Re: Intermittent hormone therapy

[Guest guest]

Sammy,

As one who has knocked you in the past, thank you for that piece. I found it very helpful indeed.

To: ProstateCancerSupport Sent: Wednesday, 7 April, 2010 1:49:00Subject: Intermittent hormone therapy

The reason for my continued survival? Diagnosed in 1996 with 'non-trivialdisease'. In my case that meant advanced metastatic PC (T3N1M0) bPSA > 50, alongwith lymph node and seminal vesicle involvement, and extracapsular spread thatrequired resection of part of the bowel. I was given 2-5 years.I did a lot of homework in those days and I didn't take anyone's word foranything. I got it all from the horse's mouth (i.e., original source - MedLineSilver Platter in those days before PubMed). It was clear to anyone who read theliterature that there was a 'fly in the ointment' with the standard castrationtherapy that limited patient survival with the onset of CRPC (castrationresistant prostate cancer). Intermittent therapy was 'experimental' and notrecommended for the majority.Anyhow, times change. IHT is now 'official', according to the EuropeanAssociation of Urology.The references did not

come through so I uploaded a PDF file. See alsohttp://fitcare. org.uk/ for full text.Sammy.Intermittent hormone therapy§The great advantage of intermittent therapy over continuous castration therapyis the biological respite from a host of unpleasant side effects. These includeloss of bone and muscle mass, decreased resistance to infection and allergy,increased anemia and tiredness along with sleep and affect disorders. Castrationmakes intermediate and advanced prostate disease a dog's life for many men, andanything to lessen the impact is to be welcomed. A return to androgen meansrecovering anabolic status and the gradual return to a normal male physiology –something to be anticipated with delight in every patient's treatment calendar.Some anecdotal reports include recovery of male erectile function during theandrogen phase

of intermittent treatment – even after radical surgery hasdamaged erectile nerves.By 1980 an accumulation of reported IHT successes resulted in one of the firstpublicationsi. A decade later a series of studies were commenced byBruchovskyii, at the Vancouver Clinic. Bruchovsky's investigation of the IHTtechnique using synthetic LHRH analogs attempts to explain why repeated cyclesof castration worked as good as, and sometimes apparently better than, a singlechronic castration episodeiii. But despite reports which are the accumulatedwisdom of decadesiv,v IHT has been until very recently regarded asexperimental by many of the great and the good in the world of prostate cancersciencevi. Not limiting IHT to early stage disease, Oliver at St. Barts hasshown that withdrawal of castration therapy in patients even with metastaticdisease can improve their survival chancesvii.Perhaps because intermittent

therapy has not sat well with the androgen causes -castration cures paradigm it has struggled to enter mainstream prostate cancerthinking. A study published in 2007 heralds the change, reporting on collecteddata from phase 2 studies of IHTviii, it presages EAU recommendations of thesame year. But after over sixty years of castration therapy embedded in thecollective medical consciousness, one wonders how much longer patients will haveto wait before more detailed recommendations can be made to determine who may beselected for IHT."Thus, it is possible to offer intermittent androgen blockade to selectedpatients, but results from randomized trials are still lacking." ixIs there a fear of the initial PSA spike produced when androgen recovery isresumed? This characteristic rapid increase, probably due to up-regulation ofthe androgen receptor, often slows down and may level out to produce a zero

PSAvelocity. Some sources will insist on undetectable ultrasensitive PSA to be thestarting point for withdrawal of chemical castration. Others have put the PSAstarting point as high as 4.0 ng/ml.Since prostate tumor is often well behaved, standard PSA kinetic algorithms canbe used to predict a ceiling PSA for cut-off purposes. Some suggest the PSAceiling during off treatment should be no higher than single figure numbers,whereas other sources venture to go much higher. One rule of thumb for the PSAceiling has been 20 ng/ml or the value at time of diagnosis – whichever was theless. However, PSA's in the region of 1000 ng/ml have been reported anecdotallywith intermittent treatment – because men need their testosterone, dislike beingcastrated, and are prepared to take the risk.Provided the situation is monitored sensibly with regular and reliable bloodtesting, IHT facilitates a much improved

quality of life at far less cost thancontinuous chemical castration.

[Guest guest]

Well, thanks for the thumbs up . My 15+ years experience of this disease

has many facets. All of them enlightening, some of them frightening, and some of

them frightfully funny.

