catch is that the immune system identifies potential threats by their
shape, which can be quite similar to the shapes of proteins and chemicals
that our own bodies produce. As a result, sometimes our bodies confuse
these naturally occurring chemicals with threats, which produces an
immune response against ourselves. Immunologists refer to our immune
system’s ability to recognise our own bodies and not attack them as self-
tolerance. When the immune system does get confused, there are lots of
fail-safe mechanisms in place to delete autoimmune repertoires, whether
B cells or T cells, so that most of the time, most of us don’t develop
autoimmune diseases.
But sometimes errors of self-tolerance can occur, and your immune
system recognises bits of your own body as if they were something
dangerous and produces an inflammatory-damaging response to them. In
many diseases, the result is that autoimmune antibodies attack parts of
your own body, such as in lupus, thyroiditis, rheumatoid arthritis (to

some extent), myasthenia gravis and various forms of nephritis and
kidney disease. In extreme instances such autoimmune diseases can result
in organ damage and death.
Patient-led research
The papers published to date provide clues about what might be going on
physiologically in Long Covid and open up avenues for future research, but
in my experience they don’t necessarily reflect what the community sees
around them in terms of who is unlucky enough to suffer.
SEX DISTRIBUTION
Published studies with huge datasets have shown women are more frequently
affected by Long Covid than men.15 , 16 And indeed, one of the most obvious
correlations between the data from my patient-led studies and the published
data is this finding. In my various studies, women have accounted for
anywhere between 70 and 86% of the patient group.
As with any data sample, there are some caveats to bear in mind in terms
of how selection bias can affect the data collected. The recruitment for my
studies happened largely on social media platforms, including Facebook,
Twitter and Slack. Most respondents came from a selection of international
Long Covid support groups on Facebook. There is likely to be a bias in terms
of the sociocultural demographic that uses these groups and these platforms,
and this bias will have an effect on the reliability of the data. For some of the
data collected, this bias is likely to be relevant; for other data it might be
much less important. With regards to the finding that more women than men
are affected by Long Covid, it is possible that women are more likely to use
the online support groups and to take part in research like mine. Therefore,
the actual proportion of women affected (relative to men) could be lower than
my data suggests. However, pretty much all the data that has been published
suggests a similar sex breakdown in the patient population, so I don’t think
the bias is too great. The lower bound of my data (i.e. 70% women, 30%
men) seems to reflect the patient group as a whole, no matter the setting.
ACTIVITY LEVEL

Unlike some of the clinical studies, which at the larger end of the spectrum
have included only a few hundred patients (the study of the data provided by
the ZOE app is a notable exception17 ), the sample size of my groups was
also larger – often between 1,500 and 2,000 respondents. My feeling is that
this data is a better representation of Long Covid in the community than was
often seen in the early clinical studies, when often only patients who had
been hospitalised during their initial Covid infection were recruited to
participate. In chapter 5 we’ll address why these mechanisms of Long Covid
might be different.
But back to the activity level. In the first of my large studies, which had
1,859 participants, I found that two-thirds of people with Long Covid were
previously highly active (exercising vigorously at least three times a
week).18 This is a slightly higher proportion than found in the general
population. Only 3.8% of participants were not physically active. So, we
were looking at a fit slice of the population who were being affected by Long
Covid – not necessarily the same demographic who were at risk of severe
illness in the acute phase (commonly understood to be people who were of
advanced age, had severe underlying conditions or were
immunocompromised).
What’s the link between fatness, fitness and immune function?
You could write a whole book on this topic. There’s an enormous amount
of research on the interface between immunology and metabolic disease.
In people who have large deposits of adipose tissue (fat), this tissue can
become a depot for poorly programmed immune cells, which can be pro-
inflammatory and can predispose people to several metabolic diseases,
notably type 2 diabetes.19
However, being fit is not necessarily good for your immune system
either. People who do a lot of physical training produce corticosteroids,
which can suppress immunity. This is one of the reasons why runners
often get ill the week after a marathon. The relationship between arduous
exercise and susceptibility to infection has been long debated, particularly
in the field of sports medicine. Among elite athletes, infections are a
close second to sports injuries as a contributor to days lost from sport.20
AGE PROFILE

The next most striking finding in my data was the age profile of the long
haulers surveyed. Although almost all age groups were represented, the
thirty-five to forty-four and forty-five to fifty-four categories were three times
more likely to appear among respondents than other ‘ten-year’ age brackets.
This ‘bulge in the middle’ has been replicated in every single one of my
studies to date, no matter which aspect of Long Covid I was researching.
Again, it is possible that selection bias may be playing a role (children, gen Z
and people over seventy use the platforms where I recruited my participants
less frequently) but these findings do seem to reflect cases in the community.
Anecdotally, while older members of society may have managed their risk of
exposure and caught Covid in lower numbers than those in middle age, the
same cannot be said of millennials, university students and children. So,
what’s going on?
How does our immune system change as we age?
Our immune systems change throughout life. Children have large, active
thymuses, the organ that acts as mission control for educating and
directing T cells, one of the key agents of the immune system. As you
grow into adulthood, the thymus shrivels up to almost nothing and puts
out far fewer T cells. Thus, as you get older, you have fewer new T cells
and more ‘exhausted’ T cells, which have gone through lots of cell
divisions and are less functional and more damaged as a result.
Another autoimmune condition that displays the ‘bulge in the middle’
age profile noted in Gez’s Long Covid dataset is new-onset rheumatoid
arthritis. This similarity between the two conditions is extremely
interesting and important.
IMMUNE CONDITIONS
The potential association between autoimmunity, other immune conditions
and Long Covid was suggested relatively early in the pandemic, so I included
a line of relevant questioning in one of my studies in November 2020, to
investigate which conditions – if any – might be risk factors.21
My approach was simple: I measured how many people in my sample were
affected by each autoimmune condition before their Covid infection, and then
compared the prevalence in my sample to that in the general population. If a
higher proportion of people were affected by a disease in my sample, then

that could suggest that the condition was a risk factor for developing Long
Covid and could give us some clues about the disease mechanism
underpinning Long Covid.
The first condition that I looked at was type 1 diabetes, in which the body’s
immune system attacks and destroys the cells in the pancreas that produce
insulin. In the UK, 2.6 million people have diabetes, and about one in ten of
these people have type 1 diabetes. This gives us a prevalence of 0.6% in the
population. (For reference, 62% of the participants in my study were from the
UK, so using UK data for comparisons seemed the most sensible, and
anyway the prevalence of the conditions I was exploring is broadly similar
across Western nations generally.) Of my sample of 824 long haulers, only
three had type 1 diabetes. To save you getting your calculator out, that
equates to 0.4% of the study sample – a similar prevalence as in the general
population. For those of you who are curious types, there were seventeen
people with type 2 diabetes in the sample (in the general population there are
around nine people with type 2 diabetes for every person with type 1). So,
whichever way you spin it, diabetes didn’t seem to be a risk factor for Long
Covid in this study’s population.
The next condition that made sense to investigate was rheumatoid arthritis.
Not to be confused with the more common osteoarthritis, which is caused by
wear and tear of joints, rheumatoid arthritis is an autoimmune condition and
can affect adults at a range of ages. Figures for the frequency of the disease in
the general population are easy to find – the prevalence is 0.44% in men and
1.16% in women.22 It’s interesting to note a similar sex distribution to what
we see in Long Covid. Balanced to the sex distribution of my sample, I
would have expected to see a prevalence of rheumatoid arthritis of around
0.9% if the disease was not associated with the probability of developing
Long Covid. However, 115 people among my sample of 824 had rheumatoid
arthritis – equating to 14%, fifteen times higher than we’d expect if the
disease was not a risk factor for developing Long Covid. Considering
Danny’s comments about the age profile similarity between Long Covid and
rheumatoid arthritis in the last boxout, this link would be one of my top picks
for future research. Are some of the same autoantibodies involved in both
Long Covid and rheumatoid arthritis? If I were a betting man, I’d definitely
have a little flutter on that one.
How about that nefarious triangle of asthma, hay fever and eczema –
known collectively as atopic conditions? As Danny described, these

conditions are largely associated with inappropriate Th2 immune responses
(which are often triggered by various allergens). Data for the proportion of
the UK population that has an atopic condition is hard to come by, but if we
add together figures for the prevalence of the individual diseases, we can
estimate that roughly 30.5% of people have at least one of asthma, hay fever
or eczema. Of course, some people might have two or all three of these
diseases and so will be counted in the data multiple times. Fortunately, I can
use my own data as a model to establish how many people have more than
one of the triumvirate and apply that to the nationwide figure. Looking at
how many people in my cohort have more than one atopic condition (and
assuming this is similar in the general population) would suggest that our
expected atopic percentage of the population is 22.2%.
So, against this expected figure of 22.2%, how many of our 824 long
haulers experienced at least one of asthma, hay fever or eczema prior to their
Covid infection? The answer is 473, or 57.4%. This is a highly striking
difference by any measure. However, we do need to compensate for the fact
that only about 38% of cases of asthma are associated with atopy (i.e. the
remainder of cases are caused by something other than Th2 immunity).23
When we remove people with non-atopic asthma from the sample, the
prevalence of at least one atopic condition falls to 52.8% – still more than
twice the proportion in the general population. This finding tallies with the
previously discussed association between Long Covid and asthma reported in
other studies and gives us plenty to go on, in terms of understanding both the
possible mechanisms of disease and which treatments might be effective.
We’ll address the related topic of MCAS in chapter 5.
POST-VIRAL FATIGUE SYNDROME (PVFS)
The final risk factor I wanted to investigate was previous post-viral fatigue
syndrome (PVFS). If people have already had their socks knocked off for
months or years after other viral infections, might that increase their risk of
developing Long Covid? First let’s consider the levels of PVFS we might
expect to see in the population at large. Between 2001 and 2013, the annual
incidence of PVFS was 12.2 cases per 100,000 people in the UK.24 We’ve
got some maths to do though to turn that into an expected proportion that we
can compare against our sample. The average age of people in our sample
was forty-five. PVFS is only really diagnosed in adulthood. Let’s be generous

