Reflections on immunity by Philip Incao, M.D.

December 11, 2002

Hi everyone-

Ok, this is long. Very, very long, and a bit heady, but it is one

of the best discourses on health, illness and immunity that I have

seen.

I hope you enjoy,

Misty.

Reflections On Immunity,

Vaccinations And Smallpox

Part 1: The Phenomenon of Immunity

Part 2: How Do Vaccinations Work?

Part 3: Smallpox And Its Vaccination

By Philip Incao, M.D.

c. 2001-3

12-10-2

Part One: The Phenomenon of Immunity

Illness is a process that everyone experiences repeatedly in one's

lifetime. Until our modern era, illnesses were classified according

to their recognizable signs and symptoms. Today, in addition to the

outward appearance of an illness, we also classify it according to

its unique features detectable with the microscope and with

biochemical tests. Thus many illnesses of similar or identical

appearance which were lumped together in the past can now be

distinguished from one another based on their microscopic or

biochemical features. For example, what for hundreds of years was

called influenza is now described as a group of " influenza-like

illnesses " , each one associated with a different virus.

On the other hand, many diseases known for centuries and

recognizable by their typical signs and symptoms have been confirmed

by modern science to be distinct entities, i.e. to be associated

each with its own particular virus or bacterium and with no other.

Measles, chicken pox and scarlet fever are examples of these.

It has long been known that in some illnesses such as these, one

experience of the illness usually confers lifelong immunity. A

second experience with measles or scarlet fever is extremely rare.

These observations by physicians and patients throughout history, as

well as careful observations of the stages in a patient's recovery

>from an acute inflammatory illness like measles or scarlet fever,

have led to certain basic concepts in medicine.

One of these concepts was formulated as " Hering's Law " in the 19th

century, although it was well-recognized and mentioned by the

ancient Greek physician Hippocrates. This law states that as an

illness resolves, its manifest signs and symptoms travel from the

inner vital organs and blood circulation to the outer surface of the

body, often visible as a rash or as a discharge of blood, mucus or

pus. In this way we " throw off " an illness.

Another basic concept arising from the phenomenology of illness,

i.e. >from observations of the directly perceptible behavior of

human illness, is the concept of immunity to or protection from an

illness that one has had before.

This immunity to second episodes of certain illnesses like measles

or scarlet fever reveals a knowing function of the human being in

relation to illness. This inner knowing allows us, without any

conscious knowledge or effort, to recognize an illness we've had

before and to thereby resist it or quickly repulse it.

Hering's law on the other hand is evidence of an innate doing

function of the human being in healing, i.e. we actively clear the

illness from our body, we get it out of our system as we heal.

These inner activities of doing and knowing work more strongly

during illness than in the healthy state, and they were clearly

recognized by the ancient physicians. Hippocrates said illness

consisted of the active element pónos (labor) as well as the

passive element pathos (suffering). Illness is intense inner work.

Hippocrates perceived this labor as a cooking and digesting (pepsis)

of our inner poisons during an inflammatory illness. Today we

regard our inner work as a battle against a hostile virus or

bacterium. The all-too-often overlooked point however, is that it

is we ourselves who inwardly, unconsciously determine whether or not

to engage in the battle. The great medical pioneer Hans Selye,

M.D., who introduced and elucidated the role of stress in health and

illness explained, " Disease is not mere surrenderbut also fight for

health; unless there is fight there is no disease (emphasis mine). " 1

The symptoms of an acute inflammatory-infectious illness begin not

when we are infected by a virus or bacterium, but when we respond.

The magnitude of our response is influenced not only by the

magnitude of the infection, but also by the inherent strength of

what is responding in us. For the ancient physicians the responder

in us was an aspect of our human spirit and our inner vitality; our

inner healing force. Today the physical basis of our inner

responder is what we call our immune system. The phenomenon of

immunity hasn't changed, but our thinking about it has.

The severity of the early symptoms of a particular illness is

directly proportional to the vigor of our immune response and

indirectly to the burden and noxiousness of the infection to which

we are responding. The surprising fact is that most of the symptoms

of an infectious disease are caused not by the germs themselves but

by our own activity of the immune system in fighting the germs. The

germ " invasion " of our body is often silent, and can take place

gradually over a long period of time without disturbing us. It is

only when our immune system decides to do battle with the

encroaching germs that we start to feel sick.

