The Inflammation Process

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The Inflammation Process

by Patrick Quanten MD

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Dealing with injury and infection is vital to survival. It is hardly

surprising then, that all animals possess mechanisms designed specifically to

deal

with wound healing and microbial defence. In mammals such as ourselves, these

mechanisms are remarkably complex and, when they function correctly, produce

an exquisitely choreographed suite of reactions which biologists are only now

beginning to fully appreciate. The first stage in this process is known as

the acute phase response, or, less technically, as inflammation.

Traditionally Western medicine has recognised the four signs of inflammation

as tumor, rubor, calor and dolor - swelling, redness, heat and pain. Besides

these physical changes, there are also important psychological ones,

including lethargy, apathy, loss of appetite and increasing sensitivity to pain

- a

suite of symptoms that are collectively known as **sickness behaviour**.

Taken together, the four classic signs of inflammation and the psychological

symptoms of sickness behaviour constitute the complex set of processes referred

to as the acute phase of response.

Pain

The value of feeling bad is nowhere better illustrated than in the case of

pain. Pain, as everyone knows, is a great protector. The acute pain, as caused

by you touching a hot stove, is obviously beneficial, making you move away

quickly from damaging objects. Even more important, however, is the second

phase of pain that tends to follow the acute pain. Acute pain is sharp and

stabbing, and ends when you are no longer in contact with the source of damage;

the second type of pain is deep and spreading, and can last for minutes, hours,

days or even months. This kind of pain is not caused by pressure or heat

from the outside world, but by chemicals released by the body itself. And,

unlike acute pain, which produces a rapid movement, the second type of pain

causes

you to keep the wounded area as still as possible, and encourages you to

take extra care to shield the area from fresh injury while the process of

repair

is completed.

Swelling

The same applies to all other aspects of the acute phase response. Swelling,

for example, is also a defensive process, caused by the leakage of plasma

and the migration of immune cells into the area of damaged tissue. All bodily

damage, whether caused by injury or infection, consists of broken cells, and

when the walls of a cell rupture, an array of molecules which would not

otherwise be released, spill out into the surrounding tissue. Some of these

molecules trigger the sensory nerves to produce the ongoing, second type of

pain

just described. The sensory nerves also react by causing the blood vessels to

widen, increasing local blood flow (Redness), and making the walls of the blood

vessels more permeable. With greater blood flow, more white blood cells, the

infantry of the immune system, can be carried to the site of the injury. The

greater permeability of the blood vessel walls enables the white blood cells

to flow out of the arteries and veins into the surrounding tissue to defend

against possible bacterial invaders. If no bacteria have found their way into

the wound, particular white blood cells known as macrophages clear up the

debris of the chattered cells by engulfing and digesting it. If bacteria have

gained a foothold and started to multiply, the white cells form a barrier to

create a pus-filled abscess in which the blood fluid, the serum, plays a key

role in healing.

Besides clearing up the debris and attacking bacteria themselves, the

macrophages also release a number of chemical messengers. These signalling

molecules, or cytokines, play a vital role in co-ordinating the acute phase

response

by facilitating both short-distance communication among the immune cells

themselves and long-distance communication between the immune cells at the

injured site and the brain.

Fever

Increasing levels of prostaglandin E2 in the brain induce an area called the

hypothalamus to turn up the body's thermostat a notch. Suddenly, the same

external temperature feels colder, and various means are employed to restore

the subjective impression of warmth. These include involuntary processes such

as shivering, which generates heat by movement, and voluntary behaviour such

as putting on more clothes, finding a warm radiator to sit next to, and so on.

Like pain and swelling, fever plays a vital part in defending the body

against infection. Many bacteria reproduce most effectively at normal body

temperature. So by raising body temperature the rate at which the bacteria can

divide is slowed down. Fever has the opposite effect on most immune cells,

causing

them to divide more quickly. So fever both slows down the spread of the

infection and accelerates the counterattack by the immune system.