and say that the average person in our group had thirty-five years (since they
were ten) to appear in this kind of statistic. That gives us an expected
prevalence of people who previously had PVFS of 0.4%. By contrast, a
whopping 23% of our sample reported previous PVFS. It’s worth
acknowledging that the quoted statistics that give us our general population
figure of 0.4% are probably on the low side, as it represents only formally
diagnosed cases, and the condition frequently goes undiagnosed. However,
with my data suggesting that the prevalence of previous PVFS was sixty-two
times higher in people with Long Covid than in the general population, it
would take a vast underestimate in the general population figure for this
result not to be extremely interesting.
There are a couple of other associations that could be important among the
Long Covid community, but they are difficult to quantify and evaluate. So, at
this stage, we move into the next level down of our evidence base, where the
connections are more speculative.
Anecdotal risk factors
In the two and a half years that I’ve been in the Long Covid community I
have spoken to hundreds – possibly thousands – of other long haulers. Each
of them has in turn spoken to many more. One of the other traits that seems to
be disproportionately common among the patient population is some kind of
connective tissue disorder. Rheumatoid arthritis fits into this category, as do
Ehlers-Danlos Syndrome, hypermobility spectrum disorders and
fibromyalgia. Previous research has noted a connection between some of
these disorders and ME/CFS,25 and so far anecdotal evidence suggests a
similar link with Long Covid.
Moving on to some more controversial territory, previous trauma of some
type and what might be unscientifically termed type A personalities (i.e.
people who could be described as workaholics, outgoing, ambitious,
organised and impatient) also seem to be common in the Long Covid
population. Now if you’ve been around the ME/CFS community for some
time, bear with me before immediately reaching for the red buzzer. Both of
these two traits have previously been cited by the biopsychosocial lobby to
support their argument that the origin of ME/CFS is psychological. For a
complete takedown of this point of view, turn to chapter 5 to read about the

biological pathways implicated in Long Covid (and ME/CFS) or chapter 7 to
learn more about the PACE trial, considered by many to have been
discredited and debunked.
So, where am I going with this? We know that people with post-traumatic
stress disorder may be more likely to develop autoimmune disease, which
suggests that trauma can have a physiological impact on the body (for more
on this see chapter 9).26 To understand how this in turn can affect behaviour,
we need to turn to the autonomic nervous system.
What is the autonomic nervous system?
At the simplest level, the autonomic nervous system is the part of the
nervous system that operates automatic bodily functions – things like
heart rate, breathing, digestion and temperature control. It is divided into
two parts: the sympathetic (which is involved in the ‘fight-or-flight’
response) and the parasympathetic nervous system (whose functions are
sometimes summarised as ‘rest and digest’ or ‘feed and breed’).
The American neuroscientist Stephen Porges elaborates further on the
autonomic system in what he terms the ‘polyvagal theory’.27 It has to be
pointed out that this hypothesis still remains firmly in the scientific realms of
theory rather than accepted medical phenomenon, but to those of us with
Long Covid the polyvagal theory makes a lot of empirical sense. In addition
to the polyvagal theory being just that – a theory – we also don’t yet have
evidence published in academic journals to link it to Long Covid. We are
simply too early in this journey for that, but I believe it is worth including
because of the remarkable way it lines up with long haulers’ experiences, and
the implications it raises for managing symptoms (see chapter 9).
Porges adds a further state, ‘immobilisation’, to the traditionally
understood parasympathetic response (i.e rest and digest). He then creates a
hierarchy between immobilisation, the traditional parasympathetic response
and the sympathetic response (i.e. fight or flight). Imagine a set of traffic
lights, where in this hierarchy the ‘safe’ state (parasympathetic response)
resides at the bottom in the place of the green light. The next state up is
termed ‘mobilisation’ (sympathetic response) and can be imagined as the
amber light, representing the cues of threat or danger, or chronic stress. The
final stage is called ‘immobilisation’, which corresponds to the red light and

represents the shutdown of the body, a ‘freeze’ state in which the focus is
purely on survival and very little active function is possible.
This state of immobilisation is probably one that sounds familiar to
everyone who’s had Long Covid. It is where we inevitably end up after
spending too long in a state of sympathetic nervous system response. In fact,
many of the symptoms of Long Covid can be attributed to autonomic
dysfunction, leading us to spend an inappropriate amount of time in ‘fight or
flight’ and not enough in ‘rest, digest and heal’.28 , 29
But what is happening physically when this is going on? During the state
of immobilisation, Porges argues that the dorsal branch of the vagus nerve
(which is the main component of the parasympathetic nervous system) enacts
the shutdown. In addition to affecting the function of the heart and lungs, the
dorsal branch affects how our body functions below the diaphragm, with
knock-on effects on the gut. So, when you’re in immobilisation expect
physiological changes too, with less frequent trips to the bathroom as your
gut function slows down.
Porges’s View of the ANS

So, how are previous experiences of trauma connected to this polyvagal
theory? I spoke to clinical psychologist (and fellow long hauler) Dr Sally
Riggs about it. She suggested that if you have a history of trauma, then it is
quite possible that you’ve spent most of your life between the states of flight
or fight and immobilisation. One of the consequences of this is that feeling
‘safe’ can actually feel ‘scary’, because it’s unfamiliar, uncomfortable and
not ‘natural’. If you consider the polyvagal hierarchy, then the route back
down to safety from immobilisation at the top has to take you through the
‘danger’ stage. For example, Dr Riggs describes how she’s observed long
haulers undertake activities like deep breathing or yoga, which are often
considered to be soothing. However, in some cases they can seem to prompt
sympathetic nervous system symptoms which are uncomfortable and
overwhelming for the body. What happens then is an immediate shutdown
that sends you straight back to immobilisation.
As far as established science is concerned, the polyvagal theory remains
just a hypothesis. It does, however, make a lot of sense to me, especially in
terms of understanding why some of us might develop Long Covid. My
argument would be that people who spent disproportionate amounts of time
with their autonomic systems under stress – however we want to define that –
are more likely to then find that a Covid infection tips this autonomic system
over into full-blown dysautonomia.30
What is dysautonomia?
Dysautonomia has been much cited in studies of people with Long Covid.
It describes the dysregulation of autonomic nervous system function and
can present as a fast or slow heart rate, postural problems on standing,
breathlessness, fatigue, headaches, anxiety, gastric issues or sleep
disruption. A specific diagnosis that’s often mentioned is PoTS (as
discussed in chapter 1), which is caused by an abnormal autonomic
response to the need to redistribute blood around the body. This state of
‘orthostatic intolerance’ (intolerance of standing upright) involves
activation of the vagus nerve in response to standing, which can lead to
tachycardia (high heart rate), low blood pressure, dizziness and fainting.
As with other aspects of Long Covid, people have described at least
two mechanistic pathways that could link the condition to this PoTS
disease profile: viral infection could cause direct cellular damage to the
autonomic nervous system, or autoantibodies targeting the receptors that

are involved in many aspects of normal parasympathetic function could
be produced in response to the infection.
We are now, fortunately, at the stage when it is becoming widely accepted by
the medical community that dysautonomia is one of the key symptom drivers
in Long Covid, with the classic symptoms of dizziness, racing heart rate and
headache also accompanied by sympathetic nervous system overdrive.
Unfortunately, however, curative treatments for dysautonomia are limited,
and most of the steps you can take revolve around management of the
condition.
GEZ: Does vaccination reduce your chances of developing Long Covid?
DANNY: It seems to reduce it – some studies say by about half 31 – but the
risk remains very real. Overall, I’d say I’ve been terribly saddened by the
devastating new Long Covid cases that have continued to pile up, even in the
post-vaccination period. If you’d asked me to predict, I’d have guessed that
Long Covid would have been largely a legacy of the severe, pre-vaccination
waves through 2020. The fact that cases have continued to accrue since then
in a largely vaccinated population shows just how little we really understand
about the causes and immune regulation of Long Covid. The UK has
acquired well over a million additional Long Covid cases in the post-
vaccination Delta to Omicron period. Surely, that’s perplexing.
GEZ: Does having Long Covid affect immunity against reinfection?
DANNY: Some long haulers have reported multiple infections. This has
become one of those questions that has become difficult to answer in the era
of Omicron: reinfection is terribly prevalent. In theory, it would be possible
to collect the data allowing one to ask whether long haulers are more or less
likely than others to be reinfected. It would be important to control for all the
many variables: different initial infecting variants, different doses and types
of vaccines. My suspicion is that the long haulers may show similar
reinfection rates to others.
GEZ: Can you develop Long Covid after a reinfection, when you recovered
fine after the first infection?

