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MARIJUANA LEGALIZATION
WHAT EVERYONE NEEDS TO KNOW®
 MARIJUANA
LEGALIZATION
WHAT EVERYONE NEEDS TO KNOW®

Second Edition

JONATHAN P. CAULKINS, BEAU KILMER,

AND MARK A. R. KLEIMAN

1
 3
Oxford University Press is a department of the University of Oxford. It furthers
the University’s objective of excellence in research, scholarship, and education
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of Oxford University Press.

Published in the United States of America by Oxford University Press

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© Oxford University Press 2016

First Edition published in 2012

Second Edition published in 2016

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and you must impose this same condition on any acquirer.

Library of Congress Cataloging-​i n-​Publication Data

Names: Caulkins, Jonathan P. (Jonathan Paul), 1965–author. | Kilmer, Beau, author. |
Kleiman, Mark A. R., author.
Title: Marijuana legalization : what everyone needs to know /​
Jonathan P. Caulkins, Beau Kilmer, Mark A. R. Kleiman.
Description: Second edition. | New York, NY : Oxford University Press, 2016.
Identifiers: LCCN 2015043342 (print) | LCCN 2015047763 (ebook) |
ISBN 978–0–19–026241–9 (hardcover : alk. paper) |
ISBN 978–0–19–026240–2 (pbk. : alk. paper) |
ISBN 978–0–19–026242–6 (Updf) | ISBN 978–0–19–026243–3 (Epub)
Subjects: LCSH: Marijuana—​United States. | Marijuana—​Law and
legislation—​United States. | Drug legalization—​United States.
Classification: LCC HV5822.M3 M2935 2016 (print) | LCC HV5822.M3 (ebook) |
DDC 362.29/​50973—​dc23
LC record available at http://​lccn.loc.gov/​2015043342

1 3 5 7 9 8 6 4 2
Printed by Courier Press, USA
 We dedicate this book to the public servants
wrestling with the difficult job
of implementing new marijuana laws
and trying to make them work for everyone.
Whether or not those laws prove to be good for the country in the end,
we all benefit from the honest and diligent efforts
of these underpaid and often unappreciated officials.
 CONTENTS

ACKNOWLEDGMENTS xvii

Introduction 1

PART I MARIJUANA AND PROHIBITION

1 What Is Marijuana? 5

What does “marijuana” mean? 5

What is marijuana legalization? 5
How does it feel to get high? 7
What are the active ingredients in marijuana? 7
What are the varieties of the cannabis plant? 8
What are the varieties of marijuana products? 9
What is industrial hemp? 10
What are the alternatives to smoking? 11
Has marijuana been getting more potent? 12
Is higher potency bad? 13
How long does intoxication last? 14
How long after use can marijuana be detected? 15
viii Contents

Is medical-marijuana the same as illegal marijuana? 16

What is synthetic marijuana (Spice or K2)? 17
Additional Reading 18

2 Who Uses Marijuana? 19

How many people use marijuana? 19

How has marijuana use changed over time? 20
How have marijuana policies changed in the past half century? 21
How much marijuana do users consume? 23
Can marijuana use lead to dependence or addiction? 24
How common is marijuana use in the United States? 25
What are typical patterns of marijuana use? 27
To what extent do heavy users dominate consumption? 29
Has heavy use become more common? 30
How much do users spend on marijuana? 31
Additional Reading 33

3 What Are the Risks of Using Marijuana? 34

Why is it difficult to measure the consequences of marijuana use? 34

How do researchers study the consequences of marijuana use? 36
What is the likelihood of becoming dependent on marijuana? 38
How bad is marijuana dependency compared to dependency
on other drugs? 40
How many users enter treatment for marijuana? 40
Does marijuana treatment work? 41
Can users experience a fatal overdose from marijuana? 43
Can users experience a nonfatal overdose from using
too much marijuana? 44
Does marijuana use cause emphysema and other
respiratory problems? 45
 Contents ix

Does marijuana use cause cancer? 46

How much harm does secondhand marijuana smoke cause? 48
Is marijuana a “gateway drug”? 49
How does marijuana affect brain development? 50
Does using marijuana lead to cognitive impairment
and a reduction in IQ? 52
Does marijuana use affect education and employment? 53
Does using marijuana cause schizophrenia and other
mental health problems? 54
Does using marijuana influence crime and delinquency? 57
Does marijuana cause automobile crashes? 58
Does mothers’ prenatal marijuana use affect their babies’ health? 60
Should mothers who use marijuana breastfeed their babies? 61
How does parental marijuana use influence child welfare? 62
Is marijuana really safer than alcohol? 63
Additional Reading 65

4 What Is Known About the Nonmedical Benefits

of Using Marijuana? 67

Why don’t we know more about the benefits of marijuana use? 68

Would there be more high-​quality research if marijuana
were legal nationally? 69
Is there a “stoned” way of thinking? 69
Is “stoned thinking” valuable? 70
Does marijuana use enhance creativity? 72
Can marijuana use enhance athletic performance? 74
What role does cannabis play in worship? 75
So there’s no real evidence of any benefits? 75
Why should mere pleasure count as a benefit? 75
Additional Reading 77
x Contents

5 What Are the Medical Benefits of Marijuana? 78

Is marijuana medicine? 78
But isn’t smoking unhealthy? 79
What did the 1999 Institute of Medicine report (really) say? 80
What is the state of the medical-marijuana literature today? 81
Does marijuana have legally recognized medical value
in the United States? 84
Why isn’t marijuana available as a regular prescription drug
in the United States? 85
What is happening with medical-marijuana outside the United States? 87
If there are pharmaceutical cannabinoids, is there any reason
to use plant material? 88
Additional Reading 90

6 How Stringent Is Marijuana Enforcement

in the United States? 91

Does it make sense for marijuana to be a Schedule I substance? 91

Who gets arrested for marijuana possession? 93
What happens after those possession arrests? 96
How harshly are marijuana producers and traffickers punished? 98
How many people are in prison for marijuana offenses? 99
Additional Reading 100

PART II NATIONAL LEGALIZATION

AND ITS CONSEQUENCES

7 What Are the Pros and Cons of

Legalization Generally? 103

What does it mean to legalize a drug? 103

What is the essential tradeoff between legalization and prohibition? 104
What are the shades of legalization? 105
 Contents xi

Why have drug laws in the first place? 107

Why even consider legalizing a substance whose use creates harm? 108
Wouldn’t the result of a policy that treated marijuana like alcohol
be an improvement over the current mess? 110
But wasn’t alcohol prohibition in the United States a complete failure? 111
How much of the increase in consumption after legalization would
reflect increased heavy use rather than increased casual use? 112
Can’t the effects of marketing be reined in by regulations and taxes? 113
What about legal availability without free trade? Couldn’t that work? 114
Isn’t it impossible to make someone better off by coercing
behavioral change? 114
If people choose to harm themselves with drugs, why is that
anyone else’s business? 116
But isn’t everyone with an addictive personality already addicted
to something? 118
If the results of legalization are uncertain, why not just try it out,
and go back to the current system if legalization doesn’t work? 119
Additional Reading 120

8 How Is Legalization of Marijuana Different

from Legalization of Other Drugs? 121

How does legalizing marijuana compare to legalizing all drugs? 121

Isn’t marijuana known to be safe? 122
If marijuana accounts for half of all drug arrests, would legalizing
marijuana free up half of our prison cells? 122
How much drug-​related crime, violence, and corruption would
marijuana legalization eliminate? 124
Would legalization increase marijuana use and dependence by as much
as legalization of crack and other drugs would increase their markets? 125
Would more marijuana use lead to more alcohol abuse, or less? 126
Would more marijuana use lead to more or less abuse
of other substances? 127
If alcohol is more dangerous than marijuana, what’s the logical
justification for one being legal and the other illegal? 128
xii Contents