All injuries and infections, as stated above, cause a fever. This might only

manifest itself in a localised heat, and does not always produce an overall

increase of the body temperature.

Lethargy, Apathy and Loss of Appetite

Fever is not cheap. The body has to work hard to raise its temperature. In

mammals, an increase of just one degree Celsius in core body temperature

requires around 10-13 per cent more energy than normal. To balance the energy

budget, savings must be made elsewhere, and the brain accordingly generates

feelings of lethargy and apathy which reduce the energy expended in behaviour.

Sick people generally do not feel like doing very much, but this is not because

they have simply " run out of energy " . They are merely saving their energy to

use in other ways.

Mechanism of the Acute Phase Response

In response to acute damage or entrance of foreign material monocytes

enlarge and synthesise increased amounts of enzymes which help to break down

the

material. In doing so they are transformed to more active phagocytes called

macrophages. Monocytes are formed in the bone marrow, enter the blood stream

and

have a longer life than neutrophils (T and B lymphocytes, " white blood

cells " ), estimated at 12 to 24 hours. Monocytes respond to chemotactic and

immobilising factors (migration inhibitory factor) excreted by lymphocytes.

This

allows them to " stick " at the debris site.

Macrophages have surface receptors for antibodies and are capable of

synthesising various proteins as messengers. An important function of the

macrophage

is the presentation of debris material to B and T cells. Large molecules or

particular substances, however, require digestion by the macrophage before

they can be recognised by the other cells of the immune system. Bits of these

materials will be displayed on the surface of the macrophage and via contact

stimulate both B and T cells into appropriate action.

Lymphocytes (including B and T cells) mainly produce immunoglobulins

(antibodies) and are also responsible for cellular immunity. Cellular immunity

is

involved in delayed hypersensitivity (allergies and various overreactions of

the body) and homograft rejection. Lymphocytes can also damage foreign cells

(bacteria, parasites, fungi, etc.). Human lymphocytes are formed chiefly in the

bone marrow. Normal T cells develop only in the presence of a normal

functioning thymus. Long lived lymphocytes are primarily T cells, that

recirculate

through the spleen and the lymph nodes, thoracic duct and bone marrow, leaving

and re-entering the circulation repeatedly. There are subpopulations of T

cells which serve to enhance (helper T) or reduce (suppressor T) B-cell

responses. It is not yet known precisely how the various surface receptors on T

and

B cells influence cell function, but they are probably involved in antigen

recognition and cell-to-cell interactions with macrophages and other

lymphocytes.

We see the various cells involved in the process under our powerful

microscopes in still pictures. We also can measure various substances at

various

points throughout the inflammation process and we can identify certain specific

sites on the cell surface. From this information we piece together the story

of cellular immunity. In fact, we tell a number of " separate " stories about

the immunological response. There is the story about how antibodies are first

formed and then used to illicit a rapid response when exposed to the same

" intruder " again. There is the story of how the immune system responds to a

bacterial, or similar, invasion. There is the story of how the immune system

creates tolerance for the prevention of immunologically induced self-injury.

There

is the story of autoimmunity, whereby antibodies are formed against the

body's own tissue, which will consequently be attacked. There is the story of

anaphylaxis, an extreme overreaction of the body defence mechanism. There is

the

story of the complement system, which consists of at least 15 plasma

proteins which interact sequentially, producing substances that mediate several

functions of inflammation. A lot of stories in which different substances and

pathways are described, but without any serious linking of the various stories

or without any knowledge as to why and how the body chooses to follow that

particular pathway on that particular occasion.