DANNY: Yes, anecdotally. Not developing Long Covid the first time is no
guarantee you won’t next time. There aren’t studies on this yet, though. One
of the obvious problems of living through this pandemic is that it throws new
research questions at us in real-time, so much faster than we can set up
research to find answers. You might perhaps imagine that mechanisms and
phenotypes of Long Covid might look a little different in the distinct immune
setting of reinfection. Also, Delta and Omicron, being such distinctive viruses
when compared to the ancestral strain, might cause somewhat differing Long
Covid. It’s still too early to know.
GEZ: The paper in Cell found that the presence of certain autoantibodies was
associated with the probability of developing Long Covid.32 Am I right in
thinking that these autoantibodies are not present in healthy people?
DANNY: You’d think that that would be a really straightforward question, but
unfortunately it’s not quite so simple to answer. Covid has provided the
biggest human immunology dataset that anybody has ever studied, but there
are enormous biases in the data, due to so many people having had an
infection. We’re finding all these exotic things but we don’t really have a pre-
Covid dataset to compare these observations against. Some French
researchers published convincing data that some people with Covid make
very damaging anti-interferon autoantibodies (which interferes with how cells
protect themselves from invaders), but we don’t know how many people
might produce these autoantibodies in the absence of Covid.33 Nevertheless
these autoantibodies are a bona-fide marker of Covid severity. The other
point raised by screening for autoantibodies (that my lab has mirrored in our
research) is the discovery of lupus autoantibodies in people with Covid.
GEZ: Does that mean that lupus shares some pathophysiology (disease process
or cause) with Long Covid?
DANNY: To answer this, it might help to explain what lupus is. Lupus is a
moderately common autoimmune disease in which the body starts to make
autoantibodies to both DNA and DNA–protein complexes. Of all things,
DNA is the one that you really don’t want to have an autoimmune response
to because it’s in every cell in your body. As a result, the autoantibodies
come in many different flavours and specificities and have incredibly diverse

impacts – that’s why lupus affects the central nervous system, kidneys, lungs,
joints and blood vessels. When you think of Long Covid, this sounds rather
familiar, doesn’t it?
GEZ: What’s different about what we know about Long Covid at the moment
and what we know about lupus?
DANNY: For lupus, we’ve never made enormous headway in identifying any
infectious agents – unlike Covid, obviously. Lupus is also very ethnically
skewed: in clinics in the UK and the USA, lupus is more commonly seen in
young, Black women. And it’s a sledgehammer, it’s very severe. If lupus is
not managed effectively, it can seriously damage your organs. We’re not
really seeing that level of severity in Long Covid, even without treatment.
GEZ: Is there anything we can see right now that differentiates Long Covid
from lupus in terms of an autoimmune signature?
DANNY: Professor Alex Richter’s team in Birmingham have been working on
autoantibody tests, and the range of autoantibodies seems much broader and
more diverse in Long Covid than in lupus.34
GEZ: So, still many more questions remaining on this front! In summary,
though, is it fair to say that we’re seeing a significant degree of autoimmunity
in Long Covid?
DANNY: I think that’s a fair statement, yes. It’s certainly part of the story.
GEZ: You earlier spoke about how extremely fit people can suppress their
immunity through steroid production, but it seems like what’s happening in
Long Covid is the opposite. When I take corticosteroids, my symptoms
subside.
DANNY: Well, it could be to do with the way your body handled the virus –
how receptive you were to it when it came in, or what kind of immune
response you had when first infected. This response would have been
affected by where you sit on the physical fitness spectrum, because people at
the opposite ends of that spectrum definitely have different immune systems.

Who’s to say what the perfect immune system is to grapple with a new virus
that we haven’t seen before?
Summary
As with just about all factors surrounding Long Covid, the science is still
developing when it comes to understanding who is at risk of the condition.
But we are starting to see some trends validated with data. If you were to
distil all the evidence (and anecdotal observations) for predisposing factors
into one fictional character, they would look a little like this: Elsie is female,
aged between thirty and fifty, and previously lived an extremely active, full-
on life. She’s not very good at taking breaks or slowing down. She has a
history of mild asthma and had glandular fever when at university. Now, of
course, not everyone will look like Elsie, but if she were a friend of mine I’d
be advising her to take it very easy in the weeks after a Covid infection. This
brings our discussion of who gets Long Covid and why to a close. But one
huge and important subpopulation deserves its own chapter, and that comes
next.

CHAPTER 3
Can Children Get Long Covid?
Early in the pandemic it was widely believed that children weren’t affected
by the novel coronavirus. This was because relatively few children needed to
be hospitalised during the acute phase of illness. Then the identification of a
small number of children with Covid who developed symptoms similar to
those of Kawasaki syndrome (a rare disease in which blood vessels are
inflamed by immune activation) suddenly made the international press. As
time has gone on, the symptoms that these children experienced became
known as paediatric multisystem inflammatory syndrome (PIMS), or
multisystem inflammatory syndrome in children (MIS-C) in the USA. PIMS
is quite rare, occurring in less than 0.5% of paediatric Covid cases.1
What has received rather less coverage in the media, and very little
research funding, is the presentation of Long Covid in children. Just how
many children are affected by Long Covid remains unclear. A wide range of
estimates have been published in the scientific literature, from 1% of those
who had an acute Covid infection at the lower bound, up to 25% in a recent
meta-analysis of 80,071 children and adolescents.2 , 3 The disparity in these
estimates is probably due to differing methodology and selection criteria for
which symptoms are considered by the researchers to constitute Long Covid,
and whether a positive PCR test is required to qualify patients for inclusion.
Whichever way you spin it, even if Long Covid only occurs in 1%, that’s still
a huge number of children, given that UK data suggests that most children
have had Covid.4
One of the reasons that people may have been slow to recognise Long
Covid in children is the continuing misapprehension, dating from the first
wave of the pandemic in early 2020, that Covid is primarily a problem for the

elderly. Each variant has affected different parts of the population and
resulted in different symptom profiles. So, while the initial wave was
dominated by discussion of care-home outbreaks, by the time we shifted from
Alpha to Delta and then to Omicron and beyond, the pandemic had become
one driven via spread in schools.
Official statistics in the UK suggest that 119,000 children and adolescents
currently have Long Covid, 21,000 of whom have had it for at least a year.
The Omicron wave was so pervasive in schools that recent Office for
National Statistics (ONS) data estimated that over 1.5% of all children in the
country have Long Covid.
And what about children who develop PIMS during the acute phase of
infection? I talked with Sammie Mcfarland, founder and CEO of the charity
Long Covid Kids. Sammie is a long hauler herself, and her daughter has had
Long Covid symptoms for more than a year. In Sammie’s experience,
children with PIMS are often discharged from hospital and classified as
having recovered, but in reality they often still have severe symptoms and
soon find their way to Long Covid Kids for help. So, essentially, children
who continue to have symptoms post-PIMS have Long Covid.
What does Long Covid typically look like in children?
Although Long Covid can manifest in as many perplexing different ways in
children as in adults, there are a few symptoms that could be grouped into a
typical paediatric presentation.5 Unsurprisingly, the most common symptom
is fatigue – just as it is in adults. Then there’s insomnia, cognitive
dysfunction, dysautonomia, anxiety and gastrointestinal disturbance, also not
unfamiliar among the adult population. Then we start to branch off with
symptoms that are more specific to young people: joint, nerve and abdominal
pain, migraines, swelling, skin rashes, temperature dysregulation and sensory
overload. Many children find overstimulation, whether auditory or visual,
difficult to tolerate. Loud or intense sounds can be very difficult for children
with Long Covid. Another frequent occurrence noted by Sammie is that
children with Long Covid demonstrate large degrees of regression. One
reported instance is that of a seventeen-year-old who had scholarships for
further study, who, after getting Covid, spent all their time in their room
playing with their Sylvanian Families toys from when they were six years

old. This kind of story seems hard to believe, but the severity of Long Covid
can lead to emotional coping mechanisms of this scale. The regression can
also present in a number of different ways, including regressive behaviour
around the rest of the family and relationships.
In extreme cases, children can have such difficulty swallowing and
tolerating food that they end up being tube-fed.6 –8 In Sammie’s experience,
once children begin to be tube-fed, they are (so far) unlikely to go back to
eating normal food. She also reports that some children with Long Covid
experience extreme muscle weakness and struggle to stand unaided. Even
after intensive physiotherapy, the improvements in some of these children are
only minor. Sammie also raises reports of children who’ve become mute
since getting Covid. This is a harder symptom to verify as it could be a result
of the psychological pressure of the illness rather than a physiological
problem. Either way, the impact is just as severe.
What do we know about long-tail viral conditions in children and
adolescents?
While post-viral conditions have been identified in children before, Long
Covid is quantitatively and qualitatively in a whole different ballpark.
That’s our starting point: no matter the age group, Long Covid is
different. There’s only really one virus relevant to children or adolescents
that’s comparable in terms of impact and that’s EBV.
EBV plays an important part of the story of human evolution – you
might say it’s our oldest foe.
Coronaviruses, like those that cause the common cold, are generally
thought of as fairly temporary infections – quick in, quick out.
Herpesviruses, such as EBV, couldn’t be more different. They tend to
persist latent in the body, often for a lifetime. Herpesviruses were the first
viruses associated with human cancers and are an incredibly successful,
almost ubiquitous pathogen.
Before the advent of modern medicine, most of the planet was walking
around with EBV in their throat, with parents passing that exposure on to
their children. Nearly all of those infections were asymptomatic. Children
grew up and went through their lives latently and persistently infected,
and most of the time nobody cared. There are rare examples in which
EBV is hugely important – it has been associated with some cancers,

including lymphomas and nasopharyngeal carcinoma – but it’s only in
recent years that we’ve been able to make that connection.
Nowadays, there are whole cohorts of adolescents who reach
adulthood and still test negative for EBV (potentially due to the increase
in protective parenting behaviours). Then, as a result of lifestyle or
environmental changes – such as moving away to university – they get
exposed to the virus. The resulting illness is what we call glandular fever
or infectious mononucleosis.
Glandular fever is one of the very few conditions in this age group that
presents similarly to Long Covid. People with glandular fever experience
fever, malaise and swollen lymph nodes, and are fatigued for a protracted
period. So, even though EBV is different from SARS-CoV-2 in many
ways, there are some very interesting commonalities. People have been
researching the impact of glandular fever on the immune system in quite
granular detail for decades. Some of the findings from that research could
help to shed light on potential pathological mechanisms in Long Covid.
In one of my favourite studies of EBV, which was done by Professor
Kristin Hogquist’s research group at the University of Minnesota, new
students at the university were tested for the virus.9 Of these students,
37% had never had EBV. During their studies, nearly half of this group of
students subsequently tested positive for EBV. The researchers were able
to assess in real time how many students developed symptoms, how
many remained asymptomatic and how many developed full-blown,
persistent glandular fever, and drilled down into the differing
immunological profiles of those groups.
To cut a long story short, when you do all the fancy immunological
investigation in those groups, you build up a picture that seems rather like
our direction of travel for Long Covid. For example, if you were to ask,
‘Was the severity of EBV infection correlated with how much virus
students had on board or the extent of their immune response?’ (pertinent
and familiar questions in the context of Long Covid), the answer would
be a bit of both. Severely affected patients often started off with a high
viral load and initially produced slightly poor antibodies against the virus,
but then ended up with massively expanded populations of persistent T
cells – sometimes even years later. These T cells were dominating their
entire immune systems, almost to the exclusion of everything else,
sometimes forming significant majorities of all lymphocytes in the blood,

