Addison`s disease causes death by a lack of steroids interfering with the metabolism.

There are only TWO known ways that this can happen. In Charles Wehner`s experience, however, there are therefore TWO kinds of Addison crisis - TWO ways to die. This was never known- because it was never thought of.

The first of these steroids is generated in the Zona Glomerulosa just under the orange coating of the adrenal glands. It is aldosterone. The crisis results in loss of sodium, and consequent loss of water. The lost sodium causes ulcers in the digestive system - and in Charles Wehner`s case, burned a small hole in the left ureter (the tube from kidney to bladder).

The loss leads to the wrong sodium-to-potassium ratio, so that the heart becomes unstable. Here is a quote from Addison himself: "...with an uncomfortable feeling of faintness or breathlessness on attempting it; the heart is readily made to palpitate;", and another from the same page: "breathlessness and palpitations being produced by the most trifling exertion or emotion; some slight œdema is probably perceived about the ankles;".

So, the mineral imbalance and thickening of the blood presents major problems. Greenhow describes: "In every case in which I have witnessed the post-mortem examination, firm, discoloured fibrinous clots were found in the right cavities of the heart,..."

The second of these steroids is generated in the Zona Fasciculata underneath the Glomerulosa. It is hydrocortisone, which - together with insulin - makes possible the combustion of sugar and fat. Without it, protein - in fact, the blood itself - is combusted. The result is anæmia. Hence Addison`s FIRST REPORT being a report of anæmia.

Limbs become heavier and heavier, until one cannot lift them. This is particularly the case when a large, or obese person suffers a sudden destruction of the Fasciculata. The weight of the limbs is as significant as the power of the muscles. Those with thin limbs tend to survive longer because they can move longer. Here is Addison`s page 3 again: "the lips, gums and tongue seem bloodless; the flabbiness of the solids increases;..." and again: "the patient can no longer rise from his bed,..."

The weakness is not due to lack of muscle - and so we have the extraordinary sight of some surprisingly muscular men becoming as weak as kittens simply because traces of chemical central to the metabolism are missing. Here is more from Addison: "the bulkiness of the general frame and the amount of obesity often present a most striking contrast to the failure and exhaustion observable in every other respect".

IN MAN THE CONDITION IS ALWAYS TUBERCULOSIS. THE WHOLE GLAND IS ALWAYS DESTROYED. THE TWO LAYERS TEND TO BE DESTROYED AT THE SAME TIME. THUS THE SODIUM CRISIS AND THE SUGAR (ENERGY) CRISIS ARE COMBINED.

Adrenal Gland External appearance. Zonæ: L: LIPOSOME G: GLOMERULOSA F: FASCICULATA R: RETICULARIS M: MEDULLA TB Right adrenal of Henry Patten. Totally destroyed. (Addison, 1855, plate 4)

On this site Charles Wehner suggests painless tests by which the sodium loss and the iron loss can be detected.

There are nowadays VERY FEW humans in the developed world with the true disease. At autopsy, the finding would be APLASIA of the entire glands - meaning that germs have DEMOLISHED the glands on both sides.

Tuberculosis mutates - that is why a MIXTURE of antibiotics has to be used against it. The Glomerulosa and Fasciculata are HOSTILE ENVIRONMENTS for germs. Therefore, it is not often that tuberculosis finds a way of living there. When it manages to occupy one gland, it always attacks the other. One can live with only one gland - but not with none.

The specific germ that has found the environmental niche of the adrenal glands could be called bacillus tuberculosis Addisonii. Other germs cannot do this. Equally, the statistical probability of cancer coincidentally attacking both glands and nothing else is absurdly low. Witness Greenhow`s splendid denunciation of a report where the sloppy reporter spoke of "cancer", even though the scalpel "grated" on the chalky TB tubercles:

"They are said to have been hard and nodulated, to have grated in places against the scalpel, and to have presented precisely the appearance of lardaceous tissue. Moreover, in order to accept as correct the report of cancer in these cases, we must admit that primary cancer had commenced simultaneously, and proceeded pari passū, in the two symmetrical organs, which is certainly a most unusual, if not absolutely unknown occurrence in the history of cancer".

In dogs, TB is known - but what are the percentages? Has a variant like bacillus tuberculosis Addisonii ever been found to have destroyed both adrenal glands in the dog?

The cause of Addison`s disease in dogs is almost invariably inheritance, due to selective breeding. But there are many breeds, and there may be many variants.

The disease develops in dogs "of a certain age", much like the menopause in human women. But the "certain age" seems to vary from breed to breed.

We know that the ovaries do not disappear in women. They just cease to produce the hormones œstrogen (estrogen) and progesterone. Similarly, it would be surprising if the adrenal glands VANISHED in the dog. It seems much more likely that they cease to produce aldosterone and hydrocortisone.

But do ALL dogs lose BOTH abilities? It is quite possible that there are dogs that lose the aldosterone capability whilst retaining the hydrocortisone - or vice-versa.

The mechanism appears to be the generation - in dogs of a "certain age" - of ANTIBODIES against certain specific proteins.

There is a good book - "Lamarck`s Signature", by Steele, Lindley and Blanden (Perseus Books), which describes the manner in which acquired antibodies become incorporated into the genome. When those antibodies are re-created in the offspring, they will gravitate to certain specific proteins - causing the T-cells ("Leucocytes") physically to DEVOUR the entire cell that has such protein.

Here again, we have an outcome of aplasia. Cells eaten up by the immune system are GONE. The mechanism may be more, or it may be less specific than the abovementioned specificity of the Adrenal TB germ.

Here we have cholesterol, which is the raw material that the adrenal glands use to create steroids. Notice the zig-zag branch of carbon atoms that sprouts at C17. That is, the piece at the top with three CH3 groups.

By comparison with aldosterone and hydrocortisone (above), it can be seen that this long branch has GONE in the steroids. The eight carbon atoms have all been "burned" off. Just like charcoal in a barbecue, these carbons will "burn". All it takes is an ENZYME. Nature has one enzyme for every chemical stage - and there are a lot of stages.

If an antibody coded for these enzymes, the T-cells would gobble up ALL cells that made them. These include cells in the ovaries and in the testes. This would be too non-selective.

To the left of C17 is C18. In aldosterone this is oxidised - by an enzyme - from CH3 to CHO. If an antibody targetted this enzyme alone, all aldosterone production would stop, but nothing else would be affected.

In such a case, it would be a SHAME to prescribe glucocorticoids - Prednisone, Prednisolone, Betamethasone or Dexamethasone - to a dog that does not need them. Before long, it would become dependent - and mistakes would lead to metabolic problems like diabetes and arthritis.

A dog MAY only need an aldosterone substitute such as Florinef. This is due to the special properties of autoimmune adrenal disease, not found in man.

The findings at pathology would be APLASIA of specific layers of the cortex - NOT of the whole gland, as in Man.

When a dog or man has been needlessly medicated, however, the finding is that the steroid-producing cells have not VANISHED, but simply SHRUNK DOWN. This is known as ATROPHY.

An animal or human with atrophied glands can rebuild them by the most gradual withdrawal of the steroids - a process known as TAPERING. The shrunken cells simply expand back to their original state.

When there is aplasia, however, this cannot work.

The purpose of Wehner`s Addison website is to publish the facts and encourage research. There are insufficient accurate diagnostic tests, and such tests as exist are not sufficiently specific. The ACTH STIMULATION TEST, for example, cannot distinguish atrophy from aplasia, of the zona fasciculata.

There is clearly a need for improved test procedures.