Prostate cancer treatments and prevention: Is nandrolone (Deca Durabolin) an untapped chemotherapy a

Prostate cancer treatments and prevention: Is nandrolone (Deca Durabolin) an untapped chemotherapy a

I will quote a brief compilation from another group, with permission.
If anyone wishes to join in the 'nandrolone debate' I'd be most
obliged if they would read the compliation FIRST - before they dive
in ;-) Bren.

" First line treatment of prostate cancer is often with the LHRH-
agonist (or, gonadotropin super agonist: lupron, zoladex, trelstar.)
or estrogens, to block the production of male androgen. Many doctors
recommend a life time of treatment (or at least many years) with
these drugs. However their primary effect of castration, with the main
symptoms hypogonadism and feminisation being extremely problematic for
many men:

The experience of mental and physical decline under androgen
deficiency is quite consistent with reports in the learned
literature[1] describing the condition of hypogonadal men: sequelae
include bone demineralisation[2], muscle wasting[3], penile
shrinkage[4], early onset Alzheimer's disease[5], metabolic
syndrome[6] and myocardial infarction[7] to name but a few.

For anyone hooked into a chemical castration loop (or indeed anyone
permanently castrated by chemical or physical procedures) , nandrolone
looks particularly promising since it is as effective as costly
alternatives for treatment of extreme debility[8]; yet it has
virilising effects that may offset the distressing feminisation[8*] of
LHRH-a and estrogens.

Nandrolone is only mildy androgenic and is not associated with a
worsening of prostate cancer markers[9]. Nandrolone induces
suppression of the HPG axis[10] with testicular[11] and prostatic
atrophy[12] that is consistent with the purpose of androgen
suppression for the control of prostatic tumour. Most importantly,
nandrolone does not cause mental or physical debility and other
significant QoL issues mentioned above.

The question also arises "Is nandrolone (Deca Durabolin) an untapped
chemotherapy preventive for prostate cancer ?"

1: Int J Impot Res. 2006 May-Jun;18(3):223-8. Male hypogonadism. Part
II: etiology, pathophysiology, and diagnosis. Seftel A. Department of
Urology, Case Western Reserve University, Cleveland, OH 44106, USA.
adsef...@aol,com

Male hypogonadism has a multifactorial etiology that includes genetic
conditions, anatomic abnormalities, infection, tumor, and injury.
Defects in the hypothalamic-pituitary-gonadal axis may also result
from type II diabetes mellitus and treatment with a range of
medications. Circulating testosterone levels have been associated with
sexual function, cognitive function, and body composition. Apart from
reduced levels of testosterone, clinical hallmarks of hypogonadism
include absence or regression of secondary sex characteristics,
reduced fertility (oligospermia, azoospermia), anemia, muscle wasting,
reduced bone mass (and bone mineral density), and/or abdominal
adiposity. Some patients, particularly those with partial androgen
deficiency of the aging male, also experience sexual dysfunction,
reduced sense of vitality, depressedmood,increased irritability,
difficulty concentrating, and/or hot flushesin certaincases of acute
onset. As many patients with male hypogonadism - likepatients with
erectile dysfunction - do not seek medical attention, it is important
for clinicians to be acquainted with the signs and symptoms of
hypogonadism, and to conduct appropriate laboratory testing and other
assessments to determine the causes and inform the treatment of this
condition. PMID: 16094414

2: J Endocrinol Invest. 2005;28(10 Suppl):73-9. Androgens,
cardiovascular disease and osteoporosis. Isidori AM, Giannetta E,
Pozza C, Bonifacio V, Isidori A. Department of Medical
Physiopathology, La Sapienza University, Rome, Italy.
andrea.isid...@uniroma1,it