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disguised as toys. The sally of cruel meaning out of what looks
harmless nonsense, or a mere verbal slip—as in the polished rebuke
of a Master of Trinity to a too confident Junior Fellow, “we are all
fallible, even the youngest of us”—has a wounding force greater
than that of a direct mode of statement. The effect is still greater
where failure and disgrace are exhibited under a thin ironical veil of
glorious achievement, as in Pope’s lines on the Lord Mayor’s Show—
said by Leigh Hunt to be the finest piece of wit he knew:— {384}
Now night descending the proud scene is o’er,
But lives in Settle’s numbers one day more.
In all such ironical inversion the satirist manages by a suggestion
of the worthy and honourable to drive home with added force the
humiliating truth; as in the remark of Cicero, apropos of an elderly
dame who said that she was but forty years old: “I must believe her,
for I have heard her say so any time these ten years”.319 The
presentation in this case of something hidden, immediately followed
by an uncovering, may evoke an echo of the “bo-peep” laugh of
infancy, which should, one supposes, tend to introduce a milder and
playful tone into the attack; yet, owing to the predominance of the
attitude of fierce derision, this very element of playfulness appears,
somehow, to give a new pungency to the satirical thrust.
Nothing could be more unlike the laughter of virulent satire than
that provoked by the expression of humour in literature. As our
analysis would lead us to expect, we find in the truly humorous
writer the mellowing influences of good nature and sympathy, and a
large understanding and acceptance of that against which he pokes
fun. While satire, sarcasm and their kind seem to be trying to push
things away, or at least to alter them, humour, curiously enough,

looks as if it were tenderly holding to the world which entertains it.
Yet while all humorous writings illustrate these tendencies, the
subjective and personal quality of humour is seen in the
circumstance that every writer brings to bear on what he sees a new
temper and attitude.
The contrast of the satirical and the humorous point of view may
be conveniently studied by glancing at the current {385} and much-
discussed distinction between wit and humour. That these do not
logically make a pair of contrasting species has been implied in our
analysis of the two. Perhaps nowhere do we find the human mind to
have been more strangely misled by the fact of the existence of two
words than in this case. Wit, as essentially a manner of deportment
of the intelligence, can stand in no simple and direct relation to an
emotional mood like humour.
No doubt there are facts which give colour to the idea of an
opposition in this case. Thus, it is indubitable that whereas humour
specially favours certain kinds of imaginative and reflective activity,
wit seems always to prefer, even in its play, something in the shape
of an incisive logical process.320 But I suspect that the deeper ground
of the distinction is to be found in the circumstance that the wit
which is most brilliant, of keenest edge, and most effective in its
stroke, appears always to grow out of, and so becomes associated
with, those moods of satire and mordant mockery, to which humour
as good-natured and tolerant is directly opposed. So it is with the wit
of Voltaire and of others of his century.
A closer examination will, however, show that there is nothing
incompatible between the humorous sentiment and the witty mode
of behaviour of the intellect. As play indeed, wit quite naturally allies

itself to the attitude of humour. It will be found that much that is
commonly described as wit discloses the softening effect of humour,
and might, indeed, just as well be called an illustration of humour.
Those who really know the Irish will sometimes hesitate whether to
speak of their wit or of their humour. The same applies, I feel sure,
to a large number of {386} Shakespeare’s “witticisms”.321 In all such
cases, the wit, which when set in the fierce mood of the satirist has
a nasty sting, not only becomes harmless, but may take on
something of positive kindliness when it is tempered by an infusion
of genial humour. The remark apropos of a very correct person, “He
has not one redeeming vice,” may illustrate the point. It may even,
in this harmless form, come into a laugh which tells against the
humorist, as in the observation of an idler, “I don’t like working
between my meals”.322
Yet though in their well-marked forms thus dissimilar, the satirical
and the humorous mood may shade one into the other in a way that
makes it difficult to draw the boundary line. Heine, in some of his
writings, e.g., the poem Deutschland, tempers his mockery with
sentiment and humour in such a way that one finds it hard to think
of it as a satire. In places, indeed, this genius, so simple-looking yet
really so profound, seems to become a consummate humorist,
bringing out with a single touch all the laughter and all the tears of
things. Was Lewis Carroll a satirist when he threw behind the fun of
his children’s stories some deeper meaning which for ever eludes us?
or was this semblance of a meaning a part of his fun, his playful way
of punishing the “grown up” for reading a child’s book? {387}
In modern literature, the interesting point to note is the growing
interpenetration of the laughing and the serious attitude, and the

coalescence of the mirthful spirit with sentiment. The two processes,
though distinct, may run on together, as we may see in
Shakespeare’s plays. The humorous element introduced by the fool
in “Lear” and elsewhere at once relieves the tragic tension, and
gives a moment’s play to that disposition towards a lighter laughing
criticism which is always active when we survey colossal folly, even
though the mental eye is at the moment focussed for its catastrophic
effects. The laughter is controlled and kept tenderly humorous and
half-sad by a large reflection, which does not lose sight, even at the
relieving moment, of the lamentable ruin. It is only another way of
combining the “fun” and the “pity” of it when the master brings a
genial humour into comedy and makes us, with his faithful follower
Bardolph, half-love and more than half-pity the faulty knight who so
merrily entertains us.
As we have seen, prose-fiction may illustrate the comic spirit and
something of the fiercer temper of satire. Yet laughter comes into it
in another form. It has to accommodate itself to the presence of
serious interests, and of a plot which involves sympathetic fear and
strain. Hence it appears in stories which have a mixed tone, as it
does indeed in comedy when this is not pure—for example, “heroic
comedy,” as illustrated by M. Rostand’s Cyrano—in the guise of
humour. That is to say, its gay treble note is complicated by an
undertone, a resonance of the sadness of its milieu. One needs only
to think how one laughs at Moses and his purchase of spectacles in
the Vicar of Wakefield, or at the disfigurement of the hero in
Cyrano.
A novel may, of course, present the grave and the gay in mere
juxtaposition, so that the interaction and {388} modification here

spoken of are only very imperfectly realised. The notion of a good
story entertained by many is of one that bears the imagination of
the reader swiftly through a series of diverse scenes, now grave and
pathetic, now gay and mirthful. A large part of modern fiction
satisfies this need. Stories of wild adventure from Gil Blas to Tom
Jones are “humorous” to the multitude in this sense. Even in the
case of a real humorist like Dickens, whose amusing figures are
there to touch the heart as well as to entertain the imagination, the
perfect harmonising of tones may sometimes seem to be wanting. A
humorist of another complexion, Laurence Sterne, seems to have
missed the judicious mixture of laughter and sentiment in his
Sentimental Journey.323
The art of humorous writing consists in part in selecting
characters, incidents and the rest in such a way as to exhibit the
intimate connections between that which amuses and that which
touches the serious sentiments, respect and pity; and to develop the
reflective consciousness which sustains the mood of humour.
Goldsmith’s history of the Vicar and his family is one of the best
examples. Scott’s Antiquary and Fielding’s Parson Adams are
characters which at once entertain and win us. Such humorous types
involve, as Leigh Hunt has pointed out, a striking contrast within the
characters, e.g., the gullible and the manly in Parson Adams;324 and
the sharpness of this contrast turns on that of the feelings excited by
the constituents. The characters selected by humorous fiction may
be consciously amusing, after the manner of the Merry Knight, or
wholly unconscious of their laughter-provoking power. A valuable
part of this amusing portraiture consists in bringing out {389} the fresh

and odd-looking characteristics not only of individuals, but of classes
and even of races.
In addition to this objective presentation of the humorous
aspects of character and its relations, the writer may further the
effect by striking now and again undertones of quaint reflection and
so introducing an element of subjective humour. The notion that
such reflection is out of place in narrative art seems strange to a
student of the history of literature. If there was room for the
comments of the onlooking chorus in Greek drama, and for the yet
deeper reflections supplied by the acting onlookers in Shakespeare’s
plays, there should be room for it in a prose narrative. In truth,
some of the best writers of fiction, Fielding, Thackeray and George
Eliot among others, make excellent use of this reflective
accompaniment. In the best works of the last-named writer we have
something of Shakespeare’s art of adding a pregnant observation
which, so far from disturbing, rather furthers the mood needed for a
due appreciation of the action.
In the great humorous writings, those of Rabelais, Cervantes and
—removed by an interval no doubt—Sterne, we appear to find
presented a largeness of subject and of treatment which makes
direct appeal as much to reflection as to perception. You must know
the Middle Ages, which are being laughingly kicked aside, before you
will even care for Gargantua; you must envisage Don Quixote and
his squire, not as two individuals or even as two types of character,
but as embodiments of two remote levels of culture, and more, of
two opposed ways of looking at the world, before you will begin to
feel all the humour of these juxtapositions. And so of the great
contrast between Mr. Shandy and his brother, the Captain. There is