Could it be reasonable to support legalizing marijuana while

keeping some other drugs illegal? 129
Can two reasonable people sensibly disagree about
marijuana legalization? 130
Additional Reading 130

9 What if We Treated Marijuana Like Alcohol? 131

What special regulations could apply to legal marijuana? 132

Could advertising be restricted in the United States? 134
How could marijuana be taxed? 136
Would regulations and taxes in practice approach
the public health ideal? 137
How much enforcement would regulation and taxation require? 138
How many marijuana-​related arrests would there be after legalization? 139
What would happen to marijuana prices after national legalization? 140
How many people would be employed in marijuana growing? 144
What would the pretax retail price be for unbranded marijuana? 145
What would the after-​tax retail price be for unbranded marijuana? 146
What would the retail price be for branded and other forms
of marijuana? 148
Would some businesses give legal marijuana away free? 150
How much would consumption increase? 151
Would legalization reduce drug violence in Mexico? 153
Does legalization pass the benefit-​cost test? 153
Additional Reading 158

10 How Would Alcohol-​Style Legalization Affect

Me Personally? 159
How would legalization affect me if I’m a typical regular adult user? 159
How would legalization affect me if I’m already dependent on marijuana? 161
How would legalization affect me if I’m an occasional marijuana user? 161
How would legalization affect me if I’m not currently a marijuana user? 162
 Contents xiii

How would legalization affect me if I’m a medical-marijuana patient? 163

How would legalization affect me if I’m a marijuana grower? 164
How would legalization affect me if I lead a Mexican drug
trafficking organization (DTO)? 165
How would legalization affect me if I’m a taxpayer? 165
How would legalization affect me if I’m an employer? 165
How would legalization affect me if I’m a parent of a teenager? 166

11 Between Marijuana Prohibition and Commercial

Legalization: Is There Any Middle Ground? 169
Are there options in between prohibition and commercial legalization? 169
What has been learned from decriminalization? 170
What about legalizing marijuana the way Portugal did (not)? 172
What about imitating the Dutch approach? 174
What about just allowing home production? 175
What about user co-​ops and collectives? 177
What about a very liberal medical-marijuana system? 179
Couldn’t users go to physicians for nonmedical-marijuana? 180
What if the government had a monopoly on the industry, or on
retail sales specifically? 181
What if the market were limited to nonprofits, “for-​benefit”
corporations, or other socially ​responsible organizations? 182
What about limiting the quantity any user can buy? 183
Why have a middle path for marijuana but not for alcohol? 185
Additional Reading 185

PART III THE CRAZY QUILT OF CONFLICTING

POLICIES TODAY

12 Where Are We, and How Did We Get Here? 189

How many states have legalized or decriminalized marijuana? 189
How did we get to the current crazy quilt of conflicting policies? 191
xiv Contents

How has support for legalization in the United States varied over time? 193
Who supports and who opposes legalization in the United States? 194
Who votes for legalization? 195
Who is funding the legalization movement? 196
Additional Reading 198

13 What’s Really Happening

in Medical-Marijuana States? 199
When did medical-marijuana get started in the United States? 199
Where does medical-marijuana come from? 201
How medical is medical-marijuana? 203
Are CBD laws really about marijuana? 205
Was there a “Sanjay Gupta” effect? 206
What is the federal government doing in states that allow
medical-marijuana? 208
Who recommends medical-marijuana to patients? 209
Was medical-marijuana invented as a wedge issue to open the gates
for full legalization? 211
Do medical-marijuana laws increase nonmedical-marijuana use? 212
What are the other population-​level consequences of
medical-marijuana laws? 213
Additional Reading 215

14 What Is Happening in Colorado

and Washington? 216
If Uruguay, Alaska, and Oregon have all legalized, why focus
on Colorado and Washington? 216
What are the key provisions common to Colorado and Washington? 217
Are revenues from taxes making a difference in state budgets? 218
Have black market sales disappeared in Colorado and Washington? 219
Are Colorado and Washington exporting marijuana to other states? 219
 Contents xv

Why pay so much attention to edibles? 220

What do Colorado and Washington tell us about the likely results
of legalization elsewhere? 221
Did legalization increase or decrease crime? 222
How did legalization affect use? 223
What is the evidence concerning effects on youth? 224
What happened to emergency department cases? 225
What has happened to traffic safety? 226
Do marijuana operations have to be cash-​only businesses? 227
How do Colorado and Washington’s medical-marijuana industries
interact with the new legal systems? 228
Additional Reading 230

15 What Is Happening in Alaska, Oregon,

Jamaica, and Uruguay? 231
What is happening in Uruguay? 231
What is happening in Jamaica? 232
How do the laws in Alaska and Oregon compare to those
in Colorado and Washington? 234
What exactly did Washington, DC, legalize? 235
What states might vote on legalization in 2016? 236
Additional Reading 238

16 What Happens When Marijuana Laws Clash? 239

Can a state legalize something that the federal government prohibits? 239
Can there be local exceptions to state marijuana laws? 240
Should local government be allowed to opt out of state legalization? 240
Is marijuana actually legal in a state that legalizes? 242
Can a state regulate and tax a substance that the federal
government prohibits? 243
What about the reverse: If the federal government legalized marijuana,
could a state still prohibit it? 243
xvi Contents

What could the federal government do in response to a state

legalizing marijuana? 244
Could federal noninterference be formalized? 246
Would marijuana legalization violate international law? 246
Does Dutch policy violate these international conventions? 248
What are the consequences of violating international conventions? 248
Could these international treaties be changed? 249
Should there be international treaties on drugs at all? 250
Additional Reading 252

PART IV THE FUTURE OF MARIJUANA LEGALIZATION

17 What Might the Future Hold? 255

Why isn’t the status quo stable? 255
Are high state taxes sustainable in the long run? 257
How much depends on 2016? 258
Will alcohol-​style commercial legalization beat out more
moderate approaches? 259
How long will it take to see all the effects of legalization
on the industry? 260
How long will it take to see all the effects of legalization on use
and dependence? 262
Will other countries legalize? 263
What is the chance all of our predictions will prove correct? 264

18 What Do the Authors Think Ought to Be Done

About Marijuana? 265

ADDITIONAL READINGS 269

INDEX 277
 ACKNOWLEDGMENTS

Partial support for this work was provided by a Harold and Colene
Brown Faculty Fellowship from the Pardee RAND Graduate School.
The views expressed imply no endorsement by any funder.
This book inherited much from our earlier Oxford University
Press books Drug Policy: What Everyone Needs to Know and
Marijuana Legalization: What Everyone Needs to Know, co-​authored
with Angela Hawken. Although other commitments prevented
Angela from fully participating in the current effort, we benefited
greatly from the insights and hard work she contributed to those
earlier books and from her comments on this version.
We received many useful comments on this volume and other assis-
tance from friends and colleagues including Alberto Aziani, James
Anderson, Martin Bouchard, Shawn Bushway, Marjorie Carlson, John
Coleman, Maria Cuellar, Steve Davenport, Tom Decorte, Michael Farrell,
Erin Flanagan, Richard Hahn, Laura Griner Hill, Kevin Haggerty,
Wayne Hall, Caitlin Hughes, Marian Jarlenski, Sam Kamin, Magdalena
Kulesza, Jonathan Kulick, Miles Light, Erin Kilmer Neel, Pat Oglesby,
Rosalie Liccardo Pacula, Mafalda Pardal, Bryce Pardo, Melissa Piccard,
Rosario Queirolo, Peter Reuter, Mark Ristich, Alison Ritter, Steve Rolles,
Sue Rusche, Eric Sevigny, Joe Vesely, Chris Wilkins, and a federal pris-
oner who prefers not to be named. We thank Jeyashree Ramamoorthy
for managing the production process. Of course none of them bears any
responsibility for our views.
We are deeply indebted to Angela Chnapko for her editorial
guidance—​and patience.
For additional information about the book and the authors, please
visit http://​www.marijuanalegalization.info.
MARIJUANA LEGALIZATION
WHAT EVERYONE NEEDS TO KNOW®
 INTRODUCTION

Should marijuana be legalized?

