Honest Money

The cause of the unprecedented deteriorations in our bodies is NOT the overuse and misuse of  what is left of our limbs.

The cause of the unprecedented deteriorations in our bodies is that we were born with too few cells in our bodies and that at middle age the number of these cells is even more reduced.

That’s what I understand. I’m no quack. Only a thalidomide monster. Here are the quotes:

Janet McCredie, “Beyond Thalidomide – Birth Defects  Explained”, London, The Royal Society of Medicine Press, 2007

§ Late-onset neuropathy in thalidomiders will be recognised as a sensory equivalent of post-polio syndrome p. 405 – 406

Since turning 40, many thalidomide victims have complained of tingling and numbness in their hands and feet.
Some also describe shooting pains.
Others describe increasing deafness, tinnitus or deteriorating vision.

The onset at middle-age of symptoms of sensory neuropathy is parallel with the experience of people who had poliomyeletis (infantile paralysis) and who suffered a second bout of motors symptoms – weakness, paralysis and wasting of muscles – with onset of middle-age.

Thalidomide attacked the embryo, not the infant.
It attacked the sensory, not the motor nerves.
The agent was chemical, not a virus.
But the response in the human body is basically similar.

p. 406
When the thalidomiders reached middle age, they also sustained the second physiological loss of neurons as normal degenerative processes took hold.
In their case, the second reduction of axon numbers may be critical.
They experience late-onset sensory symptoms in their reduced limbs
because
the second drop-out  f sensory axons depletes the population of their peripheral nerves,
perhaps below the threshold level where symptoms occur.

p. 406
Normally, our peripheral nerves contain surplus axons in reserve above the threshold number to balance any nerve damage.
What neurologists term “subclinical neuropathy”
is having less than the normal number of nerve fibres,
but enough escape with symptoms,
i.e., less than normal but more than the threshold at which symptoms appear.

Thalidomiders have coasted along for 45 years with subclinical neuropathy.
At middle age, the additional physiological degeneration of sensory nerves may deplete the axon population to a level below the symptom threshold.

A subclinical neuropathy (then becomes a clinical (symptomatic) neuropathy.

This is occurring in the thalidomiders at present.

Next alinea
There is a practical aspect in which it is important to recognise the sensory neuropathic basis of their disorder.
Medical attendants must understand that these people have neuropathic bones and joints
==>
they run the risk of poor results from surgery.
It is a well-established fact that fractures and surgery in neuropathic bones are slow to heal or may end in non-union.
The thalidomiders who present to doctors with arthritis or skeletal trauma need to be treated  conservatively, as neuropathic bones and joints.
Surgeons need to be cautious in offering joint replacements and other major procedures.
Healing is by no means assured.

p. 408 quote
… for we live, move, have a being and are subject to the actions of the elements and malice of diseases in that other world, the truest Microcosm, the Womb. of our Mother.
end of quote

p.409
The neural crest emerges from erstwhile obscurity to take its place as a highly vulnerable, extremely important stimulator of embryonic growth, and as easy target for malicious sensory neurotoxins.

END OF QUOTES

Ivo Cerckel
honestmoney@maktoob.com
http://twitter.com/ivocerckel/

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