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Hello Nick

                   Cheated the Grim ripper again!

I for one am glad As you gave me a lot of help and encouragement last winter when I fitted EFI to Spitty(still not right but have done 5000 miles so can not be that bad?)

I will have to wait until the new engine is built now!

Just overhauled a differential(I hope it does not whine or I will be on the Wine!)

Roger

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  • 2 weeks later...

Had post op consultation yesterday.  Histology fine (simple cyst) and healing well.  Discharged.   Mind you, was healing even better until an unexpected and rather violent sneeze did it a mischief Tuesday last week.  Did make my eyes water and set me back about a week.

On the mend now though.  Big backlog of work to catch up on.  If I don't get that door re-skinned before Chris get back in 10 days...... I get my ass kicked......

Roger, if you can build a diff that doesn't whine (or explode) I can find a couple for you to work your magic on.......  The one I tried (good few years ago nod) didn't go that well - howled like banshee.

Nick

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44 minutes ago, Nick Jones said:

Had post op consultation yesterday.  Histology fine (simple cyst) and healing well.  Discharged.   Mind you, was healing even better until an unexpected and rather violent sneeze did it a mischief Tuesday last week.  Did make my eyes water and set me back about a week.

On the mend now though.  Big backlog of work to catch up on.  If I don't get that door re-skinned before Chris get back in 10 days...... I get my ass kicked......

Roger, if you can build a diff that doesn't whine (or explode) I can find a couple for you to work your magic on.......  The one I tried (good few years ago nod) didn't go that well - howled like banshee.

Nick

Hello Nick

                 That is GOOD news without the sneeze(still when you get to my age you will either P***S or S****t  yourself )

My First Spitty rebuilt differential does not whine any more than before and the TR6 one I did for the brother in  law an was quiet(so he said)

So I must be lucky? whether it will prove 3 times lucky we will see!

Roger

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  • 3 months later...

..... and on to the next little "game"..... I now find myself being asked to choose the way I'd like my new prostate cancer dealt with:down:.   Not a question I wanted to be having to answer at 50 :mad:.  More positively, I'm told it's at a very early stage and can be successfully dealt with - more a case of limiting the collateral damage :ermm:.

There is nothing quite like the C word to get the vultures circling (in your mind) though due consideration, research and the very excellent Prostate Cancer UK nurse advice service has them back in the trees, if slightly nearer trees than before.....

Just something that has to be dealt with and as with most things, I prefer to make an as fully-informed decision as possible, so I'm doing my research and collecting evidence.  It occurs to me that there are many of us of an age where this is all too relevant and others may also have travelled this way. If any of you Gents have relevant experiences you are willing to share, I'd be happy to hear them - PM probably best for this!

Also, anyone over 45 who doesn't know what their PSA score is might like to consider getting it checked out - though mine is well inside the normal range as it happens.

Nick

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NIck,

There's a large literature on vitamin D3 and prostate cancer, including one trial:

https://vitamindwiki.com/Prostate+cancer+reduced+when+4000+IU+vitamin+D+was+added–+Hollis+RCT+April+2015

He refers to Maasai having low PC risk. Their serum 25OHD3 level is 115nmol/l, way more than regarded as adequate by PHE ( 50nmol/L).

Worth asking your specialist about dosing with D3.

=========

D3 is a hormone that performs widespread defensive functions, and most UK oldies are badly deficient by Maasai criteria, and by USA Inst Med standrards - see the talk I posted a a while back..

Peter

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1 hour ago, Nick Jones said:

..... and on to the next little "game"..... I now find myself being asked to choose the way I'd like my new prostate cancer dealt with:down:.   Not a question I wanted to be having to answer at 50 :mad:.  More positively, I'm told it's at a very early stage and can be successfully dealt with - more a case of limiting the collateral damage :ermm:.

Nick

Bloody hell Nick, that's no fun at all.  There's a large body of evidence on the net that PC is being over diagnosed and over treated, so tread carefully.  

But, well, Fuck, fuck, fuck, fuckity, fuck!