Wouldn't dare mention the latter. That would get me into hot water for sure

=>:-0

I wrote the book to get the frightening stuff off my chest. Obviously it is not

very digestible. However, it has helped me understand why I am still around.

Sam.

>

> Sammy,

>

> As one who has knocked you in the past, thank you for that piece.  I found it

very helpful indeed.

>

>

>

>

>

>

> ________________________________

>

> To: ProstateCancerSupport

> Sent: Wednesday, 7 April, 2010 1:49:00

> Subject: Intermittent hormone therapy

>

>  

> The reason for my continued survival? Diagnosed in 1996 with 'non-trivial

> disease'. In my case that meant advanced metastatic PC (T3N1M0) bPSA > 50,

along

> with lymph node and seminal vesicle involvement, and extracapsular spread that

> required resection of part of the bowel. I was given 2-5 years.

>

> I did a lot of homework in those days and I didn't take anyone's word for

> anything. I got it all from the horse's mouth (i.e., original source - MedLine

> Silver Platter in those days before PubMed). It was clear to anyone who read

the

> literature that there was a 'fly in the ointment' with the standard castration

> therapy that limited patient survival with the onset of CRPC (castration

> resistant prostate cancer). Intermittent therapy was 'experimental' and not

> recommended for the majority.

>

> Anyhow, times change. IHT is now 'official', according to the European

> Association of Urology.

>

> The references did not come through so I uploaded a PDF file. See also

> http://fitcare. org.uk/ for full text.

>

> Sammy.

>

> Intermittent hormone therapy§

>

> The great advantage of intermittent therapy over continuous castration therapy

> is the biological respite from a host of unpleasant side effects. These

include

> loss of bone and muscle mass, decreased resistance to infection and allergy,

> increased anemia and tiredness along with sleep and affect disorders.

Castration

> makes intermediate and advanced prostate disease a dog's life for many men,

and

> anything to lessen the impact is to be welcomed. A return to androgen means

> recovering anabolic status and the gradual return to a normal male physiology

†"

> something to be anticipated with delight in every patient's treatment

calendar.

> Some anecdotal reports include recovery of male erectile function during the

> androgen phase of intermittent treatment †" even after radical surgery has

> damaged erectile nerves.

>

> By 1980 an accumulation of reported IHT successes resulted in one of the first

> publicationsi. A decade later a series of studies were commenced by

> Bruchovskyii, at the Vancouver Clinic. Bruchovsky's investigation of the IHT

> technique using synthetic LHRH analogs attempts to explain why repeated cycles

> of castration worked as good as, and sometimes apparently better than, a

single

> chronic castration episodeiii. But despite reports which are the accumulated

> wisdom of decadesiv,v IHT has been until very recently regarded as

> experimental by many of the great and the good in the world of prostate cancer

> sciencevi. Not limiting IHT to early stage disease, Oliver at St. Barts has

> shown that withdrawal of castration therapy in patients even with metastatic

> disease can improve their survival chancesvii.

>

> Perhaps because intermittent therapy has not sat well with the androgen causes

-

> castration cures paradigm it has struggled to enter mainstream prostate cancer

> thinking. A study published in 2007 heralds the change, reporting on collected

> data from phase 2 studies of IHTviii, it presages EAU recommendations of the

> same year. But after over sixty years of castration therapy embedded in the

> collective medical consciousness, one wonders how much longer patients will

have

> to wait before more detailed recommendations can be made to determine who may

be

> selected for IHT.

>

> " Thus, it is possible to offer intermittent androgen blockade to selected

> patients, but results from randomized trials are still lacking. " ix

>

> Is there a fear of the initial PSA spike produced when androgen recovery is

> resumed? This characteristic rapid increase, probably due to up-regulation of

> the androgen receptor, often slows down and may level out to produce a zero

PSA

> velocity. Some sources will insist on undetectable ultrasensitive PSA to be

the

> starting point for withdrawal of chemical castration. Others have put the PSA

> starting point as high as 4.0 ng/ml.