no need for the interpolation of reflection: the scale, the breadth {390}
of treatment, the wealth of ideas poured out, these compel us to
reflect. The laughter which comes from the perceptions of the utter
incongruity of the mental and moral structures thus juxtaposed and
attached is saturated with this reflection. And more, so right, so
likeable, so estimable even is each of these contrasting characters,
with its well-marked temper and manière de voir, that our
sympathies go out towards both. Thus we leave the perceptual level
and the relative point of view of comedy far behind us, reaching a
standpoint near that of the thinker who embraces all particular
points of view, and yet may manage to have his own laugh in the
end. When, as in Jean Paul’s Siebenkäs, and yet more clearly in
Carlyle’s Sartor Resartus, the contrast seems to open up the great
collision in human experience between sentiment and prosaic reality,
idealism and the earth-binding instincts of practical life, we stand,
indeed, on the border-line between the humour of fiction and that of
philosophy.
Humour has its place, a respectable one too, in essays and other
forms of literature which deal directly with reality and are products
not so much of imagination as of thought. In these, the contrast
between the serious and the playful appears in transitions from a
perfectly grave to a humorous kind of reflection. Marked differences
of tone are observable here also. The humorous remark may be but
a momentary diversion of the attention, a playful side-glance, in a
serious argument. In some writings, e.g., those of Sir Thos. Browne
and of Lamb, the humorous element hardly amounts to a digression,
or even to a momentary interruption, but is fused into and half lost
to sight in the serious argument.325 Among more recent writers, too,

including some yet living, we have admirable examples of historical
narrative {391} and criticism lit up here and there with soft glow-worm
points of humour. In other cases, the humorous feature may be so
large as to modify the colour of the whole, as in Miss Kingsley’s
Travels in West Africa. An Essay, again, may be as a whole a jeu
d’esprit and the fun seem to preponderate, while the manner is
throughout that of grave argument; or, in more subtle work, as some
of Charles Lamb’s, it may be best described as fun sandwiched in
between a look of seriousness on the surface, and a real seriousness
of meaning below. The fusion of tones leaves much to be desired in
the case of many writers who are popularly regarded as skilled
humorists. A mere interruption of serious thought by a sort of playful
“aside” does not prove the existence of the gift of humour, which is
essentially the power of playing on moods not only dissimilar but
usually antagonistic in a way that avoids all shock and sense of
discontinuity.

CHAPTER XII.
ULTIMATE VALUE AND LIMITATIONS OF LAUGHTER.
Our study has taken us through various regions of research. In
looking for the germ of laughter we found ourselves in the wide and
misty plains of biological speculation. In tracing its development we
took a dip into the pleasant vales of child-psychology and
anthropology, and then tried to climb the winding paths of social
evolution. Having reached in this way the heights of modern
civilisation, we made a special investigation into the social
organisation of laughter, as represented in the art of comedy, and
into the gradual appearance of a new type of laughter, essentially
individual and independent of the social standard, to which is given
the name of humour. Throughout this voyage of discovery we have
kept in view the question of the function of the laughing spirit in the
life of the individual and of the community. It remains to determine
this function more precisely.
In order to assign its proper place and its value to a large
spiritual tendency such as runs through human mirth, we must for a
moment push our investigation into a yet more difficult and obscure
region, that of philosophy. This is necessary for more than one
reason. To begin, we can hardly hope to reach a clear view of the
worth of the laughing impulse without the help of some clearly
thought view of life as a whole; and such a “Weltanschauung” {393}
seems only to be attainable at the level of philosophic reflection.
There is, however, a second reason for entering this more remote
and private domain of knowledge. Philosophy is a carrying forward

to its highest point of development of that individual criticism of life,
with which, as we have seen, the quieter tones of laughter associate
themselves. It would thus seem to be desirable to inquire how far
along the road of philosophic speculation this companionship of the
mirthful spirit in her quieter mood is possible. This inquiry may
conveniently be pursued at once as supplementary to our discussion
of humour.
As pointed out in the chapter on the subject, reflective humour
grows out of a mutual approximation of two tendencies which seem
to the unexamining person to be directly antagonistic, namely, the
wholly serious turn for wise reflection and the playful bent towards
laughter. In philosophic humour, touched on in our survey of the
laughable in literature, this antagonism seems at first sight to be
particularly sharp. The plain man, to whom philosophic speculation
presents itself as something remote from all human interests as he
conceives of them, may well receive a shock when he hears that it
holds potentialities of a smile at least, if not of a laugh—for the
person who engages in the occupation, that is to say, and not
merely for him who looks on. It seems to be incumbent on us,
therefore, to try to make this drawing together of impulses which
look so hostile a little more intelligible.
The humorist, as we have viewed him, is able through the
development of his individuality to detach himself from many of the
common judgments and much of the common laughter of the
particular community of which he is a member. He develops his own
amusing mode of contemplation, which involves a large substitution
for the standards {394} of custom and “common-sense,” of the ideal
standards of reason. The habit of philosophic thought may be said to

complete this uplifting of the individual to ideal heights, and its
concomitant process, the expansion of the view of the irrational, the
essentially unfitting, the amusing. A word must suffice to indicate
the way in which it does this.
Philosophy, as we know, going boldly beyond the special
sciences, pushes on to a deeper knowledge of things, and of these
in their totality, of what we call the universe. In this effort it has to
envisage things in a way essentially different from that of everyday
observation. The modern philosopher may do his best to reach his
conception of the reality of things by a careful analysis of
experience; yet in the end his theory seems to have transformed our
familiar world beyond the possibility of recognition.
In this philosophic re-construction of the real world, man, his
relation to nature, and his history have to be re-considered. It
illustrates a powerful tendency to view human life and experience as
a phase of a larger cosmic movement determined by an ideal end.
The introduction of ideal conceptions, by lifting us above the actual,
seems to throw upon the latter an aspect of littleness, of futility, of
something like the dishonour of failure. The ideal requirement proves
hopelessly inapplicable to much, at least, of our everyday world; so
that, as long as we remain at its point of view, familiar things—say
the persons we happen to be thrown with, and a good deal in
ourselves, social experiments growing out of some passing trend of
“popular thought,” and even long periods of history—take on the
aspect of contradictions, of futile things that at least do not count, if
they do not actually delay the fruition of the ideal.
So, too, when philosophy becomes distinctly practical. {395}
Whether we take happiness or moral perfection or self-realisation as

the ideal end of men’s conduct, a large part of the conduct which
unfolds itself under our eyes, including much of our own, begins to
look sadly poor and shabby, as soon as we venture seriously to apply
an ideal as test. Much at least of what men praise as virtue shows
itself to be of doubtful value, and at any rate to have received a
laudation quite disproportionate to its true worth.
Lastly, this belittling effect of ideas on everyday realities is seen
when philosophy constructs for us the ideal type of human society,
and of that confederacy of civilised states of which, now and again,
it has had its dream. Under the searching rays of these ideal
conceptions even the “common-sense” to which “advanced”
communities hold so tenaciously may begin to look something
compacted rather of darkness than of light.
The situation would seem to offer room for some of those modes
of transforming the aspects of things which we have found to be
excitants of laughter. If philosophic contemplation effects a reduction
of great things to littleness, of substances to illusory shadows, of the
elevated glories of men to the level of barely passable dignities, it
should, one may reason, help men to laugh. Yet the fact that a
philosopher has been known to the ages as the laughing one
suggests that mirth has not been a common characteristic of his
kind.
In order to understand this, we must recall one or two facts. For
one thing, though seriousness may combine with a taste for the
laughable, it is and remains fundamentally opposed to the
playfulness of mirth. Philosophers are serious persons: their
constructive thought is of the most arduous of human activities, and
imposes on those who {396} undertake it an exceptional amount of

serious concentration. Little wonder, then, if we so rarely find in
them a marked fondness for the playful. The great and ineradicable
gravity of the philosopher has been sufficiently illustrated in his
theoretic treatment of our subject.
In addition to this general reason, there are others and variable
ones, differing with the kind of philosophic creed adopted, and with
the temperamental attitude of the individual towards it. To begin
with differences of creed, we must remember that a philosopher’s
doctrine, while it may invest our common world and our common life
with an aspect of indignity, may at the same time reduce these to
mere semblances by setting them in contrast to the ideal region
which it regards as the sphere of the veritable realities. In this way,
as in Plato’s Idealism, we may see a quasi-religious tendency to lift
men above the follies, deceptions and seeming evils of the world to
the sublime verities. Such a doctrine, if consistently held, reserves
but a small place for laughter—save perhaps for the happy smile of
release or escape. Plato, the thinker of many moods, was able to
adapt his doctrine to attitudes widely different from the half-poetic,
half-religious one to which on the whole he leaned; and some of
these proved to be compatible with a delicate vein of mirth. Perhaps
one may find in Plato a reflection of the different attitudes of the
gods—to communion with whom his spirit aspired—towards luckless
and erring mortals: the serene indifference of those on the height,
and a mild good-natured interest in what is seen below, which lends
itself to the softer kind of ironical banter. What is told us of the
laughter of the deities is always, perhaps, a little difficult to reconcile
with their remote altitude and the detachment of spirit which seems
proper to this; being, either in its mocking virulence, or {397} in its