The metaphor of battle is a convenient, but not fully accurate

description of the relationship between our immune system and the

proliferating viruses or bacteria during an acute

inflammatory/infectious illness. Pasteur's germ theory assumes that

disease germs have a predatory nature: that they prey on our flesh

for their own survival, while contributing nothing to us in return.

The germ theory further assumes that the harmful or lethal effects

of infectious/inflammatory diseases are a direct result of this

predation of the human body by germs.

In early microscopic studies of host tissues in acute

inflammatory/infectious diseases, Pasteur, Koch and their colleagues

repeatedly observed that germs were proliferating while many host

cells were dying. They made the critical assumption, upon which all

further thinking has been based, that the germs attack and destroy

otherwise healthy cells, thus causing direct harm to the human body.

It would have been equally justified by the observable facts to

assume that the cells were dying for inapparent biochemical reasons

and that the proliferating germs were attracted to the site of

increased cell death and decay just as flies, crows and vultures are

attracted to death in outer nature. A choice was available early on

between regarding germs as predators and regarding them as

scavengers. The nineteenth-century thinking of the time was

captivated by the Darwinian images of " Nature red in tooth and claw "

and the relentless struggle for survival. The decision to see germs

as predators was perhaps inevitable, and that has made all the

difference in our current thinking about illness and health. That

early decision by Pasteur and his followers led to medicine's

present nearly-exclusive focus on combating germs, while neglecting

all the subtle but far-reaching ways to strengthen the host against

lasting harm from inflammatory/infectious illness.

Just as flies, crows and vultures were regarded by the Native

Americans as playing a necessary and helpful role in the great chain

of Being, so too with germs which scavenge death and decay within

our bodies. The true causes of inflammatory/infectious illnesses

will ultimately be found to reside not in the germs, but in the

various human frailties which allow the forces of death and decay to

predominate in us. The scavenging germs are the markers of our

waxing and waning states of physiologic imbalance when cell death

and decay temporarily exceed their normal limits.

The metaphor of battle between immune system and germs is justified

provided we remember that our real enemies are the forces of death

and decay. The germs themselves become sacrificial victims marked

for destruction by our immune system because their role is to absorb

the products of death and decay. Germs become poisonous to us

through embodying the poisons we create. In " battling " germs, the

real battle is to overcome ourselves and to refine our nature. This

concept is implicit in the following discussion of how our immune

system does battle with germs.

Using battle as our metaphor, we can imagine three possible

scenarios. In the first, the attacking army is not strong, but the

defenders are, and the attackers are routed from the field in a

bloody but one-sided and brief battle in which the defenders suffer

no casualties. This describes a typical case of a benign but acute

inflammatory-infectious illness like roseola which usually expresses

itself in a very high fever of 105° or 106°F and an extensive rash

despite being no threat whatsoever to the host.

A second scenario would be when the opposing armies are evenly

matched and there is a fierce battle with many casualties on both

sides. This could describe an acute life-threatening inflammatory

illness like septicemia or an overwhelming pneumonia, in which

recovery or death is equally likely.

In the third scenario, the war reporter arrives late at the

battlefield and finds no carnage, in fact little or no evidence of

any previous battle. The defending army is quiet and no attackers

can be seen. The reporter at first concludes that it was a very

quick and easy victory for the defenders and the attackers have

fled. On closer investigation, however, he finds that no battle

took place because the defenders were unable or unwilling to fight.

What our reporter at first thought was the defending army in reality

consists of non-combatant defenders who have been quietly and

massively infiltrated by the attackers. The attackers blend in,

occupying the defenders' homeland, and any defenders who would fight

them have gone underground where they intermittently harass and

provoke the occupying enemy.

The point of this elaborate metaphor is to demonstrate by analogy

that the absence of fevers and other symptoms and signs of

inflammatory illness (the absence of a battle) does not always mean

that our immune system (the defending army) has been victorious!

Today it is more often the case that when we don't fight our battles

vigorously and often enough, i.e. when our fevers and discharging

inflammations are very seldom and mild, then we are liable to be

infiltrated by the enemy in disguise and suffer from chronic

allergic or autoimmune disorders. This concept today is called the

hygiene hypothesis. In the 1920's Rudolf Steiner expounded

essentially the same concept as a mutual interplay between opposing

forces of inflammation and of sclerosis, in which the healthy state

is a dynamic balance between the two.

