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1. Foreword
2. Preface
1. Conventions Used in This Book
2. Using Code Examples
3. Safari® Books Online
4. How to Contact Us
5. Acknowledgments

3. 1. Bootcamp: Introducing Spring Boot
1. Getting Started with the Spring Tool Suite
1. Installing Spring Tool Suite
2. Spring Boot Starters
3. Getting Started with the Spring Initializr
1. Generating Spring Boot applications
4. The Spring Guides
5. Auto-Configuration
1. Spring Boot Configuration
4. 2. The Cloud Native Application
1. Platforms
1. Building Platforms
2. The Patterns
3. Netflix’s Story
1. Splitting the Monolith
2. Netflix OSS
4. The Twelve Factors
5. 3. 12-Factor Application Style Configuration
1. The Confusing Conflation of “Configuration”
2. Support in Spring framework
1. The PropertyPlaceholderConfigurer
2. The Environment Abstraction and @Value
3. Profiles
3. Bootiful Configuration
4. Centralized, Journaled Configuration with the Spring Cloud
Configuration Server
1. Security
5. Refreshable Configuration
6. Next Steps
6. 4. Testing
1. Testing in Spring Boot
2. Integration Testing
1. Test Slices
2. Mocking in Tests
3. Testing Annotations
3. End-to-end Testing
1. Testing Distributed Systems

2. Consumer-driven Contract Testing
3. Spring Cloud Contracts
4. Continuous Integration
5. Functional Testing
4. Behavior-driven Testing
7. 5. REST APIs
1. Leonard Richardson’s Maturity Model
2. Simple REST APIs with Spring MVC
3. Content Negotiation
1. Reading and Writing Binary Data
2. Using Google Protocol Buffers
4. Error Handling
5. Hypermedia
1. Media Type and Schema
6. API Versioning
7. Documenting REST APIs
8. The Client Side
1. REST Clients for Ad-Hoc Exploration and Interaction
2. The RestTemplate
8. 6. Managing Data
1. Modeling Data
1. RDBMS
2. NoSQL
2. Spring Data
1. Structure of a Spring Data Application
2. Domain Class
3. Repositories
4. Organizing Java Packages for Domain Data
3. Auto-configuration
4. Bootstrapping Datasource Dependencies
1. Datasource Connections
5. JDBC Template
6. Spring Data Examples
7. Spring Data JPA
8. Spring Data MongoDB
9. Spring Data Neo4j
10. Spring Data Redis

1. Caching
11. Next Steps
9. 7. Data Integration
1. Distributed Transactions
2. The Saga Pattern
3. Batch workloads with Spring Batch
4. Scheduling
5. Isolating Failures and Graceful Degradation
6. Task Management
7. Process-Centric Integration with Workflow
8. Event Driven Architectures with Spring Integration
1. Messaging Endpoints
2. From Simple Components, Complex Systems
9. Message Brokers, Bridges, the Competing Consumer Pattern and
Event-Sourcing
10. Spring Cloud Stream
1. A Stream Producer
2. A Stream Consumer
11. Spring Cloud Data flow
1. Streams
2. Tasks
12. Next Steps
10. 8. Using Spring Boot with Java EE
1. Compatibility and Stability
2. Dependency Injection with JSR 330 (and JSR 250)
3. Building REST APIs with JAX-RS (Jersey)
4. JTA and XA Transaction Management
1. Resource-Local Transactons with Spring’s
PlatformTransactionManager
2. Global Transactions with the Java Transaction API (JTA)
5. Deployment in a Java EE Environment
6. Final Word
11. 9. Service Brokers
1. Cloud Foundry
2. Services Marketplace
1. Creating Services
2. Binding Applications

3. Cloud Foundry Service Brokers
3. Cloud Controller
4. Service Broker API
5. Implementing a Service Broker with Spring Boot
1. Amazon S3 Service Broker
2. The Service Catalog
3. Service Instances
4. Service Bindings
6. Deploying the Service Broker
1. Releasing with BOSH
2. Releasing with Cloud Foundry
3. Consuming Service Instances
4. Extending Spring Boot
12. 10. The Forklifted Application
1. The Contract
2. Migrating Application Environments
1. the Out-of-the-Box Buildpacks
2. Customizing Buildpacks
3. Containerized Applications
3. Soft-Touch Refactoring to get your application into the cloud
1. Talking to Backing Services
2. Achieving Service Parity with Spring
4. Next Steps
13. 11. The Observable System
1. The New Deal
2. Visibility and Transparency
14. 12. Push vs. Pull Observability and Resolution
1. Capturing an Application’s Present Status with Actuator
2. Metrics
3. Identifying Your Service with the /info Endpoint
4. Health Checks
5. Application Logging
6. Distributed Tracing
1. Finding Clues with Spring Cloud Sleuth
2. How Much Data is Enough?
3. OpenZipkin: a Picture is worth a Thousand Traces
4. The OpenTracing Initiative

7. Dashboards
1. Monitoring Potentially Risky Service Calls with the Hystrix
Dashboard
2. Codecentric’s Spring Boot Admin
3. Ordina Microservices Dashboard
8. Remediation
9. Next Steps
15. 13. The Application Centric Cloud
1. Portable Applications
2. Cattle
3. Containerized Workloads
1. Scheduler
2. Service Discovery
4. The Application Framework
1. Spring Boot
2. Spring Cloud
16. 14. Continuous Delivery
1. Start Here
2. Every Build is a Release Candidate
3. Version Control Everything
17. 15. Edge Services
1. Greetings
2. A Simple Edge Service
3. Netflix Feign
4. Reactive Programming
5. Proxies with Netflix Zuul
1. A Custom Zuul Filter
6. Security on the Edge
1. OAuth
2. Building an OAuth Authorization Server
3. Building an Implicit OAuth Client with Angular.js
4. Building a Social OAuth Authorization Server
18. 16. Routing
1. Locational Decoupling with Service Registration and Discovery
2. The DiscoveryClient Abstraction
3. Cloud Foundry Route Services
4. Next Steps