Be well Bud.

C.

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19 minutes ago, GT6MK3 said:

There's a large body of evidence on the net that PC is being over diagnosed and over treated, so tread carefully.

Well yeah.....  I've read quite a bit of it I think.  One of the options I've been given is "active surveillance" where they do nothing but repeat testing on a regular basis. Though one of the tests is something that you REALLY don't want to repeat too often (!), this has the benefits of no collateral damage, though ultimately it's just kicking the can up the track a bit as treatment will almost inevitably be needed eventually.  I do appreciate the sense and value of this approach as I do understand that the PCa itself is not the cause of (longstanding) symptoms and is in fact an incidental finding.  I could have had it 5 years already and might have 5 - 10 years more before it's a real issue in it's own right.

However, the reason I actually got fully tested this time is that my old man (78) has apparently gone from "no evidence of PCa" 3 years ago after much testing, to stage 4 with extensive bone mets now....  Whether this is due to an unusual progression in his case, or failed testing is not clear at this point, but it colours my thinking quite considerably as you may imagine! 

To quote a medical friend "the only good carcinoma is the one in the bucket" - though that option appears to carry the greatest risk of significant collateral damage so the choice is not clear cut!

Shit happens........ could be much worse.

Nick

 

PS.  Peter, my understanding is that persons of African heritage have a very significantly increased PCa risk compared to us palefaces?  I know the Masai (and a couple of other tribes in that region) have VERY unusual diets, but even so.......  I will add to my question list though.

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1 hour ago, Nick Jones said:

 

 

 

PS.  Peter, my understanding is that persons of African heritage have a very significantly increased PCa risk compared to us palefaces?  I know the Masai (and a couple of other tribes in that region) have VERY unusual diets, but even so.......  I will add to my question list though.

Nick,

The point about the Maasai is their serum D3 level: 115nmol'L. That is the best indication of what a western, indistrial, heliophobic level should be. For reasons that I find susoect, the UK sets a very low standard, whereas the USA recently set 100-120 nmo/'L - as adequate.  Low D3 is widely associated with PC , and may other chronic disease states. It has promonved effct on the immune system and hence on ellimination/control of cancerous cells. Gut cancers especially. VitaminDwiki is the best introductory site. And you can measure your serum level through the post. Best clinical expertise with D3 will be from an up to date cancer immmunologist.

USA Afrocaribbeans do have hgh PC incidence and lower serum D3. Dark skin deepresses D3 synthesis, and their diet tends to lack D3 , and they live wellaway from the equator. No data on Maasai prostates as far as I know, but I'm interesrted in their Parkinsons/Alzheimer/dementia/MS stats so if  I find anything I'll post it. 'Maasai males have very high iron loads, but other equatorial pastoral tribal comunities also have ca 115 D3, and dont drink blood. Year-round sun, no sunblock and sensible learned behaviuor re sun exposure contrast with our slip-slap-slop and a D3 -deficient diet.  I shall not be at all surprised to learn in a few years time that D3 deficicncy proves to be a significnat risk factor in many western chrnnic diseases. Supplementaion with D3 might  tip the balance post-diagnosis.

You could scan Google Scholar over say past 5 years for "prostate + vitamin D3  + supplement". 

Peter.

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My sympathy, Nick!   But no opinion, none at all, this isn't my specialty.

But I have, AFAIK and so far, the benign form of prostate enlargement, and I'm on a similar 'surveillance' programme, so I know what you mean about certain tests or examinations!     

John

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In UK BARTS are starting a prospective study

http://www.ejso.com/article/S0748-7983(18)30562-6/abstract

-might be a possibility of enrolling in a trial.

 

===

This points to benefcial effct of D3

https://www.ncbi.nlm.nih.gov/pubmed/17241782?dopt=Abstract

D3 itself will need a higher than normal dose, probably higher than the 4000 IU used above. This is because the proinflammatory transciption factor NFkappaB reduces VDReceptor expression and block activation of 25OHD3 by the 1hydroxylase. Serum levels needed in health may be far too low to  reverse inflammation. So BXL628 shows the way , high D3 may well be an effective alternative, and safer. 10,000 IU pd is regarded as NOAEL, and is what I take for Parkinsons.... as an experiment.