Returning to the acute phase response, the story we are particularly

interested in, we know that there are many different cytokines (messengers)

involved. One of the first cytokines to be released by the macrophages on

detecting

signs of injury or infection is known as interleukin-1ß (IL-1ß). It diffuses

into the tissue surrounding the damaged cells, where it triggers a second wave

of cytokines which cause other types of immune cells such as neutrophils and

monocytes to migrate to the injured site. The IL-1ß released by the

macrophages also enters the blood stream, where it is carried to the brain, but

is

prevented from entering the brain directly by a layer of cells known as the

blood-brain barrier. It therefore adopts a more cunning route into the central

nervous system. First, the IL-1ß molecules attach themselves to specially

designed receptors on the surface of the cells in the blood-brain barrier. When

these receptors are activated, a chain reaction is initiated that eventually

leads to the manufacturing of a molecule known as prostaglandin E2, which,

unlike IL-1ß, is capable of passing through the blood-brain barrier. When it

enters the brain, prostaglandin E2 activates the receptors on both neurons and

microglia (immune cells in the brain), which can then initiate the other

components of the acute phase response: fever, lethargy, apathy, loss of

appetite,

anxiety, and increased sensitivity to pain in other areas of the body. But

the story does not end there. Once inside the brain, prostaglandin E2

encourages the microglia to manufacture IL-1ß. The net result is that, although

IL-1ß

cannot cross the blood-brain barrier directly, a build-up of IL-1ß in the

blood stream leads to a build-up of IL-1ß in the brain and the cerebrospinal

fluid. To complete the cycle, the IL-1ß leads to further synthesis of

prostaglandin E2 in the brain, which in turn augments the various components of

sickness behaviour.

To compensate for the decreased supply of new calories caused by the loss of

appetite, the body starts to unleash old calories that have been stored up

for just such times of emergencies. These calories are stored in fat deposits

around the body, but before the fat can be used as a source of energy it must

be broken down into glucose. So another crucial component of the acute phase

response is the secretion of glucocorticoids, which trigger the process of

converting fat to glucose. The key glucocorticoid in humans is cortisol, which

is released by the adrenal glands in response to a cascade of chemical

signals initiated in the brain by IL-1ß. First, the IL-1ß stimulates the

hypothalamus to secrete a chemical called corticotrophin releasing hormone

(CRH). The

CRH travels to the pituitary gland, just below the brain, where it triggers

the release of another chemical called adrenocorticotrophic hormone (ACTH).

Finally, the ACTH reaches the adrenal glands, which secrete the cortisol.

Because of their close interconnections, the three anatomical structures

involved

in this chemical cascade are known collectively as the

hypothalamo-pituitary-adrenal axis.

You do appreciate that the story presented here is a simplified version -

nobody knows exactly what happens in all directions at any given moment in time

- but it helps us to concentrate on that part of the story that we are

particularly interested in. And here is a very interesting part of the story:

the

fight-flight response, which enables vertebrates to respond to large

predators, evolved by co-opting the biological systems underlying the acute

phase

response. Both the innate immune response to infection and the fight-flight

response to large predators activate the same immune-brain circuits. When a

monkey or a human spots a lion moving rapidly towards them, for example, the

hypothalamo-pituitary-adrenal axis is activated, just as it is by IL-1ß in the

acute phase response. In both cases, the HPA axis responds with the same

chemical cascade leading to the release of cortisol by the adrenal glands. This

makes good sense, since cortisol breaks down the body's fat reserves into

glucose that provides vital energy. It is of interest also to note that this

whole

system immediately reverses as soon as the danger has subsided. That may

occur because the lion starts to run away from us, or because we all of the

sudden recognise the " lion " as our favourite dog!

Problems I have with it

Let's go through the phases again.

The acute phase response, as is the fight-flight response, has to be an

instantaneous response in order to keep you alive. The first thing that happens

in damaged tissue or infection is a response from the macrophages, or the

monocytes - this is not quite clear from the science. How many damaged cells,

or

how many bacteria, viruses or parasites, are required to trigger off this set

of events? Macrophages and monocytes are floating around in the blood stream.