Returning to our third scenario, there are of course times when the

absence of a battle, i.e. absence of obvious disease symptoms,

indeed does mean that the defending army has easily routed the enemy

and is truly immune from further attack. Thus we see that two

entirely opposite outcomes, 1. immunity from attack and 2. quiet

infiltration by the attackers into the defenders' homeland (the host

body) can have the exact same appearance superficially. This

analogy applies precisely to another pair of similar-appearing but

inwardly opposite states, i.e. the true immunity conferred by

overcoming illness as opposed to the apparent immunity conferred by

vaccination. In both cases the host appears to be healthy due to

the absence of illness, but true health is much more than the

absence of overt illness. We will illustrate this point further

when we discuss smallpox in part 3.

To complete our phenomenological description of immunity, we must

note that in addition to the functions of clearing illnesses from

the body and of recognizing the illnesses it has previously

encountered, the immune system has another cognitive or knowing

capacity. This is the discrimination of self from non-self and the

ability to " tolerate " , i.e. to not treat as foreign and to not react

to, any elements of self. This remarkable knowing of the immune

system also extends to its ability to tolerate, in pregnancy, a

massive foreign presence in the body, the fetus, without reacting to

it at all.

Thus we see the incredible skill and apparent purposefulness of

doing and the discriminating capacity of knowing possessed by the

immune system. Although modern science rarely uses the

words " knowing " and " doing " in its descriptions of the immune

system, nevertheless distinct knowing and doing functions are very

clearly and unavoidably implied in all scientific writing on

immunology. Science prefers to focus on the molecular level, hoping

to find in molecular events the elusive key to understanding, if not

why, at least how the immune system does what it does.

Today the immune system is most often described in articles and

textbooks as comprising those bodily organs, cells and functions

which discriminate between self and non-self. The molecules of self

or non-self which the immune system can recognize are called

antigens. One branch of the immune system, called the humoral

immune system, consists primarily of antibodies which are protein

molecules made by the body to specifically interact with foreign

antigens. Antibodies attach themselves to any foreign antigens like

bacteria or parasites which may exist in blood or body fluids

outside of the body's cells. Antibodies are attracted to such

extracellular antigens and usually coat these antigens as one step

in the complex process of the destruction, digestion and elimination

of foreign matter in us by our immune system.

We come now to a beginner's question, one seldom or never asked in

the science of immunology. It is, why does our immune system work

in such an inconsistent way, providing for permanent immunity from

recurrence only after certain illnesses and not after others?

A " why " question such as this is usually considered irrelevant in

modern science, while the equivalent " how " question is actively

pursued. In the case of immunity to illness, it is the " how "

questions that have led science to the idea and the practice of

vaccination.

For science the pertinent question is, how can we imitate nature and

bring about lifelong immunity to an infectious-inflammatory illness,

but without having to experience the illness first? The first task

would be to learn exactly how nature itself manages to maintain

permanent immunity in us after a first experience of illness. What

is this process of lifelong maintenance of resistance to a

particular illness? Can science duplicate it?

Part Two: How Do Vaccinations Work?

It is an interesting fact that sometimes a practical scientific

breakthrough happens out of an intuition, a hunch, long before the

discoverer or anyone else is able to explain just how and why this

particular breakthrough works. This is true of the work of Jenner

and Pasteur, the great initiators of the practice of vaccination.

Astoundingly, in our modern era when vaccinations are so widely

acclaimed and practiced, science still cannot explain how they work.

In the New Scientist magazine of May 27, 2000, an article on AIDS

vaccine research quotes the following from two scientists: " I'm

amazed by the amount of basic science we don't know, " and " the

assumption that successful vaccines work by simply producing

antibodies is almost certainly wrong. " The article then describes

how one vaccine researcher found that in a certain viral disease of

horses, vaccination was successful in inducing antibodies against

the virus, nevertheless the vaccinated horses died faster than the

unvaccinated ones! Referring to our present ignorance as to just why

these vaccinated horses would succumb, he stated, " It's an issue

people haven't wanted to think about, but we might have to. "

Vaccine science and practice have always been based on certain

assumptions, which we are only now beginning to examine. One of

these is that antibodies in the blood (humoral immunity) confer

protection against an illness, and that the level of antibodies

correlates with the degree of protection. This relationship between

measurable antibodies in the blood and apparent protection >from

illness has been observed for decades in many types of infectious

diseases. It is not known however whether the antibodies persisting

in the blood for months or years after an infectious disease are

themselves responsible for protecting us from recurrences of that

disease or whether they are merely markers of a protection that is

accomplished by another part of the immune system. It is also not

known whether the apparent protection associated with vaccination-

induced antibodies is a benefit pure and simple or whether a hidden

cost to the immune system is involved. The idea of a hidden cost is

considered unthinkable by vaccine researchers for obvious practical

reasons, yet it continues to be a nagging doubt among an ever-

widening circle of parents, consumer advocates, chiropractors,

holistic physicians and other discerning people.