 You need to find a specialist who understands the science. The science of D3 is  moving ahead far faster than most clinicians can keep up. I'd ask if that BARTs trial is going to use 10,000 IU pd !!!

Peter

 

https://www.harvardprostateknowledge.org/low-vitamin-d-tied-aggressive-prostate-cancer

 

 

Edited by PeterC
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2 hours ago, GT6Steve said:

Sorry to hear that Nick, I too anm on active surveiilance and will the invasive biopsy again in two weeks.  Definately one of the most "interesting" events of my life LOL  Good luck to you, 

 

Thanks Steve.  And my commiserations to you also.  "Biopsy" and "again"...... :blink:  Didn't rate very high on my "must do that again" list!

Good luck with that - how often do they repeat it?  I've been led to believe that MRI is the first line check here, with biopsy only if the MRI shows progression. (good reason to get on the Vit D and aspirin maybe?)

Nick

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Hi Nick

Really sorry to read this and I suppose that the small consolation is that you discovered it early enough to decide how to proceed.  You noted that your PSA was/is well within normal limits and I just wondered how you ended up being diagnosed.

During my 2017 MOT, I was seen by a doctor who recommended that the PSA test was cross-referenced with the index finger test, but when I had this year's general inspection following January's bout of pneumonia, a different doctor dismissed any fallibility of PSA out of hand.

Well done for posting - received wisdom appears to be that men do not talk enough about the disease.  The breakthrough with breast cancer is increasingly associated with ceasing to regard it as a taboo subject, on the basis that the more it is discussed, the more likely it is to be caught early.

All the best

Paul

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I've had symptoms for many years.  Decades even.  Semi-diagnosed as chronic prostatitis.  In the early days the balance was" mostly ok with bad patches", but it's swung the other way in recent years being mainly "not great" interspersed with "bad" and the occasional "good" just to remind me how it should be.

I have had previous consultant-level involvement 4 or 5 times over the years, but never got anywhere much with it as the way the NHS system works, by the time you get to see the big guys the flare-up has subsided.  Never had any treatment for it. This time I actually got into the system for another urological reason (which had a happy ending) and the prostate happened to be kicking off at the time and got a mention under "any other business".  This led to a digital exam and the usual "oh, that's a bit big".  However, the difference this time around was that my father was diagnosed with late stage PCa last year and this increased my perceived risk factor significantly as there is a familial link. 

Even then, my PSA history (latest result 2.5) and age meant that I didn't really fit the criteria for further testing (MRI), but I was offered it.  That showed something of minor interest and I was again given the option to go further with biopsy, which I did.  In a way it's an incidental finding as although the cancer may be a consequence of whatever causes my symptoms, it is not (I'm told) the cause of them.

It could be argued that there is an increasing body of evidence that a fair chunk of the male population of my age and upwards (and some younger) who have no symptoms at all, might actually have similar cancer levels if tested to this extent.  Some will go on to develop more serious disease, but others may live another 30 years, and die of old age, still unaware of it.

Active surveillance is real and sensible option for many diagnosed early with non-aggressive forms.  As this is a relatively new approach, the number of studies and evidence base is still relatively small, but survival rates seem as good as those going for active intervention and "collateral damage" rates very much lower.  Obviously many do go on to have active intervention, but it can be 5 or 10 years down the line and some don't seem to progress much at all and remain untreated.

But for my father's disease I would almost certainly still be untested.  I don't know if that would be better or worse......  I definitely don't ever want to be in Dads position though.  That is a whole different animal. 

I also had a colleague, not much older than I at first diagnosis, who was already well past the curable stage when diagnosed.  He lasted 6 more years which was about 4 years longer than the Doctors thought he'd last.  Very determined man and fought it to the end.

The common-ness of it does at least mean that it's pretty well understood now and the science / treatments are moving quite fast. 