Cloud Native Java
First Edition
Designing Resilient Systems with Spring Boot, Spring Cloud, and Cloud
Foundry
Josh Long & Kenny Bastani

Cloud Native Java
by Josh Long, Kenny Bastani
Copyright © 2016 Josh Long, Kenny Bastani. All rights reserved.
Printed in the United States of America.
Published by O’Reilly Media, Inc., 1005 Gravenstein Highway North,
Sebastopol, CA 95472.
O’Reilly books may be purchased for educational, business, or sales
promotional use. Online editions are also available for most titles
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or corporate@oreilly.com.
Editor: Brian Foster
Developmental Editor: Nan Barber
Month Year: First Edition

Revision History for the First
Edition
2015-11-15: First Early Release
2015-12-14: Second Early Release
2016-01-21: Third Early Release
2016-03-01: Fourth Early Release
2016-04-20: Fifth Early Release
2016-05-13: Sixth Early Release
2016-05-31: Seventh Early Release
2016-09-23: Eighth Early Release
2016-10-31: Ninth Early Release
See http://oreilly.com/catalog/errata.csp?isbn=9781449370787 for release
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While the publisher and the authors have used good faith efforts to ensure
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Conventions Used in This Book
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Indicates new terms, URLs, email addresses, filenames, and file
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Chapter 1. Bootcamp: Introducing
Spring Boot
Spring Boot provides a way to create production-ready Spring applications
with minimal setup time. The primary goals behind the creation of the Spring
Boot project are central to the idea that users should be able to get up and
running quickly with Spring. Spring Boot also takes an opinionated view of
the Spring platform and third-party libraries.
An opinionated view means that Spring Boot lays out a framework of
abstractions that are common to all Spring projects. This opinionated view
provides the plumbing that all projects need but without getting in the way of
the developer. By doing this, Spring Boot makes it simple to swap
components when project requirements change.
This chapter will introduce you to building Spring Boot applications. The
topics we will go over are:
The Spring Tool Suite
Spring Initializr
Starter Projects
The Spring Guides
Auto-configuration

Getting Started with the Spring
Tool Suite
The Spring Tool Suite (STS) is an Eclipse distribution that is customized for
developing Spring applications. STS is a freely available IDE under the terms
of the Eclipse Public License. While there are many IDE options available for
developing your Spring applications, STS provides a set of features that are
tailored for Spring-based development.

Installing Spring Tool Suite
Let’s get started with downloading and installing the Spring Tool Suite,
available from http://www.spring.io.
Go to https://spring.io/tools/sts
Choose Download STS
Download, extract, and run STS
After you have downloaded, extracted, and have run the STS program, you
will be prompted to choose a workspace location.
Figure 1-1. Choose your desired workspace location
Choose your desired workspace location and click OK. If you plan to use the
same workspace location each time you run STS, click on the option "Use
this as the default and do not ask again“.
After you have provided a workspace location and clicked OK, the STS IDE
will load for the first time.

Figure 1-2. The STS dashboard
Your first Spring Boot application
Let’s now use STS to create our first Spring Boot application. We’re going to
create a simple Hello World web service using the Spring Boot starter project
for web.
To create a new Spring Boot application using a Spring Boot Starter project,
choose from the menu File > New > Spring Boot Starter Project.

Figure 1-3. Create a new Spring Boot Starter Project
After choosing to create a new Spring Boot Starter Project, you will be
presented with a dialog to configure your new Spring Boot application.

Figure 1-4. Configure your new Spring Boot Starter Project
You can configure your options, but for the purposes of this simple
walkthrough, let’s use the defaults and click Next. After clicking Next, you
will be provided with a set of Spring Boot Starter projects that you can
choose for your new Spring Boot application. For our first application we’re
going to choose the Spring Boot Starter Web project.

Figure 1-5. Choose your Spring Boot Start Project
From the list of sections, choose Web to expand its list of options. Now from
the Web section, choose the option Web and click Finish. After you click
Finish, your Spring Boot application with the Spring Boot Starter Web
project dependency will be created.
Now that your project has been created and imported into the STS IDE, you
will notice that a new project is available in your package explorer area.

Figure 1-6. Expand the demo project from the package explorer
If you haven’t already, expand the demo [boot] project and view the project

contents as shown in the screenshot above. From the expanded project files,
navigate to src/main/java/com/example/DemoApplication.java.
Figure 1-7. Navigate to DemoApplication.java
This is your main application class for your new Spring Boot application.
STS has configured this project as a Spring Boot starter project with the
spring-boot-starter-web dependency. If you navigate to your pom.xml file in
your Package Explorer you will find that the following dependencies have
been added.
<dependencies>
<dependency>
<groupId>org.springframework.boot</groupId>
<artifactId>spring-boot-starter-web</artifactId>
</dependency>
<dependency>
<groupId>org.springframework.boot</groupId>
<artifactId>spring-boot-starter-test</artifactId>
<scope>test</scope>
</dependency>
</dependencies>
The starter project for Web

A starter project for unit testing
Now that we understand the makeup of our Spring Boot application, let’s
create our first RESTful service by modifying DemoApplication.java. In
DemoApplication.java, modify the contents so that it looks like the
following example.
package com.example;
import org.springframework.boot.SpringApplication;
import org.springframework.boot.autoconfigure.SpringBootApplication
import org.springframework.web.bind.annotation.RequestMapping;
import org.springframework.web.bind.annotation.RequestParam;
import org.springframework.web.bind.annotation.RestController;
@SpringBootApplication
public class DemoApplication {
public static void main(String[] args) {
SpringApplication.run(DemoApplication.class, args);
}
@RestController
public static class Hello {
@RequestMapping(value = "/hello")
public String hello(
@RequestParam(value = "name", defaultValue = "World")
return "Hello, " + name;
}
}
}
Annotates a class as a Spring Boot application
This starts the Spring Boot application

Annotates a class as a REST controller
This maps a URL route to a controller method
This method has a query string parameter with a default value
Now that we have our code for a basic RESTful web service, let’s go ahead
and run the application. Run the application from the Run > Run menu.
Figure 1-8. Run the Spring Boot application
After choosing the Run option from the menu, you’ll be presented with a
Save and Launch dialog. Choose the DemoApplication.java option and click
OK.