The AIDS research quoted at the beginning of this article suggests

that it's not the antibodies which protect us, but rather it's the

cellular immune system. Also called the cell-mediated immune

system, it comprises the white blood cells, all the lymph nodes and

lymphatic tissue throughout the body and is concentrated in the

thymus, tonsils, adenoids, spleen and bone marrow. It is generally

agreed that the primary function of the cellular immune system is to

destroy foreign intracellular antigens like viruses and some

bacteria as well as the cells that harbor them. This is

accomplished by the various white blood cells which are able to move

inside, outside and through the walls of our blood vessels and to

access every part of the body.

In the past I have been tempted to assign the immune system's doing

function to the cell-mediated branch and its knowing function to the

humoral antibody-mediated branch. This neat division of function is

not borne out by the facts. Research shows us that each branch

participates in functions of both knowing and doing, although most

of the immune system's muscle to destroy, digest and drive out

intruders is flexed by its cell-mediated branch. Thus, while immune

system functions of knowing and doing may be conceptually distinct,

in the physical reality they are overlapping in an exceedingly

complex orchestration of organs, cells, molecules, hormones and

chemical messengers.

There are also other aspects of the immune system which are beyond

the scope of this article. Reading a modern textbook of immunology

can be frustrating as one finds a bewildering array of cellular,

molecular and antibody-mediated processes which science has

discovered without knowing how they all fit together and manage to

cooperate in health and in illness in the human being. It's

something like hoping to find an understanding of how an automobile

performs by studying its disassembled parts in an auto parts shop.

At the present time, it is thought that the encounter between self

and non-self, that is, between the immune system and a

foreign " invader " like a virus or bacterium begins in the domain of

the cellular immune system with a cell called the antigen-presenting

cell. If the foreign guests are not great in number or in their

noxiousness, the cellular immune system is able to dispatch them,

digest them and clear them from the body without ever calling into

action its coworker the humoral or antibody-mediated immune system.

This explains the very important fact that without our awareness we

are continually infected with many small numbers of different germs

in our body, some of them nasty, and the cells of our immune system

continually shepherd them and keep them in check without the

assistance of antibodies.

Like dust and other unseen debris, these microorganisms enter our

bodies as we breathe, eat and drink. Only when the number or rate

of growth of germs exceeds a certain threshold are they then

recognized by the humoral immune system, resulting in the formation

of antibodies specific to the particular provocative bug. At this

stage we may have only mild fleeting symptoms or none whatsoever.

This explains how we may be found to have antibodies against

illnesses we don't remember ever having had! This is

called " subclinical infection " , i.e. infection without symptoms, and

it happens commonly.

Thus science has discerned three levels of infection. The lowest

level is our steady-state equilibrium of everyday life in which we

peacefully co-exist with our inner menagerie of germs without

needing to form detectable antibodies against them. At this lowest

level our cellular immune system is quietly busy keeping our bugs in

line and when necessary pruning the flock. Thus, although small

numbers of disease agents are within us, out cellular immune system

sees to it that we remain well and free of disease symptoms, and

that our germs are under control.

At the second level of infection, we temporarily relax our vigilance

and allow a certain group of germs to begin rapidly multiplying to

the point where the humoral immune system is alerted and begins to

produce antibodies against the offending bugs. This sets off a

cascade of immune system functions which succeed in fairly quickly

quelling our rebelling germs, so quickly that the person hosting all

these inner happenings is unaware of having just gone through a

subclinical illness. The identity of the wayward germ can

afterwards be diagnosed by the presence in the blood serum of the

specific antibodies produced against it by the humoral immune

system.