Epidemiological studies correlated the age-related decline of serum
testosterone levels to the concomitant increase of cardiovascular
diseases, osteoporosis and bone fractures. For this reason,
testosterone replacement therapy (TRT) in older men with late-onset
hypogonadism has been advocated. Testosterone has an anti-resorptive
effect that may increase bone density at lumbar spine. Androgens may
also have cardio-protective effects by improving endothelial function
and reducing the risk factors for atherosclerosis. It has been
proposed thatatherosclerosis and osteoporosis share common
pathophysiologicalmechanisms. Therole of inflammatory cells, citokynes
and calcium deposition into thevascular walls has been reviewed to
explore the causal nexus betweenthese frequently associated diseases.
Experimental studies indicatethat a deregulation in the commitment of
pluripotent mesenchimal stemcells toward specialized phenotypes might
participate in thedevelopment of these conditions. The crossed-over
beneficial effect ofbisphosphonate on the cardiovascular system and
statins on bonemetabolism supports the research for a unitary
pharmacologicalapproach to both conditions. The findings that
androgens regulatemesenchimal celldifferentiation, as well as body
composition, lipid profile and bonemetabolism, have claimed a role for
TRT in aging men with late onset-hypogonadism. PMID: 16550728

3: J Clin Endocrinol Metab. 1996 Oct;81(10):3654-62. Sublingual
testosterone replacement improves muscle mass and strength, decreases
bone resorption, and increases bone formation markers in hypogonadal
men-a clinical research center study. Wang C, Eyre DR, Clark R,
Kleinberg D, Newman C, Iranmanesh A, Veldhuis J, Dudley RE, Berman N,
Davidson T, Barstow TJ, Sinow R, Alexander G, Swerdloff RS. Department
of Medicine, Harbor-University of California-Los Angeles Medical
Center, Torrance 90509-2910, USA. W...@HARBOR6.HUMC.EDU

To study the effects of androgen replacement therapy on muscle mass
and strength and bone turnover markers in hypogonadal men, we
administered sublingual testosterone (T) cyclodextrin (SLT; 5 mg,
three times daily) to 67 hypogonadal men (baseline serum T, < 8.4 mol/
L) recruited from 4 centers in the U.S.: Torrance (n = 34), Durham (n
= 12), New York (n = 9), and Salem (n = 12). Subjects who had received
prior T therapy were withdrawn from injections for at least 6 weeks
and from oral therapy for 4 weeks. Body composition, muscle
strength, and serum and urinary bone turnover markers were measured
before and after 6 months of SLT. We have shown previously that this
regimen for 60 days will maintain adequate serum T levels and restore
sexual function. Total body (P = 0.0104) and lean body mass (P 0.007) increased with SLT treatment in the 34 subjects in whom body
composition was assessed. There was no significant change in total
body fat or percent fat. The increase in lean body mass was mainly in
the legs; the right leg lean mass increased from 8.9 +/- 0.3 kg at 0
months to 9.2 +/- 0.3 kg at 6 months (P = 0.0008). This increase in
leg lean mass wasassociated with increased leg muscle strength,
assessed by leg press(0 months, 139.0 +/- 4.0 kg; 6 months, 147.7 +/-
4.2 kg; P = 0.0038).SLT replacement in hypogonadal men led to small,
but significant,decreases in serum Ca (P = 0.0029) and the urinary
calcium/creatinineratio (P = 0.0066), which were associated with
increases in serum PTH(P = 0.0001). At baseline, the urinary type I
collagen-cross linked N-telopeptides/creatinine ratio [75.6 +/- 7.9
nmol bone collagenequivalents (BCE/mmol] was twice the normal adult
male mean (41.0 +/-3.6 nmol BCE/mmol) and was significantly decreased
in response to SLTtreatment at 6 months (68.2 +/- 7.7 nmol BCE/mmol; P
= 0.0304) withoutsignificant changes in urinary creatinine. Serum
skeletal alkalinephosphatase did not change. In addition, SLT
replacement causedsignificant increases in serum osteocalcin (P 0.0001) and type Iprocollagen (P = 0.0012). Bone mineral
density did not change during the 6 months of SLT treatment. We
conclude that SLT replacement therapy resulted in increases in lean
muscle mass and muscle strength. Like estrogen replacement in
hypogonadal postmenopausal females, androgen replacement therapy led
to decreased bone resorption and urinary calcium excretion. Moreover,
androgen replacement therapy may have the additional benefit of
increasing bone formation. A longer term study for several years
duration would be necessary to demonstrate whether these changes in
bone turnover marker levels will result in increased bone mineral
density decreasedfracture risks, and reduced frailty in hypogonadal
men. PMID: 8855818