If you picked up this book in search of a clear yes or no answer,
consider putting it back on the shelf. We won’t tell you how you
should vote. We instead want to help you reach your own informed
conclusion and appreciate that the issues are more nuanced than
advocates on either side of the debate will usually acknowledge.
The consequences of legalization are unpredictable: no one can
say for sure how much more marijuana might be used after legal-
ization, how much of that additional consumption would involve
teenagers or people with serious drug problems, or whether heavy
drinking, tobacco smoking, and other substance-​abuse problems
would increase or decrease as a result. That isn’t to say that we have
to decide entirely in the dark: a vast amount is known about the use
of marijuana, about the use of other psychoactive chemicals, and
that store of knowledge contains some valuable hints about likely
futures. But the uncertainties remain.
Even people who agree in their predictions might still disagree
about the desirability of legalization, because they value the pro-
jected outcomes differently.
And even if we had perfect foresight and agreed entirely about
values, the question “Should marijuana be legalized?” would still
not be answerable, because “legalization” doesn’t describe a specific
alternative. Allowing home-​growing is one form of legalization; so
is a completely free market that allows joints to be sold like corn-
flakes. There’s no reason to expect someone who likes (or dislikes)
one form of legalization to like (or dislike) all the others.
Moreover, the alternative to “legalization” is “prohibition,” but
that, too, comes in a variety of flavors and colors. There is tremen-
dous variation in the intensity of marijuana enforcement and sanc-
tions for violations, even within the United States.
2 Introduction

So the smart response to “Are you for marijuana legalization?”

would be a pair of questions: “What kind of legalization?” and
“Compared to what kind of prohibition?”
That does not keep most Americans from answering the poll-
sters’ question “Do you favor legalizing marijuana use?” Four years
ago, when we wrote the first edition of this book, public opinion was
just about evenly split, representing a remarkable upsurge in sup-
port for legalization over the previous twenty years. Opinion has
continued to shift in a pro-​legalization direction: supporters now
usually outnumber opponents by more than ten percentage points.
In the interim, four states have replaced their prohibition poli-
cies with commercial legalization, giving us for the first time actual
evidence about some of the early consequences of letting companies
supply marijuana to any adult. Also, in 2013 Uruguay embarked
on a very different approach, with co-​ ops, home-​ growing, and
government-​controlled distribution, but not the commercialization.
Jamaica is setting up an odd hybrid model, medical on the surface
but aggressively commercial underneath.
Marijuana remains forbidden by federal law and by international
treaties (as well as laws in the other forty-​six states). But there is
continued demand for change.
The goal of this book is not to persuade you to support or oppose
legalization; as c­ hapter 18 shows, the three of us—​colleagues and
friends, in general agreement about the facts and with very similar
world-​views in many ways—​differ on what ought to be done. Our
goal instead is to provide the raw material needed for you to develop
informed opinions by presenting the issues fairly and sweeping
away the myths and fallacies common to these discussions.
We have been studying marijuana and marijuana policy for a
combined total of nearly seventy years, but what we know is only
a fraction of what is known, let alone the vast amount that remains
unknown. A thorough understanding would draw on ideas from
agronomy, anthropology, botany, chemistry, cognitive science, eco-
nomics, history, international relations, law, management, medi-
cine, neurobiology, operations analysis, pharmacology, philosophy,
policy analysis, political science, psychology, public administration,
sociology, and statistics.
In the face of all this complexity, we have done our best. The rest
is up to you.
 PART I
MARIJUANA AND PROHIBITION
 1
WHAT IS MARIJUANA?

What does “marijuana” mean?

“Marijuana” is the common (and legal) American term for the dried
flowers and leaves of the plant Cannabis sativa, and for the plant itself.
The flowers contain concentrated amounts of psychoactive (mood-​
altering) chemicals known as cannabinoids (produced only by this
plant), terpenoids, and flavonoids; the leaves that have become the
symbol of marijuana contain lesser quantities of the same chemicals.
The amounts and mixtures of these molecules vary with the genet-
ics of the plant, growing practices, and the timing of the harvest.
Most of the rest of the world (and most of the scientific litera-
ture) refers to marijuana as “herbal cannabis” and hashish—​which
is made by extracting the cannabinoid-​rich trichomes—​as “canna-
bis resin,” with “cannabis” being a catchall term that includes both
products.

What is marijuana legalization?

Marijuana is the most commonly used illegal drug in the world;
various forms have been used for thousands of years for their
medicinal, social, and aesthetic effects, in addition to the industrial
use of other parts of the cannabis plant for food, fuel, and fiber.
International treaties and the laws of most countries forbid grow-
ing, selling, and possessing marijuana. That makes lawbreakers out
of the more than 125 million people who have used the drug in the
past year, and also those who supply them. It creates illicit markets
with a total value in the tens of billions of dollars per year—​in the
ballpark of $40 billion per year in the United States alone. Some of
that illicit activity leads to violence and to the corruption of public
6 Marijuana and Prohibition

officials. Millions of users are arrested for possessing the drug,

and smaller but substantial numbers go to prison for growing and
selling it.
The legalization question concerns whether to change the laws
to make it legal to produce, sell, and possess (nonindustrial) mari-
juana, and, if so, what rules should apply.
Legalization would replace illicit market production and distri-
bution with an aboveboard industry. There could still be rules and
regulations, just as there are rules and regulations governing pro-
duction and distribution of alcohol, or for that matter of automo-
biles and avocados. But the bulk of the trade would be conducted by
farmers and merchants and retail clerks, not by criminals.
There are many ways to liberalize marijuana policy short of
legalization. Use could be tolerated but production and sale still for-
bidden, or possession of small amounts could be treated as a civil
violation rather than as a crime; that’s the policy confusingly called
“decriminalization.” Use and sale of small quantities could be toler-
ated while production and wholesale distribution remained forbid-
den; that’s the current policy in the Netherlands.
There are also many options for legal supply without jumping
to a commercial market along the lines of alcohol. Production, sale,
and use could be permitted only for certain specific medical pur-
poses. Or the whole activity could be restricted to noncommercial
channels, with users growing their own or forming cooperatives.
Even commercial legalization could include more or fewer
restrictions on sale and use. Alcohol can only be sold to adults and
by licensed sellers, while caffeine—​in the form of coffee or cola
drinks—​ is sold without restriction. Thinking about marijuana
legalization, then, involves an exercise in policy design. Repealing
current laws is simple in concept; what’s complex is figuring out
what might replace those laws.
Legalization of most currently banned drugs has little political
support. Marijuana is different. Public opinion polls typically find
that more than half of all Americans support legalizing the drug,
and four states have already created legal for-​ profit marijuana
industries (Colorado and Washington in 2012; Alaska and Oregon in
2014). Other states are considering marijuana legalization, including
California. Change in federal law, too, seems much closer now than
it did just a few years ago.
 What Is Marijuana? 7

How does it feel to get high?