At the third level of infection things get seriously out of control

and all our inner alarm bells go off as a tribe of germs

proliferates wildly and provokes the full defensive reaction of our

immune system. This is called the " acute inflammatory response " ,

which usually includes fever, release of stress hormones by the

adrenal glands, increased flow of blood, lymph, mucus, and a

streaming of white blood cells to the inflamed area. The human host

of these wisdom-filled events now feels sick and may experience

pain, nausea, vomiting, diarrhea, weakness, chills and fever. We

have now emerged from the realm of the subclinical to a full-blown

clinical illness, with all of its intense and often frightening

symptoms. It is critical to a healthy understanding of these things

to realize that we never merely suffer through an illness in a

passive, one-dimensional way. In an acute illness, parts of us that

in health are most active, like our mind and our muscles, are

subdued, while other parts like our blood, glands and immune system

are much more active than normal. Thus every illness rouses us to

become more inwardly active than usual, and this inner activity of

ours is the cooking through, the sweating out and the throwing off

of the illness. This is hard work, and every illness calls upon and

exercises capacities in us which otherwise would have remained

dormant. Adults often notice these new capacities as a change in

attitude or outlook after an illness. Children often manifest

positive changes in their behavior or development after overcoming

an acute inflammation or fever.

Having successfully passed the challenge of a particular illness, we

may not need to experience it again. Something about the illness and

our response to it has made us immune to its recurrence. If we knew

what that something was, perhaps we could learn how to use it to

create health and prevent illness. Of course, this is the basic

concept of vaccination, but the all-important question is, does

vaccination accomplish what we think it does?

We've already suggested that it's probably the cellular immune

system, and not antibodies, which protect us against illness.

Surely antibodies can have no role in either preventing or

overcoming first bouts of infectious-inflammatory illness, because

they are formed only after the illness has peaked. It must be the

cellular immune system which confers the resistance to, as well as

the capacity to overcome, both first episodes and subsequent

episodes of infectious disease. To understand how this might

happen, it is helpful to examine more closely the very illness and

its vaccination which started the whole debate: smallpox.

Part Three: Smallpox And Its Vaccination

That vaccines can confer a degree of protection from certain

infectious-inflammatory illnesses is clear. What is not clear, as

mentioned earlier, is exactly what vaccinations do to the immune

system to bring about their protective effect. Researchers

generally agree that vaccines do not prevent the particular virus or

bacterium from entering the body nor from beginning to multiply

within it. It is thought instead that the vaccines stimulate

or " prime " the immune system to quickly eradicate the offending germ

soon after it begins to infect the host.

Let us consider how this process might work in the case of

smallpox. Our knowledge about smallpox and its vaccination is based

on over 200 years of study of this dramatic and much-feared illness

by physicians in many countries.

The natural course of the illness begins when one " catches " smallpox

from someone with a smallpox rash or from the mucus or pus of

smallpox on a patient's bedclothes or dressings. For the next

twelve days there are no signs or symptoms at all and the new

patient is not contagious even though the smallpox virus is

multiplying within the body. On or about the twelfth day large

numbers of smallpox virus enter the blood (viremia) and

the " toxemic " phase of the illness begins, meaning a poisoning or

contamination of the blood circulation. This blood poisoning of

smallpox is the beginning of the overt illness, with symptoms of

fever, prostration, severe headache, backache, limb pains and

sometimes vomiting. After three or four days of these symptoms the

typical smallpox rash begins to erupt and in the next one to two

days the fever falls to almost normal and the patient feels much

better.

The skin eruption begins as red spots which over the next few days

evolve into raised pimples, which then change to blisters which then

become pus-filled (pustules). On the 11th to 13th day of the

illness the pustules begin to dry up and form crusts or scabs which

then fall off by the end of the third week of the illness. The

fever usually returns, less severely, after the pustules appear and

then becomes normal as the crusts and scabs form. If one dies >from

smallpox, it may be in the first week of the illness if the toxemia

is very severe, but most smallpox deaths have occurred toward the

end of the second week after the pustules appear.

The majority of smallpox patients survive, and the falling away of

the dried-up scabs from the skin signifies the final stage of

healing, approximately 33 days after catching the infection. The

dramatic course of smallpox illustrates very well some of the

concepts discussed earlier in this article. The twelve-day

incubation period during which the smallpox virus actively

multiplies in the body without provoking the slightest symptom

confirms the point that it is our response to infection, not the

infection itself, which causes the typical disease symptoms of

fever, aches and pains and extreme weakness.

The fact that the fever drops and the patient feels much better

after the rash breaks out illustrates Hering's Law. The poisons

circulating in the blood during the toxemic phase cause the most

severe symptoms of smallpox. These symptoms improve considerably

once the blood clears out its poisons by discharging them through

the skin, producing the typical pus-filled blisters of smallpox.