>

> Since prostate tumor is often well behaved, standard PSA kinetic algorithms

can

> be used to predict a ceiling PSA for cut-off purposes. Some suggest the PSA

> ceiling during off treatment should be no higher than single figure numbers,

> whereas other sources venture to go much higher. One rule of thumb for the PSA

> ceiling has been 20 ng/ml or the value at time of diagnosis †" whichever was

the

> less. However, PSA's in the region of 1000 ng/ml have been reported

anecdotally

> with intermittent treatment †" because men need their testosterone, dislike

being

> castrated, and are prepared to take the risk.

>

> Provided the situation is monitored sensibly with regular and reliable blood

> testing, IHT facilitates a much improved quality of life at far less cost than

> continuous chemical castration.

>

[Guest guest]

Alan asked:>What was your experience with intermittent HT? Can you tell us how long your on and off periods were, how low your PSA got, how high and fast it rose on the off periods, and what yourtestosterone levels were?ON-OFF between one year and two on average, some less. I have done over a dozen cycles.>Are you still doing well with it?I still base my treatment around IHT.>I know that you may not have data on all this unless your doctor was very aggressive in testing you, but if you've got any useful data, I'd love to hear it.Actually, I have data from 1996 onward and use a spreadsheet to graph different parameters to make sens e of what is happening. I have plots for PSAV vs androgen (T, DHT) for instance for most of the period.>I know some guys do extremely well on intermittent HT and some don't. But the ones who do well certainly appear to suffer less.I certainly could not have survived 15 years on castration therapy. It would have either killed me outright or sent me mad. .... This is a long term sentence with increasingly acute

treatment side effects. The medical

castrate does

not have the same hormonal status as the eunuch. Indeed, the medical

castrate is actively prevented from acquiring the hormonal status of

a eunuch. It is necessary to be very clear about the difference in

terms of reduced quality of life and increased morbidity that the

medical castrate will have to endure. The

effects of profound chronic medical castration are consistent with

reports in the literaturei

describing the condition of hypogonadal men. Bone demineralisation,

muscle wastingii,

early onset Alzheimer's diseaseiii,

cognitive impairmentiv,

metabolic syndromev

and myocardial infarction are all part of the course. D'Amico and

others have

shown that cardiac mortality increases significantly after just 6

months of medical castration treatmentvi.

Hitherto,

the

insidious side effects of medical castration have not been recognised

as a systemic response

of the human body to the reduction of anabolic hormones. There has

been a failure to acknowledge the patients' need for dedicated

support on a number of fronts: from maintaining bone, blood and

muscle health to management of cognitive and psychological changes

that put them at risk. The harsh truth

goes against the happy image portrayed by social medicine that

castration is without side effects, and may even be desirablevii.

i

Seftel

A.

Male hypogonadism. Part II: etiology, pathophysiology, and

diagnosis. Int

J Impot Res. 2006 May-Jun;18(3):223-8. PubMed:16094414

ii

Basaria

S.

Androgen Deprivation Therapy, Insulin Resistance and Cardiovascular

Mortality: An Inconvenient Truth. J

Androl. 2008 Jun 20. PubMed:18567642

iii

Hogervorst E, Combrinck M,

AD. Testosterone and

gonadotropin levels in men with dementia. Neuro

Endocrinol Lett. 2003 Jun-Aug;24(3-4):203-8. PubMed:14523358

iv

Jim HS, Small BJ, S, Salup R, sen PB. Cognitive

impairment in men treated with luteinizing hormone-releasing hormone

agonists for prostate cancer: a controlled comparison. Support

Care Cancer. 2009 Apr 3. PubMed:19343369.

v

Lunenfeld B. Testosterone

deficiency and the metabolic syndrome.AgingMale.

2007Jun;10(2):536. PubMed:17558968

vi D'Amico AV, Denham JW, Crook J, Chen MH, Goldhaber SZ, Lamb DS, ph D, Tai KH, Malone S, Ludgate C, Steigler A, Kantoff PW. Influence of androgen suppression therapy for prostate cancer on the frequency and timing of fatal myocardial infarctions. J Clin Oncol. 2007 Jun 10;25(17):2420-5. PubMed:17557956.

vii

Wassersug RJ, TW.

Modern-day eunuchs: motivations for and consequences of contemporary

castration. Perspect Biol Med.