good-natured familiarity, rather too suggestive of a close attachment
to our race; for which reason, by the way, philosophers, if they wish
to soar god-wards and still to keep a laughing down-glance on their
fellows, should beware lest they soar too high.
How high-pitched speculation tends to silence laughter by
withdrawing the philosopher too far from the human scene may
easily be seen by a glance at the historical schools. The Stoic and
the Epicurean alike, widely dissimilar as were their views of the good
and their moral tempers, took into seclusion the philosophic life
which Aristotle had bidden them combine with a discreet
participation in the social life about them; seeking, each in his own
manner, to realise its self-sufficiency and its consolations. There, no
doubt, they reflected much on the follies of the unwise who
remained in the crowd. Yet the Stoical temper, with its striving after
a passionless imperturbability, excluded the idea of a laughing, quite
as much as of a pitying, survey. On the other hand, the Epicurean,
though his theory of life accentuated the value of the tranquil
pleasures, did not apparently find in his Garden a corner for the
quiet amusement of a laughter-bringing contemplation.
In this way philosophy, by substituting a new and ideal mode of
thought and life for the common mode, is apt to dismiss it as void of
significance and unreal, and so to be unable to laugh at ordinary
humanity just because it has ceased to be interested in it. Yet all
philosophising does not thus belittle the realm of reality, as common
men regard it. Philosophers have been known to regard as realities
the same particular things that Plato contemned as mere shadows,
and to reconstruct and to justify as rational what the plain man
accepts as his world. When {398} this goes so far as to insist on the

goodness of things human, and to say that the world as a whole is
as perfect as it can be, and thus in a new way, as it would seem, to
break away from the common view, it seriously threatens the locus
standi of the laugher. Nothing, indeed, in the way of a theory of life
would appear to be more fatal to a mirthful temper of the mind than
an out-and-out optimism. At most, laughter would take on the
aspect of the serene gaiety of a happy and thoughtless girl; as it
does, I suspect, in the case of Abraham Tucker, for whom Sir Leslie
Stephen claims the character of a “metaphysical humorist”.326 It is
true, as I have elsewhere shown,327 that a genial and tolerant
laughter may predispose a man, should he begin to philosophise, to
adopt an optimistic theory of the world. Nevertheless, I believe that
a firm grasp of such a theory would tend to reduce very considerably
the scope of his laughter. It is just as well, perhaps, that R. L.
Stevenson—whose predominant inclination to a hopeful and cheerful
view of things is clearly shown in his idea that every man carries his
ideal hidden away, as the Scotch boys used to carry lanterns in a
silent ecstasy—did not go farther than his letters show him to have
gone, along the path of philosophic construction.
If, on the other hand, the manner of philosophic speculation at
once accepts the common facts of life as real, and yet as inherently
and hopelessly bad, laughter is even more effectually excluded.
There may, it is true, be room in the pessimist’s creed for a grim
irony, of which, indeed, we find a trace now and again in the
writings of Schopenhauer and his followers; but for laughter pure
and simple, or even for laughter mellowed by the compassion which
the {399} pessimist bids us cultivate, there seems to be no breathing-
space. The state of things is too tragic to allow even of a smile.

It remains to determine the relation of one other tendency in this
high thinking to the possibilities of laughter. In philosophic
scepticism, with its insistence on the relativity of our knowledge and
on the impossibility of attaining to rational certainty, we seem to find
a denial of all philosophy rather than a particular species of it;
nevertheless, as the history of the subject shows, it is the outcome
of a distinct and recurrent attitude of the philosophic mind. Now
scepticism does undoubtedly seem to wear a rather malicious smile.
This smile may be said to express an amusement at the spectacle of
illusions pricked, which tells at least as much against the high-
soaring thinker as against the man of common day who relies on the
intuitions of his “common-sense”. The sceptic’s attitude leans,
indeed, more towards that of common-sense, in so far that, while
destroying the hope of absolute knowledge, it urges the practical
sufficiency of such conjectural opinion as we are able to reach.
Scepticism thus introduces another standpoint for the laugher
and adds to the sum of laughable things. This is the standpoint of
the practical man and of what we call common-sense, so far as this
is knowledge shaped for the guidance of men in the ordinary affairs
of life. This common-sense, as its name plainly tells us, is essentially
a social phenomenon. Here, then, within the group of tendencies
underlying reflection—that is to say, the kind of intellectual activity
which marks the highest development of the individual point of view
—we encounter the contrast between this and the social point of
view. So far as we are able in our philosophic moments to “see the
fun of it,” as R. {400} L. Stevenson says apropos of a modern
philosopher, we join the choir of common-sense laughers—the
laughing realists as distinguished from the laughing idealists.328 From

their point of view, as the history of comedy plainly illustrates, all
highly abstract speculation looks amusing because of its quaint
remoteness from their familiar realities and interests; because, too,
of a keen suspicion of its being a vain attempt to soar above the
heads of common mortals. To pull down the speculative soarer to his
proper footing on our humble earthcrust is always a gratifying
occupation to the lovers of mirth. Even the soarers themselves will
sometimes give one another a kick downwards, the man of science
loving to have his joke at the expense of the unverifiable
conceptions of the metaphysician, and the latter being sometimes
lucky enough to turn the tables by showing how physical science
itself may, by its abstract methods, manage to strip material things,
the properties and laws of which it sets out to explain, of the last
shreds of reality.329
A word may serve to define the relation of philosophic humour to
the tendencies just indicated. Humour, we have found, is
characterised by an inclination to reflect, and to take the large views
of things which embrace relations; further, by a mirthful caprice of
fancy in choosing for play-ground the confines of issues felt all the
time to be serious. It grows distinctly philosophic when, as in Jean
Paul or his disciple, Carlyle, the contemplation of things breaks
through the limitations of the viewer’s particular world-corner,
surmounts “relative” points of view, and regards humanity as a
whole, with oneself projected into the spectacle, as nearly as
possible as disinterested spectator. {401}
We need not look for the philosophic humorist among zealous
adherents of the schools. In these, as elsewhere, a fervid devotion
tends, through its narrowing effect on ideas and its rigid fixation of

the point of view, to shut out humour, which even in its most serious
vein loves an ample reserve of space for free wanderings in search
of new aspects of things. The humorist is much more likely to be
found among students of philosophy who retain a measure of
scholarly impartiality in relation to the competing creeds.
A full development of humour in the philosopher seems to be
impossible, save where the amusing aspects of speculative soaring
are dimly recognised. This may come through a study of the history
of the subject; for it is hard not to smile at the spectacle of a man
refurbishing and possibly adding a new handle to one of the
“systems” which have had their day (and more, perhaps) and
undertaking once more to use it as a deadly weapon against the
adversary. A dash of the sceptical spirit, also an ability now and
again to see the pretentiousness of it all, would appear to be needful
for a large humorous enjoyment. One should have, too, at least a
side-glance for the fun of the proceeding when the human pygmy
tries the giant’s stride by offering us a definition of the absolute.
It would seem, then, as if the philosophic humorist needed to
combine two opposed points of view; that of the thinker who
criticises actual life in the light of ideas, and that of the practical man
who takes his stand on the fact of primal human needs and seeks an
interpretation of things which will satisfy these. He should be able to
soar with the Platonist to the realm of Ideas, so as to enjoy the droll
aspect which men’s behaviour assumes as soon as a glimmer of light
is made to fall on it from the Universal Forms; {402} and he should be
no less capable of taking up the standpoint of everyday reality and
common-sense, so far as to discern the element of a practical
irrationality which lurks in any undue insistence on these Ideas.

This combination in philosophic humour of two opposed
tendencies is illustrated in its attitude towards the question of the
worth of life. Since a humorist is characterised by a certain depth
and range of sympathy, he is not likely to accept the optimist’s easy
way of getting rid of the sufferings of humanity. At this point, at
least, he will be alive to the obstinate and inexpugnable reality of
our concrete experiences. Yet, just because he insists on never
losing his hold on his buoyant laughter, he will not sink into the
pessimists depths of complaint. He will see that even the large
spectacle of human struggle, in which there is much to sadden a
compassionate heart, begins to wear the shimmer of a smile as soon
as we envisage it as a sort of game played by destiny against our
race. Just as a glimpse of the provoking, almost malicious aspects of
the circumstances which irritate us in our smaller world may stifle
the rising imprecation, by bringing up a smile or even a sotto voce
laugh; so, when a philosophic humorist looks out upon the larger
human scene, he may find the starting sigh checked by a glance at
the playful irony of things. The reflective mind will indeed readily
find in the scheme of the world traces of an impish spirit that must
have its practical joke, cost what it may. With a fair appearance of
wise purpose, the destinies have contrived to combine just the
amount of bungling needed to convey an intention of playful though
slightly malicious teasing.
Thus, in the final evaluation of the world, humour may find its
place. Perhaps it is not too much to say that the {403} last word on
man and his destiny leaves an opening for the humorous smile. So
quaintly do the rational and the irrational elements seem to be
interwoven in the structure of our world, that a humorist, for whom,

as we have seen, the spectacle must always count as much, might
almost construct a new Theodicy and say: “The world is at least the
best possible for amusing contemplation”.330
We have spoken of philosophy as hovering aloof from our
common life, and this idea might seem to exclude all possibility of a
utility in the exercise of a philosophic humour. Yet even when men
philosophise and so appear to erect about them a new cosmos, they
remain in their human world and are doing something towards
shaping their relations to it; so that, after all, we may not
unreasonably look here, too, for some self-corrective function in
laughter, some aid rendered by it to that adjustment of the self to its
surroundings, which is enforced on us all—the exalted thinker no
less, let us say, than his faithful quadruped, whose world his
master’s strange habits make sadly complex.
The first service of such a philosophic humour is to complete the
process of a laughing self-correction. It is only when we rise to the
higher point of view of a philosophic reflection and see our own
figure projected into the larger whole, that we are able to estimate
ourselves and our concerns with some approximation to justness. As
we look down the vast time perspective we first fully discern our
flitting part in the world. And the glimpse of the dwarfed figure we
cut in the vast assemblage of things, followed by the reflection how
well it can work out its {404} hidden purpose whether or not we
happen to be on the scene, may suffice fully to reveal to us the
absurdity in the crude exaggerations of our dignity, of our usefulness
and of our troubles, and bring to the lips the corrective smile, even if
it fail to evoke the yet more valuable self-purifying laugh.