The chief danger of smallpox consists in the degree of blood

poisoning and in the huge and exhausting effort required for the

immune system to push the poisons out of the blood and through the

skin. When the toxemia, the poisons, are overwhelming and the

patient lacks the strength to discharge them out of the body, then

the patient may die in the effort, either before the eruption ever

appears or else, utterly spent, afterwards.

The patients who survive smallpox will have lifelong neutralizing

antibodies to smallpox virus in their blood and permanent immunity

to a second episode of the illness. What does this mean?

Using the battle metaphor from part one, we could say that the

victorious defending army has acquired much valuable skill, know-

how, and confidence through its combat experience as well as certain

medals awarded to acknowledge their participation in combat. The

first three attributes are comparable to the inner strengthening of

the cellular immune system which is attained through overcoming an

illness like smallpox. The medals as visible tokens of achievement

are roughly comparable to the antibodies visible on simple blood

tests indicating that the host has already won that battle and is

likely to be immune to future attacks of the same illness.

If a foolish general were under the illusion that merely wearing a

combat medal actually conferred the know-how, skill and confidence

gained in battle, then he might propose pinning medals on soldiers

with no combat experience to make them immune to dangerous future

battles. That would bestow the same outward appearance to the

seasoned and unseasoned soldiers alike, belying their experience.

In the same way, science bestows antibodies through vaccination and

mistakenly assumes that it is bestowing the immune strength that can

only be developed through the experience of illness. In equating

the significance of vaccine-induced antibodies with that of illness-

induced antibodies, science confuses the outer sign of the battle

experience with the experience itself. Antibodies arising through

illness are markers of immunity and (unlike the medals in our battle

metaphor) also contribute to immunity, but antibodies alone are not

sufficient to confer lasting immunity to a particular illness.

There are several diseases which may recur repeatedly, such as

herpes outbreaks, despite high antibody levels. The evidence

suggests that it is our cellular immune system which confers lasting

immunity, with antibodies playing a secondary role in the process.

Immunity is really the result of our experience, of having gone

through, along with our cellular immune system, an active process

(the combat in the metaphor) of learning and strengthening. The

immune system is a limb of us, and it learns from experience just as

we do. Antibodies signify that we've had experience of illness,

often repeatedly, but not necessarily that we've gained anything

from the experience. When on some level we respond with greater

initiative to our experience of illness, actively processing,

digesting and ultimately learning from such experience, then we are

usually immune from having to repeat it. In such cases our cellular

immune system has strengthened itself through its active encounter

with, and overcoming of, the illness. In this view, immunity is the

result of having successfully met the challenge of a particular

illness and having gained mastery over it. It is like learning a

particular skill, such as riding a horse, which is then usually

retained for life. On the physiologic level, the skill and mastery

we gain in overcoming illness accrue to our cellular immune system.

This active process of acquiring mastery cannot be replaced by a

vaccination unless the host's immune response to the vaccination is

essentially identical to its response to the illness itself, even

though reduced in intensity. This would mean that in order to

produce genuine cellular immunity, a vaccination would have to

reproduce the experience of the illness, causing some of the same

signs and symptoms, though milder, that are caused by the illness.

To see if this is true, let us look at smallpox vaccination.

The vaccination consists of introducing live cowpox (vaccinia) virus

into the skin by multiple superficial punctures in a small area

about 1/8 inch diameter on the upper arm. The vaccination site is

then inspected twice after 3 and 9 days to determine if the

vaccination " takes " or not. A primary reaction or " take " evolves as

follows: for three days after the vaccination there is no

reaction whatsoever. On the fourth day a small red pimple appears

which gradually grows into a blister which becomes pus-filled,

surrounded by a zone of redness and often with tender, swollen

glands in the armpit and mild fever. This reaction peaks on the 8th

to 10th day, after which the pustule gradually dries up and forms a

scab which eventually falls off leaving a scar.

Clearly the primary " take " reproduces the experience of smallpox

itself described earlier, but of course in a very limited way so as

to generate only one pock rather than many dozens of them. The

cellular immunity produced by smallpox vaccination is also limited,

lasting from six months to three years. This immunity probably

coincides with the length of time that the exercised " muscle " of the

cellular immune system remains strengthened from its labor of

discharging the single cow pock resulting from the vaccination. The

antibodies appearing in the blood after primary smallpox vaccination

may remain for over ten years, but these antibodies cannot be taken

as a trustworthy sign of immunity. The official description of the

currently available smallpox vaccine in the U.S., which was

manufactured by Wyeth Laboratories, states vaguely " the level of

antibody that protects against smallpox infection is unknown " 2 If

we can state blandly that the protective level of antibody is still

unknown after having assumed for several decades that protection is

directly correlated with antibody level, then surely it is time to

rethink that assumption.