Nick

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Hello Nick

                 As someone  I regard as a friend I do not know what to say!

But it is right us men do not talk about these things enough! which does not help.

I wish you well in what ever treatment you go for and tell the Grim Reaper you are just a kid(well compared to me! and lots of TRIUMPH miles to go)

Roger

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I had a look at the genetic risks associated with PCa.  There are around 50-60 SNPs ( 'mutations' if you like) discovered to date but no single one stands out, apart from a gene controlling MYC. eg see this 2018 article:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5849176/

" We successfully identified SNPs within 29 loci. Rs1447295 was among 8 SNPs in the 8q24 hotspot and was found to be significantly associated with aggressive PCa in three studies [45, 44, 41], and adverse pathology in one low-grade GWAS study [37]. The effect of rs1447295 modulating MYC could be heightened by a gain or amplification at this locus, indicating the selective susceptibility of this hotspot to aggressive progression of the disease. Similar genomic hotspots of germline and somatic aberration alignments have been noted in breast cancer where tandem duplications were found to peak where two germline susceptibility loci were present on MYC [88]. Such regions are more prone to double stranded breaksand rely on faulty repair mechanisms that generate large tandem duplications [88]. We postulate that these hotspots and SCNAs, which are present in ~25% of patients with low-grade PCas [20], could be used to select patients whose disease might progress towards a more aggressive phenotype, deeming them worthy for further investigation in a clinical setting."

MYC is a gene that plays a controling role in the cell cycle: https://en.wikipedia.org/wiki/Myc

 

I think I would want to know if I carried that genetic variant, rs1447295.  Most of the authors of that paper are in London universities, whcih might help PCa specialist.

Peter

Edited by PeterC
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Thanks, Nick.

10 hours ago, Nick Jones said:

It could be argued that there is an increasing body of evidence that a fair chunk of the male population of my age and upwards (and some younger) who have no symptoms at all, might actually have similar cancer levels if tested to this extent.  Some will go on to develop more serious disease, but others may live another 30 years, and die of old age, still unaware of it.
 

Indeed.  The digitally-oriented doctor I saw last year observed sagely that its prevalence can be measured by the probability that far more men die with PCa than of it.

Paul

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The single most neglected and unrecognised insult to our health and longevity may well be a life-long deficiency in D3

http://europepmc.org/articles/PMC4536937

Videos from this UCSD conference are here:  https://ucsd.tv/vitamin-d-public-health/

including D3 and prostate trial by Hollis:  https://ucsd.tv/search-details.aspx?showID=29079

It is only in the past 20 years that the revolution in genomics has revealed the astonshingly wide effects of D3 on gene expression. controlling about 2% of our genes, and providing broadly speaking a defensive function. If you follow the   Slip-Slap-Slop mantra you really do need to read this.

Clinicians globally cannot agree on the 'correct adequate serum level of D3 - its like fittng angels on the tip of a pin. But UK trails the field by regarding 50nmol/L as adequate.  To me the ebst measure comes from African, near-equatorial, agrarian/.pastoral, preindustrial societies:

"" Two African tribes, the pastoral Masai and the hunter–gatherer Hadza, have been shown to have serum 25(OH)D concentrations averaging 46 ng/mL [26]. Both tribes live in equatorial East Africa, where humans are thought to have originated, and have daily sun exposure approximating that of ancestral humans. ""

Note: Multiply ng/ml by 2.5 to get UK and EU units of nmol/L.  So Maasai have  115nmol/L.  

Peter

============

I can make a cogent argument that D3 deficincy in past decades has resulted in my idiopathic Parkinson's at age 72. When I started ny my high D3 regime, as serum lecel rose from 100 towards 170nmol/L ,I noticed several improvements in : urinary urgency, nocturia, early morning leg cramps, psoriasis, muscle aches after garage work, leg muscle 'termbling' weakness, a rosier less depressed more motivated outlook.  Even at 100 nmol/L winter coughs and colds were abolished.

D3 is not a f****ng vitamin its a hormone !!

Edited by PeterC
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