Figure 1-9. Choose DemoApplication.java and launch the application
Your Spring Boot application will now start up. If you look at your STS
console, you should see the iconic Spring Boot ASCII art and the version of
Spring Boot as it starts up. The log output of the Spring Boot application can

Random documents with unrelated
content Scribd suggests to you:

"Continuing the study of these analogies which, if not enough to
prove a common origin, are enough to justify further study of the
question, I find in one of my patients a morbid condition due to an
arthritic source, i.e., an urticaria alternating with asthmatic coryza
(hay fever), the latter appearing with symptoms such as injection
and itching and tumefaction of the eyes which recall the cutaneous
affection to which it had succeeded." (Italics mine. Here is my
urticaria theory expressed in 1868. G. F. L.)
"Behind a vast number of nervous troubles, behind a vast number of
bizarre functional anomalies stamped with a nervous imprint, we find
arthritism." (Italics mine. Here is my pet theory of the gouty origin of
neurasthenia and perhaps Beard's neurotic constitution, beloved of
rhinologists. G. F. L.)
"As to analogies between summer catarrh and urticaria, I wish to
draw no conclusions from them. If it be admitted that both are due
to arthritism, their succession and the analogy in their local
development can be understood." (My urticarial nature of the lesion
again. G. F. L.)
I might add that de Mussy reports success in preventing the
appearance of the symptoms by the use of quinine for seven or
eight days before the expected attack. During the attack he used
sulphur and arsenic for the catarrh.
In the next chapter we will consider the fate of de Mussy's theory of
gout as the underlying cause of hay fever.

CHAPTER VIII
HAY FEVER AS GOUT
In the last chapter we read that the theory of a gouty diathesis as
the constitutional basis for hay fever originated with Dr. Gueneau de
Mussy, in 1868, on account of the many resemblances that he found
between the symptoms of gout and the symptoms of hay fever. We
have now to consider the fate of the de Mussy doctrine in those
countries where hay fever is best known and has been most closely
studied, Great Britain and America, Germany and France.
De Mussy in Great Britain and America. If any specialist on the
nose and throat in England or America ever heard of de Mussy and
his theory that hay fever is rooted in a gouty diathesis, he is keeping
the secret well, for it does not appear in any of the books that he
writes; but in every book I find the disease attributed to the neurotic
constitution first suggested by Beard. In this statement I do not
include several references to "uric acid poisoning" which is not the
same thing as gout, as will be explained in Chapter IX, on the Uric
Acid Theory.
After reading de Mussy's argument for the dependence of hay fever
on a gouty diathesis, I turned first to the English books. For
centuries, England has been famous as the home of gout and, since
the Englishman, Bostock's, account of his own case, hay fever, too,
like parliamentary government and gout, has been recognized as an
inheritance of the Anglo-Saxon race. As British physicians see more
gout than any other physicians in the world and as, for many years,
they have had the best opportunities for the study of hay fever, I
turned first to the English books, thinking that if there was any truth
in the gouty theory, the British physicians would have found it out

long ago. To my surprise I searched book after book by both British
and American authors, but in not one instance did I find hay fever
associated with gout. These books included Allbutt's System of
Medicine, F. T. Robert's Practice, Lennox Browne, Morell Mackenzie in
England and, in this country, Ballenger, Bosworth, Coakley, Kyle,
Solis-Cohen, Ivins and Vehslage and Hallett.
No one is more saturated with the traditions of British medicine than
Sir William Osler, but, in his Practice of Medicine, in discussing the
constitutional causes of hay fever, he seems to know nothing of the
gouty theory.
Besides the article on hay fever in his Diseases of the Nose and
Throat, Sir Morell Mackenzie wrote a comprehensive work on Hay
Fever and Paroxysmal Sneezing that ran through five editions and
bears on the flyleaf the admiring comment of the London Lancet
that it "must be regarded as one of the most complete expositions of
our knowledge of this curious complaint in our language." It is a
wicked joy to catch such a scholarly writer as Mackenzie napping. In
a footnote he even refers to the de Mussy lecture in the Gazette
hebdomadaire, Jan. 5, 1872, as calling the disease spasmodic
rhinobronchitis, with which name the disease is still known in
France. One suspects that the learned Doctor was very busy that
day and that the footnotes were looked up by somebody else; for,
though he gives "the most complete exposition in our language," as
the Lancet puts it, of the constitutional causes underlying hay fever,
there is never a word of de Mussy's theory of gout.
In Osler and McCrae's Modern Medicine the article on Hay Fever is
written by Professor Dunbar, of Hamburg, deviser of pollantin. Here
at last we get away from British insularity, for, in spite of his Scotch
name, Dunbar is a German. On page 863 he writes:
"For a long time it has been believed that the predisposition to hay
fever rests on a gouty diathesis. This view is not on the face of it
inconsistent with the pollen theory. Inquiries, however, have shown
that gouty persons form only a small portion of hay fever patients."