The sensation of being under the influence of marijuana varies with
the type and quantity consumed, the person and his or her experi-
ence and purpose in using, and the social circumstances (“drug, set,
and setting”).
Science has little to say about the feelings generated by marijuana
intoxication or about how those feelings compare with the feelings
generated by other drugs. The marijuana experience is complex.
Most drugs taken for other-​than-​medical use can be classified as
either central-​nervous-​system (CNS) stimulants (such as caffeine,
cocaine, amphetamines, and MDMA) or CNS depressants (such as
alcohol and the opiate pain relievers, including morphine, oxyco-
done, and heroin), but marijuana is neither. While most psychoactive
drugs used for pleasure influence the systems pertaining to one or
more of three neurotransmitters—​dopamine, serotonin, or GABA—​
the chemicals in cannabis react with two other systems (CB1 and
CB2). And—​again unlike most recreational drugs—​marijuana con-
tains a large variety of psychoactive molecules, not just one. This
complicates efforts to define a dose or the marijuana equivalent of a
“standard drink” (roughly half an ounce of pure alcohol, whether as
a can of beer, a glass of wine, or a shot of spirits).
The effects of those actions and interactions are multiple and
oddly assorted: focusing attention on sensory experience, impairing
short-​term memory and the “executive function” in ways that inter-
fere with absorbing complex information and managing divided
attention, suppressing nausea, enhancing appetite for some foods,
and making users more receptive to humor and more attentive to
music. The effects are not always pleasant; users can experience
intense anxiety and panic attacks (see ­chapters 3, 4, and 5).

What are the active ingredients in marijuana?

Until recently, most discussion about the effects of marijuana
focused on a single chemical: delta-​9-​tetrahydrocannabinol, better
known as THC. THC is the main psychoactive ingredient in mari-
juana, and the one most responsible for its intoxicating effects.
The THC in the living plant occurs mostly in a nonpsychoac-
tive form called THC-A, which is converted to THC by drying and
8 Marijuana and Prohibition

heating. Once in the body, THC is further converted into scores of

metabolites, some of which are also themselves psychoactive. Many
common tests for “marijuana” in the human body actually mea-
sure these metabolites. As to the plant material, the percentage of
THC (including THC-A) by weight is a good measure of intoxicating
potency.
The effects of the other cannabinoids are less well understood
than those of THC. As far as is now known, none of them produces a
“high” in the absence of THC, but they interact with THC to alter its
impact in a variety of ways: enhancing or attenuating it, speeding up
or slowing down its onset, and influencing how long the effect lasts.
One compound drawing increasing attention from both scientists
and medical-marijuana providers is cannabidiol (CBD). CBD is not
intoxicating—​CBD alone doesn’t produce a high—​but there is evi-
dence it can blunt the anxiety sometimes produced by high doses of
THC, and it may also have independent anti-​anxiety, antipsychotic,
and antiseizure actions that might make it therapeutically useful. It
seems likely that marijuana with a lower ratio of THC to CBD may
pose less risk of overintoxication and dependency than the high-​
THC, low-​CBD strains now typical of expensive marijuana, but the
science remains unresolved.
Most marijuana users—​even those who know what CBD is—​
cannot detect its presence or absence in the material they use, and
even in stores in states where marijuana commerce is legal, the labels
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 Spread of Influenza in 1889–90.

Month. 1889–90.
First (October) St. Petersburg, Moscow, Courland, Livonia, Finland.
Second Berlin, Paris, Vienna, Sweden, Denmark.
Third London, Holland, Belgium, Balkan States, North America.
Fourth Capetown, Egypt, Honolulu, Mexico, Japan, Hong Kong.
Fifth San Francisco, Buenos Ayres, India, Sierra Leone, Scilly Islands.
Sixth Chili, Kamerun, Zanzibar, Basutoland, Tasmania.
Seventh British Bechuanaland, Barbados.
Eighth Gold Cost, Natal.
Ninth Trinidad.
Tenth Iceland, Madagascar, China, Senegal.
Eleventh Kashmir, Katunga.