4: : World J Urol. 2006 Dec;24(6):639-44. Treatment of sexual
dysfunction of hypogonadal patients with long-acting testosterone
undecanoate (Nebido). Yassin AA, Saad F.Clinic of Urology/Andrology,
Segeberger Kliniken, Norderstedt-Hamburg, Germany. yas...@t-online.de

Recently, testosterone undecanoate (TU), a new parenteral testosterone
(T) preparation has been introduced. Two of its distinctive features
are (a) its prolonged action: after two initial loading injections 6
weeks apart, usually only one injection every 12 weeks is needed (b)
over the full interval between two injections, plasma T levels are in
the physiological range. New research presents convincing evidence
that T has profound effects on tissues of the penisinvolved in the
mechanism of erection and that testosterone deficiencyimpairs the
anatomical and physiological substrate of erectilecapacity, which is,
at least, in part reversible upon androgentherapy. Our studies with TU
demonstrated that venous leakage could becorrected with T treatment in
a number of patients. We further couldshow that sexual functions, in a
substantial number of elderly men,can be restored with treatment with
T only. So, these results arguefor determination of T levels in
elderly men with sexual problems. Ifthe levels are subnormal, T
treatment is warranted. PMID: 17048032

5: Neuro Endocrinol Lett. 2003 Jun-Aug;24(3-4):203-8. Testosterone and
gonadotropin levels in men with dementia. Hogervorst E, Combrinck M,
Smith AD.Oxford Project To Investigate Memory and Ageing, Department
of Pharmacology,University of Oxford, Oxford, UK.
eva.hogervo...@pharm.ox.ac.uk

OBJECTIVES: Sex steroids such as testosterone and estradiol might
protect the brain against Alzheimer's disease (AD). We previously
found lower levels of testosterone in men with AD compared with
controls. We wanted to assess levels of pituitary gonadotropins that
regulate sex steroid levels, to determine whether primary or secondary
hypogonadism was responsible for low levels of testosterone in cases.
METHOD: We included 45 men with AD (McKhann, 1987), 15 men with other
types of dementia and 133 elderly controls from the Oxford Project to
investigate Memory and Ageing. Gonadotropins (follicle stimulating
hormone or FSH and luteinizing hormone or LH), sex hormone binding
globulin (SHBG, which determines the amount of free testosterone) and
testosterone were measured using enzyme immunoassays. RESULTS: We
found no difference in average LH (8.7 +/- 9 UI/L), FSH (13 +/- 17 UI/
L) or SHBG (44 +/- 18 nmol/L) levels between AD cases and controls.
Similar to our earlier findings, testosterone levels were
significantly lower in men with AD (13 +/- 6 nmol/L) compared with
controls (17 +/- 8, O.R. = 0.92, 95% C.I. = 0.87 to 0.97, p<0.005).
Results were unchanged when controlled for age, SHBG and gonadotropin
levels. CONCLUSION: Although normal, the levels of gonadotropins were
inappropriately low for the levels of testosterone. Our results
support a preliminary conclusion that secondary hypogonadism occurs in
men with AD. This could be a consequence of brain degeneration. This
is contrary to an earlier study (Bowen, 1999) that found raised levels
of gonadotropins in cases with AD, suggesting primary hypogonadism.
Our cohort was younger than theirs and gonadotropin levels increase
with age. We are enlarging our data set to investigate whether primary
hypogonadism occurs in older cases with AD or whether secondary
hypogonadism precedes cognitive dysfunction in men at risk for AD. If
this is true, testosterone replacement therapy for hypogonadal men at
risk for dementia may be indicated. PMID: 14523358

6: Aging Male. 2007;10(2):53-56. Testosterone deficiency and the
metabolic syndrome. Lunenfeld B Faculty Of Life Sciences. Faculty of
Life Sciences, Bar-Ilan University. Ramat Gan. Israel.