Finally, in the great Edinburgh Encyclopædia Medica, 1900, Volume
4, Greville MacDonald, of London, in the article on Hay Fever, seems
to know nothing of the gouty theory and says innocently at the end
of the article, "No special dietary is indicated, seeing that these
patients present no tendency to lithæmia, etc." He makes the
extraordinary suggestion that, in relieving the attack of hay fever,
"rather than give the patient cocaine, it might be wise to allow the
opium pipe." In the early prescriptions for hay fever, opium sprays
and nasal douches were common enough, but this is the only time I
ever heard a reputable physician and a teacher, at that, advising a
patient to "hit the pipe."
I think that, from the evidence examined, we may say that British
and American authors know nothing of de Mussy and his theory.
Next, I looked up the gout authorities, Ewart, Ebstein, Garrod,
Falkenstein, Lancereaux, Lecorche, each of whom wrote a bulky
treatise on Gout, but there is never a word on Hay Fever.
De Mussy in Germany. For many years, whenever I have wanted
to know anything from the bottom up, historically, linguistically,
philosophically, I have turned to a German book and have always
found what I was looking for, if it is known to man. Where an
American or British author will skim over or touch a subject
carelessly, not seeming to care where the idea comes from or its
relation to other ideas in different times or countries, a German will
plow steadily through the matter from Hammurabi to Wilhelm III
and lay bare all the collateral tributaries and branches, always with
an index at the end.
First I tried Heymann's Handbuch der Laryngologie und Rhinologie
(Wien, 1900) and found hay fever described in the article on Die
Nasalen Reflexneurosen, by Professor Jurasz in Heidelberg; but there
was no mention of gout. By this, I was truly convinced that nothing
was known on the subject. If a Heidelberg Herr Professor does not
know it, it does not exist. And "Professor Jurasz in Heidelberg" had
failed me.

However, looking further in Heymann, my faith in German
thoroughness and all-inclusiveness revived. Hay fever appears also
in the article on Acute Rhinitis, by P. H. Gerber, of Königsberg, and
here, on page 371, we find a complete "Literatur" spread out in true
Teutonic style from Bostock to date. However, Gerber does not
discuss the matter of gout in the text, but says merely, "Recently
Bishop asserts that the nervous disturbances of hay fever are due to
an excess of uric acid in the blood."
The gouty theory of hay fever receives scanty recognition from most
German writers. Strümpell does not mention it. In his Handbuch der
Specielle Pathologie und Therapie, Berlin and Wien, 1904, Eichorst
says skeptically, page 326, "It has been stated often that gouty
families are especially apt to develop hay fever," and on page 330
"Grote saw hay fever patients of gouty families cured (?) by a course
of waters at Neuenahr."
In Eulenberg's Real-Encyclopædie der gesammten Heilkunde, 1887,
page 509, article Hay Fever, we read:
"Of general diseases, malaria and gout have been advanced as the
basis of hay fever, but without convincing proof."
We may conclude, then, that while British and American physicians
know nothing about the gout theory, German physicians know about
it but do not believe it.
Finally, in my wanderings through German encyclopædias, I came to
the many-volumed Nothnagel and here, at last, found a modern
writer who knew de Mussy and recognized the importance of his
observations. At the end of Volume 4 there is a monograph on Hay
Fever by Dr. George Sticker, of the University of Giessen, the most
thorough and satisfactory book on the subject that I have found. It
may be read in English in the American edition of Nothnagel,
Philadelphia, 1902. Sticker resists the impulse to begin with Galen,
though he notes rather wistfully that John Mackenzie of Baltimore
succumbs to it. He gives the most complete statement in any

modern book of the gout theory of hay fever, but, alas, Sticker
misses the pearl in the oyster. He says nothing of de Mussy's
recognition of the urticarial nature of the lesion in hay fever.
As this volume of Nothnagel may not be easily available to the
gentle reader, I copy a paragraph from Sticker for his or her benefit.
Nothnagel's Specielle Pathologie und Therapie, Band 4, 1896. Article
Bostock's Catarrh, by Dr. George Sticker, page 118. "In the last few
years convincing proofs are accumulating that there is a certain
constitutional disorder on which the individual tendency to hay fever
depends. Though further careful proof is desirable, it can scarcely be
doubted that the pathogenesis of hay fever is based on that
constitution that the English and French describe as arthritic, which
expresses itself in a hereditary or family tendency to rheumatism,
gout, diabetes, obesity, migraine, furunculosis, bronchitis, asthma,
etc. Bostock himself mentioned his gouty tendency. Phœbus found it
in many patients. But it was Gueneau de Mussy who first recognized
the prevalence and necessary basis of the disease in the arthritism
of the hay fever patient; and his teaching has been accepted and
enriched with new material by Herbert, Leflaive, Lermoyez, Ruault,
de Dreyfus-Brissac, Rendu, Molinie.... And so it is probably no
coincidence that, like gout, the morbus principum of Sydenham, so
also the aristocratic hay fever is a prerogative of the Anglo-Saxon
race."
Reading this praise of Englishmen and Frenchmen by a German
makes one sad to-day. Hasten the day when the old hearty
comradeship in science will return, the day when German and
Frenchman and Englishman will again praise one another's
achievements ungrudgingly and each learn eagerly as of old what
the other had to teach.
De Mussy in France. As might be expected, among French
rhinologists and writers on general medicine, de Mussy's teaching is
well known and has many advocates. Note that the writers
mentioned by Stickerare all Frenchmen. The usual view is well

expressed by André Castex in his Maladies du Larynx, du Nez et des
Oreilles. Paris, 1907, page 425.
"Hay fever attacks especially those who belong to an arthritic stock,
whose parents have had or who themselves have migraine, gravel,
eczema. This explains its frequency in England and America; for the
Anglo-Saxon race is especially subject to arthritic disorders. In
France it exists but is infrequent. In this way also we must explain
why hay fever is rare among the laboring classes who frequent the
hospitals and is observed almost exclusively among wealthy patients,
people of sedentary habits and sluggish digestion (nutrition
ralentie)."
In Brouardel and Gilbert's Traité de Médicine et de Thérapeutique,
Volume 27, page 66, another André, André Cartaz, expresses mild
skepticism as to the proof offered.
"The presence of an arthritic diathesis is accepted by many authors.
Leflaive thinks it the sole predisposing cause, especially gout. During
the attack he has demonstrated, as I would say, and that is proof for
him, an appreciable decrease in the quantity of urine and percentage
of urea, an increase in uric acid and, in one case, the presence of
indican."
Lermoyez also advises caution in accepting the gouty theory to the
neglect of known remedies for the disease. I abstract his sensible
remarks from his Thérapeutique des Maladies des Fosses Nasales,
Paris, 1896. Article Rhinites spasmodiques, rhume des foins, page
300.
"It would be a mistake to hold with the German school that the
nasal lesions were the only cause of hay fever; for these lesions are
completely absent in many true cases of the disease and, on the
other hand, many people affected with hypertrophic rhinitis breathe
air full of pollen without showing symptoms of hay fever. There is
certainly a general predisposition. In hay fever certain patients
present a peculiar idiosyncrasy, often inherited, almost always