What makes them aware of damaged tissue or foreign materials? Is it by sheer

luck that they come across these? And if so, how do they get to damaged

cells deep in an organ or structure, when they are mainly floating around in

the

blood? Whatever the answers to these questions, one thing looks likely: it is

going to take time.

From here on, a number of different cells and a whole string of " messengers "

are involved in the process. Let's follow just one line.

The macrophages, once they have located the problem, release IL-1ß which

" diffuses into the tissues surrounding the damaged cells " . This interleukin

leaks from the macrophages into its outer-environment. In other words, for the

time being, it remains local. After some time, it drifts into the blood stream.

Via the blood stream it is taken up to the brain. That journey takes time.

Of course, the blood stream will take the IL-1ß to all other places in the

body too but as we have no information on what it might do there, we are better

off totally ignoring that fact! If IL-1ß triggers off a second wave of

cytokins which cause other immune cells to migrate to the site, why doesn't

this

happen anywhere else in the body whilst IL-1ß is travelling throughout the

whole body? And furthermore, why isn't IL-1ß picked up by any of the

elimination

systems it travels past? How do the kidneys or the liver know when a

molecule is needed or obsolete?

Now IL-1ß arrives at the brain, but finds that it can't enter. It attaches

itself to specific receptors on the membrane of the blood-brain barrier. This

is said to trigger a chain reaction on the other side of the barrier, i.e. in

the brain. How many IL-1ß molecules are needed in order to trigger this

reaction? What is the proportion between the number of molecules attached to

the

outside and the extent of the reaction? What is the regulatory mechanism and

what will stop it? Finding an appropriate receptor site, reading the message

and performing the reaction on the other side surely, all of that takes time.

One of the responses from the brain is to produce prostaglandin E2.

Producing something in response to a direct order surely will take time.

Prostaglandin E2 is now capable of pushing through the blood-brain barrier.

Passing through a check point surely takes time.

Once inside the brain prostaglandin E2 has to find very specific receptors

on two different cells, the neurons and the microglia. Once this has been

done, the other aspects of the acute phase response are put in motion. How many

molecules of prostaglandin E2 are required to illicit such a response? How is

the response, once it has been triggered, controlled? For the nervous cells

to carry out these instructions to put in place " loss of appetite, fever,

lethargy and increased sensitivity to pain in other parts of the body " , is

surely

going to take time.

Also, prostaglandin is now encouraging the microglia to produce IL-1ß. This

production of material in response to a very specific order must take time.

Oh nearly forgot, IL-1ß also travels to the hypothalamus, a particular part

of the brain. This journey must take time. Once there, it stimulates the

hypothalamus to produce the corticothrophin releasing hormone (CRH). This

hormone

travels to the pituitary gland, which is on the outskirts of the brain. This

journey must take time. Do all these molecules know exactly where to travel

to? If so, how? Otherwise, what happens to all the stuff that goes astray?

And aren't we lucky that nowhere else except where it is required, tissues

exist that possibly could respond to these drifters?

In the pituitary gland the CRH stimulates the production of the

adrenocorticothrophic hormone (ACTH). Surely, the production of this must take

time.

The ACTH is now released into the blood stream. Don't ask how? Are we now

all of the sudden outside the blood-brain barrier? How did that happen; we

didn't have the same fuss coming out as we had going in, did we? Via the blood

the ACTH travels to the adrenal glands. Well, in fact, of course, it travels

anywhere and everywhere in the body. Why is it only the adrenal glands that

recognise this molecule? How does a cell that is part of a gland, and can't

move, make contact with a single molecule that happens to be floating by in the

blood stream? How many molecules are needed to trigger the response? How will

the manufacturing and the amount required be regulated? The journey must have

taken time.

The adrenal gland now produces cortisol. That production must take time.

Now you are ready for that lion that is running towards you. And guess what,

if it turns out not to be a lion, you will turn this whole mechanism off

straightaway and all the effects will be immediately reversed.