Between the years 1889 and 1893 according to Leichtenstern there was no period
altogether free from influenza. Here and there individual cases or small epidemics
sharply localized were observed. In 1893 another epidemic appeared in many places and
became quite widespread. There was not, according to this author, the definite
geographic progression that had been observed in 1889. This was but a recrudescence, a
lighting up from endemic foci remaining after the first wide spread. In the first half of
1893 there was a light spring epidemic, and in November of the same year a larger
epidemic swept over the whole of Europe. The height of the latter was reached chiefly in
December.
The influenza incidence subsequent to 1893 will be discussed later.
 TABLE I.
Influenza epidemics previous to 1889.
Date. General Site of origin. Direction of Localities Rapidity of
features. spread. affected. spread.
1173 Rather meagre Unknown. Described in Not known.
description. Italy, Germany,
England.
1239 Described by Described in Invaded all of
1311 Zeviani. France. France.
Records not
definite. Not
generally
accepted.
1323 Mentioned by
Hirsch, Gluge
and Zeviani.
Most believes
it was a
typhoid
epidemic.
1327 Mentioned by Described in
Zeviani, Italy.
Hirsch and
Gluge. Rather
doubtful.
1358 Described by Savoy, Germany,
Zeviani. Not France,
generally Catalonia.
accepted.
1387 (Zeviani, Italy. Italy, France,
Schweich, Strasbourg,
Gluge, Hirsch Southern
and Germany.
Ripperger.)
Characteristic
description.
1403 A very short France. Described in
epidemic. France. In 1404
(Gluge, it invaded
Ripperger, Flanders and
Pasquier.) Germany
(Hirsch).
1411 Described only Described only Described by
in Paris. in Paris. Pasquier as in
Extent Paris.
unknown.
1414 Characteristic In Italy and
description. France in
February and
March. In the
Danube district
between
January and
April.
1427 Very Described in
 characteristic France.
description.
1438 Cited only by Described in
Zeviani. Italy.
1482 Very limited
description
by Mezeray.
1510 Widespread Malta (?) Generally, from Malta, Sicily,
over all of (Webster and South to Spain and
Europe. Hancock North. Portugal, Italy,
report that it France,
began in Hungary,
Africa). Germany,
Holland,
England,
Norway.
1557 All of Europe. Conflicting General direction Asia, 4 months from
information from South to Constantinople, Italy to
(Asia?). North in Sicily, Italy, Netherlands.
Europe. Spain, Sicily in June.
Dalmatia, Nimes in July.
Switzerland, Italy in August.
France, Madrid in
Netherlands, August.
England. Dalmatia in
September.
Netherlands in
October.
1562 Uncertain Only small
1563 information. epidemics at
most.
1580 True pandemic Orient (Hirsch) From Asia to Orient, North France in May.
covering the Africa and Constantinople Africa, Germany and
Orient, Africa Malta and in Europe Constantinople, Hungary in
and Europe. (Pechlin). from South to Malta, Venice, August.
North. Sicily, Italy, England and
Spain, Hungary Rhine Valley in
and Germany September.
to the Baltic, Saxony in
Bohemia, October.
France,
Belgium,
England,
Denmark,
Sweden.
1587 Apparently Described in Italy
quite and Germany.
localized.
1591 High mortality.
Indefinite
information.
1593 Spread over a Said to have Uncertain.
wide area in commenced
Europe. in Belgium,
“following a
violent
 earthquake,”
and gradually
extended over
all the cities of
Europe.
1626 Local. Described in
Italy.
1627 In America. Spread from
North America
to West Indies
and Chili.
1647 In America
(Webster).
1658 Local. England (?). Described in
England and in
Treptow near
Stettin.
1675 Over Western Germany (?). Germany, Germany in
Europe. Hungary, September,
England, England and
France. France in
October and
November.
1688 Apparently England(?). Described only in
localized in England and
Great Britain Ireland.
and Ireland.
1693 England and Dublin(?). Dublin, Oxford, One month from
the adjacent London, Dublin to
continent. Holland, London.
Flanders.
1709 A period of In 1712, onset in 1712, spread Italy, France, Six months from
1712 extensive Germany. from Germany Belgium, Germany to
endemics. to Holland and Germany, Italy.
Italy. Denmark.
1729 First epidemic Usually Russia through Moscow, Sweden, Moscow in April,
said to have designated as Sweden, Poland, Silesia, 1729. Sweden
originated in Russia Poland, Austria, in September,
Russia and (Moscow). F. Germany, etc. Hungary, England in
first Hoffman to Italy and England, November.
described as claimed to perhaps North Switzerland, Paris in
entering have seen the America. France, Italy, December.
Europe from epidemic in Iceland. Rome in
the Northeast Halle in February,
rather than February, 1730.
the 1729.
Southeast.
First spread.
Pandemic
period.
1732 Second spread. Over Europe and Germany in
Pandemic America. November.
period. According to France in
Pelargus it January, 1733.
again followed Spain and Italy
the route from in February.
 Russia through
the North of
Europe and
then South.
1737 Not generally England, North
recognized. America,
Barbados,
France.
1742 Slow spread Began either on Occurred in Germany, Germany in
1743 from the shores of Germany in Switzerland, January, 1742.
Germany. the Baltic Sea Jan. and Feb., Italy, France, England in
Recurrences or in single 1742, and then Holland, April, 1743.
in Germany cities in disappeared to Belgium,
up until 1745. Germany. reappear in England.
Switzerland in
the spring.
1757 A period of Began either France, Scotland, Barbados, Villalba states
1758 related first in North America, Germany, that the
1761 epidemics America and Finkler states Austria, epidemic in
1762 with spread thence that in 1762 Hungary, 1767 had
1767 complicated to Europe or influenza first Denmark, traveled over
geographic else began started in England, the whole of
pictures and spontaneously Germany and Ireland, Alsace. Europe in a
without clear in both spread thence period of two
cut direction hemispheres. in a very months.
of spread. irregular way
over Western
Europe. Gluge
and Hirsch
state that in
1767 the
disease
appeared
simultaneously
in Europe and
North
America.
1775 Slow spread First First spread to Germany, Italy, Invaded Vienna
1776 through appearances Vienna, and Austria, in June. Made
Western in Autumn of after a England, appearance in
Europe. 1775 in village quiescence Ireland, France. Italy in
of Clausthal in broke out in September. In
the Harz France and England and
mountains. England and France in
possibly October,
spread to November and
America and December.
China.
1780 Western January, 1780 in Spread to Alsace, Three months
1781 Europe and France. Germany and from France to
possibly Italy, and in Brazil.
Brazil and March
China. reported in Rio
de Janiero.
Appeared in
Sept. 1780 on
 Southern coast
of China.
1781 One of the most China and Through Siberia China, India, Moscow,
1782 widespread perhaps India and Russia to America, January, 1782.
pandemics. in Autumn of Petrograd, Russia, Riga, Riga,
Abundant 1781 (Hirsch). Finland, Riga, Germany, February.
literature. English Germany, etc. England, Germany,
writers Scotland, March.
connect onset Netherlands, England, April.
with Ireland, France, Scotland, May.
occurrence of Italy, Spain. Ireland,
influenza in France and
the British Italy, June.
Army in India, Spain, August.
Nov., 1781.
Wittwer and
others begin
its history in
Petrograd in
January, 1782.
1788 Throughout all Russia, in West and South. Russia, Germany, Seven months
1789 of Europe. March, 1788. Spread in Hungary, required to
One year “Apparently America in Denmark, cover this
later in independent 1789 England, territory.
America. origin in throughout Scotland,
America in United States France, Italy,
Sept., 1789.” from New York Switzerland.
North and
South and
finally
touching the
West Indies,
South America
and Nova
Scotia.
Recurrences in
single cities of
U. S. in 1790.
1799 Local epidemic Origin in Russia. Spread West and Russia, Galicia,
1800 confined to South. Poland,
Northeastern Germany,
Europe. Denmark.
1802 Local endemic First reported in No clear cut France, Germany,
1803 outbreaks France. direction. Italy, England,
covering Recurrences Switzerland,
considerable until 1805–08. Central Europe.
territory General
which follow dissemination
the last throughout
period by a North America
quiescence of in 1807.
five months.
There
appears to
have been an
unassociated
epidemic
 early in 1800
in China and
one in Brazil.
1811 Several 1807, onset in Usually from North and South 1815, one month
1815 epidemics in Massachusetts New England America. from Boston to
1816 North in February. West and New York, and
1824 America and 1815, onset in South. five months to
1826 to some Boston in South Carolina
extent in September. and Brazil.
South 1824, onset in 1824, three
America. Boston in months from
October. Boston to
Georgia.
1827 Widespread
epidemics
throughout
Eastern
Russia and
Siberia.
1830 Extensive China in To Manila in Entire earth. Ten months from
1833 influenza January, September, China to
period made 1830. 1830. Later to Russia. Four
up of two or South Sea months from
three Islands and Russia to
pandemic India. Germany. Two
periods. Appearance in additional
Russia in months
October, 1830, through
with France,
subsequent England,
spread West Scotland,
and South and Sweden,
on to North Belgium,
America (Feb., Switzerland.
1832). Six months
from Germany
to Italy.
1833 Second Probably Asia. After an interval Europe. (America Petrograd in
pandemic in of one year appears to have January.
above period. Europe was escaped this Berlin and
again visited second Constantinople
with an epidemic.) in March.
extensive Denmark and
plague which Sweden,
attacked the France and
same countries Great Britain