Evidence is presented to link components of the metabolic syndrome to
testosterone deficiency and obesity. Testosterone deficiency in
hypogonadism or testosterone deprivation in normo-gonadotropic men
increases fat mass as well as fasting insulin levels. Testosterone
supplementation (TS) in a dose dependent manner, increase lean body
mass (LBM), reduces fat mass, body mass index (BMI) and waist hip
ratio in both young and elderly hypogonadal men. A negative
association between T and insulin resistance as well as impaired
glucose intolerance has been demonstrated and in type 2 diabetic men
TS improves metabolic parameters. TS improves most components of the
metabolic syndrome and also reduces inflammatory cytokines. PMID:
17558968

7 : J Clin Oncol. 2007 Jun 10;25(17):2420-5. Influence of androgen
suppression therapy for prostate cancer on the frequency and timing of
fatal myocardial infarctions. D'Amico AV, Denham JW, Crook J, Chen MH,
Goldhaber SZ, Lamb DS, Joseph D, Tai KH, Malone S, Ludgate C, Steigler
A, Kantoff PW. Departments of Radiation Oncology and Medicine,
Cardiovascular Division, Brigham and Women's Hospital and Lank Center
for Genitourinary Oncology, Dana-Farber Cancer Institute, Boston, MA
02215, USA. adam...@lroc.harvard.edu

PURPOSE: We evaluated whether the timing of fatal myocardial
infarction (MI) was influenced by the administration of androgen
suppression therapy (AST). PATIENTS AND METHODS: The study cohort
comprised 1,372 men who were enrolled onto three randomized trials
between February 1995 and June 2001. In the three trials, the men were
randomly assigned to receive radiation therapy with 0 versus 3 versus
6, 3 versus 8, or 0 versus 6 months of AST. Fine and Gray's regression
was used to determine the clinical factors associated with the time to
fatal MI, and estimates of time to fatal MI were calculated using a
cumulative incidence method. When comparing the cumulative incidence
estimates using Gray's k-sample P values, increased weight was
ascribed to the earlier data because recovery of testosterone is
expected for most men within 2 years after short-course AST. RESULTS:
Men age 65 years or older who received 6 months of AST experienced
shorter times to fatal MIs compared with men in this age group who did
not receive AST (P = .017) and men younger than 65 years (P = .016).
No significant difference (P = .97) was observed in the time to fatal
MIs in men age 65 years or older who received 6 to 8 months of AST
compared with 3 months of AST. CONCLUSION: The use of AST is
associated with earlier onset of fatal MIs in men age 65 years or
older who are treated for 6 months compared with men who are not
treated with AST. PMID: 17557956

8: Scand J Urol Nephrol. 1996 Oct;30(5):403-8. Androgen therapy for
anaemia of chronic renal failure. Indications in the erythropoietin
era. Teruel JL, Aguilera A, Marcen R, Navarro Antolin J, Garcia Otero
G, Ortuno J.Department of Nephrology, Hospital Ramon y Cajal, Madrid,
Spain.

The high cost of recombinant human erythropoietin has led us to
consider the existing indications for androgen treatment of anaemia in
patients with chronicrenal failure. In the present work, we have tried
to identify those patients on haemodialysis for whom androgens could
constitute a therapeutic alternative. The evolution of haemoglobin
concentration was analysed in 84 patients (67 males and17 females)
treated with a cycle of nandrolone decanoate (200 mg per week given
intramuscularly, for six