How much time do you reckon that will take?

And There is More

The main questions these theories throw up are about the time consumed in

all these chemical reactions as well as the time spent travelling, and the very

precision of the connections made. Don't forget that all of this can be

switch off and on in a blink of an eye.

However, when we look around we find that there is more evidence we need to

consider if we want to have a better understanding of the functioning of our

body.

* Blalock found that lymphocytes were secreting the mood-altering

brain peptide endorphin, as well as ACTH, a stress hormone thought to be made

exclusively by the pituitary gland. How can a cell of the immune system produce

and secrete a hormone that relates to our moods? Candace Pert found that

every neuropeptide they identified in the brain was also found on the surface

of

the human lymphocyte. These emotion-affecting peptides actually appear to

control the routing and migration of monocytes, which are very pivotal to the

overall health of the organism. They communicate with the other lymphocytes,

called B cells and T cells, by interacting through peptides and their

receptors, thus enabling the immune system to launch a well-coordinated attack

against

disease. How can specific brain peptides not only get to the cells of the

immune system, but then actually tell them what to do?

But immune cells don't just have receptors on their surfaces for the various

neuropeptides. As demonstrated by the paradigm-shaking research of Ed

Blalock at the University of Texas in the early eighties, and confirmed by

research

done by Michael Ruff, Sharon and Larry Wahl and Candace Pert (Department of

Physiology and Biophysics at Georgetown University Medical Center in

Washington, D.C.), immune cells also make, store and secrete neuropeptides

themselves. In other words, the immune cells are making the same chemicals that

we

conceive of as controlling mood in the brain. So, immune cells not only control

the tissue integrity of the body (defence system), but they also manufacture

information chemicals that can regulate mood or emotion (mental state)

* Consider CCK, a neuropeptide governing hunger and satiety, which was

first discovered and sequenced by chemists who were exploring its first

action on the gut. If you were given doses of CCK, you would not want to eat,

regardless of how long it had been since your last meal. Only recently have we

been able to show that both the brain and the spleen, which can be described

as the brain of the immune system, also contain receptors for CCK. So brain,

gut and immune system are all being integrated by the action of the CCK.

There are nerves that contain CCK all along the digestive tract and in and

around the gallbladder. After a meal, when the fat content is moving through

the digestive system to your gallbladder, you experience a feeling of

satisfaction, or satiety, thanks to the signal CCK sends to your brain. CCK

also

signals your gallbladder to go to work on the fat in the meal, which enhances

the

feeling of fullness. The CCK system also signals your immune system to slow

down whilst the food is still digesting. How can a brain chemical directly

regulate the way the digestion works, and co-ordinate this with the function

of the gallbladder and the immune system, all at the same time?

* Scientists have also established that when you intend to bite into a

lemon, the digestive system is already releasing the required juices to deal

with the lemon. These enzymes are specific for the type of food you are

about to put in your mouth. How does the stomach know what it coming its way

even

before it gets there? If all the communication is of a chemical nature how

can a cell produce and release specific enzymes without any part of the body

being in contact with the food item? Equally, it has been demonstrated in

seriously dehydrated people that the first sip of water they take, knowing that

there is more available, already releases the blockade on the kidneys and that

all systems instantaneously start to act as if they had enough water. If the

body works as a bag of chemicals, it would be logical to assume that the

dehydration emergency state would not be lifted until the sensor found that

enough water was available inside the body.

* Deepak Chopra MD sums it all up. " At the very instant that you

think, " I am happy " , a chemical messenger translates your emotion, which has no

solid existence whatever in the material world, into a bit of matter,

perfectly attuned to your desire, that literally every cell in your body learns

of

your happiness and joins in. The fact that you can instantly talk to 50

trillion cells in their own language is just as inexplicable as the moment when

nature created the first photon out of empty space. " Every thought is instantly

translated into a balance of chemicals which direct every cell of the body to

express this thought in a co-ordinated and appropriate way.