neuroarthritic. But to say with the French school that the arthritic
diathesis (trivial diathesis, commonplace diathesis, diathèse banale)
is the only cause of hay fever is to make a mistake that leads to
inefficient treatment."
Conclusion. How this discussion of the gouty nature of hay fever
escaped English and American authors is a strange thing. British
physicians frequent French hospitals and are familiar with French
medical writings. In 1868 American physicians studied in Paris as
they went later to Vienna and Berlin. It is strange that they never
brought back with them this French theory of the gouty nature of
hay fever and that no British or American author seems to have
quoted from their books.
I must make one partial exception to this statement. In his Diseases
of the Nose, Throat, and Ear, Philadelphia, 1906, Professor Grayson
says that, in hay fever, there is "some diathetic state that is rooted in
defective nutrition. Whether we term this lithæmia or gout or uric
acid diathesis is immaterial, the central fact being that through
intestinal toxæmia or some disturbance of normal metabolism we
have resulting a persistent poisoning of the blood-current."
Now this is simply substituting one theory for another without proof
of either; for the origin of hay fever in auto-intoxication is as little
proved as its origin in gout or uric acid. Auto-intoxication has simply
replaced uric acid in the Doctor's mental picture gallery; for, like uric
acid, auto-intoxication often exists in the imagination of the
physician and not in the patient. For further discussion of this point,
the reader is referred to the next chapter, on the Uric Acid Theory.
A novel and interesting article in Grayson is the description of
angioneurotic œdema as affecting the nose and throat, page 182.
He writes:
"I have no doubt that in this disease, as in hay fever, the gastro-
intestinal tract is the birthplace of the toxic material. Although the
disease may occur in gouty or rheumatic individuals, there is

scarcely sufficient reason for ascribing any pathological connection
between it and these other affections."
The comment on this is that, until we know what gout is, which we
do not at present, we cannot argue satisfactorily either way. Some
day I shall tell a listening world what I know about gout. I shall
elaborate my favorite theory that the American neurasthenia, now
rapidly increasing in other countries, is a form of gout, a gout of the
nervous system. And here, too, I find that Frenchman, de Mussy,
anticipating me in his remark that "Behind a vast number of nervous
troubles, behind a vast number of functional anomalies stamped
with a nervous imprint, we find arthritism." The name neurasthenia
was not known in de Mussy's day, but he hit off the condition neatly
as "functional anomalies stamped with a nervous imprint."
The defect in all these discussions of the gouty or non-gouty nature
of hay fever or of neurasthenia is our lack of a sure diagnostic sign
of the disease gout. Gout occurs in two forms, typical and atypical,
irregular gout. In typical gout, with the deposits of urates in the
joints and cartilages, the diagnosis may be easy. In atypical or
irregular gout we may have a group of inflammations or functional
disturbances in any tissue of the body. From their frequent
occurrence in gouty people, we suspect them to be gouty, but can
prove nothing. When they appear in people who have never had
typical gout we can only say that a gouty origin is probable. There is
no sign in the blood or in the urine or anywhere else by which we
can say that gout is or is not present. It is in this class of atypical
gout that hay fever and neurasthenia belong, if they be gouty at all.
Until somebody discovers a diagnostic sign of gout that is available
in these irregular cases, the evidence of the gouty nature of hay
fever and neurasthenia must remain exactly what it was to de Mussy
fifty years ago, analogies of symptom groups, and not an exact
laboratory diagnosis based on physiological or chemical tests such as
we have come to depend upon with such confidence in recent years.
One matter that should be made clear in the reader's mind is that
the so-called uric acid poisoning or uricacidæmia is not the same

thing as gout by any means, though Grayson confuses it with gout,
as do nearly all American authors. For fuller discussion of this point,
we will pass to the next chapter.

CHAPTER IX
THE URIC ACID THEORY
Uric acid is a substance about which more has been written and less
understood than many others in medicine and that is saying a great
deal. As a basis of the suboxidation theory of Bence Jones' day, as
the cause of gout with Garrod, as a step in our knowledge of
metabolism and as a popular fad, uric acid in its time has played
many parts.
Uric Acid in Hay Fever. In 1893, Dr. Seth Bishop announced
before the American Medical Association that "excess of uric acid in
the blood causes hay fever and nervous catarrh;" and advised
elimination and control of the uric acid as the principle of treatment.
The article may be found in the Journal of the American Medical
Association, 1893, and abstracted with an interesting discussion on
the treatment of hay fever, in the Philadelphia Medical News, 1894.
This position, of course, is also that of Haig (Uric Acid, seventh
edition, page 386) and his followers.
Now, in 1893, the theory of uric acid poisoning flourished like a
green bay tree and all sorts of queer and misunderstood pathological
processes came and roosted in its branches. Patients came to our
offices, not complaining of headache or lumbago or cough, but
asking for "something for that uric acid." As patients will, they had
already made the diagnosis from the newspapers and wished our
advice only for the remedy.
As the basis of hay fever, this theory of uric acid poisoning has
apparently made as little impression as de Mussy's theory of gout on
the nose and throat specialists of this country and Great Britain; for I