A like helpfulness is brought us by philosophic humour when we
contemplate the whole human lot. In estimating our world as a
dwelling-place for man, there is surely room for the exaggeration
which comes from a natural indignation at what hurts us, or from a
natural impatience at being able to do so little to better our estate.
Similarly, when we undertake to pronounce on the moral worth of
our species. It is, after all, our world, and, so far as we know, our
only one; and a side-glance at the requirements of a practical
wisdom may suffice to bring the smile which instantly corrects a
disposition to decry it overmuch. Such a glance may save us alike
from the sentimentalities of the cultivator of Weltschmerz, from the
foolish bitterness of the misanthrope, and from the sadly
unbecoming vanity of the “philosopher” who teaches that the world
and the institutions of human society exist for the sake of the man
of genius. A friend of Carlyle tells me that the gloomy sage would
sometimes, after pouring out one of his long and savage tirades
against things in general, suddenly hold breath, and then let himself
be swiftly borne downwards to more familiar levels on the rapid of a
huge laugh, almost as voluminous, perhaps, as that of
Teufelsdröckh, which he has so vividly described for us. In this way,
one conjectures, there came to him a moment of perfect lucidity, in
which he saw the absurdity of the overstrained attitude likely to be
produced by undue violence of emotion, aided by an irrepressible
turn for preaching to one’s fellows; {405} a moment when, perhaps,
the stubborn realities, which his words had made a show of
demolishing, were seen securely standing and ironically smiling at
his impotent rage.

In the foregoing account of laughter and its uses, we have
sharply separated the individual from the social point of view. Fifty
years ago, such a distinction would have required no justification. It
seems, however, just now to be the fashion to think of the individual
as merely an anatomical detail, too small to be really distinguished,
of the “social organism,” and of his part on the earthly scene as
consisting merely in making a small contribution, which at its best is
a negligible quantity, to the efficiency of this organism.
This is not the place to argue so serious a matter. At the risk of
appearing unfashionable, one may venture to keep to the old notion
that in counting human values we must assign a high one to
individuality; that, for the sake of the community itself, a proper
freedom for the full development of a man’s own mind, tastes, and
character, is something which should be secured even at great cost;
and that, were this not so, society’s claims on the individual have
well-defined limits, beyond which every man has the right, and owes
it to himself as a primal duty, to develop himself in the way which his
natural inclinations enlightened by reflection may suggest to him. To
insist further on this point would almost be to cast a slur on our
literature, which contains some of the masterly pleadings for
individual liberty.
This freedom for individual self-development clearly includes a
perfect right to form one’s own view of one’s world, and to derive as
much amusement as one can from a humorous contemplation of it.
It could only be something akin to an awe-struck flunkeyism which
would make a {406} person hesitate here. To one who has cultivated
the requisite observation and taste in the fellowship of one or two
congenial friends, the following of the tortuous movements of the

laughable in all domains of human industry and of human indolence
is one of the crowning felicities of life: the fun is always old in its
essence, wherefore we respond so quickly; yet it is always new in its
embodiments, wherefore we go on relishing it with an unabated
keenness.
The indulgence in this mode of amusing contemplation is, I
readily grant, in a sense anti-social, that is to say, opposed to what
the laugher’s community at the moment accepts as fitting and as
good. When a tranquil observer of his social world laughs at the
pretences, at the futilities, or it may be at the vagaries of its high
dignitaries, he may not improbably feel half-terrified at the sound of
his laugh; so firmly has our early schooling set in us a tendency to
regard as insolent upstarts all small things when they challenge big
ones: whether a “cheeky” schoolboy standing up to his big senior, or
a small country confronting a big one, or a “petty” anti-war minority
facing a “practically unanimous” people. Insolence it may be, yet
perhaps to the eye of reason not more contemptible than the
genuine ὕβρις in which great things are wont to indulge freely as
well within their right. It is indisputable, as urged above, that the
verdicts of the many, when they appear to fix the permanent
demands of social life, or to store away some of the precious fruit of
experience slowly maturing with the ages, are entitled to respect;
and a wise man will not hastily dismiss any popular opinion which
promises to have persistence. On the other hand, it is no less clear
that the views of minorities—whether singular or plural in number—
are exposed to special risks of their own. Yet this, and more, does
not affect the contention that popular opinion, just because it is {407}
popular, is almost completely relieved of that necessity of finding

reasons for its assertions which presses heavily upon a minority;
and, what is more serious, is subject to various and potent
influences which are just as likely to lead to error as to truth. An
opinion which may be seen to result from a mental process palpably
warped by prejudice does not grow valid merely by multiplying the
number of those who adopt it; for the increase may easily be the
result, either of the simultaneous working of a like prejudice, or of
the contagion which propagates psychical states, as well as physical,
among perfectly inert members of a crowd.
At the risk of appearing insolent, then, one must urge that the
individual and the society have their reciprocal claims. The most
extravagant adulator of his community would, perhaps, allow that
she has her favourites, and that some of the obscure “Judes” have
no particular reason for bearing her affection. The limbs of the body
politic which find themselves emaciated by under-feeding, while the
belly is bloated with over-feeding, may perhaps be forgiven for not
joining in the pæans on the glories of the social organism. Yet one
need not urge this line of remark. Little chance, alas, of our Judes or
our starvelings betaking themselves to a laughter which even
approaches that with which we are now dealing. Those who would
enter the gateway of this haunt of quiet amusement must leave
outside all grudging and sense of failure. Happy he who having
played the social game and lost can, with a merry shrug of the
shoulders, and at least half a laugh, betake himself to such a calm
retreat. He will find one into which the garden of Epicurus may be
said to open, where he can gather about him, at any rate, the
congenial friends who are always ready to hold sweet discourse with
him through their books; patient friends whom he cannot offend by

an {408} unwise interruption, though unhappily they are out of reach
of the gratitude which he would fain tender them. Here he may now
and again glance through the loopholes in the wall and see each
new day enough of the drolleries of the social scene to deepen his
content.
The evolutionist has accustomed us to the idea of the survival of
the socially fit, and the elimination of the socially unfit sort of
person. But more forces are at work in the world than our men of
science dream of. There is, oddly enough, a force which favours the
survival of the unfit, widely different from that supplied by others’
preservative benevolence: the impulse to adapt one’s environment to
the peculiarities of one’s organism by turning the world into a
plaything. How many men in one of the highly civilised communities
of to-day may have learned to keep their heads above the water by
the practice of a gentle laughter, no one knows or will ever know. It
is enough to say that there are such, and that after fully cultivating
their gift of humour they have found a world worth coming back to,
with their part in which they will be perfectly contented. Some of
these, who would probably be called social failures by the faithful
adherent to conventional standards, have been known to me, and
have been reckoned among the most delightful of my companions
and most valued of my friends. Society’s neglect of them, or their
neglect of society, has at least permitted them to develop the gift of
a wise and entertaining discourse.
I am far from suggesting, however, that this gay solitude—à
deux, or à peu de gens—is only for the social failure. Even in our
much-extolled age a philosopher will sometimes be found who is
perverse enough to hold with Plato that the mass of society are

wrongheaded, and that he will best consult his well-being by seeking
a wall for shelter from the {409} hurricane of wind and dust. Such an
one may do worse than betake himself to our retreat. And a wise
man who, like Montaigne, feels that he has lived “enough for others”
and desires to “live out the small remnant of life” for himself may
appropriately draw towards its entrance, not minding the shouts of
“Old fogey!” which come from behind. Nay, more, as already hinted,
a man who feels that his place is in the world may be advised now
and again to enter the retreat, if haply he may find admission as a
guest.
It may, however, be objected that even when a man thus
detaches himself as spectator from his society he perforce remains
at the social point of view in this sense, that the critical inspection
which brings the coveted laugh involves a reference to an ideal
community. The objector might find colour for his statement in the
fact that it is Frenchmen, that is to say, members of the most
sociable of modern races, who have chiefly dwelt on the delights of
retirement from the crowd. I am not greatly concerned to dispute
with such an objector; it is enough for my purpose to say that the
point of view of our supposed contemplator is far-removed from that
habitually adopted in any community which one could instance. As
such, it stands clearly enough marked off as individualistic. To this it
may be added that in that kind of laughter at the social spectacle
which presupposes philosophic reflection, the point of view is no
longer in any sense that of a particular community: it has become
that of a human being, and so a citizen of that system of
communities which composes the civilised world.