This is only possible, on the huge scale that we are talking about, if each

individual cell " knows " the thought and produces whatever is necessary to

express that thought itself.

 

This leads to two serious consequences. One is the fact that somehow there

must be a way that each cell has a direct line to our mind. A thought is not a

physical thing until a cell produces something to make it physical. Yet,

somehow the thought is " captured " by each and every cell and it is this thought

that tells the cell what to do. Or in other words, a non-physical thing is

heard and read by all cells and they react exactly to what is the essence of

that non-physical entity. This must mean that all cells are highly sensitive to

" a mood " , to " something in the air " , to " an atmosphere " , " a sense of " or " an

energetic alteration " . As the mind changes, so does the function of each and

every cell in the body; and only according to the state the mind is in. Be

happy and all your cells are happy. Be angry and tense and all your cells are

angry and tense. From the moment you think something is doing you good, it

is. When you think something is damaging you, it is. It is the thought that

provokes the effect, not the substance or the situation.

And secondly, it means that the immediate cell reaction we see is organised

by the cell itself, producing all required attributes itself. Once these

chemicals, proteins, peptides, hormones, etc. have done their job they are

discarded into the surrounding tissue and dumped into the blood stream. As a

reaction of the cell's activity, not as the cause of, the levels of these

substances within the surrounding tissues and the blood itself will now start

to rise.

Along the banks of these extensive waterways a variety of anti-pollution

plants (glands, organs) are available, which identify specific materials and

filter them out of the blood circulation. These materials now accumulate inside

the glands where they are destroyed and the building blocks recycled.

Hormones, enzymes, chemicals, etc. are not produced by glands but collected and

destroyed by them.

* Insulin, a hormone always identified with the pancreas, is now known

to be produced by the brain also, just as brain chemicals like transferon

and CCK are produced by the stomach.

* If the spleen and lymph nodes are the places where the cells of the

immune system are woken up and directed, we would expect to see these sites

swollen and most active in the early stages of an infection. In fact, the

swelling of the lymph glands is most often a secondary phase in the development

of the disease and appears later on. Equally, in the advanced stages of

chronic destructive diseases, such as tuberculosis, you would expect to find

the

highest number of leucocytes and phagocytes circulating in the blood in order

to put up the maximum of fight. However, the opposite is true: numbers of

circulating leucocytes are well down at the advanced stage, but the lymph nodes

are engorged with leucocytes!

Once we know that all cells have receptors for all chemicals the body will

ever use, and is capable of making these chemicals, we can now understand why

everything always has an effect on every part of the body. From the

fight-flight response to the influence of stress or the effect of hearing bad

news,

the effects of every aspect of our life is immediately felt in every nook and

cranny of the body.

* Doctors prescribe steroids to someone who is suffering from a

difficult case of arthritis. The steroids will bring down the inflammation in

the

joints dramatically, but then a host of strange things might happen. The

person could begin to complain of being fatigued and depressed. Abnormal fatty

deposits might begin to show under the skin and the blood vessels could become

so brittle that he/she would develop large bruises that are very slow to heal.

What would link these entirely divergent symptoms?

The answer lies at the level of the receptors. Corticosteroids replace some

of the secretions of the adrenal cortex, a yellowish pad on the top of the

adrenal glands. At the same time, they suppress the other adrenal hormones as

well as the secretions from the pituitary gland, which is located in the

brain. As soon as it is given, the steroids rush in and flood all the receptors

throughout the body that are " listening " for a certain message. When the

receptors become filled, what follows is not a simple action. The cell can

interpret the adrenal message in many ways, depending on how long the site

stays

filled. In this case, the receptor stays filled indefinitely. Equally important

is the fact that other messages are not being received due to the blockage of

receptor sites, as is the loss of innumerable connections with the other

endocrine glands.