in about the in April, Italy
same order. in May.
1836 Third spread in Origin rather West and South Europe, Faroe Almost
1837 above period. obscure, as previously. Islands, simultaneous
possibly in Mexico,(?) invasion at
Russia. India, Java. Petrograd,
Sweden,
Denmark,
Germany and
England;
Egypt, Syria,
 France,
Ireland,
Holland, and
Switzerland
one month
later. Italy,
Spain and
Portugal yet
another month
later.
1838 Every year in 1838, February;
1847 this period Island of
with the Bourbon and
exception of Iceland.
1840 showed, 1838,
according to November;
Hirsch, some Australia and
local New Zealand.
epidemic. 1839,
Abyssinia.
1841, Germany,
Hungary,
Ireland.
1842, Belgium,
England,
France, Egypt,
Chili.
1843, Germany,
England,
Iceland,
France, Siberia,
the United
States.
1844, Germany,
England,
Switzerland,
Cayenne.
1845, Germany
and
Switzerland.
1846–1847,
France, Russia,
Constantinople,
Brazil,
England,
Denmark,
Belgium,
Switzerland.
1847 Epidemic Origin Spread not All of the
1848 period uncertain. definite, North countries of
throughout America in Western
Europe 1848. Europe, West
without clear Indies, New
cut direction Zealand,
of spread. Newfoundland,
Sandwich
Islands, Egypt,
 Algiers, West
Coast of Africa.
1850 Epidemics 1857, began in 1850–51, 1855, only one
1889 covering August in particularly month
larger or Panama and throughout the between
smaller spread to West whole Western Petrograd and
territory Indies and up coast of South Italy.
every year, and down the America with
but none to Pacific Coast. later spread to
compare in Prevailed in California &
intensity with Europe in Europe.
those of 1831, December. 1852, Australia,
1833, 1836 Tasmania,
and 1847. South America.
1853, Faroe
Islands.
1854, Bavaria.
1855, Europe,
spreading
rapidly West
and South from
Petrograd.
Later in same
year, Brazil.
1857–58,
widespread
epidemic in
both
hemispheres.
1860–70, very
irregular
appearances in
Australia,
Tasmania,
Philadelphia,
the Bermudas,
Holland,
California,
France,
Switzerland,
Africa,
Germany,
Belgium,
Russia,
Denmark,
Sweden and
Turkey.
1874–75,
Extensive
spread in
America,
Germany and
France, with
recurrence one
year later in
eleven areas of
the United
 States.
1879, America.
1885–88, Re-
appeared each
year in
Petrograd.
1889, (Spring)
Greenland and
Hudson Bay
territory. (May)
Bokhara in
Turkestan from
where the great
pandemic of
1889–90 is
usually said to
have taken its
origin.
Table I shows that prior to 1510 the information was so limited as to be not entirely
conclusive. We must rely upon the fragmentary descriptions of writers located usually in
or near the intellectual centers who described the disease as they saw it in their city or
country. We have no way of ascertaining what other countries were invaded, and we
possess no method by which we may enumerate the “silent areas,” countries which in
the absence of a chronicler have not been able to transmit their story.
There have been fourteen very widespread epidemics since 1510, all of which might
appropriately be designated as pandemics. They are those of 1510, 1557, 1580, 1593,
1729, 1732, 1762, 1782, 1788, 1830, 1833, 1836, 1847, 1889 and 1918. Some of these have
spread farther than others according to the records, but in nearly all we have reports of
influenza being present in practically every country provided with a historian. We may
find from the table another group in which there have been more or less extensive
epidemics, apparently related, but without any general direction of spread. Such are the
epidemics of 1709–12, 1757–67, 1802–03, 1838–47 and the period 1850–59. Finally,
there are at least ten periods during which relatively small areas have been affected with
epidemic influenza. Such for instance is the year 1688 when the disease was apparently
localized in Great Britain and Ireland; in the year 1693 when England and the adjacent
continent were involved, with little spread elsewhere; and again in 1742, when there was
a slow spread through Germany into adjacent countries with recurrences in the former
up until 1745.
In England the following epidemics have been recorded, some of them in great detail:
1510 and 1557, described by Thomas Short; 1658 by Willis; 1675, by Sydenham; 1729–
1743 by Huxham; 1732–33 by Arbuthnot; 1758 by Whytt; 1762 by Baker and Rutty; 1767
by Heberden; 1775 by Fothergill, who collected observations from many physicians; in
1782 by Gray, Haygath and Carmichael Smith; 1803 by Pearson and Falconer, and a
great number of others; 1833 by Hingeston and others; 1837 by Streeten, Graves, and
Bryson, etc.; 1847 by Peacock, Laycock and many others; also those of 1855 and 1889–
93.
According to Stallybrass, epidemic crests have been reached in England in 1789–90,
1802–03, 1830–32, 1840–41, 1848–51, 1854, 1869–70, 1879, 1890–91, 1898 and 1918
to 1920. The periodicity in multiples of ten years in this latter group is remarkable.
The disease appears to have visited North America in the years 1627, 1647, 1729, 1732,
1737, 1762, 1782, 1789, 1811, 1832, 1850, 1857, 1860, 1874, 1879, 1889, 1900, 1915–1916
and 1918–20. Abbott speaks particularly of the years 1647, 1655 and 1697–98, 1732,
1762 and 1782 and 1889 as being years of especial epidemic prevalence in this country.
 Clinical and Epidemiologic Identification.
Up to the present time we have discovered no one characteristic by which we may say
that a case or an epidemic is positively influenza. We have had to rely on the general
symptomatology, which indeed is sufficiently characteristic, although so nearly like the
symptoms of certain other diseases as to make us hesitate to make an absolute
diagnosis, and on the epidemic characteristics. The necessity of an absolute criterion in
the clinical diagnosis is particularly felt in the presence of an isolated interepidemic
case, or a small endemic outbreak. It is at this point that the opinions of epidemiologists
diverge, a divergence which results in two schools of thought in the explanation of the
endemic source of epidemic influenza. Are the interepidemic cases and the small
localized epidemics due to the virus which causes the great pandemics; are they
influenza vera, or are they entirely different diseases with similar symptomatology,
caused by some other microorganism and should they be designated by some other
name? Thus Leichtenstern remarks: “When we go over the records of the years 1173 to
1875, and particularly those of the last century, when the information has been more
extensive and more accurate, we find that scarcely a year has passed without news of the
epidemic occurrence of influenza at some point or other of the earth. Some of these local
and territorial epidemics are merely endemic recurrences of the great pandemics which
have left the germ deposited in the various localities. Others of these small epidemics
probably have nothing to do with influenza vera, but are local outbreaks of catarrhal
fever.”
Contrary to the usual belief, influenza is a disease of quite definite and distinct
characteristics, both clinical and epidemiological. The symptoms are clear cut, with
sudden onset, severe prostration out of all proportion to the clinical symptoms and to
the fever, headache and pain in the back, general body pains, and fever of greater or less
degree. There is usually a lack of leucocytosis or a true leucopenia. In uncomplicated
influenza there are as a rule no localizing symptoms. There may be a slight soreness of
the throat, or a slight cough, but these are at best mild. The fever lasts from three to five
days and disappears, while at the same time all of the symptoms clear up with the
exception of the profound prostration, which as a rule continues for some time,
rendering convalescence surprisingly slow. The pain in the back may remain for a week
or so. This is the description of uncomplicated influenza.
The manner of spread of epidemic influenza is constant in a primary epidemic and the
epidemic as a whole has certain features which render it characteristic. The sporadic
case has as a rule the same quite clear cut clinical symptomatology, but it fails to
manifest the one feature most characteristic of epidemic influenza—a high degree of
contagiousness. Further, although the symptoms in themselves are characteristic, there
is no one pathognomonic sign by which one may say, “this is a case of influenza,” and,
finally other disease conditions such as tonsillitis, frequently resemble it so much as to
cause error in diagnosis.
This becomes, then, one of the problems in the study of influenza epidemiology. It is a
matter of first importance to determine once and for all whether true influenza is with us
always, or whether it appears only at the time of the great pandemics. Upon the answer
to this question more than upon any other one thing rests our choice of methods of
eradication. Any procedures of preventive medicine that may be undertaken on the
assumption that the source of pandemic influenza is to be found in one or a few endemic
foci, such as the one supposed to exist in Turkestan, would fail utterly should the true
condition be that of a universal distribution of a relatively avirulent virus which from
time to time from some unknown cause assumes a highly increased virulence.
Before becoming involved in this very complicated question, let us familiarize
ourselves completely with the characteristics of the pandemic and epidemic variety of
the disease.
 General Characteristics of Early Epidemic
Outbreaks.
We have described the symptomatology of uncomplicated influenza. It is rare that this
clinical picture is seen alone during the height of an epidemic. Complications, chiefly of
the respiratory tract, as a rule occur in such a large proportion of individuals that they