find no mention of it in their books, except the brief reference of
Professor Grayson quoted in the preceding chapter. In the Virginia
Medical Monthly, however, I find an interesting paper by Dr. John
Dunn, Professor of Diseases of the Nose and Throat in the University
Medical College of Richmond, Virginia. Following the suggestions of
Dr. Bishop, Dr. Dunn treated his patients with diet and alkalies
according to the uric acid theory and reports excellent results.
It may be pointed out that the successful results of the treatment by
no means prove that the condition was due to uric acid; for the diet
may be doing many other things besides controlling the movements
of the uric acid and it is probable that the effect of an alkali in the
blood is not a simple neutralizing of an acid but that it sets in motion
a train of chemical changes of great complexity. None the less, Dr.
Dunn's paper is well worth reading by every physician for its
practical suggestions in the treatment of hay fever.
The cardinal error made by the advocates of the uric acid poisoning
is that they name the poison. If the theory were stated that an
unknown poison or poisons circulate in the blood and cause many
symptoms of disease, as headache, gouty pains, bilious vomiting,
and so on, we would all agree that this is so. Call it the X-poison, if
you will, as Roentgen did with his unknown ray. But when you name
the poison uric acid, you challenge the chemist and the physiologist
to test your doctrine by chemical analysis, and when the uric acid
doctrine is tested in this way it is found sadly wanting.
It is true that uric acid in the form of urates is found in the blood in
varying quantities, but there is no proof that it does any harm there.
In fact, there is good evidence that it does not. In the disease,
leukæmia, there is an enormous amount of uric acid in the blood, far
more than was ever demonstrated in gout or the so-called uric-acid
disorders; yet, in leukæmia, there are no symptoms of gout or any
other symptoms that have been attributed to uric acid poisoning.
A second error of the uric acid advocates, flowing from their first
error of naming the poison, is to pour their acids and alkalies into

the blood with the childlike faith that, like good children, the acids
and alkalies will go in there and do just what they were told to do,
neutralize the uric acid, and get out. They assume that the chemistry
of the acids and alkalies is as simple inside of the body as it is
outside of it and that the blood is simply a passive mixture of
chemicals.
A third error of the uricacidites is to talk so glibly of the chemistry of
the blood and the influence of this or that food or medicine on its
chemical changes. The chemistry of blood! A subject of which the
ablest physiological chemists have but touched the fringe,—is that a
knot to be unloosed familiar as his garter by an amateur with a
watch-glass and a thread?
In his Lehrbuch der Organischen Chemie für Mediciner, Leipzig,
1906, Bunge observes slyly that he had "sometimes had occasion to
remark in private that the less a physiologist knew about chemistry,
the more irresistible was his impulse to undertake the most difficult
subjects."
When the uric acid amateur chemist comes to study the real poisons
of the blood, he will be confronted with a problem even more
intricate than uric acid, though that one is intricate enough and still
unsolved. For there are "poisons in the blood," though it is
improbable that uric acid is one of them. These poisons are the
blood-proteins, so many that the physiologist has never counted
them, so minute in quantity that no chemist has ever isolated them,
so complex in structure that the ablest chemists of the world stand
appalled before a molecule that contains sixty atoms of carbon,[1] so
powerful that an undetermined fraction smaller than one-third of a
grain will kill ten thousand guinea pigs or one hundred thousand
mice, and so perfectly under control that they circulate harmlessly in
the normal blood. The marvel is that any animal remains alive; and
no animal would remain alive were it not for a system of protection
by which these poisons are rendered harmless, usually by a slight

rearrangement of the atoms in their molecule which is one of the
wonders of organic chemistry.
We are far from knowing just what happens when we pour acids and
alkalies and foods into this witches' cauldron of blood. Rather than
impudently announcing the changes that are about to take place in
the blood when we administer a certain food or medicine, we should
stand in reverent awe before one of the most intricate and
marvelous puzzles with which nature ever challenged the chemist
and the physiologist.
Shall we therefore stop using acids and alkalies as medicines
because we do not know each step in their mode of action? By no
means. We do not know each step in the mode of action of any
medicine or of our foods, either, for that matter; but we do not for
that reason stop eating. We should still use the acids and alkalies for
their effect on the patient as far as we can see it just as we shall still
go on eating food because it nourishes us; but we shall be wise to
stop talking so glibly about what we cannot see and do not yet
know, the effect of those acids and alkalies on the chemistry of the
blood.
Uricacidæmia and Gout. Now, why do I speak with respect of de
Mussy's theory of gout as a cause of hay fever and so disrespectfully
of the uric acid doctrine? Are not gout and uric acid poisoning the
same thing? No. They are not; though the two ideas are usually
confused by medical men since Garrod's time and his demonstration
of the increase and decrease of uric acid in the blood of gouty
patients. Gout is something more than a simple accumulation of uric
acid in the blood because of its imperfect elimination by the kidneys.
What that something is, we do not know; but gout is, at least, a
clinical entity, a definite group of symptoms known since
Hippocrates' time. Take away the uric acid theory and you still have
the disease, gout, that any of us can recognize, as the Greeks and
Romans recognized it when the word uric acid was unknown. It is on
these symptoms of gout, the clinical picture of disease, not on any
hypothetical uric acid, that de Mussy based his theory and thus far

he is on solid ground. On the other hand, uric acid poisoning is
largely a figment of the imagination. Take away the uric acid, which
has never been satisfactorily proved to be there, and there is
nothing left. In not one one-hundredth part of the cases of so-called
uric acid poisoning is it proved that uric acid has anything to do with
the case.
The Deposits of Uric Acid in Gout. The deposit of uric acid in the
form of urates in the gouty joint has always been a strong argument
for the theory that gout, at least, is due to an excess of uric acid
(urates) in the blood. At one time, in a humble way, I was a
pathologist, and this theory of a blood overloaded with uric acid as
the only thinkable cause of its deposition in the joints never
impressed me as pathologically sound. I often compared these
deposits of urates in the joints with the deposits of lime salts so
often found at autopsies in caseous glands or small necrotic areas.
The superficial observer says:
"See what an excess of lime salts there must have been in the
blood." He is thinking of laboratory glassware and the ground
around a mineral spring that becomes encrusted with salts as the
solutions evaporate. But, in animal pathology, this is a false
conclusion. The animal body is not a test-tube and, in it, the laws of
physics are modified by those of physiology. Lime salts are deposited
in the caseous gland or tubercle not because they are in excess in
the blood but because lime salts are attracted to all caseous material
from normal blood. Whether or not this calcification is an intentional
provision of nature to protect the body, to petrify the necrotic
material and make it harmless, is not the question here, though the
calcification has this effect. The point here is that calcification of
caseous glands or necrotic areas does not presuppose an excess of
lime salts in the blood. The first step is not an excess of lime in the
blood but a necrosis, after which the lime salts will be deposited
from normal blood.
So, it has seemed to me that the deposit of urates in and around a
joint is no proof of their excess in the blood. Just as in calcification,