I do not doubt that during this laughing contemplation of the
social whole, of which at the moment he is not serious enough to
regard himself as a part, the individual will feel society pulling at his
heels. The detachment {410} from his community, though it fall far
short of the abandonment of the recluse, will, as already hinted, be
felt to be a revolt. When, glancing back at the crowd wreathing itself
in a dust-cloud, he laughs with his large laugh free from rancour, he
may catch a glimpse of the absurdity of his critical performances.
Here, again, we meet the final contradiction between ideal
conceptions and obdurate everyday facts. It is a droll encounter
when the foot of pure intellect, just as it is parting from the solid
earth, strikes against the sturdy frame of philistine common-sense,
of “that which subdues us all,” philosophers included. The
individualism of the point of view in a laughing contemplation of
one’s social world is only surmounted when a large philosophic
humour thus draws the laughers self into the amusing scene.
We may now better define the attitude of the humorist in its
relation to that of the comedian and of the satirist. The comic spirit,
placing itself at the social point of view, projects as laughable show
an eccentric individual, or group of individuals. Satire, when it
attacks the manners of an age, may be said to project the society,
turning it into an object of derision. Humour, as we have seen,
sometimes does the like, though in its laughter at the social scene it
is neither passionately vindictive nor concerned with the practical
problem of reforming a world. To this may be now added that as a
sentiment nourished by sympathy it tends, when something of
philosophic width of contemplation is reached, to combine the social

and the individual mode of projection by taking up the self into the
spectacle of the whole.
Enough has been said, perhaps, on the developments of
individual laughter. Its point of view seems on inquiry {411} to justify
itself as a distinct and a legitimate one. With some idea of the ways
of this, as well as of the larger laughter of societies and groups, we
should be able to form an estimate of the final significance and
utility of the laughing impulse.
Laughter, born of play, has been seen above to possess a social
character. Throughout the evolution of communities, from the first
savage-like tribes upwards, we have observed it taking a
considerable part in the common life, helping to smooth over
difficulties of intercourse, to maintain what is valued, and to correct
defects. It remains to ask under this head, what is its whole value
to-day as a social force, and what indications of the future can be
discovered in the tendencies which we note in its later social
developments.
These questions appear to be best approached by a reference to
the results of our study of comedy. This, in its higher forms, has
shown itself to be the clear expression of the attitude of a
community, when it would laugh away something in its members
which it sees to be unfitting, though it may not regard it as serious
enough to call for a more violent mode of ejection. That which is
thus lightly dismissed is always something which looks anti-social,
whether or not it takes on for moral reflection the aspect of a vice.
A common tendency among writers on comedy is to claim for it
the value of a moral purgative, to attribute to it the power of

effecting directly a process of self-correction in the spectator. Even
Congreve and Vanbrugh, in their defence of their plays against
Jeremy Collier, pretended that they were reformers of the world.
This agreeable supposition will not, one fears, bear critical
inspection. One objection, just touched on, is that comedy {412} does
not deal a blow straight at the immoral, as the language of Aristotle
and of some of his citers appears to suggest. This circumstance
seems to stand seriously in the way of its effecting a moral
purification. Nor does the holding up to merry contemplation of the
tendency of men to stray too far from the customary social type,
imply a serious purpose of correction behind. Though she may wear
a shrewishly corrective expression, the Comic Muse is at heart too
gay to insist on any direct instruction of her audience. A glance at
her stern-eyed sister, Satire, will convince us of this. On the other
side, we meet with another and more fatal objection: the mental
pose of the spectator at the comic show makes it extremely unlikely
that he should at the moment apply the object-lesson so as to
discern the laughable side of his own shortcomings. One remembers
here that a man is all too slow in making such a self-application even
in the serious surroundings of a church, where a remark, pointed
perhaps with a significant turn of the finger (I speak of ruder times),
is recognised by all but himself as specially aimed at him; and if so,
how can we expect a spectator at a comedy, in the playful mood
which has no room for any serious thought, to rub in the moral
medicament supplied him?
Such purification as is possible can, it is plain, be only indirect.
When Lessing writes “the whole of morality has no more powerful
and effective preservative than the laughable” he seems to imply

this indirectness. So far as the provocative lurks in the immoral, we
can say that our laughter at the comic exhibition may serve as a
useful prophylactic. By tracing out, with the guidance of the comic
poet, the unsuspected developments and effects of a failing, we may
be furthering our moral salvation through the setting up of a new
internal safeguard. If the tendencies should {413} later on thrust up
their ugly forms in ourselves, the fact of our having laughed at them
may make a considerable difference in the swiftness and energy of
the movement of repression. The fear of becoming ridiculous, which
grows better defined and so more serviceable in one who has made
acquaintance with comedy, is a valuable side-support of what we call
moderation and reasonableness in men; and comedy is entitled to
her modest meed as one of our health-preservers.
Yet we may easily go wrong here, doing an offence to our gay
enchantress by taking her words too seriously. She looks, at any
rate, as if she wanted much more to please us than to improve us.
In considering her aim one is reminded, through a relation of
contrast, of what Aristotle said about the connection between
pleasure and virtue. The good man, he tells us, though aiming at
virtue, will be the more satisfied if pleasure comes by the way, giving
a kind of unexpected finish to the virtuous achievement. The art of
comedy merely reverses the order: she aims directly at pleasure, but
is far too good-natured and too wise to object to furthering virtue if
this comes as a collateral result of her entertainment.331
The comedy, at once wise and gay, of a past age seems to have
parted from us; and one would look in vain to newer developments
of the art for any considerable instruction in the lesser social
obligations. Nor is the corrective function of a large communal

laughter likely to be carried on by such new forms of art as our
“social satire,” in so far as these can be said to keep at the point of
view of the good sense of a community. The tendency to-day seems
to be rather to force a laugh from us at some bizarre extravagance
of manners, which we could never {414} think of as a possibility for
ourselves; or, on the other hand, to bring us near a cynical point of
view, at which the current of our laughter becomes shallow and
slightly acidulated, a point of view which has little, if any, promise of
a moral stiffening of the self against insidious attack.
In spite of this, laughter, or the potentiality of it, remains a social
force. A measure of faith enables one to believe that even a political
leader is sometimes checked by the fear of laughter—on the other
side. It is probable that the men of good sense in every community
are kept right more than they know by the faintly heard echo of the
“dread laugh”. If there is a danger just now of a conspiracy between
a half-affected over-seriousness on the one side and an ignorant
pretentiousness on the other, in order to banish the full genial laugh
of other days, we may be allowed to pray fervently for its failure.
We have seen a tendency to claim too much in the way of
serious function for the laughter of comedy. This desire to emphasise
its practical utility, which is to be looked for perhaps in a people too
pragmatic to seize the value of light things, is illustrated in a curious
and mostly forgotten dispute as to the fitness of ridicule to be a test
of truth. The debate was opened by Shaftesbury, who maintained its
fitness, and was carried on by Warburton, Karnes and others. Much
of it reads quaintly naïve to-day. Shaftesbury’s paradox almost
sounds like a malicious attempt to caricature the theory of Prof. W.
James, referred to in an earlier chapter of this work. To suggest that

we know a piece of folly, say that of Malvolio, to be folly because we
laugh at it, is surely to be thrusting on our laughter a dignity which
is quite unmerited, and, one may add, does not become it. This
point was not held to in the discussion, which, as I have {415} shown
elsewhere, soon became a contest about the rights and the
restraints of laughter.332
There is a like risk of exaggerating the useful function in
estimating the service of laughter to the individual. No deep
penetration of mind is needed for perceiving that a lively sensibility
to the touch of the ludicrous will expose a man to considerable loss.
To all of us, so far as we have to live in the world and consort with
those who, being both solemn and dull, are likely to take offence, if
not with those who, like Mr. Meredith’s entertaining ladies, cultivate
the fine shades, a quick eye for drolleries is likely to bring situations
of danger. This drawback must be considered in appraising the total
value of laughter to a man.
With respect to its function as aiding the individual in a healthy
self-correction, enough has been said. It is, in truth, no small
advantage to be able to blow away some carking care with a good
explosion of mirth. And if the world is much with us, we shall be
likely to need laughter now and again as a protection from contact
with much that is silly and much that is unwholesome. Yet, in this
case, too, the chief value seems to reside in its immediate result, the
gladdening and refreshing influence on the laugher, which has in it a
virtue at once conciliatory and consolatory. This it is which makes it
so good to step aside now and again from the throng, in which we
too may have to “wink and sweat,” so as to secure the gleeful
pastime of turning our tiresome world for the nonce into an

entertaining spectacle; amusing ourselves, not merely as {416}
Aristotle teaches,333 in order that we may be serious, but because
our chosen form of amusement has its own value and excellence.
It is one thing to assign to laughter a definite ethical or logical
function, another to ask whether it has its place among the worthier
human qualities. We have seen how some have denounced it,
indiscriminately as it would seem, as a thing irreverent if not
unclean. That view does not come further into the present
discussion. We have only to ask what kind of dignity it has.
It is assumed here that we exclude the more malignant and the
coarser sorts of laughter. A considerable capacity for the pure mirth
which the child loves—and comedy may be said to provide for the
man who keeps something of the child in him—supplemented by a
turn for the humorous contemplation of things is, I venture to think,
not merely compatible with the recognised virtues, but, in itself and
in the tendencies which it implies, among the human excellences.
This is certainly suggested by the saying of Carlyle: “No man who
has once heartily and wholly laughed can be altogether irreclaimably
bad”.334 We may not be able to rise to the point of view of R. L.
Stevenson, when he wrote, “As laborare so joculari est orare;”335 yet
we may be inclined to think that it is impossible to construct the idea
of a man who can be described as decently complete without
endowing him with a measure of humour. Whatever our view of the
“Good,” reasonable men of all schools appear to allow some value to
a capacity for pleasure, especially the social pleasures, among which
laughter, even when it seems to retire into solitude, always keeps a
high place. On its intellectual side, again, as the {417} play of mind,
the mirthful disposition has an intimate relation to such valuable

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The Long Covid Handbook Gez Medinger Danny Altmann

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