very nearly dominate the picture. Although caused by various microorganisms, all of
which appear to be secondary factors the results are so characteristic that in the past,
descriptions of influenza epidemics have usually been descriptions of the complications
of epidemic influenza. Most influenza epidemics are complicated. But we do know from
the experience of recent years as well as from history that relatively uncomplicated
epidemics of influenza have occurred, and that when they do so occur a predominant
characteristic has been the extreme mildness.
It is a fundamental characteristic of pandemic influenza that early cases in widespread
epidemics, as well as in “pre-epidemic increases” are very mild, with a minimum of
respiratory complications and with exceedingly low mortality. It is because we are better
acquainted with the more severe variety that, when these mild precursors appear we are
always in doubt for a time as to their true identity.
In spite of our 20th century erudition, the influenza when it first appeared in mild
form in the American Expeditionary Forces in 1918, for a lack of better knowledge as to
its cause was called “three-day fever.” In Italy in the same year the designation of the
disease progressed from pappataci fever through “Spanish grip” and “summer
influenza,” until finally it was designated influenza, pure and simple. Sampietro in Italy
particularly discussed the possibility of the disease being pappataci fever.
Belogu and Saccone, who wrote in May of 1918, decided that the epidemic was not
influenza in spite of the manifest clinical similarity, chiefly because of the absence of
signs of secondary invasion, such as nervous symptoms, gastro-intestinal symptoms,
and pneumonia, and especially because of the rapid recovery after defervescence. They
also considered the possibility of pappataci fever and dengue, and ruled out both. They
discussed calling the condition “influenza nostras,” but reached no definite conclusion.
Trench fever was also considered by some. United States Public Health Reports for 1918
record that dengue was reported prevalent at Chefoo, China, during the two weeks
ended June 15th, 1918. One week later there was a paragraph stating, “Prevalence of a
disease resembling dengue and affecting about fifty per cent. of the population was
reported at Shanghai, China, June 15, 1918.” It is not impossible that this was influenza.
Zinsser reminds us that Hayfelder, when he saw the influenza as it spread in
Petrograd in November of 1889, remarked its close clinical similarity to the description
of an epidemic of dengue which had prevailed in Constantinople during the preceding
September. Hayfelder, in studying the 1889 epidemic at its onset in Russia and the East,
wrote of “Sibirisches Fieber” which was first looked upon as malaria owing to the
apparently complete absence of the complicating lesions habitually associated in our
minds with influenza.
The same difficulty in early identification was experienced in this country in 1918. At
the end of March of that year the author who was stationed at Camp Sevier, South
Carolina, was one of a Board of Officers appointed to investigate a disease which had
broken out among troops stationed at that camp. At that time the line troops consisted
of three infantry regiments and three machine gun battalions. On the day following a
parade in the city of Greenville a considerable number of men in three out of the six
organizations suddenly took ill. There were a few isolated cases in other organizations,
but in the one infantry regiment and two machine gun battalions the regimental
infirmaries were filled, and some cases were sent to the base hospital. Nearly all were
very mildly ill and exhibited the symptoms of pure uncomplicated influenza as described
above. The onset was sudden, there were the usual pains and aches, the bowels were
regular, there was a feeling of discomfort in the pit of the stomach in many instances,
and there were no sore throats and very little cough. Recovery was as a rule very rapid,
although about a dozen of the entire number developed pneumonia and some of these
died. Physical examination of those only mildly ill and who remained in the regimental
infirmary showed as a rule nothing, but in some instances scattered fine moist rales near
the hilus of the lungs. In some of the organizations the disease was definitely spread
down rows of company tents. Careful bacteriologic examination was made at the time
and the predominating organisms were found to be a gram-negative coccus resembling
micrococcus catarrhalis, and a non-hemolytic streptococcus. This was in uncomplicated
cases.
The Board decided that the disease should be called influenza, but our only basis for
such decision were the clinical symptoms and the contagious character. At that time
none of us dreamed of any possible connection with a severe epidemic to occur later,
and laboratory search for influenza bacilli which was carefully made in view of the
clinical diagnosis showed none of these organisms to be present.
At about the same time a similar epidemic was being experienced at Fort Oglethorpe,
Ga. V. C. Vaughan, in describing this epidemic, remarks: “A disease strongly resembling
influenza became prevalent in the Oglethorpe Camp about March 18, 1918. It soon
assumed pandemic proportions. Within two weeks every organization in Camp Forrest
and the Reserve Officers Training Camp was affected.
“The symptoms were as follows: Headache, pain in the bones and muscles, especially
the muscles of the back, marked prostration, fever, sometimes as high as 104 degrees.
Sometimes there was conjunctivitis, coryza, a rash and possibly nausea, recovery taking
place in a few days.
“In all organizations the epidemic was first located in companies before it became
general.
“The incubation period was short, not over one or two days.
“Some organizations suffered more than others for no apparent reason.
“It is probable that the epidemic disease was recently brought to these camps. If it is
genuine influenza, and the epidemiological features no less than the leading symptoms
seem to point to that disease, there is here offered the most reasonable explanation of
the outbreak which is now possible. No other disease spreads so fast or is so prostrating,
considering its symptoms.”
We will quote at some length from the report of Zinsser of the Chaumont epidemic in
France in 1918, because of the excellence of the description, and particularly because
Zinsser has followed three successive epidemics with successive increases in the
complications and corresponding transformations in the clinical picture. It is worthy of
special note that he has remarked that the influenza, as first seen at Chaumont, showed
nothing in the symptoms that would suggest a predominant respiratory tract infection.
 “It will be useful to discuss briefly the early cases as we saw them during the
Chaumont epidemic, not because the observations made there add much that is new
from a clinical point of view, but because they will remove any possible ambiguity
concerning our conception of influenza in its pure uncomplicated form.
“As far as we can judge the little outbreak at headquarters was typical of the first
advent of epidemic influenza in many places. The population of the town, at the time,
consisted of a large office personnel attached to the military administration, scattered as
to billets and places of work; of military units living in barracks and eating at common
messes; and of the townspeople. The epidemic descended upon individual military units
with the suddenness of a storm, striking a considerable percentage of the men, perhaps
most of the susceptible material, within less than a week, and ending almost as abruptly,
with only a few isolated cases trailing behind. Among the more scattered office workers
and among the townspeople it was disseminated more gradually and trailed along for a
longer period.
“These early cases were clinically so uniform that a diagnosis could be made from the
history alone. The onset was almost uniformly abrupt. Typical cases would become ill
suddenly during the night or at a given hour in the day. A patient who had been perfectly
well on going to bed, would suddenly awake with a severe headache, chilliness, malaise
and fever. Others would arise feeling perfectly well in the morning, and at some time
during the day would become aware of headache and pains in the somatic muscles.
“The typical course of these cases may be exemplified by that of J. T. W., a draftsman
attached to the 29th Engineers. He was perfectly well until May 20th, working regularly,
his bowels and appetite normal, considering himself healthy. On May 21st, at 4:30 A.M.
he awoke with a severe headache. He arose, forced himself to eat breakfast and tried to
go to work. He began to feel feverish and chilly. At the same time his headache became
worse, with pains in the back, and burning in the eye balls. At 2 P.M. he reported sick,
and was taken to the hospital with a temperature of 102.8 degrees. At midnight his
temperature dropped to 101.6 degrees, and came down to normal by noon of the 22d. As
he recovered he developed a slight sore throat, great soreness of the legs and a very
slight cough. He recovered completely within a few days.
“These cases with a few exceptions developed no rashes. One or two of them had
blotchy red eruptions which we felt incompetent to characterize dermatologically. The
leucocyte counts ranged from 5,000 to 9,000. A very few went above this. Sometimes
there was a relative increase of lymphocytes, but this was by no means regular. The few