so in gout, the first step may be a minute area of necrosis or other
local degeneration that attracts the urates that are always present in
normal blood; or the secret of the gouty inflammation, like that of
urticaria and hay fever, may at last be found in Anaphylaxis, as
described in the next chapter.
FOOTNOTES:
[1] Wenn mehr als 60 Atome Kohlenstoff im Molekül sind, dann
ueberlasse ich das Object zu andern. Bunge, page 262, quoting
"einen hervorragenden Forscher auf dem Gebiete der organischen
Chemie." See Bunge for authority of these statements.

CHAPTER X
HAY FEVER AS ANAPHYLAXIS THE
GOUTY DIATHESIS REAPPEARS
Fifty years ago de Mussy pointed to the resemblance between hay
fever and gout and claimed hay fever as a manifestation of the
gouty diathesis. As related in Chapter VII, he based his theory on
the resemblance between the history and symptoms of hay fever
patients with those of gouty patients. In his day he found both hay
fever and gout confined to the Anglo-Saxon race, both hereditary
and familial, both exhibiting urticaria, eczema, and asthma, and he
recognized that the lesion in the eyes and nose of the hay fever
patient was not a true catarrh but an urticaria.
On the other hand, Wolff-Eisner declared that hay fever is an
anaphylaxis and this idea has been developed and confirmed by
Koessler and others so fully that we must accept it as proven. Let us
examine this matter of anaphylaxis to determine whether after all
there is any essential difference between the two views of hay fever.
Anaphylaxis. The conception anaphylaxis or lack of protection
begins with the discovery that a harmless protein injected into a dog
will so sensitize him that, after ten days or so, another injection of
the same protein will kill him. The point is that the change has
occurred in the animal, not in the protein injected. The protein is the
same as before and can be injected once into any number of dogs
without harm. In this way we explain the cases in which drugs and
foods that are harmless to most people may be virulent poisons to
those who happen to have been sensitized by a former overdose.
The widespread use of antitoxin in diphtheria gave abundant

opportunity to study the phenomena of sensitizing a human being
with one dose and killing him with another dose of the same thing.
The symptoms of anaphylaxis first observed were urticaria, arthritis,
and dyspnœa. Then Bruck showed that what we used to call
idiosyncrasy to drugs and foods that are harmless to most people is
really an anaphylaxis, attributable to a former overdose of the same
thing. Next, it was learned that anaphylaxis may persist through life
and be transmitted to the offspring of rabbits and guinea-pigs,
illustrating the cases in human families where sensitiveness to a
certain food or drug runs down through several generations. Then
the dermatologist brought in a list of skin eruptions, urticaria in the
lead, as examples of anaphylaxis to certain foods or to poisons
generated within the body, especially in the intestines. Then asthma
was included among the anaphylactic reactions and, finally, Wolff-
Eisner pointed out that the lesion of hay fever is an anaphylaxis. I
may add here that this view of hay fever confirms my observation
that the lesion is not a catarrhal inflammation but an urticaria.
So we have a picture of anaphylaxis as a sensitiveness to bacterial
poisons or to foods or drugs that are harmless to most people
expressing itself as an urticaria, an arthritis, an asthma or hay fever.
But this is the very group of symptoms on which de Mussy based his
theory of gout. When we add that this sensitiveness or anaphylaxis
is hereditary and that it is aggravated by foods, drugs, or pollens
that are harmless to most people, I submit that we have a pretty
picture of the gouty diathesis; for the gouty diathesis, too, is a
susceptibility to arthritis, to urticaria, and to asthma from causes
that do not trouble other people, and in gout, too, this weakness is
hereditary. One thinks of the gouty patient who cannot take iron or
digitalis because it aggravates the gouty pain and of the attack of
gout that is brought on by a glass of champagne or a piece of beef
or a few strawberries that the majority of mankind can take freely
without harm. Now, if urticaria, eczema, arthritis, asthma and hay
fever form a picture of anaphylaxis, and if these symptoms also form
the picture of the gouty diathesis, is it not probable that one of

these pictures can be explained in the terms of the other? If the
anaphylaxis to the diphtheria antitoxin, horse serum, can develop
arthritis, is it not probable that the most striking feature of gout, the
inflammation of the joint, is also an anaphylaxis to poisons yet
unknown to us but the same poisons that make the gouty urticaria
and asthma?
What if gout should prove to be a sensitization or anaphylaxis to uric
acid that does not exist in the non-gouty? This would explain the
puzzle of one patient full of gouty pains with very little uric acid in
his blood while another patient, like the leukæmic, has a blood full of
uric acid that does not trouble him.
The Mechanism of Anaphylaxis in Hay Fever. The anaphylaxis
theory of hay fever is based on the observation that the epithelial
cells of the mucous membranes of the eyes, nose, and throat have
not lost their primitive power of digesting foreign protein.
Ages ago, when we were amœbæ or little drops of protoplasm, we
had no eyes or nose or separate stomach for digesting food. The
one little cell body did everything. One of the most important powers
of that cell body was its power of digesting and assimilating food,
and its most important food was the nitrogenous food or protein
from which it built up its own body substance. Now, foreign or food
protein cannot be simply absorbed as such. Foreign protein is a
poison and never tolerated in the blood. The foreign protein used as
food must first be changed into the special kind of protein that the
body can use. The foreign protein is changed by splitting its
molecule into its simplest parts and then recombining them in the
desired form. The complex protein molecule, containing those sixty
atoms of carbon that gave the Schrecklichkeit to the German
professor of chemistry as related on page 71, is split up again and
again into simpler forms. The end products are harmless, but the
early splittings produce both poisonous and non-poisonous products.
The end-results of these successive splittings, the splinters, as it
were, are then combined by the amœba to form its own kind of
protein or body substance.