In practice antibody levels were seldom used in the smallpox era as

a measure of immunity. Anyone not vaccinated in the previous three

years was considered to be susceptible to smallpox, regardless of

their antibody level.

The all-important question is how to interpret the meaning of

reactions to smallpox vaccination which are milder and briefer than

the primary " take " which peaks in ten days, and which does result in

a genuine though short-lived immunity of the cell-mediated system.

Since the early 1970's only two types of reactions to smallpox

vaccination have been officially recognized, as recommended by the

World Health Organization (WHO). For purposes of greater clarity,

in this discussion I will be referring to the older classification

which recognized three types of normal reactions to smallpox

vaccination.

The second type of normal skin reaction to smallpox vaccination was

called the accelerated or vaccinoid reaction, usually in people who

had some immunity to smallpox at the time of vaccination, either

from a previous experience of the disease or from a previous

smallpox vaccination. In the accelerated reaction, the skin blister

which forms is smaller and reaches its maximum size and intensity

between the 3rd and 7th day after the vaccination. This reaction

works in exactly the same way as the primary reaction but to a

lesser degree, boosting the cell-mediated immunity that is already

present, but waning, from the previous vaccination.

It is the third type of reaction to smallpox vaccination that in my

opinion has created all the problems, that has been at the root of a

200 year old controversy over the usefulness of smallpox

vaccination. This stems from the fact that this reaction for years

was interpreted as indicating immunity to smallpox, when it often

meant exactly the opposite. In many cases the bearers of this

reaction may have had a suppressed cellular immunity, making them on

repeated revaccination more susceptible to smallpox than an

unvaccinated person!

This third type of reaction to smallpox vaccination was originally

called an immune reaction, then later renamed an early or immediate

reaction. A small pimple forms at the vaccination site which may

evolve into a tiny blister, peaking on the second or third day and

diminishing thereafter. An earlier textbook of viral diseases >from

the smallpox era states the following: " The early or immediate

reaction is an indication of sensitivity to the virus and may be

given by persons who are either susceptible or immune to smallpox.

[it] cannot be regarded as a successful result and cannot be

guaranteed to induce or increase the person's resistance to

smallpox. " 3 This is a typical scientific understatement that

glosses over years of devastating results of smallpox vaccination in

which thousands of vaccinated people who were thought to be immune

based on their so-called " immune reaction " to vaccination later

caught smallpox and died.

Ian Sinclair, writing on the history of smallpox, states:

" After an intensive four-year effort to vaccinate the entire

population between the ages of 2 and 50, the Chief Medical Officer

of England announced in May 1871 that 97.5% had been vaccinated. In

the following year, 1872, England experienced its worst ever

smallpox epidemic which claimed 44,840 lives.In the Philippines,

prior to U.S. takeover in 1905, case mortality [death rate] from

smallpox was about 10%.In 1918-1919, with over 95% of the population

vaccinated, the worst epidemic in the Philippines' history occurred

resulting in a case mortality of 65%.The 1920 Report of the

Philippines Health Service [stated] 'hundreds of thousands of people

were yearly vaccinated with the most unfortunate result that the

1918 epidemic looks prima facie as a flagrant failure of the classic

immunization toward future epidemics.' " 4

How can this be? How can these historical facts be reconciled with

my earlier statement that a primary take in response to a first

smallpox vaccination results in genuine cellular immunity for up to

three years? The usual explanation offered is that the vaccine used

was inactive due to loss of potency in storage, but this clearly

cannot be the whole answer to the many documented instances of

failure of smallpox vaccination to protect from smallpox.

The answer is an open secret which has been very well known for

years, but never fully understood: that many first recipients of

smallpox vaccine fail to produce a take (primary reaction) and

continue to fail to do so even when revaccinated many times. The

textbook states,

" Easton (1945) records of one man who died of confluent smallpox

that vaccination had been attempted at birth, again in 1941 and ten

times in 1943 without a take, thus emphasizing the danger of

accepting even repeated unsuccessful vaccination as evidence of

insusceptibility to smallpox.. " 5

This is an excellent example of a vitally important observation

leading to an irrelevant, though not incorrect, conclusion. This

example begs the question: how many repeated failures to react does

it take to justify the concern that continuing to revaccinate may be

doing more harm than good?