spinal fluids that were examined were normal. As to enlargement of the spleen, we can
say nothing definitely.
“Soon after this we observed the disease in a Division, the 42d, then holding a part of
the line in front of Baccarat. Here it had already developed a somewhat different nature,
due, we believe, to the fact that the men of this Division were not, as were those at
Chaumont, living in a rest area, but were actively engaged in military operations,
working, sleeping, and eating under conditions that involved greater fatigue, less
protection against weather, and greater crowding in sleeping quarters. The Baccarat
cases were much more frequently catarrhal; sore throats, coughs and more serious
respiratory complications were more common. However, they were usually coupled
unmistakably with an underlying typical influenzal attack, sudden onset, pains and short
lived fever. Moreover, there were a great many of the entirely uncomplicated cases
interspersed with the others.
 “Still later, in September, October and November, respiratory complications were so
frequent and severe, came on so early in the disease, and the pneumonia mortality
became so high, that the fundamental identity of these later cases with the early three-
day fever might easily have been lost sight of by observers who had not followed the
gradual transformation.
“In consideration of these facts, it is apparent that etiological or other investigations
can throw no light upon the problems of influenza unless they are carried out with
clearer understanding of the differentiation between the complications and the basic
disease.
“The serious respiratory infections of the bronchi and lungs we can set down with
reasonable certainty as complications due, certainly in the overwhelming majority of
cases, to secondary bacterial invaders. It is a matter of considerable difficulty, however,
to know exactly where the basic disease stops and the complications begin; and whether
we must regard the mild sore throat and conjunctival injection which so often
accompany the simple cases as a part of this basic clinical picture, or as the simplest
variety of complication. This is much more than an academic question, since, as we shall
see, the bacteriological analyses of such lesions have played an important role in
etiological investigations.”
 Symptoms in Former Epidemics.
The difficulty in making a decision in the presence of an epidemic is very similar to
that of deciding whether the epidemics of former times were in each case influenza.
Some few have been recorded in which the description has corresponded fairly well to
that of primary uncomplicated influenza. Thus, concerning the epidemic of 1557 in
Spain, Thomas Short wrote as follows: “At Mantua Carpentaria, three miles from
Madrid, the epidemic began in August.... There it began with a roughness of the jaws,
small cough, then a strong fever with a pain of the head, back, and legs. Some felt as
though they were corded over the breast and had a weight at the stomach, all of which
continued to the third day at furthest. Then the fever went off, with a sweat or bleeding
at the nose. In some few, it turned to a pleurisy or fatal peripneumony.”
Most of the descriptions, however, have been of a general character and include
descriptions of the complicated periods of the epidemic. One of the more complete of the
early descriptions was that by Lobineau in 1414, who wrote: “C’était une espèce de
rhume, qui causa un tel enrouement que les chastelets furent obligez d’interrompre leurs
séances; on dormoit peu et l’on souffroit de grandes douleurs à la teste, aux reins et par
tout le reste du corps; mais le mal ne fut mortel que pour les vieilles gens de toute
condition.”
With this exception we possess no very good or complete description of influenza
prior to the epidemic of 1510. After that time they have as a rule been detailed enough to
enable identification. Hirsch bases his conclusions concerning the year 1173 chiefly on
the following quotation: “Sub hisdem diebus universus orbus infectus ex aeris nebulosa
corruptione, stomacho catarrhum causante generalem tussim, ad singulorum perniciem,
ad mortem etiam plurimorum immissam vehementer expavite.” Nearly all that we have
to go on in this description is the widespread incidence of the disease and the presence
of respiratory symptoms, particularly cough. In 1323 the description emphasizes only
the high morbidity. Thus, Pietro Buoninsegni writes: “In questo anno e d’Agosto fu un
vento pestilenzia le per lo quale amalò di freddo e di febbre per alcuni dì quasi tutte le
persone in Firenze e questo madesimo fu quais per tutta Italia.” The same author
describes the epidemic of 1327, emphasizing again the high morbidity and in addition
the low death rate: “In detto anno e mese fu quasi per tutto Italia corruzione di febbre
per freddo; ma pochi ne morirono.” Again in 1387, he emphasizes the same two features.
Pasquier, in writing of the epidemic of 1403 in France, says: “En Registres de
Parlement on trouve que le vingt-sixième jour d’avril 1403 y eut une maladie de teste et
de toux, qui courut universellement si grande, que ce jour-là le Greffier ne pût rien
enrégistrer et fut-on contraint d’abandonner le plaidoyé.” Here the high morbidity and
the symptoms, particularly cough and pain, are emphasized. In 1414, Baliolanus
describes again the high morbidity and symptoms, particularly cough and hoarseness:
“Eoque frigore humanis corporibus concepto ... tussis maxima atque raucitas orta unde
nullus pene ordo, aetas et sexus liber evasit.” In 1411, Pasquier writes the following: “En
1411 y eut une autre sorte de maladie dont une infinité de personnes furent touchez, par
laquelle l’on perdoit le boire, le manger et le dormir ... toujours trembloit et avec le estoit
si las et rompu que l’on ne l’osoit toucher en quelques parts. Sans qu’aucune personne
en mourut.”
 Subsequent to 1510 descriptions have been as a rule more definite. There are,
however, exceptions to this statement and these fall in the epidemics concerning which
there is some dispute.
 Manner of Spread.
More characteristic and more important from an epidemiologic standpoint than the
symptomatology in general, as we have discussed it, is the mode of development of the
epidemic as a whole.
Human intercourse.—Before the days of bacteriology the contagiousness of the
disease was little discussed. Its infectiveness was in fact not universally established until
the epidemic of 1889–1890. One of the first writers who attempted to see in the
influenza a contagious disease was Ch. Calenus who wrote in 1579: “Contagiosum dico
morbum, quia etsi quidem ab occulta quadam coeli influentia, principaliter eum profisci
haud dubium est ... eo in loco quo jam grassabatur inter homines citius eos invadabat,
qui cum affectis frequenter conversabantur, quam eos, qui a consuetudine affectorum
studiose abstinebant.” This keen observer saw that those who carelessly exposed
themselves to close contact with cases of influenza were more likely to develop the
disease than those who protected themselves in every way possible. The “contagious”
school first developed in England, where Haygarth, Hamilton, Gray, Hull, Duggard,
Bardsley, and others, in 1775–1803 described the disease as being not in the air, but in a
specific contagion. Others who considered influenza a contagious disease were Simonin,
Lombard, Petit de Corbeil (1837), Blanc (1860), and Bertholle (1876).
Watson (1847) quotes Cullen as saying that this species of catarrh proceeds from
contagion. He, himself, is not convinced of this fact. He says the visitation is too sudden
and too widely spread to be capable of explanation in that way. “There are facts in the
history of influenza which furnish a strong presumption that the exciting cause of the
disorder is material, not a mere quality of the atmosphere; and that it is at least
portable. The instances are very numerous, too numerous to be attributed to mere
chance, in which the complaint has first broken out in those particular houses of a town
at which travelers have recently arrived from infected places.... What I wish to point out
now is the fact that the influenza pervades large tracts of country in a manner much too
sudden and simultaneous to be consistent with the notion that its prevalence depends
exclusively upon any contagious properties that it may possess.”
Parkes, writing in Reynolds’ System of Medicine in 1876, views the subject more as we
see it today: “The rapidity of the spread would seem at once to negative any connection
between human intercourse and the propagation of the disease; yet there is some
affirmative evidence. It does not appear to follow the great lines of commerce; but when
it has entered towns and villages in which the investigation can be carried on, it is
curious how frequently the first cases have been introduced, and how often the
townspeople nearest the invalids have been first affected. In this country especially,
Haygarth in 1775 and 1782, and Falconer in 1802, collected so many instances of this
that they became convinced that its propagation was due entirely to human intercourse.
So also, when it passes through a house, it occasionally attacks one person after another.
But if it is introduced in this way it afterwards develops with marvelous rapidity, for we
cannot discredit the accounts of many thousands of persons being attacked within a day
or two, which is quite different from the comparatively slow spread of the contagious
diseases. This sudden invasion of a community makes it, to many persons, appear highly
improbable that any effluvia passing off from the sick should thus so rapidly
contaminate the atmosphere of a whole town.