As we rose in the animal scale, instead of being an amœba of a
single cell, we became constructed of millions of tiny cells and began
to set aside certain groups of cells to do special work, the eyes for
seeing, the ears for hearing, the lungs for breathing, the digestive
organs to prepare our food and a sheath of harder cells over the
outside of the body that we call our skin and mucous membranes.
Specialized as those cells have been for many generations, they
have never forgotten that a foreign protein is a food or, perhaps, an
enemy, to be split up and decomposed at sight. So, the epithelial
cells of the mucous membrane of the nose and eyes, though they
have no longer anything to do with digesting our food, secrete a
ferment or enzyme that can split up any protein that may happen
along. This process is called parenteral digestion or digestion outside
of the intestines; and this theory of the parenteral digestion of
protein is the foundation of the anaphylaxis theory of hay fever.
During the growing months of the year the air is full of pollen that is
blown in everybody's eyes and nose. In that pollen is a proteid that
is digested by the secretion of those mucous membranes,
proceeding exactly as food is digested in the stomach and intestines,
splitting up the complex proteid molecule into simpler groups, and
forming both poisonous and non-poisonous substances. In the
normal eyes and nose this splitting of the protein proceeds slowly,
forming only minute amounts of poison. As absorption from the eyes
and nose is slight, no unpleasant effects are produced.
The first step in the development of hay fever is supposed to be a
disturbance in this digestion of protein in the eyes and nose, by
which larger amounts of poison are formed and absorbed by the
mucous membrane, producing the first poisoning, which, like the
first injection into the dog, sensitizes the mucous membrane to other
doses of the same poison. It is supposed that disturbance in the
protein digestion may be caused by stoppage of the nasal passages,
with excessive accumulation of proteid, inhalation of excessive
amounts of pollen, forming excessive amounts of poison, or,
perhaps, insufficient secretion, so that the splitting-up process is not

hastened to its conclusion of harmless products. The anaphylaxis
theory halts a little at this point and is not exactly clear about the
mechanism of that first poisoning.
After the first poisoning, the epithelia are permanently injured and
remain more permeable to protein. They also develop the power of
making large amounts of the digesting enzyme, which is absorbed
into the blood and is supplied to all the tissues of the body, so that
all tissues, including the skin, can decompose the pollen protein.
Advantage is taken of this distribution of the protective enzyme in
the skin reaction, in which a small area of skin denuded of its
superficial epithelia reacts in the form of a hive-like swelling when
the pollen that originally affected the patient is brought in contact
with it.
The next time that the pollen reaches the eyes and nose the mucous
membrane is ready for it with an abundant secretion of enzymes to
destroy it. In this intense digestion of the proteid, quantities of the
poisonous substances are formed which irritate the eyes and nose
worse than before, explaining why hay fever becomes worse with
successive attacks.
The inherited form of hay fever is explained by the well-known
transmission of anaphylaxis to the offspring. The first case in the line
of descent must start with a severe poisoning that lays the
foundation of the anaphylactic inheritance.
I would submit to the enthusiastic immunologist that this first
sensitization which he takes for granted but cannot prove is the
weak spot in his hypothesis. This is the point where he needs help,
and it is at just this point that de Mussy's neglected theory of gout
completes the picture. The immunologist has not explained why I, a
boy growing up with other boys, inhaling the same amounts of
pollen as they, catching no more colds than they, and never having
any serious illness, became sensitive to pollen while the others did
not. There is no recollection of any "first poisoning" by pollen that
might have started the anaphylaxis. But, says the immunologist, it

was your parents who were sensitized and you inherited the
anaphylaxis. Now, my parents lived to old age and had no sign of
hay fever, though my brother had it and my children are beginning
to sneeze and rub their eyes suspiciously in June and August. But if
you associate hay fever with the gouty diathesis, as the clinical
histories seem to justify, you enlarge immensely your opportunity to
prove ancestral sensitization to whatever unknown poison originally
produced the gouty sensitization. This view does not restrict you to
ancestral hay fever, but extends it to gout or to any equivalent of
gout.
The best work in English on hay fever as an anaphylaxis is the
monograph of Karl K. Koessler in Forchheimer's Therapeusis of
Internal Disease, 1914, Volume 5, page 671, to which the reader is
referred for a full discussion of the subject. The same author gives
an abstract of his work in the Illinois Medical Journal, 1914, page
120. This article in Forchheimer is the most complete that has been
written since Sticker's time and covers the ground from Sticker, who
knew not anaphylaxis, to Wolff-Eisner, who is not available in
English.
I was gratified to find in Koessler a sympathetic soul. He thinks, as I
did, that the monograph of Sticker in Nothnagel is the best review of
hay fever that we have. He calls it "a remarkable monograph and
the standard work on the subject." But why, oh why, K. K. K., in your
own masterly article in Forchheimer, did you follow Sticker all
through his historical chapter but leave out all that he says of de
Mussy's theory of gout or arthritism as the constitutional basis of hay
fever and also leave de Mussy and every reference to his work out of
your list of Literature? The German books are more liberal. While
most of them ignore de Mussy and his theory in their text, they all
list his writings in the Literatur. Has the microbe of bacteriology and
the laboratory bitten you so virulently that you can find no place for
the gouty diathesis even in an index?
I know that the gouty diathesis is out of date. In fact, all diatheses
are out of fashion. Nobody speaks of them now. They went out with

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