They are affections
of muscles, tendons, nerves, articulations
(cartilages, meniscuses) and bones. The most
frequent affections are:
lumbagos |
pain in the cervical region
of the spìne |
pains of the articulations |
tendinitises |
carpal tunnel
syndrome |
The parts of the body most frequently touched are:
the spinal column |
upper limbs (shoulder,
elbow, wrist) |
knees |
STIFFNESS, LIMITATION OF THE MOVEMENTS
AND ARTHROSIS
With aging the
connective tissue loss its elasticity and its
constitution is changed in a worse structure.
According to Ladislas
Robert, Research Director at the CNRS and
Director of the Laboratory of biochemistry of
the connective tissue from the Medicine Faculty
of Paris-XII, the elementary fibers of collagen
are linked by chemical bridges. The increase of
the resistance of collagen with aging is the
consequence of an increase of the quantity of
bridges or
from an alteration of their structure.
This phenomenon is increased by the chemical
affinity of glucose for the collagen tissue (1).
The loss of male hormone lead to hyperglycemia
as we have seen above. There is why the
sweetened middle aged man becomes stiff.
At the same time the
ground substance of the connective tissue is
altered and the oxygenation of the connective
cells is compromised. The rarefaction of the
normal ground substance is the consequence of
the loss of male hormones as demonstrated, in
1958, by Harry Sobel and Jessie Marmorston, from
the University of Southern California in Los
Angeles (2).
Those phenomenon
added with overweight lead to arthrosis.
The detection of
androgens' insufficiency is done by the study of
the pool of
androgens.
OSTEOARTICULAR DISEASES
In France,
occupational doctors diagnosed an explosion of
bone diseases between 1991 and 1994, with growth
of 160 % compared to preceding years.
Back trouble, which
is a major cause of disability, accounts for six
million consultations a year, a third of
rehabilitation prescriptions, 13 % of
occupational accidents, 7% of work stoppages due
to illness and 2,5% of non-hospital
prescriptions. The deterioration of the
muscular-bone-articular system is continually
ignored.
Rheumatoid arthritis -
Pool of
androgens
In 2011,
a Japanese study showed that dihydrotestosterone
is a negative regulator of
rheumatoid arthritis' pathogenesis by decreasing
the inflammatory reactions.
pdf. (11).
The detection of
androgens' insufficiency is done by the study of
the
pool of
androgens.
OSTEOPOROSIS
In 1978, Daniel Baran
and his collaborators, from the department of
Medicine and Pathology, Division of Bone and
Mineral Metabolism from the Washington
University School of Medicine, reported the
positive effect of testosterone therapy on bone
formation in a hypogonadic male with
osteoporosis (3).
In 1981, Delmas and
Meunier from the Research Laboratory on
histodynamics of the bones and the Alexis Carrel
Faculty of Lyon in France, reported eight cases
of osteoporosis in eight men with low levels of
male hormones (4).
In 1983, Gérard
Milhaud from the University hospital Saint
Antoine in Paris, has reported the fragility of
the bones in climacteric women but also in
climacteric man according studies on the mineral
constitution of their bones (5). The rapidity of
the mineral loss in man is slower than in women.
The same year, Doctor
Foresta and his collaborators reported in the
scientific revue Hormone Metabolic Research the
linear relation between testosterone plasmatic
levels and bones' density (6).
In 2000,
Vanderschueren
and Vandenput from the Louvain University,
Belgium, confirmed
the essential action
of testosterone on bone growth
(8) pdf.
summary.
In
2004 and 2011, publications of searchers from
the Louvain University, Belgium, confirmed again
the essential action of testosterone on bone
growth
:
2004 (download summary) (download
full text) (9) and 2011 (download
full text) (10)
The detection of
androgens' insufficiency is done by the study of
the
pool of
androgens.
AMYOTROPHY
The metabolism of the muscle is influenced by
testosterone which increases the quantity of
specific contractile proteins as seen above.
Testosterone increases also the input of
glycogen into the muscle cells. Glycogen
constitutes fuel or energy for the muscle's
contraction. The link between glycogen and
testosterone during exercise is reported by F.
Plas from the University Hospital
Pitié-Salpêtrière in Paris, in 1978 (7).
During the andropause disease the muscles are
weak and exercise aggravates the loss of
testosterone. In this situation any intensive
sport is dangerous even the jogging. The heart
which is also a muscle is deprived of its fuel
and heart attacks and even sudden death may
occur at any moment.
The detection of
androgens' insufficiency is done by the study of
the
pool of
androgens.
Bibliography
11. Jian XU,Yuka ITOH, Hidetoshi HAYASHI, Takemasa TAKII,
Keiji MIYAZAWA, and Kikuo ONOZAKI. Dihydrotestosterone Inhibits Interleukin-1a
or Tumor Necrosis Factor a-Induced Proinflammatory Cytokine Production via Androgen Receptor-Dependent Inhibition of Nuclear Factor-k B Activation in Rheumatoid Fibroblast-Like Synovial Cell Line. Biol. Pharm. Bull. 34(11)
1724—1730 (2011)
10. Mieke Sinnesael, Steven Boonen,Frank Claessens,
Evelien Gielen, and Dirk Vanderschueren.
Testosterone and theMale Skeleton: A DualMode of
Action : Journal of Osteoporosis. Volume 2011, Article ID 240328, 7 pages
9. Vanderschueren D,
Vandenput L, Boonen S, Lindberg MK, Bouillon R, Ohlsson C.
Androgens
and bone :
Endocr Rev. 2004 Jun;25(3):389-425.
8.
Vanderschueren D, Vandenput L.
Androgens and osteoporosis : Andrologia. 2000
May;32(3):125
1. ROBERT L. Les Horloges Biologiques. Nouvelle Bibliothèque
Scientifique Flammarion, 1989.
2.
SOBEL H. AND MARMORSTON J. Hormonal Influences Upon Connective Tissue Changes of
Aging, in : PINCUS G (ed) Recent Progress in Hormone Research, vol 14. Academic
New York
1958.
3.
BARAN D.T., M.A. BERGFELD,S.T. TEITELBAUM AND L.V. AVIOLI. Effect of
testosterone therapy on bone formation in an osteoporotic hypogonadal male.
Calcif.
Tiss. Res. 2§ : 103-106, 1978.
4. DELMAS P. ET MEUNIER P.J. L'Ostéoporose au cours du
Syndrome de Klinefelter.La Nouvelle Presse Médicale, 10 : 687-690, 1981.
5. MILHAUD G. Mécanisme d' Action de la Calcitonine au
Niveau de la Matrice Calcifiable, in : L. Robert et H. Greiling Eds.
Pharmacologie Cellulaire et Moléculaire des Maladies du Tissu
Conjonctif :
227-239. Boehringer. Ingelheim. Mannheim. Reims,
1983.
6.
FORESTA C., BURNARDO B., RUZZA G. et al. Lower Calcitonin Levels in Young
Hypogonadic Men with Osteoporosis :
Horm. Metab. Res., 15 : 206, 1983.
7.
PLAS F. -Variations de la Fonction Androgénique au
cour des Efforts Prolongés : Bull.
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Nat. Méd., 162,6 : 494-499, 1978.