Giving steroids to an arthritis patient involves trillions of molecules and

receptor sites. That is why the blood vessels, skin, brain, fat cells and so

on, all exhibit their different responses. The long-term consequences of

staying on steroids include diabetes, osteoporosis, suppression of the immune

system (making a person more susceptible to infections and cancer), peptic

ulcers, internal bleeding, elevated cholesterol, and much more. One might even

include death amongst these side effects, because taking steroids for a long

period causes the adrenal cortex to shrivel. If the steroid is withdrawn too

quickly, the adrenal gland does not have time to regenerate. The person is left

with inadequate defences against stress, which adrenal hormones help to

buffer.

Take all these details together, and what you see is that steroids can cause

literally anything to happen. They may be the immediate cause or just the

first domino - the distinction makes little difference to the person involved.

All drugs affect all systems of the body and can never be made to be

specific.

* In the body's own biochemical chain reactions cortisol (a steroid)

plays a major part in the activation of the inflammation process in order to

assist the body in its efforts to clean up damaged cells or invading foreign

materials (bacteria, fungi, parasites). The same steroids are prescribed by

doctors as a power weapon against inflammation. How can this be? - In the

natural cellular process steroids are produced in minute quantities and locally

by

each cell wherever the steroids are needed. They also have a very short life

span. The " homeopathic " quantities have an strong inflammatory effect.

However, used in huge doses and indiscriminately steroids (artificially made)

become anti-inflammatory by blocking a number of inappropriate receptor sites

for

a long period of time.

And then there is the problem of the white blood cells of our immune system,

the gallant defenders of the tissues. We have already asked questions about

the time and very specific actions of these cells. If they are floating in

the blood stream waiting for a call about some damage or invasion, how would

that message " catch " these constantly moving targets, and how quickly would

they be able to respond in adequate numbers?

It seems there are other problems relating to our white blood cells.

* The white blood cell is a living cell, which has a nucleus, and it

has an amoeboid action, which means that it is seen to develop protrusions

that are said to be the way the white blood cell moves forward. Dr Powel has

found clear evidence, however, that the white blood cell is not a living cell,

but a mere compact form of pathogenic material (a sophisticated rubbish bag!).

When first formed the leucocytes are neither granular nor nucleated and are

referred to as " young cells " or " round cells " . As the cell progresses further

it looks as if a " nucleus " appears, but soon further " nuclei " are added (You

would only expect one nucleus per cell). As time advances these foci

increase in size as well as in number. The constituents thereof becoming

susceptible

first to one dye and then to another (The nucleus, the brain of the cell,

changes format?). Sometimes they undergo fatty degeneration, and are then

called myelocytes.

The distortions on which the migratory or amoeboid movement of the leucocyte

depend and which seem to indicate that it is endowed with life, are chiefly

attributable to the action of the carbon dioxide gas which is generated

within it as it passes into decay.

Dr Powel affirms that every nucleus or nucleolus in a leucocyte is simply a

collection of residual matter (debris from damaged cells and foreign

material) and is to be regarded, therefore, as a focus of decay. He further

states

that the segmentation of the leucocyte is not a matter of " vital duplication "

as has been supposed, but of progressive disintegration of the morbid

material. The leucocyte is not a destroyer but it is the thing destroyed.

* Five types of circulating leucocytes can be identified: neutrophils,

lymphocytes, monocytes, eosinophils and basophils. It is generally accepted

that all these leucocyte types derive from a common pluripotent stem cell.

Apart from this common origin the various types are totally independent. None

of these leucocytes divide as all other living cells do.

Precursors of the neutrophils are myeloblasts and promyelocytes. The primary

granules found in these cells contain specific enzymes and proteins. With

further development the cells become myelocytes and have secondary granules,

containing different enzymes. From here the neutrophilic cells become condensed

and the nucleus segmented.