2007 Autumn;50(4):544-56. PubMed:17951888.

> >> > Sammy,> > > > As one who has knocked you in the past, thank you for that piece. I found it very helpful indeed.> > > > > > > > > > > > > > ________________________________> > From: sammy_bates sammy_bates@> > To: ProstateCancerSupport > > Sent: Wednesday, 7 April, 2010 1:49:00> > Subject: Intermittent hormone therapy> > > >  > > The reason for my continued survival? Diagnosed in 1996 with 'non-trivial> > disease'. In my case that meant advanced metastatic PC (T3N1M0) bPSA > 50, along> > with lymph node and seminal vesicle involvement, and extracapsular spread that> > required resection of part of the bowel. I was given 2-5 years.> > > > I did a lot of homework in those days and I didn't take anyone's word for> > anything. I got it all from the horse's mouth (i.e., original source - MedLine> > Silver Platter in those days before PubMed). It was clear to anyone who read the> > literature that there was a 'fly in the ointment' with the standard castration> > therapy that limited patient survival with the onset of CRPC (castration> > resistant prostate cancer). Intermittent therapy was 'experimental' and not> > recommended for the majority.> > > > Anyhow, times change. IHT is now 'official', according to the European> > Association of Urology.> > > > The references did not come through so I uploaded a PDF file. See also> > http://fitcare. org.uk/ for full text.> > > > Sammy.> > > > Intermittent hormone therapy§> > > > The great advantage of intermittent therapy over continuous castration therapy> > is the biological respite from a host of unpleasant side effects. These include> > loss of bone and muscle mass, decreased resistance to infection and allergy,> > increased anemia and tiredness along with sleep and affect disorders. Castration> > makes intermediate and advanced prostate disease a dog's life for many men, and> > anything to lessen the impact is to be welcomed. A return to androgen means> > recovering anabolic status and the gradual return to a normal male physiology â€"> > something to be anticipated with delight in every patient's treatment calendar.> > Some anecdotal reports include recovery of male erectile function during the> > androgen phase of intermittent treatment â€" even after radical surgery has> > damaged erectile nerves.> > > > By 1980 an accumulation of reported IHT successes resulted in one of the first> > publicationsi. A decade later a series of studies were commenced by> > Bruchovskyii, at the Vancouver Clinic. Bruchovsky's investigation of the IHT> > technique using synthetic LHRH analogs attempts to explain why repeated cycles> > of castration worked as good as, and sometimes apparently better than, a single> > chronic castration episodeiii. But despite reports which are the accumulated> > wisdom of decadesiv,v IHT has been until very recently regarded as> > experimental by many of the great and the good in the world of prostate cancer> > sciencevi. Not limiting IHT to early stage disease, Oliver at St. Barts has> > shown that withdrawal of castration therapy in patients even with metastatic> > disease can improve their survival chancesvii.> > > > Perhaps because intermittent therapy has not sat well with the androgen causes -> > castration cures paradigm it has struggled to enter mainstream prostate cancer> > thinking. A study published in 2007 heralds the change, reporting on collected> > data from phase 2 studies of IHTviii, it presages EAU recommendations of the> > same year. But after over sixty years of castration therapy embedded in the> > collective medical consciousness, one wonders how much longer patients will have> > to wait before more detailed recommendations can be made to determine who may be> > selected for IHT.> > > > "Thus, it is possible to offer intermittent androgen blockade to selected> > patients, but results from randomized trials are still lacking." ix> > > > Is there a fear of the initial PSA spike produced when androgen recovery is> > resumed? This characteristic rapid increase, probably due to up-regulation of> > the androgen receptor, often slows down and may level out to produce a zero PSA> > velocity. Some sources will insist on undetectable ultrasensitive PSA to be the> > starting point for withdrawal of chemical castration. Others have put the PSA> > starting point as high as 4.0 ng/ml.> > > > Since prostate tumor is often well behaved, standard PSA kinetic algorithms can> > be used to predict a ceiling PSA for cut-off purposes. Some suggest the PSA> > ceiling during off treatment should be no higher than single figure numbers,> > whereas other sources venture to go much higher. One rule of thumb for the PSA> > ceiling has been 20 ng/ml or the value at time of diagnosis â€" whichever was the> > less. However, PSA's in the region of 1000 ng/ml have been reported anecdotally> > with intermittent treatment â€" because men need their testosterone, dislike being> > castrated, and are prepared to take the risk.> > > > Provided the situation is monitored sensibly with regular and reliable blood> > testing, IHT facilitates a much improved quality of life at far less cost than> > continuous chemical castration.> >>