The relevant conclusion, in my opinion, is that due to differences

in immune response capability among individual human beings at the

time of first vaccination, in some individuals the cellular immune

system lacks the muscle to push out the single pock eruption that is

the primary take. The scratching of the virus into the skin of the

arm is a strong challenge to the immune system. A successful take

depends on the ability of the cellular immune system to respond to

that challenge in an equally vigorous way, to push the intruding

virus right back out of the body. It is a simple matter of action

and reaction, of challenge and response. If Charles Atlas

challenges a 97-pound weakling to arm wrestling and his opponent's

arm immediately collapses, we would not think that the challenge

ought to be repeated indefinitely if the weak condition of the

responder had no means of improving! Yet in thousands of

individuals in the last 200 years who may have been weakened through

stress, poor nutrition and poverty, whose cellular immune systems

were not vigorous enough to respond to smallpox vaccination with a

take, the effect of repeated revaccination, which was commonly

practiced, was to weaken these individuals' immune systems still

further, making them no doubt more vulnerable to smallpox than they

had been before vaccination! This would explain the disastrous

results of the above-mentioned smallpox vaccination campaigns in

England, the Philippines and in many other countries as well.

The ambivalent nature of the early reaction to smallpox vaccination

is analogous to the third battle scenario mentioned in part one of

this article. When little or no signs of battle (reaction) are

visible, it may mean that the defenders were easily victorious (the

host is immune) or contrariwise it may mean that the defenders

lacked the strength to fight and their homeland was subsequently

quietly infiltrated by the attackers. When a smallpox vaccine

recipient lacks the immune muscle to respond to the viral intrusion

of his or her body with a vigorous pock-forming discharge, then we

might expect that most of the intruding virus has remained in the

body. With each revaccination the burden of vaccinia virus in the

body increases, and the suppressive effect of this viral burden on

the cellular immune system also increases, eventually resulting in a

dangerous state of immunosuppresion. This may also explain the

occasional catastrophic effects that were observed resulting from a

brief medical fad in the 1970's: treating recurrent herpes

infections with repeated smallpox vaccinations.

The disease smallpox and its vaccination are fruitful subjects to

study in order to understand how the immune system works, because we

can observe what happens on the skin as vital clues to what might be

happening inside the body. The main lesson from this study is the

exceedingly important fact that a lack of a vaccine reaction, and by

extension a lack of illness symptoms, can by no means be taken as a

sign of immunity or of health.

The other critical fact confirmed by our historical experience with

smallpox vaccination is that individual differences in response to

vaccination are extremely important. One size most definitely does

not fit all. It is clear that although the smallpox vaccine was

effective in conferring a temporary immunity in some individuals, an

unknown number of other individuals were probably harmed by the

vaccine. With the smallpox vaccination the adverse effects were

fairly obvious, they often appeared on the skin. With other

vaccines in use today the adverse effects may not be so obvious.

We've seen with smallpox that the same vaccination procedure which

temporarily strengthened the cellular immune system in some

individuals probably weakened it in others, especially upon repeated

revaccination.

The possibility, that the up to 39 doses of 12 different vaccines

which children today receive by school entry may be impacting the

cellular immune systems of many individual children in a negative

way, suggests itself to the open mind. Science has most of the

knowledge and the tools it needs to investigate and to find answers

to these unanswered questions. All it needs now is the will. May

it come soon, for our children's sake.

1 Selye, Hans. The Stress of Life. New York: McGraw-Hill, 1978,

p.12

2 http://www.cdc.gov/ mmwr/preview/mmwrthml/rr5010a1.htm

3 Rivers, T.M., and Horsfall, F.L., Jr. Viral and Rickettsial

Infections of Man. Philadelphia: Lippincott, 1959, p.686.

4 http://www.whale.to/cvaccines /sinclair.html

5 Rivers, T.M., and Horsfall, F.L., Jr. Viral and Rickettsial

Infections of Man. Philadelphia: Lippincott, 1959, p.687.

http://www.vaccineinfo.net/issues/how_vaccines_work.htm

December 11, 2002

Thanks, Misty.

It is great to see others joining to help educate the public. I took a tiny

part out and posted it on the BB in hopes to attract lots to your 'site.

Perhaps posting the entire thing in installments, on the BB, would reach

more people and also, incidentally, show off your 'site.

Namaste`

Walt

-

<mistytrepke

Tuesday, December 10, 2002 11:31 PM

Reflections on immunity by Philip Incao,

M.D.