Lymphocytes are a reasonably homogeneous collection of singular nucleus

cells; the nucleus surrounded with only a few granules. There are two main

types,

T and B cells.

Monocytes are formed in the bone marrow from promonocytes, containing

granules with specific enzymes. As a result of ingesting foreign material these

monocytes transform into macrophages.

Eosinophils have a characteristic granule containing a unique peroxidase.

Basophils have distinctive deep-blue granules, characteristically obscuring

the cell nucleus, and rich in histamine.

All together we can count twelve different cells that are said to make up

our mobile defence unit. Only the very early stem cells, which live mainly in

the bone marrow, divide. It is from these cells that red blood cells and

platelets are made. None of the five types of circulating leucocytes know cell

division. The duplication of cells through the process of cell division is the

most normal way of proliferation in any living cell. No intact cell DNA has

ever been extracted from any of the five types of leucocytes.

If these front-runners of our defence system do not produce any copies of

themselves, how can we then explain the rapid proliferation of leucocytes in

case of infection?

How can we explain the increasing numbers of leucocytes at the site of a

localised infection or tissue damage without a corresponding increase in blood

numbers, knowing that the white blood cells can not proliferate?

If leucocytes have a memory of all the foreign material it has ever dealt

with (used in the secondary phase of the cellular immunity), but the cells

never divide, never produce offspring, and just die, how can we explain the

passing on of the memory to these new leucocytes? Remember, the life span of

lymphocytes is between 12 and 24 hours.

 

What does all this mean?

For over twenty years now scientists have proven that every cell in our body

can produce any enzyme, hormone or protein it needs, including " messengers " .

At the same time, every cell in our body has receptors for all the

messengers, so that it communicates with its immediate environment.

The rapid and very precise response of the body to any situation leads us to

believe, in view of all that scientific evidence, that every cell of the

body is capable of " picking up " energetic signals and respond immediately and

precisely to it. Every cell of the body " listens out " for signals in the air,

not unlike the human-made radio system. It registers what it " hears " by

producing the appropriate chemicals, which in turn set off a chain reaction as

a

direct result of the energetic environment the cell, and the whole body, finds

itself in.

These chemicals, enzymes, hormones, proteins, have a very short shelf-life

and are washed away into the lymphatic fluid that surrounds each and every

cell, and into the blood stream. They are excreted by the cell and are

essentially cell waste. Here it drifts around until an organ, a gland,

" recognises "

the material through its own specific receptors, captures it and draws it out

of the blood stream. Within the inner workings of each gland or organ the

mechanism for dismantling the chemical and recycling the building materials

such

as small molecules and basic elements is put to work. The higher the blood

concentration of the specific substance the harder the gland has to work. It

may even become swollen under a high workload pressure!

Within this system we also know that each cell produces its own

anti-invasion chemicals, such as interferon and the lytic enzymes. In case of

damage to

the tissue or the invasion of bacteria (see _ " The Origin of Germs " _

(http://freespace.virgin.net/ahcare.qua/literature/medical/originofgerms.html) )

the

surrounding cells start the clean up process by producing the enzymes needed

for the destruction and disintegration of the failing tissue. The rubbish that

is consequently produced is " bagged up " in various cell-like structures, each

equipped with the appropriate enzymes to break down the specific material it

is carrying. It is a mobile recycling unit on its way to the depot, the

spleen and lymph nodes. Here the " bags " are totally disintegrated, broken down

into its basic components and recycled.

The conclusion is that:

* glands don't produce hormones, they collect them and break them

down.

* lymph glands don't produce white blood cells; they collect the

" bags " that we have come to know as " white blood cells " and recycle the basic

elements.

* swollen glands are not a response from the cellular immune system to

a spreading infection; they are a sign of a detoxification system under

pressure.

 

Call me crazy! But before you do, take a long and hard look at the available

research science. Don't be afraid to change your mind if you find that the

truth lies outside your long-standing, and widely endorsed, beliefs.